Principles of Skin Care: A Guide for Nurses and Health Care ...

This page intentionally left blank

Principles of Skin Care


Principles of Skin CareA Guide for Nurses and OtherHealth Care ProfessionalsRebecca Penzer RN, BSc(Hons), PGDipEd, MScCommunity Dermatology Nurse Specialist, Norfolk Community Health and CareDermatology Nurse Specialist, Queen Elizabeth Hospital, King’s LynnDeputy Chair, International Skin Care Nursing GroupSteven J. Ersser RGN, BSc (Hons), PhD (Lond), CertTHEdProfessor of Nursing Development & Skin Care ResearchDirector, Centre for Wellbeing & Quality of LifeSchool of Health & Social CareBournemouth University, UKChair, International Skin Care Nursing Advisory BoardWith contributions from:Julie Van Onselen BA(Hons), DipN, DipMar, RGN, RSCN, ENB 998, N25(DermN)JVO Consultancy-education in dermatology and Dermatology Nurse, Oxon PCTRachel Duncan MPhil, BN (Hons), PGCE, ENB 237, RGNMacmillan Clinical Nurse Specialist – Skin CancerSt Helens and Knowsley Teaching Hospitals NHS TrustJean Robinson RGN, RSCN, MAClinical Nurse Specialist Children’s DermatologyBarts and The London NHS Trust

This edition first published 2010© 2010 Rebecca Penzer and Steven J. ErsserBlackwell Publishing was acquired by John Wiley & Sons in February 2007. Blackwell’spublishing programme has been merged with Wiley’s global Scientific, Technical, and Medicalbusiness to form Wiley-Blackwell.Registered officeJohn Wiley & Sons Ltd, The Atrium, Southern Gate, Chichester, West Sussex, PO19 8SQ, United KingdomEditorial offices9600 Garsington Road, Oxford, OX4 2DQ, United Kingdom2121 State Avenue, Ames, Iowa 50014-8300, USAFor details of our global editorial offices, for customer services and for information abouthow to apply for permission to reuse the copyright material in this book please see our websiteat www.wiley.com/wiley-blackwell.The right of the author to be identified as the author of this work has been asserted in accordance with theCopyright, Designs and Patents Act 1988.All rights reserved. No part of this publication may be reproduced, stored in a retrieval system,or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording orotherwise, except as permitted by the UK Copyright, Designs and Patents Act 1988, without the priorpermission of the publisher.Wiley also publishes its books in a variety of electronic formats. Some content that appears in print maynot be available in electronic books.Designations used by companies to distinguish their products are often claimed as trademarks. All brandnames and product names used in this book are trade names, service marks, trademarks or registeredtrademarks of their respective owners. The publisher is not associated with any product or vendormentioned in this book. This publication is designed to provide accurate and authoritative informationin regard to the subject matter covered. It is sold on the understanding that the publisher is not engaged inrendering professional services. If professional advice or other expert assistance is required, the services of acompetent professional should be sought.Library of Congress Cataloging-in-Publication DataPenzer, Rebecca.Principles of skin care : a guide for nurses and other health care professionals / Rebecca Penzer, Steven J.Ersser ; with contributions from Julie Van Onselen, Rachel Duncan, Jean Robinson.p. ; cm.Includes bibliographical references and index.ISBN 978-1-4051-7087-1 (pbk. : alk. paper)1. Dermatologic nursing. 2. Skin—Care and hygiene. I. Ersser, Steven. II. Title.[DNLM: 1. Skin Diseases—nursing. 2. Skin Care—nursing. WY 154.5 P419p 2010]RL125.P46 2010616.50231—dc222009033608A catalogue record for this book is available from the British Library.Set in 10/12 pt Sabon by MPS Limited, A Macmillan CompanyPrinted in Malaysia1 2010

ContentsAcknowledgementsChapter 1 Introduction 1What is skin? 1Skin health 2What is in this book 7Conclusion 8References 8Part 1 Fundamental principles ofmanaging the skin 9Chapter 2 Biology of the skin 11Introduction 11Skin structure 11Functions of the skin 20Skin and ageing 24Conclusion 28References 28Chapter 3 Assessment and planning care 29Introduction 29Assessment 30Planning care 42Intervention 44Evaluation 45Conclusion 46References 46ixChapter 4 Protecting the skin andpreventing breakdown 49Introduction 49The concept of skin vulnerability 49What causes skin breakdown? 50Preventative practices 55Nursing intervention to supportbehavioural change (prevention) inrelation to sun exposure 60Nutrition to support skinintegrity 61Preventing skin damage byscratching 63Conclusion 64References 64Chapter 5 Emollients 71Introduction 71Definition 71Constituents of emollients 72Potential side effects 73Emollient formulations 75How emollients work? 80Considerations that willeffect how patients useemollients 82Conclusion 83References 83

vi ContentsChapter 6 Psychological and socialaspects of skin care 85Introduction 85Social impacts 85Psychological impact 88Nursing interventions 92Conclusion 100References 100Chapter 7 Helping patients make themost of their treatment 103Introduction 103Self-management and patientsupport 103The challenge of promotingtreatment adherence 109Prescribing skin-related productsand opportunities for medicineseducation 112Conclusion 115References 115Part 2 Principles of illnessmanagement 119Chapter 8 Psoriasis 121Introduction 121History of psoriasis 121Who gets psoriasis? 122Biology of psoriasis 122Comorbidities associated withpsoriasis 123Clinical variants of psoriasis 124Physical symptoms that accompanypsoriasis 128Trigger factors in psoriasis 130Treatments for psoriasis 131Measuring quality of life 145Conclusion 145References 147Chapter 9 Eczema 151Introduction 151What is eczema? 151Atopic eczema 154What is eczema commonlymistaken for? 157Eczema severity assessment 158Caring for children with eczema 159Other forms of eczema inadulthood 160Contact dermatitis 161Treatment options for eczema 163Conclusion 173References 173Chapter 10 Acne 179Introduction 179What is acne? 179Who gets acne and distribution 184Treatments 185Psychological impact 192Conclusion 193References 193Chapter 11 Skin cancer and itsprevention 195Introduction 195Skin cancer epidemiology: thescale of the problem 195Pre-malignant skin lesions 196Non-melanoma skin lesions 198Introduction to melanoma 202Surgery 207Causation, risk prevention and earlydetection 208Nursing intervention andpromoting self-examination 209Conclusion 213References 214Chapter 12 Infective skin conditions andinfestations 221Introduction 221Bacterial skin infections 222Viral infections 226Fungal infections 233Infestations 240Conclusion 242References 243Chapter 13 Less common skinconditions 247Introduction 247Blistering conditions 247Connective tissue disorders 251

Contents viiDrug reactions 252Lichen planus 255Pityriasis rosea 257Primary cutaneous T-celllymphomas 258Rosacea 260Urticaria 262Vitiligo 265Conclusion 266References 266Appendices 269Appendix 1 – The psoriasis areaseverity index (PASI) 269Appendix 2 – The SCORAD index 271Appendix 3 – Examples of emollientswith excipients 272Index 273


AcknowledgementsWe would like to thank the following people for their help and support inwriting this book: Dr David Paige, Dr Mike Cork, Professor Eugene Healy,Professor Terence Ryan, Dave Roberts, Dr Elizabeth Norton, Andrew Kerr andAlison Jackson. Thanks also to the Wessex Cancer Trust.


Introduction 3However, adornment, decoration and displayhave other important sociological implicationsindicating belonging to group and tribes or converselyto show rebellion and individuality.Signals given through the skin can indicate awide range of social norms and values. The obviousones include religious observance reflectedby the amount of skin and hair covered andby what types of garments are worn. Clothingand adornments vitally allow humans to fit intotheir own social system and indicate a senseof belonging. The social norms in relation todisplaying the skin are time dependent. Thus aBritish woman living in Victorian times mighthave felt it disgraceful to expose her ankles,whereas in the 21st century this is not generallyconsidered scandalous behaviour! Piercingand tattooing give a wide range of social signalsincluding membership of certain groups.However, once again, in the 21st century theserules too are becoming more blurred and lessstrictly adhered to with a wide cross section ofsociety choosing to have tattoos and variousbody piercings.As with other organs of the body, humans areprone to abuse their skin. Fair skinned peopleaim for the perfect sun-tan and in the process ofgetting to this point put themselves at risk ofboth malignant and non-malignant skin cancers.It is becoming an increasingly common practicefor people with darker skins to want to lightenthem. This is done through a number of unregulatedmechanisms including the use of potenttopical steroids, which cause a range of otherhealth problems, as well as the desired skinlightening. Depending on the extent and timeframe of steroid use, these effects may alsobecome systemic.Abuse and discriminationWhatever the context of skin decoration andskin adornment, it is usually done in order tomake a personal statement. However there areinstances when skin marking and/or skin alterationis abusive and detrimental to personalhealth. For example, the tattooing of numbersonto the arms of prisoners in concentrationcamps was designed to dehumanise and depersonalisepeople. Individuals became a numberrather than a name. Female genital mutilationis another example of a practice which is abusive.Whilst some people within cultural groupsaccept the practice as part of becoming a woman,it is widely condemned as an abusive, dangerousand unnecessary practice.The course of human history is littered withtragedies of discriminatory behaviour broughton by false judgements made because of thecolour of the skin. Discriminatory behaviourdue to skin colour is now illegal in many partsof the world and the last 20 years have witnessedmassively significant events in the questfor racial equality. The ending of apartheid inSouth Africa and the election of an AfricanAmerican as President of the United States ofAmerica are two examples of this. But discriminatorybehaviour because of skin colour doesstill exist. A recent Health Care Commissionhighlighted that many Trust institutions withinthe British National Health Service were stillnot meeting their obligations as equal opportunitiesemployers. It states that althoughethnic minority groups make up 16% of theworkforce only 10% are in senior managementpositions and 1% in a chief executive position(Commission for Healthcare Audit andInspection, 2009).For one group of people racism, ignoranceand misunderstanding because of the colour oftheir skin, remains life threatening. There are asignificant number of people living with albinismin East Africa. Albinism is a geneticallyinherited condition where the pigment of theskin, hair and eyes is either reduced or missingaltogether. Whilst albinism does occur inthe Caucasian population, it is more prevalentand more noticeable in black Americans. Someestimates put the number of those with albinismat 1 in 4000 in Tanzania, whilst the figuresfor the European population is more like 1 in20,000 (Smith, 2008). Life for an African withalbinism is curtailed due to hugely increased riskof skin cancer; however recent urbanisation ofthe population has led to an increase in murderand mutilation. It is thought that possessing abody part of someone who has albinism acts as

Introduction 5Box 1.2 Lymphatic filariasisLymphatic filariasis is a mosquito bornedisease in which parasites known as filarialworms damage the lymphatic system.Small microfilariae are transmitted frommosquitoes to humans when the insecttakes a blood meal. The microscopic parasitesgrow into worms which can reach10 cm in length. These live in ‘nests’ inthe lymphatic system causing significantdamage. As a result lymphatic function isaffected causing swelling and compromisedskin function which, over time, canlead to elephantiasis. As a result of thesehuge limbs and grotesque skin changes,many people experience significant morbidityand disability. Working can becomedifficult or impossible. Undertaking activitiesof daily living is a challenge. Manypeople are ostracised from their communitiesand feel socially unacceptable. Thegood news, however, is that the diseasecan be eliminated through distributionof anti-parasitic drugs. This alongside a programmeof managing the morbidity causedby lymphoedema and skin changes is aglobal health programme. For more detailssee www.filariasis.org.CosmeticIf we accept that skin is healthy only if the individualis content with the way their skin looks,feels and functions, cosmetic and aesthetic considerationsbecome part of skin health.Currently in the UK cosmetic dermatologyremains a relatively small proportion of a dermatologist’swork and most of what is done is as partof private practice. However in other countries,for example the United States of America, officebaseddermatologists provide extensive cosmeticservices with nurses providing significant supportand education to patients and technical assistanceto their medical colleagues. For many the marchtowards dermatologists doing more cosmeticwork is an inevitable part of the modern age.If we accept the fact that skin health includesthe psychological well-being which comes as partof feeling good about oneself, this shift mayseem acceptable. However, in a national healthservice with limited resources, providing cosmeticcare within that system is generally consideredinappropriate. Indeed when dermatologists’skills are at a premium in order to managechronic skin disease and skin cancer, it may beconsidered immoral to use those skills for nondermatologicaldisease procedures.It can be a challenge to determine when a skinproblem is ‘purely cosmetic’ and when it is a dermatologicaldisease requiring treatment. Forexample, removal of a skin tag (which is harmlessto physical health) may be seen as a cosmeticprocedure and therefore not a treatment to becarried out as part of a national (public) healthservice. However, if the skin tag is exactly in aposition which catches on a bra-strap and causespain and discomfort each day, a case may bemade for its removal. Likewise a skin tag onthe neck may cause acute embarrassment andpsychological damage for an individual and thusseeing its removal as part of a treatment process,is a relevant approach. The first example mayseem more clear cut, but that is because prioritiesin health care are usually given to problemsthat give physical rather than emotional pain.It is easy to see that the line between cosmesisand treatment is blurred and often fraught withcontroversy.The beauty industry focuses on the attributesof young looking skin and works hard to persuadea youth oriented world that those attributesare positive and desirable. These messages are soeffective that individuals will go to considerablelengths to achieve younger looking skin. Table1.2 gives some examples of beauty treatmentswith their intended outcomes, methods of workingand possible side effects. In general youthenhancing treatments aim to reduce signs ofageing by smoothing and/or filling wrinkles andimproving texture and colouring. Any nursesinterested in working in the field of aestheticswould do well to read the latest Royal Collegeof Nursing Guidance (2008) (Royal College ofNursing, 2008).

6 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 1.2 Examples of cosmetic procedures.Type of treatment How it works Outcome Possible side effectsBotulinumtoxinThe toxin botulinum isproduced by the bacteriaClostridium botulinum.A purified formulation of thetoxin (tradename Botox) canbe injected into facialmuscles and cause paralysisby preventing the release ofacetylcholine from motor nerveendings. It also controlssweating by blockingsympathetic nerve fibres.It is used particularlyon the face to reducefrown lines and crowsfeet. The muscle paralysismeans that the skin lookssmoother. The effect willlast for several weeksand individuals may optto have treatments every3–6 months.Bruising at the injection site;Eyelid droop if the botulinumtoxin tracks down into theeyelid muscle.Headache.ExfoliationPhysically removing theoutermost layer of deadkeratinocytes using arough substance, eithera cleanser or a roughcloth/sponge. This is amild non-invasive treatment,easily carried out at home.A filler smoothes out theskin surface, usually bythe injection of a substanceinto the skin. Substancessuch as collagen andhyaluronic acid areinjectable and need tobe redone to maintaineffect as they are absorbedinto the body over time.The skin will appear‘brighter’ and smoother.Soreness and discomfortespecially for people whohave very sensitive skin.FillersThe skin will appearsmoother. It can be usedto reduce facial linesand can also be used ondepressed acne scarsNumbness;Allergic reactions;Bleeding and bruising.Laser resurfacingThere are different methods oflaser resurfacing. Non-ablativemethods have fewer unwantedside effects and treat onlythe dermis without affectingthe epidermis. Ablativemethods are more effectivebut associated with morerisk and a longerrecovery timeA type of exfoliationusing a variety of techniquesincluding ‘crystal’ and‘diamond’ microdermabrasion.Often carried out inspas but increasinglymarketed to the homeenvironment.The skin is rejuvenatedwith fewer wrinkles,lines and blemishes.It may also be helpfulin removing scars.Few side effects areassociated with non-ablativemethods. Ablative methodsare likely to lead toerythema, swelling,soreness and potentialfor infection.MicrodermabrasionAs with exfoliation. Oftena series of treatments willbe recommended.As with exfoliation above.(continued)

Introduction 7Table 1.2 (continued)Type of treatment How it works Outcome Possible side effectsPeelsChemicals are applied to theskin surface to remove the toplayers of skin, the extent ofepidermal removal dependson the strength of the peel.Smoothes the skin surfaceand also improves skintone. It may also behelpful in treating mildacne scarringA mild peel is describedas being like sunburn andmay cause skin scaling; amore severe peel will leadto blistering, swelling andconsiderable discomfort andpossible skin infection.May lead to scarring.RetinolCreams containing retinol orpro-retinol (a form of vitamin A)are thought to increase levelsof glycosaminoglycan andprocollagen. This leads togreater skin strength and areduction in the appearance ofageing.Threads with small ‘teeth’ onthem are passed throughsubcutaneous fat just belowthe skin, with a needle. Thethreads are then pulled tightand secured with a suture.Reduces fine lines andwrinkles.Skin redness and soreness;increased sensitivity to sunexposure.Thread face-liftSagging or wrinkled skin issmoothed out, but it willnot change the shape ofthe face. The change ispermanent but the skincontinues to age so theeffect lasts for about 5 years.Possible bruising; infectionis a risk. If not carried outwell facial asymmetry mayresult.What is in this bookThis book is split into two broad sections:‘Fundamental principles of managing the skin’and ‘Principles of illness management’. In thefirst section, some of the core nursing issues thatare relevant across the board of dermatologicalcare are addressed. In order to be able to addressthe health needs of patients with dermatologicalconditions, the authors feel that it is importantto get to grips with these fundamental issues.Thus Chapter 2 provides an in-depth look atthe biology of the skin and its appendages. It isdifficult to understand, never mind to explainto patients, what is going wrong with their skinwithout this core knowledge. Whichever fieldof nursing is being discussed, planning care is acritical nursing activity. Chapter 3 looks at theprocess of patient assessment, planning careand monitoring interventions. As nursing rolesdevelop, increasing numbers of practitionerswill be independent prescribers and this is alsoexplored in this chapter.In this introductory chapter there is a focus on theimportance of skin health. Chapter 4 takes a genericlook at what happens when the skin becomes vulnerableand fails, in other words skin health is compromised.It provides an in-depth examination ofthe nursing activities needed to prevent skin breakdown and thus promote skin health.Emollient therapy remains one of the mainstaysof chronic skin disease management. It isimportant for both preventive care and treatmentand as such could perhaps have beenplaced in either section of this book. However,as a generic topic which is relevant across somany disease areas emollient therapy warrantedits own chapter. In Chapter 5, detailed examinationis given to how emollients work and howthey should be used.

8 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsUniquely this text book has chosen to devotetwo chapters to topics which are often touchedupon in dermatology but rarely given a significantamount of attention. Chapter 6 looks at thepsychological and social impacts of skin diseaseemphasising the nursing role in helping patientswith the mental difficulties that skin diseasescan impose. Chapter 7 takes some of the themesfrom Chapter 6 and develops them specificallyto consider how nurses can help patients toimprove their adherence with treatment. In bothchapters, theories are related to practice to enablethe practitioner to develop their skills in themost useful way.The second section will be more familiarto most readers in that it covers the dermatologicalconditions most commonly seen in practice:Chapter 8 psoriasis, Chapter 9 eczema, Chapter 10acne, Chapter 11 skin cancer, Chapter 12 infectivedisorders and Chapter 13 more uncommon skinconditions. In each chapter pathological processeshave been considered in some detail and thentreatments and nursing interventions. Evidencehas been widely used, particularly systematicreviews when they are available. Whilst most ofthe conditions in Chapter 13 are indeed moreuncommon, some of them are not that uncommonbut they do not fit into any of the otherchapters so they need to appear here!Before concluding it is important to mentionclinical images. Throughout the text the authorshave attempted to provide clinical images thathelp to illustrate disease appearance and distribution.However, we would strongly recommendthat you supplement these pictures bylooking at websites that provide an excellentarray of visual resources (see Box 1.3)Box 1.3 Websites for dermatologyimageswww.dermnet.comwww.dermatlas.orgwww.dermnetnz.orgwww.dermis.netConclusionThe authors have aimed to create a book whichhelps nurses and other health care practitioners topractice in a way that is as evidence-based as possible.We also hope that this book helps to developpractitioners who work with compassion, recognisingthat patients with skin disease are oftenaffected in many dimensions of their lives. Thismay be through physical discomfort, psychologicalpain or social exclusion. Whatever the impacton individual patients, nurses who understand skindisease are well placed to alleviate suffering. Thismay be through direct intervention to treat adisease condition or through health promotion toimprove skin health and prevent skin disease.ReferencesCommission for Healthcare Audit and Inspection(2009). Tackling the Challenge: PromotingRace Equality in the NHS in England.London: The Healthcare Commission.Earth Observatory (2009). Ultraviolet Radiation:How it Affects Life on Earth. NASA. http://earthobservatory.nasa.gov/Features/UVB/uvb_radiation2.php last accessed 24/11/09Global Alliance for the Elimination of LymphaticFilariasis (2004). A Future Free of LF. Retrieved15 April 2009, from www.filariasis.org.Royal College of Nursing (2008). AestheticNursing: RCN Guidance on Best Practice.London: Royal College of Nursing.Sherriff, A., J. Golding, ALSPAC study teamet al. (2002). Hygiene levels in a contemporarypopulation cohort are associated withwheezing and atopic eczema in preschoolinfants. Archives of Disabled Child, 87: 26–29.Smith, A. (2008). Albino Africans live in fearafter witch-doctor butchery. The Observer, 35.http://www.guardian.co.uk/world/2008/nov/16/tanzania-humanrights last accessed 24/11/09Strachan, D. (2000). Family size, infectionand atopy: The first decade of the “hygienehypothesis”. Thorax 55(Suppl 1): S2–S10.Williams, H.C. (1997). Dermatology HealthCare Needs Assessment. Oxford: RadcliffeMedical Press.

Part1Fundamental principlesof managing the skin


Biology of the skin2Rebecca PenzerIntroductionThe skin is the largest organ of the body weighingbetween 2 and 4.5 kg (16% of body weight)and covering approximately 2 m 2 (Tortora andDerrickson, 2006). The skin is between 1 and2 mm thick, depending on the part of thebody that is being considered. It is dynamicand changing, capable of healing itself andresponding to the external environment in sucha way that ensures human survival. Like allother organs, the skin is capable of failure, theresults of which can be physically and psychologicallydebilitating and potentially lethal.To understand how to care for the skin, itis necessary to have an understanding of skinbiology. Therefore this chapter will cover:■■■Skin structure and function;Skin changes from pre-birth to old age;Ethnic differences.environment. It is considerably thinner than thedermis, approximately 10% of total skin thickness.The dermis is the powerhouse of the skin,providing the supportive structures to allow theepidermis to function.EpidermisThe epidermis, which forms the top layer ofskin, is constantly shedding millions of deadDermisEpidermisHair shaftDermal papillaSebaceous glandSweat glandSkin structureArrector pili muscleThe skin is composed of two main layers(Figure 2.1). The epidermis is the outer layerwhich comes into contact with the externalSubcutaneous fatHair bulbFigure 2.1 Structure of the skin. (Source: Reprinted fromGraham-Brown and Burns, 2006.)

Biology of the skin 15Intermediatefilament(keratin)PlaqueTransmembraneglycoprotein (integrin)in extracellular spacePlasma membraneBasementmembraneFigure 2.4 Hemidesmosome. (Source: Reprinted fromTortora and Derrickson, 2006.)rete ridges of the epidermis interdigitate withthe dermal papillae providing further stability.The effectiveness with which the two layersof the skin hold together can be compromisedin some genetically inherited disorders, forexample epidermolysis bullosa, or by diseasesthat develop later in life, for example bullouspemphigoid (see Chapter 13 for furtherdetails).This ground substance plays an importantrole in providing bulk for the dermis which actsas a shock absorber and a lubricant between thecollagen and elastin (protein) fibres when theskin moves. Due to its high viscosity, hormones,waste products and nutrients may pass throughit; however, it is difficult for bacteria to movethrough.The protein component of the dermis is largelymade up of collagen and elastin. Fibroblasts,which are found extensively throughout the dermis,are responsible for the production of collagenand elastin. The fibres that make up collagenare tough and resist stretching but they are flexibleand as such they give structural strength tothe skin. Bundles of collagen lie parallel to oneanother throughout the dermis forming cleavageor tension lines (Figure 2.5). Surgical incisionsthat are made parallel to these lines aremuch less likely to gape and will heal more effectively,than those that are made across tensionDermisLying between the epidermis and the subcutaneousfat, the dermis is the support system for theepidermis, providing it with nutrients and oxygenand removing waste products. It consistslargely of connective tissue.Connective tissue consists of a ground substancewith protein fibres distributed throughoutit. The ground substance contains waterand a mixture of large organic molecules whichare a combination of polysaccharides (complexcarbohydrates) and proteins. The most commontype of polysaccharides in connective tissue isglycosaminoglycans (GAGS). These help to trapmoisture, making the ground substance morejelly-like and viscous. GAGS include hyaluronicacid which binds cells together, lubricates jointsand shapes the eyeball.(a)Front(b)BackFigure 2.5 Relaxed skin tension lines. On the head andneck (a) these are readily identified by following the existingwrinkle or skin-crease lines. On the limbs the lines tend torun obliquely around rather than along the limb (b).

Biology of the skin 17Appendageal structuresWhilst these emerge from the skin through theepidermis and are considered epidermal appendages,most of them lie within the dermis or thesubcutis. As such they include hair, nails, sebaceousand sweat glands.HairThe surface of the skin is virtually completelycovered by invaginations of the epidermis,known as hair follicles. An invagination can bedescribed as the folding of something so that anexternal surface becomes an internal surface.Thus in the case of the epidermis, the surfaceof a hair follicle is covered in the same cells asthe surface of the external skin. Out of the folliclea keratin tube grows known as hair. Theonly parts of the skin surface that are not coveredin hair are the lips, the palms of the handsand the soles of the feet – these parts of the skinare described as glabrous. For our early ancestorshair was vital for protection and for insulation.Now, as we have evolved into relativelyhair-free beings, hair is much more about display,representation of cultural norms and sexualattraction. Hair does still offer some elementof insulation and protection for the scalp, butclothing now provides most of the warmth andprotection for the body.Hair growthHair growth occurs in three phases. The activegrowth phase, known as anagen, is usuallyabout 3 years for head hair (although it can beup to 9 years – see later). This allows the hair onthe head to grow to some considerable length;pubic and eyebrow hair have shorter growthphases (usually around a month). This meansthey fall out before they get very long. The restingphase, known as catagen, is when the hairsits in the follicle but is not actively growing andis followed by telogen when the hair is shed. Itis normal for an individual to shed 70–80 hairsa day. When removing terminal hairs by pluckingor waxing, the phase that the hair is in willeffect, how hard the hair is to remove and howlong it will take to grow back. Thus if the hair isin catagen or telogen it will come out relativelyeasily, but the growth phase starts again relativelyquickly. If the hair is plucked during anagen,it is harder to remove but will take longerto grow back.Types of hairThere are three different types of hair, terminal,vellus and lanugo. Lanugo hairs are present inutero but are shed in early childhood. Vellushairs are the fine downy hairs that cover mostof the body, particularly in women and children.Terminal hairs are generally much coarser andthicker and include those which cover the scalp,beard, chest hair and pubic areas. The quantityand texture of hair is determined largely bygenetic make-up, but hormonal changes can alsoinfluence hair growth and hair loss.Terminal hair shape varies depending on theethnic origin of an individual. In terms of hairtype, three ethnic groups can be considered: black(Afro-Caribbean), Caucasian and Indo-Chinese.■■■Afro-Caribbean: when cut in cross-section,the hair is thin and a flattish oval in shape. Thehair is twisted and curly causing it to be comeeasily tangled and broken. The pigmentswithin black hair are a combination of blackand red, with around 40% of black womenhaving near black hair, 50% black/brown hairand around 10% having auburn shades.Caucasian: a cross-section shows a slightlyfatter oval shape than for black hair, generallybeing fine textured and varying fromwavy to straight. It is the only ethnic groupwith a wide variety of pigment varying fromwhite blonde to reds to black.Indo-Chinese: the cross-section shows analmost perfectly round shape and the hairis generally straight or very slightly wavy.It is a very strong type of hair with a greatcapacity for growth. The anagen phase canbe twice as long as that of other hair typesand the shedding rates less. This means thathead hair can grow to the waist or below(Kingsley, 2003).The basic structure of the hair is the sameregardless of ethnic variations. It starts growth

18 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsCuticleMedullaCortexFigure 2.6 Structure of a hair. (Source: Reprinted fromGraham-Brown and Burns, 2006.)from the dermal papilla at the base of the hairshaft, where the keratinocytes divide, differentiateand gradually keratinise as the hair growsup the hair follicle. The hair bulb also containsmelanocytes which will determine the pigmentof the hair. Each hair consists of three distinctlayers (Figure 2.6). The medulla running throughthe centre of the hair shaft consists of cells inwhich air is incorporated. The cortex is similarto the prickle cell layer of the skin, althoughkeratinisation is further advanced. This is wherethe colour of the hair lies. The outer layer, orcuticle, is made up of overlapping keratinisedplates, like tiles on a roof. The cuticle helps individualstrands of hair to stay separate and notto matt together. Where the hair is subject tothe greatest abrasion (at the tip), the cuticle maywear away allowing the keratin fibrils of the cortexand medulla to frizz out leading to split ends.Conditioners smooth the roughened surfaceof the cuticle helping the hair to look shinier.The structure of the hair is very strong and canstretch to up to 30% of its length.Sebaceous glandsEach hair follicle has a sebaceous gland partway along its length. Sebaceous glands are simplebranched alveolar glands which are foundall over the body, except on the palms and soles.They are larger on the face, neck and upperchest and smaller on the limbs and trunk. Thegland releases sebum onto the hair surface, thuslubricating it and the skin surface. The centralcells of the alveoli accumulate oily lipids untilthey become so engorged that they burst, thegland is thus made up of cells that must ‘die’ asthey release their secretory product. The cellsare replaced by underlying cells.Sebaceous glands are stimulated by hormones,particularly androgens, and therefore are key tothe development of acne (see Chapter 10).Attached to the hair follicle is a bundle ofmuscle called the arrector pili muscle. Thesecontract when an individual is cold and pullthe hair into an upright position. This causesgoosebumps and is one of the body’s ways ofconserving heat. The erect hair traps warmair next to the skin surface. This biologicalphenomenon was much more effective whenhumans were hairier, now body hair is sparseand fine, this mechanism for keeping warm isrelatively ineffective.NailsNails provide protection for the delicate digitalends and make fine motor operations of the fingersmore effective. Although humans do notrely on the use of their nails for scratching andgrooming (as other primates do), they remaina useful tool for scratching when the skin isitchy!Like the hair follicle, the nail bed and nailfold are formed from an invagination of the epidermis.Cell division (mitosis) occurs in the nailmatrix and at the proximal end of the nail; newcells are then added to the nail plate. The processof growth is complex ensuring that the nailgrows flat rather than as a claw (primates beingthe only other mammal with nails rather thanclaws) (Figure 2.7). Nails allow humans andprimates to make much more delicate manoeuvreswith their fingers. In humans, fingernailsand toenails grow through the same mechanism;however, fingernails grow at the rate of1 mm per week and toenails more slowly. Thenail bed is highly vascularised and thus pink incolour. The ‘half moon’ white area that occursjust above the cuticle (the lunule) appears palerbecause a thicker basal layer obscures the dermalblood vessels from view. The shape andcolour of the nail can be adversely affected by

Biology of the skin 19Proximal nail foldNail plateTable 2.2 Nail anatomy.Nail partDefinitionLunulaProximal nailfoldNail bedNail matrixNail plateCuticleFigure 2.7 Nail structure. (Source: Reprinted from Graham-Brown and Burns, 2006.)trauma or inflammation. Table 2.2 gives furtherdetails on nail anatomy.Sweat glandsIt is estimated that there are around 2.6 millionsweat glands in the skin, women have more thanmen but those in men are more active. There aretwo different types of sweat glands, eccrine andapocrine.Eccrine sweat glandsEccrine sweat glands are widely distributedacross the skin surface, although concentrated inpalms, soles, forehead and axillae. This type ofsweat gland excretes a mildly salty fluid (99%water with small amounts of salts, ammonia,urea and uric acid) directly onto the surface ofthe skin when the skin surface temperature risesabove 35°C (Hinchcliffe et al., 1999). The mainpurpose of this is to encourage heat loss. Theevaporation of 1 L of sweat requires 580 kcal(2,400 KJ) of energy. Heat provides this energy,thus using it up and cooling the skin. Sweat willNail bedNail plateRootBodyFree edgeHyponychiumNail foldEponychiumNail matrixLunuleSource: Adapted from Saladin (2001).The skin on which the nail platerestsThe clear keratinised part of thenailProximal end of the nail, underlyingthe nail foldPortion of the nail plate overlyingthe nail bedPortion of the nail plate that extendsbeyond the end of the fingerThe space beneath the free edgeof the nail plateThe fold of skin around the marginsof the nail plateDead epidermis that covers theproximal end of the nail: cuticleThe growth zone of the proximalend of the nail. This correspondsto the stratum basale of theepidermisWhite crescent at the base ofthe nailnot evaporate in a very humid climate as theatmosphere is already laden with water.About 400–500 mL of fluid is lost per daymostly through sweat, although a small amountdirectly through the surface of the skin, lungs andbucal mucosa, known as insensible water loss. Ifthe ambient temperature is particularly hot orthe person is exercising, fluid loss may rise to asmuch as 12 L. Sweating from eccrine glands isalso stimulated by fear particularly on the palmsand soles; this phenomenon forms the basis of liedetector tests. Hot, spicy foods may also inducesweating, known as gustatory sweating.Apocrine sweat glandsApocrine sweat glands open into the hair follicleand are found mainly around the nipples, scalpin the groin and axillae. They are inactive inchildhood, being activated during puberty underthe influence of androgens.

20 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsThe glands are affected by the sympatheticnervous system, during times of stress, pain orsexual arousal. The secretion is basically thesame as eccrine sweat with the addition of proteinsand fatty substances which make a thicker,stickier substance. Although this is odourless, itis vulnerable to the activities of bacteria foundon the skin, and it is this action that makes themusty smell commonly known as body odour.It is thought that apocrine sweat is the humanequivalent of a scent gland which, whilst vitalfor other animals, seems to have become less sofor humans.Mammary glands that produce breast milkand ceruminous glands that produce ear wax inthe ear canal are modified apocrine glands.Functions of the skinThe skin is a multifunction organ. Its structureis uniquely designed to enable it to undertakeeach of these functions and cope with a range ofenvironments.Barrier functionThe skin is an incredibly effective barrier to theoutside world – at its simplest, it keeps the outsideworld out and the inside in – quite literallyit holds the human body together. However, theskin is not just a simple inert envelope; the barrierit provides is complex and offers physical,chemical and immunological protection.Physical protectionThe analogy that is most commonly used todescribe the physical barrier properties of theskin is that of a brick wall. In this instance, thelayer that really is of interest is the horny layerof the epidermis. Corneocytes form the top layerof skin, these heavily keratinised cells need tobe well-hydrated to form a complete barrier –they are the bricks in the wall. These bricks are‘cemented’ with lipids. As the skin is constantlyshedding, it is physically difficult for pathogenicorganisms to take hold.When intact, this brick wall is very effective atkeeping out allergens and pathogens. If the barrierfunction is compromised (and it only has tobe relatively mildly damaged through an excoriation),pathogens or allergens can penetrateleading to an infection or an allergic reaction.Moving in the opposite direction, a break inthe barrier also allows moisture and lipid to belost. A more severe break in the skin barrier, forexample following a burn, can be catastrophic,indeed life threatening, as the body struggles tocope with the challenge of extensive infectionand imbalanced homeostasis.Chemical protectionThe surface of the skin is covered in commensalorganisms. These ‘friendly’ bacteria and fungilive in harmony with humans and indeed offera level of protection from pathogenic or disease-causingorganisms. The commensals haveevolved to be able to thrive in the slightly acidicenvironment of the skin surface (pH of 4.5–6).Skin cells are provided with inbuilt protectionfrom UV radiation by melanin. In the upperlayers of the epidermis, melanin is scatteredthroughout the cells providing protection, whilstin the lower layers the protection is specificallytargeted as the melanin granules form ‘umbrellas’over the nuclei of the basal and spinous cells.Physical and chemical barriers form part ofthe body’s innate defence system.Immunological surveillanceUnderstanding of the role that the skin playswithin the immune system is ever increasing.The role of specialised cells such as Langerhanscells has already been discussed. However, othercells also have a role within immunological surveillance.For example, epidermal keratinocytescan, in certain circumstances, express immunologicalmarkers on their surface and producecytokines which are known as signalling molecules(examples include immunomodulatingagents such as interleukins) which in turn inducean inflammatory response.Immunity is distinguished from innate nonspecificresistance in two ways. Firstly, antigensare recognised and produce a specific

Biology of the skin 21response, which also involves distinguishingnon-self molecules. Secondly, the body remembersprevious encounters with antigens so thatsubsequent encounters prompt more rapid andvigorous responses. Generally the immune systemworks to protect the body from unwantedvisitors (pathogens and allergens); however, if anindividual is genetically predisposed to certainchronic skin conditions, the immune system canbe triggered to produce responses that are notdesired. For example, in psoriasis, T-cells areactivated by the production of inflammatorymediators leading to hyperproliferation of skincells and inflammation (see Chapter 9).StorageThe skin acts as an organ of energy storagewhich can be drawn upon under physicallychallenging situations such as starvation anddehydration. The layer of fat acts as a reservewhich can be metabolised to produce energy.This process involves fats being broken downinto fatty acids which are in turn broken downinto acetyl CoA which can feed directly into theKrebs cycle to produce energy.Babies have a specialised type of fat knownas brown fat which yields energy more easilythan other types of fat. They also have a higherproportion of their body weight given over tofat than adults. This is important as babies havea large surface area relative to their weight andare unable to shiver; this makes them vulnerableto heat loss. Breakdown of this brown fatproduces the energy required to stay warm. Asa child develops muscular control and can usethis muscular activity to generate warmth, theimportance of the brown fat lessens. Generallyadults do not have brown fat.Temperature regulationThe skin is the organ of temperature regulation.Whilst thermoregulation (the maintenanceof core body temperature at 37°C) is under thecontrol of the hypothalamus, the receptors fortemperature are found in the skin and likewiseit is the structures within the skin that allow forheat conservation or heat loss. The mechanisminvolves stimulation of peripheral temperaturereceptors in the skin, which in turn affectthe hypothalamus and the sympathetic nervoussystem which acts directly on the peripheralblood vessels in the skin. Vasoconstriction of theperipheral vasculature leads to heat conservationand vasodilation to heat loss.Heat lossThere are four different mechanisms by whichheat can be lost from the skin.RadiationDescribes the movement of heat directly throughthe air and this can be a mechanism for heat lossif the skin is warmer than the surrounding air.However, on a sunny day the skin can be directlywarmed by the sun’s rays through radiation.ConvectionIf there is movement in the air or of the body,hot air will rise and be replaced by cooler air.This mechanism is hampered by the presence ofclothes (which will therefore keep a body warm)and facilitated by a fan.ConductionThis simply describes the movement of heatthrough an object that the body comes into contactwith.EvaporationWhen eccrine sweat is excreted onto the skin,the heat from the skin is used to evaporate itaway into the atmosphere. The net effect is tocool the surface of the skin (see section on sweatglands for more details).SensationTouch, a social phenomenonThe skin is the organ of physical sensation; itallows humans to experience the pleasure of

22 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalssensual touch and the unpleasantness of pain.Heat, cold and pressure are all experiencedthrough the skin. The skin is rich in sensorynerve endings, particularly the fingers, toes andlips. Touch is not only a physical experience butalso a personal and social phenomenon; it is theway we connect physically to other humans andthe way that we express a vast range of humanexperiences including power, love, abuse andcaring. (Classen, 2005) describes touch as:…a fundamental medium for the expression,experience and contestation of social valueand hierarchy. The culture of touch involvesall of culture. (Classen, 2005, p. 1)Different cultures have unique ways of describingtheir experience of how the skin interactswith the world around it. The Cashinuahuatribe of Eastern Peru describes ‘skin knowledge’as the knowledge of the world one acquiresthrough the skin, through the feel of the sun,the wind, the rain and the forest. This allowsthem to find their way through the jungle andto locate the animals that they hunt for.Western culture would advocate close contactbetween mother and baby as vital for bonding;however, this has not always been the case. Inthe late 19th and early 20th century, Dr L.EHolt wrote that babies should not be rockedand only kissed infrequently on the forehead.Dr Watson wrote in his 1928 book entitledPsychological care of infant and child:Mothers just don’t know, when they kiss theirchildren and pick them up and rock them,caress them and jiggle them upon their knee,that they are slowly building up a humanbeing totally unable to cope with the world itmust later live in (p. 42)Thus, attitudes towards touch are not justrelated to cultural norms but also to time.Sensation as a physical experienceThe skin is part of the sensory nervous systemand as such contains a number of mechanismsfor sensation including touch, pressure, vibration,itch and tickle.TouchTouch sensation can either be crude or fine.Crude implies that there is knowledge that theskin has been touched but the exact location andsize of stimulus may not be determined. Finetouch means that the exact part of the body,shape, size, texture and source of the stimuli canbe distinguished.Fine touch is experienced through the stimulationof Meissner’s corpuscles which are foundin hairless skin. They are an egg-shaped mass ofdendrites enclosed in a capsule of connective tissue.These are rapid acting and generate nerveimpulses at the beginning of a touch. They areabundant in fingertips, hands, eyelids, tip of thetongue, lips, nipples, soles, clitoris and the tip ofthe penis. Crude touch is experienced throughthe stimulation of hair-root plexuses. Againthis produces a rapid response when movementon the surface of the skin which disturbs hairsstimulates free nerve endings wrapped aroundhair follicles.Slowly adapting touch receptors are generallymore sensitive to pressure, vibration and stretching.Type I receptors (Merkel discs) are saucershapedfree nerve endings that contact Merkelcells in the epidermis. They are particularlyprevalent in fingertips, hands, lips and externalgenitalia. Type II (Ruffini corpuscles) are elongated,encapsulated receptors found deep in thedermis (particularly in hands and soles) andin ligaments and tendons; they are sensitive tostretching.ItchCutaneous itch is caused by the stimulationof free nerve endings of C fibres. These unmyelinatedC fibres transmit impulses relativelyslowly and although functionally they are thesame as those that transmit pain, functionallythey are distinct. There are a number of mediatorswhich lead to the stimulation of these fibresand the consequent sensation of itch. Theseinclude histamine, cytokines, neuropeptides andprostaglandins.Tickle is a curious sensation as it only occurswhen an individual is touched by someoneelse. It is thought to be mediated by free nerveendings and lamellated corpuscles.

Biology of the skin 23PainWhilst pain is generally considered an unpleasantexperience, its biological functions are firstlyto help protect us from noxious substances ordangerous situations and to help pinpoint anunderlying cause of disease.Nociceptors are free nerve endings which arefound all over the body, except in the brain.Tissue irritation or injury releases chemicalssuch as potassium, prostaglandins and kinins,all of which can stimulate nociceptors. Thepain may continue long after the stimulus isremoved as the pain-stimulating chemicals maypersist and the nociceptors exhibit very littleadaptation.Pain may be experienced as fast or slow pain,the sensation being determined by the type offibres transmitting the pain impulses. Perceptionof fast pain occurs 0.1 seconds after the stimulusas impulses are sent along medium-diametermyelinated A fibres. This generates an acute,sharp, pricking pain. Generally fast pain is notfelt in deeper tissues of the body. Slow painbegins a second or more after the stimuli hasbeen applied and builds up in intensity over secondsor minutes. The impulses are transmittedby small-diameter unmyelinated A fibres andgenerate a more chronic, throbbing, burning oraching sensation. Pain can occur in skin, deepertissues and internal organs.Biochemical reactions in the skinThe most commonly reported biochemical functionof the skin is the synthesis of vitamin D.This occurs mainly in the prickle and basal layerswhere UV light stimulates the conversion of7-dehydrocholesterol to vitamin D3. VitaminD is essential for the skeletal development as itcontrols the balance of calcium and phosphorousabsorbed through the small intestine andmobilised from the bone. The amount of melaninin the skin affects the exposure time requiredto synthesise the vitamin; black skin requires 12times the length of exposure to UVB than whiteskin. This is probably due to the fact that only2–5% of UVB penetrates the epidermis in blackskin whereas in white skin this is 20–30%.Androgen metabolism also occurs in the skin;testosterone is converted to 5α-dihydrotestosteroneby the enzyme 5α-reductase.PsychosocialThe skin is the organ of display, it is howhumans present themselves to the world, andoften judgements are made (rightly or wrongly)on appearance. The skin is often adorned ina multitude of ways in order to produce socialsignals of cultural significance. This may bethrough permanent marks such as tattooing,piercing and scarification or temporary decorationsuch as make-up and jewellery. The amountof skin that is displayed allows others to makejudgements about lifestyle choices or religiousconvictions. Often one can determine racialgroupings by the colour of the skin or hair, andage may be guessed by noting wrinkles, skin toneand hair colour. Of course, all judgements madeon the basis of appearance may be wildly wrong,but this does not stop people making them!In an appearance-based society, to appear‘abnormal’ can have an enormous impact on anindividual’s psychological well-being. The feelingof being unwelcome or discriminated againstbecause of the skin is a potentially devastatingexperience that means individuals have a rangeof negative responses including withdrawal fromsociety, developing low self-esteem, having mentalhealth problems or failing to achieve theirfull potential.The profound almost instinctive distaste oftenengendered by skin disease, which more-oftenthan-notis totally out of proportion to its objectivemanifestation, may be related to a deeplyheld, almost primeval fear of contagious infectionor infestation. It is clear through historic documents,including the Bible, that those with signsof disease through the skin were outcast, leprosybeing the prime example of this. It is thoughtthat many of those who were labelled as lepersactually had other skin diseases such as psoriasis.As communities who did not have the benefit ofunderstanding of the modes of disease transmission,an outward sign such as a diseased skin wasan obvious thing to ‘blame’. These issues will beexamined in more detail in Chapter 6.

24 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsIn summary, our skin and hair can reflect bothour physical and mental well-being. A ‘bad hairday’ can mean a day where everything seems to gowrong and where a person feels unprepossessingand incapable. Conversely, a new hair style canboost confidence and make an individual feelyounger and more confident. General health willalso affect the health of the skin, when someoneis relaxed and healthy their skin is more likelyto ‘glow’. Good skin health not only means thatthe physical attributes of the skin are functioningwell, but also that an individual feels psychologicallycomfortable in his/her own skin.Skin and ageingThe skin structure and function changesthroughout the human lifespan. The changesdescribed in this section should be seen as inevitablebiological processes, although it may bepossible to slow down ageing, no one has yetworked out how to stop it happening altogether!Table 2.3 shows some terms which may be usedto describe skin growth and skin death.Table 2.3 Skin growth and skin death.Skin deathAtrophyNecrosisGangreneSkin growthHyperplasiaHypertrophyNeoplasiaDefinitionSkin shrinking or reducing due toloss of cells either in size or number.This can be either through lack of use(disuse atrophy) or old age (senileatrophy)Premature, pathological death oftissue caused by trauma, infectionsor toxinsTissue necrosis resulting frominsufficient blood supplyMultiplication of cellsEnlargement of existing cellsTumour composed of abnormalnon-functional tissuePre-birthDuring embryogenesis, layers of cells known asgerm cells are formed. Skin will eventually beformed by the cells in two of these layers; theectoderm forming (amongst other structures) theepidermis and the mesoderm the dermis.The baby is protected in utero by a thicklayer of vernix caseosa, a very effective greasysubstance which protects the infant’s skin fromthe watery environment of the amniotic fluid.The words vernix caseosa come from a Latinderivation, vernix, meaning ‘varnish’ and caseosa‘cheesy’. The vernix is composed of sebum,which is secreted from the baby’s sebaceousglands from around 20 weeks, and skin cells asthey desquamate. Further protection is providedby the fine, downy hair known as lanugo. Thisfalls out soon after birth to be replaced withvellus and terminal hairs.At birthIf a baby is born after its due date, the vernixcaseosa would have mostly gone which meansthe skin tends to be dry and peeling as it has notbeen effectively protected in the watery environmentof the womb. If a baby is born prematurely,its skin will be more vulnerable as it would nothave had chance to mature completely, making itmore prone to infection and trauma. This beingsaid, the skin of a newborn is generally quite vulnerabledue to the immaturity of the skin barrier.It has not developed a complete flora and fauna,so does not have full protection of the commensalbacteria nor has it developed the acid mantle.For the first 6 weeks of life, it is recommendedthat water alone is used to cleanse the skin.Subsequently, any products that are used shouldhave minimal levels of perfume and colourantsin them. Bland emollients (see Chapter 5) maybe helpful if a baby’s skin gets dry.Babies in neonatal units have particularlyvulnerable skin. A survey carried out at theUniversity of Southampton suggests that despitethis fact, many neonates have their skin overlycleansed and frequently damaged with tape anddressings (Rapley, 2007).

Biology of the skin 25Post-birth/early monthsThere are a number of skin changes in the earlymonths which can be considered ‘normal’ thatdo not usually require any intervention exceptreassurance.MiliaThese are tiny white spots which appear over thenose and face of babies; they are common. Theirformation is probably related to the stimulus ofthe sebaceous glands which become temporarilyblocked. There is no need to squeeze them as theywill resolve of their own accord. The sebaceousglands become small and inactive soon after birthand as they do the milia resolve. The sebaceousglands remain inactive until puberty.Mongolian blue spotThese are also relatively common in babies ofIndo-Asian or Afro-Caribbean origin and occurin over 90% of children of Mongolian extraction.They consist of a blue grey patch on theskin which often occurs on the sacrum but canoccur anywhere on the body. The skin surfaceis normal. The cause is thought to be elongatedmelanocyte precursor cells in the dermis. Theycan be mistaken as trauma from non-accidentalinjury, so should be documented in the notes. Formost children these patches will fade as they getolder, some however will persist into adulthood.Benign acquired melanocytic lesionsBoth freckles and lentigo can be described asbenign acquired melanocytic lesions. Frecklesare areas of skin where melanocytes are seen tobe more active than in neighbouring areas. As aresult, small (less than 5 mm in diameter), flatareas of pigmentation appear, generally scatteredover the face, neck and arms, appearing ina variety of shades depending on the individualand the time of the year (darker in summer).Lentigo (plural being lentigenes) are also flatand a similar variety of sizes as the freckles,but they do not vary with sun exposure. Unlikefreckles where there is no increase in the numberof melanocytes, in lentigo there are.Congenital melanocytic naeviThese lesions may be small or giant and occurin approximately 1% of births. The surface ofthe lesion may be smooth or rough and warty;there may be one or more hair follicles in thelesion. Giant congenital melanocytic naevi(those that cover a large area of the body andmay be accompanied by thousands of smallerlesions) are associated with malignant melanomasand parents will need careful counsellingabout what action to take. Sometimes, thelesions are too large to consider surgicalexcision and grafting.Vascular naeviVascular naevi are caused by dilated and tortuous,but otherwise normal blood vessels. Wherecapillary vessels are involved, a superficial ordeep type may be described.The superficial capillary naevi are caused byabnormal dilated vessels in the superficial dermisleading to salmon-coloured patches oftenon the face that will fade quite quickly. Theyare relatively common, occurring in approximately50% of all neonates. The deeper capillarynaevi are known as ‘port wine stains’,and because the vascular abnormality extendsdeeper into the dermis, these do not resolve andmay even extend throughout life. The colour ofthe patches varies from pale pinkish red to darkpurple; the colours will deepen with age. Thesechanges can be associated with intracranial vascularchanges and neurological pathology, soany child with a facial port wine stain should beinvestigated.Arterial naeviOtherwise known as superficial angiomatousnaevi or strawberry birth marks, these occurin around 10% of children by the age of 1.Commonly, they start growing within a fewdays to a few weeks of birth and are usually relativelysoft and irregular in outline. Sometimesthere is a deeper component to these naeviwhere the subcutis is involved, in these instancesthe changes may lead to a distortion of normalanatomy. Growth of the lesion usually stops

26 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsat around 6 months and resolution is usuallyspontaneous and complete, although if thelesion was particularly large, lose skin or atrophymay be left. The following rule of thumb isusually quite accurate:Forty percent are gone by the age of 4 years;50% by 5 years; 60% by 6 years; 70% by7 years; 80% by 8 years and 90% by 9 years.(Graham-Brown and Bourke, 1998).If the lesion interferes with feeding, breathingor sight, treatment may be recommended. Forsmaller areas, this is likely to be a steroid injection,but other options may be necessary includinglaser therapy. These types of naevi usually occuron the head, neck, buttocks or perineal areas. Ifthey are associated with the lower back, sacrumor buttocks, a scan is usually recommended toexclude problems of tethering of the spinal cord.Physiological jaundice (icterus neonatorum)At about 2 days of age, parents may noticethat their newborn is a yellowish colour. Thisis quite normal and results from the breakdownof the excess red blood cells that thechild needed when they were in utero. As thechild breaths following delivery, it no longerhas any need of these red blood cells, so theybreak down leading to high serum bilirubin levelsand the consequent yellow colour. This typeof jaundice should not be confused with pathologicjaundice which occurs within 24 hours ofbirth and may be indicative of ABO or rhesusincompatibilities.PubertyPuberty is the time at which reproductive organsbecome functionally active. In both males andfemales, it is accompanied by the developmentof the secondary sexual characteristics includingthe growth of pubic hair and axillary hair andfacial hair in boys. These changes are due to alarge increase in the secretion of gonadal sexhormones. Androgens have a powerful effect onthe hair follicle stimulating the sebaceous glandthat has lain dormant since shortly after birth.This leads to an increased production of sebumcausing teenage skin and hair to be greasierthan prior to puberty. For some, this change inthe sebaceous gland functioning will mean theappearance of acne. Most teenagers experiencecomedones, others will experience more extremeacne with pustule or even nodule formation.Chapter 10 discusses acne in greater depth. Theapocrine glands are also stimulated leading tothe experience of body odour for the first time.Teenage years are also a time when youngadults start to take a real interest in theirappearance and is a good time to encouragehealthy skin behaviour, including protectionfrom UV radiation (see Chapter 4).PregnancyHormonal changes throughout the menstrualcycle can influence the skin and hair for somewomen. It is during the second half of themenstrual cycle, following ovulation when theprogesterone levels peak, that women noticechanges in their skin and those with a skin conditioncan experience an exacerbation.During pregnancy some specific changes dooccur, specifically a deepening of the normalpigmentation of the nipple, the areola, the genitalarea and the midline of the abdominal wall.Following delivery this pigmentation will fade,but seldom back to the usual colour. For a proportionof women (around 70%), the secondhalf of pregnancy sees chloasmal pigmentationwhich is characterised by an irregular, sharplymarginated area of pigmentation which developsin a symmetrical pattern over the cheeks and/orforehead. It is also common for women to seetheir moles darken whilst pregnant and it is alsopossible for new moles to appear. It is advisablefor pregnant women to take additional precautionswhen going out into the sun; they shouldwear a hat and use a high factor sunscreen.Vascular changes mean that women noticeflushing of the palms of the hands and spidernaevi appear on the face, upper trunk and arms.Oedema of the lower legs and increased appearanceof varicose veins occur due to a rise in

Biology of the skin 27venous pressure caused by the increased pressureof the growing foetus impeding venous return.Dermal changes include stretch marks whichoccur due to weakened tensile strength of dermalfibres (caused by the increase corticosteroidoutput) and the stretching of the skin due to thegrowing foetus. A study carried out in SouthernIndia showed that nearly 80% of women experiencedstretch marks following pregnancy(Kumari et al., 2007). Marks appear as raisedreddish/purple lines during and just after pregnancy,which fade to more skin- coloured slightlydepressed shiny lines. Avoiding stretch marksduring pregnancy may be down to genetic goodfortune; however, the following strategies mayhelp decrease the likelihood of stretch marks orat least their severity:■■■Gradual and moderate weight gain duringpregnancy (a woman with a normal bodymass index should aim to gain between 25and 35 lbs during pregnancy.);Gentle exercise;A Cochrane review considered studies thatlooked at topical products which might alleviatestretch marks. The review highlightsone product containing Centella asiaticaextract, alpha tocopherol and collagen–elastinhydrolysates, which when compared to aplacebo was associated with women developingfewer stretch marks. A second studysuggested that a product containing tocopherol,panthenol, hyaluronic acid, elastin andmenthol was associated with women developingfewer stretch marks. But this study didnot include a control and the improvementsmay have been associated with the massage(Young and Jewell, 1996).Old ageAs humans get older, the skin becomes thinner,less elastic, drier and more finely wrinkled. Thedegree to which the skin becomes visibly aged isrelated largely to genetics and photo-ageing. Inother words, wrinkle formation is determined bythe traits inherited from parents and the extentto which someone has exposed themselves tosunshine over their lifetime. Intrinsic ageingdescribes the natural biological processes whichit is not possible to control and extrinsic ageingthe impact that the environment and exposureto it has on the skin. It is possible to get a senseof the impact of extrinsic factors by comparingthe skin of a sun-exposed and non-sun-exposedsite. In an elderly person, particularly, there isa marked difference between the texture andcolouring, the former being much smoother andless wrinkled.The changes highlighted in Table 2.4 meanthat older skin is increasingly sensitive and lessable to cope with external stressors on the skin.Thus the skin has less innate ability to cope withexternal agents such as perfumes in topical products,extremes of temperature, urine and faeces.These factors are discussed further in Chapter 4.Overexposure to UV radiation is responsiblenot only for the effects of ageing but also moreworryingly for skin cancers. Basal and squamouscell carcinomas are both closely associatedwith prolonged sun exposure and whilst theyare rarely life threatening, they can be locallydestructive and need to be properly diagnosedand treated. Malignant melanomas are alsoassociated with sun exposure, although burningis generally thought to be a high risk factor. Skinmalignancies are discussed later in Chapter 11.Table 2.4 Skin changes caused by ageing.Changes in the skinEpidermal turnoverslowsLess effective barrierfunctionLess flexible andtough collagenLess evenly distributedmelaninFewer sweat glandsLess sebumproductionConsequenceThinner skinMore prone to infection/drynessMore prone to wrinkles andsheeringMore prone to sun damageLess effective temperaturecontrolIncreased skin dryness

28 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsConclusionThe skin provides humans with a flexible anddynamic outer layer. Its complex structure andfunction create a unique environment whichprotects the inner functionings of the body andprovides an incredible interface with which tointeract with the outside world. This chapterhas formed the basis of a biological understandingof the skin; the rest of the book will look atwhat happens when skin fails, from a number ofdifferent perspectives.ReferencesClassen, C., Ed. (2005). The Book of Touch.Oxford: Berg Publishers.Graham-Brown, R. and J.F. Bourke(1998). Mosby’s Color Atlas and Text ofDermatology. London: Mosby.Graham-Brown, R. and T. Burns (1996).Lecture Notes in Dermatology (7th edition).Oxford: Blackwell Science.Graham-Brown, R. and T. Burns (2006).Lecture Notes: Dermatology (9th edition).Oxford: Blackwell Science.Grimes, P., B. Edison, B.A. Green andR.H. Wildnauer et al. (2004). Evaluationof inherent differences between AfricanAmerican and white skin surface propertiesusing subjective and objective measures.Cutis, 73(6): 392–396.Hinchcliffe, S., S. Montague and R. Watsonet al. (1999). Physiology for Nursing Practice.London: Bailiere Tindall.Hoffjan, S. and S. Stemmler (2007). On therole of the epidermal differentiation complexin ichthyosis vulgaris, atopic dermatitis andpsoriasis. British Journal of Dermatology,157(3): 441–449.Kingsley, P. (2003). The Hair Bible: A CompleteGuide to Health and Care. London: AurumPress Ltd.Kumari, R., T. Jaisankar and D.M. Thappaet al. (2007). A clinical study of skin changesin pregnancy. Indian Journal of DermatologyVenereology and Leprology, 73(2): 141.Lydyard, P., A. Whelan et al. (2000). InstantNotes on Immunology. Guildford: Bios.Marieb, E. and K. Hoehn (2007). HumanAnatomy and Physiology (7th edition).San Francisco: Pearson BenjaminCummings.Rapley, S. (2007). A National Survey ofNeonatal Skin Care Practices. Universityof Southampton, School of Nursing andMidwifery. Unpublished report.Roitt, E. and P. Delves (2001). Roitt’sEssential Immunology. Oxford: BlackwellScience.Saladin, K. (2001). Anatomy and Physiology –The Unity of Form and Function. New York:Magraw Hill.Tortora, G. and B. Derrickson. (2006).Principles of Anatomy and Physiology(11th edition). New Jersey: John Wiley andSons Inc.Wesley, N. and H. Maibach (2003). Racial(ethnic) differences in skin properties: Theobjective data. American Journal of ClinicalDermatology, 4(12): 843–860.Young, G. and D. Jewell (1996). Creams forpreventing stretch marks in pregnancy.Cochrane Database of Systematic Reviews1(Art No.CD000066).

Assessment andplanning care3Steven J. ErsserIntroductionThis chapter will outline a systematic approachto assessment, introducing key concepts, theirapplication and both physical and psychologicalassessment tools. Key principles and issues regardingthe planning of care and relevant factors willbe summarised. Details of the assessment processrelated to specific conditions in the relevant conditionrelated chapters are provided. An overviewwill be given of common dermatological interventionsand related psychological and educationalinterventions, although the detail will be discussedand signposted to the relevant chapters elsewhere.Finally, some issues of evaluation and the use ofevaluative strategies are highlighted.An effective plan of care requires careful assessment,the related planning of interventions and asystematic evaluation of its consequences. As thelargest organ of the body, and the most visual, theskin is highly accessible to assessment, althoughthe process is complex. The challenge of assessingabnormal changes in the skin is the sheer numberof variation that may occur in site, colour, textureor surface features and the type of lesionsthat may be present. This chapter builds on theprevious one on skin biology. Effective planningof care requires an understanding of normalstructure and function, its disruption by diseaseprocesses and the influence of psychosocial factors.The International Classification of Disease(ICD-10) index of dermatological diagnosesconveys the considerable and complex range ofdermatological conditions, listing several hundred(www.who.int/classifications/icd/en/); however,the British Association of DermatologistsDiagnostic Index has over 4,000 preferred terms,with highly differentiated dermatological diagnoses.Many of these are rare in nature. Themost common conditions fall into nine categories:skin cancer, atopic eczema, contact dermatitisand other eczemas, psoriasis, acne, blisteringconditions, viral warts, other infective disorders,benign tumours and vascular lesions, leg ulceration(Williams, 1997). Indeed, a person may nothave a skin disease per se, but a problem such asdryness (xerosis), which can be both uncomfortableand disruptive, leads to other problems withthe skin barrier.The purpose of assessment is to determine thenature of the clinical problem, its relative priorityand the possible need for referral, given the natureand complexity of the person’s condition. If theclinician does not have a diagnostic role then skillis required to accurately describe any changes

30 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsobserved that aid effective communication withclinical colleagues, and in particular to ensureappropriate referral. It is necessary to approachskin assessment in a systematic and holistic way,reviewing not only physical changes but also anypsychological and social impact on the personand their family. This must also embrace a reviewof the impact on the quality of life of the personand their family. Assessment is not a one-off activitybut rather an ongoing process, which involvesmonitoring changes in the patient’s condition,their response to such changes and those relatedto treatment effects that are either therapeutic oradverse in nature.AssessmentNormal skinAn assessment of a range of typical skin typesis made by examining the person’s tendency toburn and tan, using the following guide (Table3.1). This is useful to assess and convey whenappraising sun/ultraviolet (UV) damage, riskprior to phototherapy, or when providing aguide when engaging in health education relatedto UV exposure risk awareness. Key considerationsin a person’s skin typing include a person’spigmentation and erythema history and theirgenetic history (Leach et al., 1996). Those withfair skin, which includes types 1 and 2, are morelikely to develop skin cancer.Table 3.1 Normal skin – skin typing.An assessment approach has been adopted thatis suitable for use by a wide range of dermatologyprofessionals and primary care staff based onthe framework provided by Leach et al. (1996)and Ashton and Leppard (2005) to aid diagnosis,although it will also enable the clinician todescribe and assess more precisely the conditionof the skin, to aid effective team working, by enablingthe referer to describe the lesion or rash inthe absence of an established diagnosis.Racial variationsRacial variations in skin are reflected in Table 3.1;these have implications for assessment, such asdetermining lesion colour and in the estimationof UV protection related to the presenceof melanin (see Chapter 2). The most lightlypigmented (European, Chinese and Mexican)skin types have approximately half as much epidermalmelanin as the most darkly pigmented(African and Indian) skin types. Research byAlaluf et al. (2002) highlights the analysis ofmelanosome size, which revealed a significantand progressive variation in size with ethnicity:African skin having the largest melanosomesfollowed in turn by Indian, Mexican, Chineseand European. Based on these findings, theypropose that variation in skin pigmentation isstrongly influenced by both the amount and thecomposition (or colour) of the melanin in theepidermis. Variation in melanosome size mayalso play a significant role. Further details ofthe relationship of skin typing to the person’sgenetic history and social heritage are given inLeach et al. (1996) and on racial influences onskin disease in Gawkrodger (1998).Skin typeIIIIIIIVVVICharacteristicsAlways burns, never tansSometimes burn, rarely tanRarely burns, easily tansNever burns, always tansAsian peopleAfro-Caribbean/Black AfricanpeopleBody surface areaAs highlighted in the previous chapter, theskin covers an extensive surface area, coveringapproximately 2 m² of the body (Tortora andDerrickson, 2006). An important element of skinassessment is to determine the extent to whichthe body surface area (BSA) is affected by thedisease and the nature and pattern of lesions. Itis commonplace to use a simple body map proforma in clinical practice to document the distributionof rashes and track their variations with

Assessment and planning care 314½%4½%4½%18%4½%4½%18%4½%1%9% 9%9% 9%Figure 3.1 Body map.time. Figure 3.1 shows a body map depicting thefront and back of the body, where the distributionof lesions (the affected area) may be crudelyreflected by the degree of shading completed. Itis possible to record on the body map the BSAaffected, as a percentage.The BSA can be estimated in various ways(Ashcroft et al., 1999). The use of the flat handpalm provides an indicator of 1% of total BSA,whilst often accepted in clinical practice technicalestimates put the area as up to 0.76% of the BSA.Another approach, the rule of nines, estimates differentareas of the body comprising of 9% coveragefor each of the following: head, anterior trunk(upper and lower each 9%), posterior trunk (upperand lower each 9%), each leg (anterior and posterioreach 9%), each arm (4.5% each) and genitalia(1%) (see Figure 3.2). However, untrained observerstend to overestimate the extent of lesions, suchas small psoriasis plaques. A challenge in dermatologicalassessment is securing sufficient consensuson the area of skin affected by disease, which isthe variation between assessors or observers. Highinter-observer variability is a problem of calculatingBSA amongst clinicians (Ashcroft et al., 1999).Clinical monitoring of the course of diseaseover time may involve the documentationof the distribution of the affected area of skin;this is achieved by shading the affected area.AnteriorFigure 3.2 Rule of nines.PosteriorIncreasingly, estimates of body surface are usedin the assessment of disease severity measures,such as the PASI or Psoriasis Area Severity Index,which are discussed in more detail later in thischapter. Errors made in the estimation of BSAmay well affect the severity score and, in turn,this may have implications for treatment decisionsbased on clinical protocols. For this reason,the estimation of BSA and the related calculationof severity measures require training and oversightwithin clinical teams, to ensure practitionerachieve a satisfactory standard of consistency andaccuracy.Understanding and describing lesionsWith the very high number of dermatologicaldiagnoses, it is particularly useful to be able tounderstand and systematically describe the differentfeatures and observable patterns of theunderlying lesion or rash. This has the benefit

32 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsof highlighting its observable features andenabling referral to other health professionalswithout a diagnosis. However, if undertakeneffectively it should be an indication of a differentialdiagnosis for those with the appropriatetraining. Documenting the appearance ofa lesion or rash can be challenging given theirpattern of distribution and the sublety of theirsurface features. As such, it is necessary to gainfamiliarity with the typical types of lesions seenand rash patterns; these are introduced below.The process of describing lesions is therefore aprecursor to making a full assessment and anysubsequent differential diagnosis or the basisfor referral. Guidance on how to describe skinlesions is summarised in Table 3.2.Describing rashesA rash is a change in the colour or texture ofthe skin and as such reflects the nature andpattern of a collection of individual lesions. Amajor consideration in dermatological assessmentis to determine the specific patterns ofsuch rashes and their specific characteristics asan aid to diagnosis. Some of the dimensions ofTable 3.3 A framework for skin assessment and lesiondescription.1. Site2. Erythematous, i.e. reddened skin (blanches on pressure)or non-erythematous3. Acute (2 weeks duration) or chronic (2 weeksduration)4. Surface featuresa. Normal/smooth (i.e. same as surrounding skin)b. Scalyc. Hyperkeratoticd. Wartye. Crustf. Exudateg. Excoriated5. Type of lesiona. Flat: macules and patchesb. Raised: papules, plaques and nodulesc. Fluid-filled: vesicles, bullae and pustulesd. Surface broken: erosions, ulcers and fissuresIf non-erythematous describe the6. Coloura. Due to blood: pink, purple, mauveb. Due to pigment: brown, black and bluec. Due to lack of blood/pigment: whited. Other colours: yellow, orange, greySource: Based on Ashton and Leppard (2005).Table 3.2 Guidance on describing skin lesions.1. Look first to identify:a. Sites involved: specify body areab. Number of lesions: single, multiplec. Distribution: includes symmetrical or not, localisedor generalisedd. Arrangement: includes discrete, coalescing,disseminated, linear, annular2. Feel the lesions by:a. Surface palpation: with finger tips – smooth,uneven, roughb. Deep palpation: by squeezing between finger andthumb – soft, firm, hard3. Describe a typical lesion using the following headings:a. Type of lesion (see Table 3.3)b. Surface features (see Table 3.3)c. Colour, including erythematous or non-erythematousd. Border of rash/lesion: well/poorly defined or anaccentuated edgee. Size and shape of individual lesion: includes round,irregular, serpiginousSource: Based on Ashton and Leppard (2005).skin assessment are specified in Table 3.3. Theseinclude site, colour, acuity, surface features andtype of lesion.Owing to the wide-ranging nature of lesions,it is helpful to understand their different types.Therefore, specific definitions and clinical examplesof particular surface features and lesions arenow summarised in Table 3.4.A useful distinction is also made of primaryand secondary lesions. Primary lesions are causeddirectly by the disease process; this includes macules,papules, nodules, plaques, wheals, vesicles,bulla, pustules and cysts (Figures 3.3–3.8).Secondary lesions refer to the consequences ofthe disease process; these include scale, crust,fissures, lichenification, erosion, ulcers, excoriation,scar and atrophy (Johannsen, 1998).Further details of physical signs in dermatology,with excellent illustrative photographs, can befound in Lawrence and Cox (2002). Many skin

Assessment and planning care 33Table 3.4 Types and definitions: Surface features and lesions.Types of lesionNormalScalyHyperkeratoticWartyCrustExcoriatedExudateFlat: maculeFlat: patchRaised: papuleRaised: plaqueRaised: noduleFluid-filled: vesicleFluid-filled: bullaeFluid-filled: pustuleDue to broken surface:ulcerDue to broken surface:erosionDue to broken surface:fissureColour: due to bloodColour: due to pigmentColour: due to lack ofblood/pigmentColour: otherSmooth, the absence of other surface featuresExcess dead epidermal scales produced by shedding from the stratum corneum orabnormal keratinisation (e.g. erythrodermic psoriasis)Increased keratinisation (cornification) of the epidermis, which appears clinicallyas thickened and rough skin or mucous membrane (e.g. foot psoriasis)A wart-like lesion consisting of finger-like projections (e.g. filiform wart)Dried exudate (comprised of dried serum, bacteria and possibly blood, mixed withepidermal debris – e.g. impetigo)A superficial linear erosion caused by excessive scratching (e.g. atopic eczema)A leakage of fluid from blood vessels into nearby tissue (e.g. acute eczema)A flat lesion circumscribed area of altered skin colour 1 cm in diameter(e.g. vitiligo, solar lentigo)A flat lesion 1 cm in diameter (e.g. port wine stain)A raised lesion 1 cm in diameter (e.g. compound naevus)A slightly raised flat-topped lesion 1 cm in diameter of surface skin(e.g. plaque psoriasis, pityriasis rosea)A solid palpable mass that is larger than 1 cm whose greater part lies beneath theskin (e.g. erythema nodosum, basal cell carcinoma)A small lesion 5 mm in diameter, fluid-containing elevation (e.g. herpes simplex,eczema herpeticum)A lesion 5 mm in diameter, fluid-containing elevation (e.g. bullous pemphigoid)A lesion 1 cm filled with pus (e.g. acne vulgaris)Loss of epidermis and dermis (e.g. ducibitus [pressure] ulcer)Loss of epidermis only (e.g. intertrigo – a rash in body folds)Linear split in skin: foot psoriasis (e.g. a heel fissure)Petechia (pin head size) (e.g. Meningococcal disease – that do not disappear whenpressure if applied) – they are purpuric lesions up to 2 mm across; Purpura(2.5 mm): red, purple or orange/brown colour due to blood leaking from bloodvessels (does not blanche under pressure) (e.g. drug eruption, allergic vasculitis);Haematoma (bruise); Telangiectasia: spider-like capillaries (e.g. due to chronictreatment with topical corticosteroids)May be due to increase in melanin pigment following epidermal inflammation(e.g. lichen planus)Depigmentation: complete loss of melanin (e.g. vitiligo)Hypopigmentation: partial melanin loss due to epidermal inflammation(e.g. eczema)Yellow (e.g. xanthelasma)

34 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsFigure 3.3 Macule. (Source: Reprinted from Graham-Brown and Burns, 2006.)Figure 3.4 Plaque. (Source: Reprinted from Graham-Brownand Burns, 2006.)Figure 3.5 Papule. (Source: Reprinted from Graham-Brownand Burns, 2006.)Figure 3.6 Vesicle. (Source: Reprinted from Graham-Brownand Burns, 2006.)Figure 3.7 Bullae. (Source: Reprinted from Graham-Brownand Burns, 2006.)

Assessment and planning care 35Figure 3.8 Nodule. (Source: Reprinted from Graham-Brown and Burns, 2006.)diseases have a classic distribution which aidsdiagnosis; this is illustrated in Figure 3.9.The process of skin assessmentand history takingSkin examinationThe visual examination of the skin requiresadequate light to ensure that the subtle changesin surface texture and colour are visible. Ideallynatural sunlight is preferred, although additionalartificial light may be used, such as a focusedlamp with a magnification facility. Before examiningfor lesions, it is necessary to assess the generalcondition of the skin. One important generalfeature is skin turgor, which provides an indicatorof hydration – by pulling the skin together ina gentle pinch-like movement and then examiningthe rapidity with which it returns to its originalposition – elasticity and moisture level. Goodsites to test the skin turgor include the back ofthe hand and between the thumb and forefinger.A delayed period over which it returns to its normalshape may be an indication of dehydration.This is distinct but related to the elasticity ofthe skin, which is also dependant on its proteinstructure.It is also necessary to assess the skin appendagessuch as nails and hair, which may providean indication of generalised disease such as psoriasisor localised pathology. For example, nailinfections (paronychia) can cause distortionand brittleness to finger and toenails and scalppsoriasis produces scalp scaling. Abnormalitiesin the appendages may also provide clues asto general health; for example clubbed nailsmay be an indication of poor nutritional statusor disease such as pulmonary or inflammatorybowel disease (Fawcett et al., 2004).Palpation is important to distinguish somesurface features such as warty, degree of scalingand the solidity of a lesion. Colour changesreflect the presence of factors such as the localmicrocirculation and inflammatory changes tothe existence or absence of certain pigments,such as melanin (e.g. as in vitiligo). Other colourchanges may be due to the presence of pigmentssuch as haemosiderin, a brown-pigmentedmaterial found in skin affected by venous isease.To determine abnormal variations in colourchange, it is often useful to examine the extremitiessuch as the nails, lips and ear lobes, whichcan provide acces sible indications of colourchange. Technological aids may also enhanceskin assessment; these are discussed later inthis chapter.History takingHistory taking is more effective if undertakensystematically. Key areas to address are outlinedin Table 3.5, with an illustration of twoframeworks, which provide simple contrastingapproaches to assessment and the use or not ofa mnemonic reminder. These can be very usefulwhen documenting a patient history, as say anurse prescriber, as they prompt areas to exploreand can aid clear reporting.History taking is of course dependant on theability of the patient to give an account oftheir medical history. A number of factors maylimit this process, such as developmental stage,sensory impairment or mental health. Carersand parents can assist in the process. Patientsmay also be affected by their social confidencein disclosing information about their skin; forexample they may be too embarrassed to discussgenital rashes or symptoms affecting sensitiveareas or the effect of a skin condition onsexual activity. Aside to the use of empathy,receptiveness and sensitivity, continuity of contactwith a health professional is desirable to

36 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsAtopic dermatitisPsoriasisAcne vulgarisLight-sensitive eruptionsSeborrhoeic dermatitisPityriasis roseaFigure 3.9 Classic lesion distribution in common skin disorders (Mackie, 2003).develop a relationship and trust. This may leadto a greater willingness for patients to disclosesensitive information. The organisation ofservices may not permit such continuity, however,where possible it should be planned toensure continuity of care; nurse-led clinics withagreed caseloads can assist this process. Consultationskills, within which history takingfalls, are a neglected aspect of dermatologycare and, indeed, they are an issue that hasbeen given very limited attention in the speciality.Effective consultation skills provide a key

Assessment and planning care 37Table 3.5 History taking frameworks.Generalbasis upon which patients may be willing todisclose information relevant to their conditionand how they are coping with it. Adequateattention needs to be given to the ability of thepractitioner to create a helping or therapeuticrelationship, including factors such as empathy,genuineness, self-awareness, ability tonegotiate care with the patient, trust buildingand warmth (Ersser, 1997). This provides akey basis for effective support and education.Consultation skills are discussed further inChapters 6 and 7.Nursing diagnosesOldcarts (mnemonic)1. Presenting complaint 1. Onset2. Previous history of2. Locationpresenting problem3. Previous medical history 3. Duration4. Drug therapy 4. Character5. Personal and social history 5. Aggravating factors6. Systems review 6. Relieving factors7. Overall appearance on 7. Timingexamination8. SeverityMedical diagnoses are but one basis uponwhich health professionals may be guided tointervene in response to a health care need.Since 1973 work has been undertaken bythe National Group for the Classificationof Nursing Diagnosis in the USA to developa system of nursing diagnoses. They refer toactual or potential health problems whichnurses by virtue of their education and experienceare capable and licensed to treat(Gordon, 1976). The benefit of this systemis that it provides a method of framingpatients’ needs for nursing in ways other thanby medical diagnosis alone, giving a partialindication of the implications for nursing interventionto aid the process of care planning.It is also a reminder that nursing care of theskin is a fundamental consideration and transcendsthe scope of dermatological disease, byhighlighting the range of causes of impairedskin integrity and skin at risk of impairment.The classification system has progressivelydeveloped taxonomy of nursing diagnosessince 1973. The development of nursing diagnosesis directed towards standardising nursingterminology; this process is now ledby the North American Nursing DiagnosisAssociation (NANDA). This process aims toachieve the following outcomes (NANDA-International, 2007):■■■■name client responses to actual or potentialhealth problems, life processes andwellness;documentation of nursing care;contribute to the development of informaticsand information standards, ensuring theinclusion of nursing terminology in electronichealth care records; andfacilitates the study of the phenomena ofconcern to nurses to improve patient care.Related developments have been led by theInternational Council of Nurses (ICN) to developthe International Classification for NursingPractice (ICNP ® ).The system used within the NANDA-I taxonomyutilises what are termed axes, whichare defined as a dimension of the humanresponse that is considered in the diagnosticprocess (NANDA-International, 2007). Theseinclude: (1) the diagnostic concept (fundamentalroot of the diagnostic statement), for exampleskin integrity, mucous membrane, bathinghygiene self-care; (2) the subject of diagnosis(individual, family and community); (3) judgement(impaired, ineffective); (4) location (e.g.skin); (5) age (infant, child, adult); (6) time(chronic, acute, intermittent); and (7) status ofdiagnosis (actual, risk, wellness, health promotion).Those nursing diagnoses directly relatedto skin care (NANDA-International, 2007) aresummarised in Table 3.6.

38 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 3.6 Nursing diagnoses directed related to skin health (NANDA-International, 2007).Nursing diagnosis Definition Defining characteristics Related or risk factorsImpaired skinintegrityAltered epidermisand/or dermisDestruction of skin layersDisruption of skin surfaceInvasion of body structuresRelated external factors: chemical substance,extremes of age, humidity, hyperthermia,hypothermia, mechanical factors (e.g. shearingforces, pressure, restraint), medications,moisture, physical immobilisation, radiation.Related internal factors: Change in fluid status,changes in pigmentation, changes in turgor,developmental factors, imbalanced nutritionalstatus, immunological deficit, impairedcirculation, impaired metabolic state, impairedsensation, skeletal prominence.Risk for impairedskin integrityAt risk for skinbeing adverselyalteredRelated risk external factors: chemicalsubstance, extremes of age, humidity,hyperthermia, hypothermia, mechanical factors,medications, moisture, physical immobilisation,radiation, secretions.Related risk internal factors: Change in fluidstatus, changes in pigmentation, changes inturgor, developmental factors, imbalanced nutritionalstatus, immunological factors, impairedcirculation, impaired metabolic state, impairedsensation, skeletal prominence,medication, psychogenic factors.Of course, given the range of nursing diagnoses,generic needs for nursing may be manifestedin a person with a skin health problem. Forexample, in supporting a child with severeatopic eczema, there may also be considerationsregarding the following nursing diagnosticareas: for example, parenting, parental–childattachment, parental role conflict, caregiver rolestrain, infant feeding pattern, self-esteem, socialisolation, anxiety and sleep deprivation – toname only some possible dimensions. Considerationof nursing diagnoses within a skin/dermatologicalnursing context may highlight abroader range of needs for nursing that mayarise from a pathological problem (dermatologicaldisease or other condition impacting on theskin) for which there may be a wide range ofhuman responses and scope for nursing interventionthrough care planning.Assessment toolsA variety of tools may be used to aid moreeffective assessment of the condition of the skinand patients responses to it; this includes physicalassessment of lesions and clinical severityand psychological assessment. The former isdiscussed here and the latter (mainly diseaserelatedquality of life measures) is examined inChapter 6. Tools that examine the impact onthe family, for example The Dermatitis FamilyImpact Questionnaire (Lawson et al., 1998),reflect the wider psychosocial impact of chronicskin disease.Severity toolsTools to assess disease severity are importantboth in skin assessment and the evaluation

Assessment and planning care 39of treatment effectiveness. Developed tools arenow widely used for common chronic inflammatoryskin conditions such as eczema andpsoriasis. It is important to try to use validand reliable standardised tools to ensure rigorousmeasurement. Valid tools measure whatthey are intended to measure and reliabletools ensure that the measure gained underthe same conditions (such as degree of severity)is derived consistently. In addition, it isnecessary to practise and develop skill in usingsome tools, for example the assessment of aPASI score to ensure reliability of assessmentacross observers and by the same clinician,under the similar clinical conditions. Detailsof commonly accepted valid tools are outlinedin Table 3.7; copies of the PASI and SCORADtools are reproduced in the Appendices 1 and2 respectively. Acne severity is a core complexarea for scoring; a recent review paper identifiedas many as 25 scales for the global assessmentof acne, which indicates the lack ofconsensus on the issue and a gold standard(Lehmann et al., 2002).Table 3.7 Common chronic skin severity tools.Tool Disease parameters Source materialPASI: Psoriasis AreaSeverity IndexSCORAD IndexThis is the most widely used tool to assesspsoriasis disease severity. The estimate is based onthe percentage area affected of four body regions –head, trunk, upper and lower extremities – whichis given a value of 0 (no psoriasis) to 6 (90%present). The following clinical parameters arealso used within a 0–4 scale – ranging from nosymptoms to very marked symptoms, again for thedifferent body areas.1. Erythema (redness)2. Induration (thickness)3. Scaling (flaking or desquamation)4. BSA affectedA formula is used to calculate the PASI score.PASI scores: 1–10: mild to moderate; 11–20: moderateto severe and 20 severe; the theoretical maximumscore being 72 (see Appendix 1).The European Task Force on Atopic Dermatitishas developed the SCORAD (SCORing AD)index to create a consensus on assessment methodsfor AD.1. Objective items:a. Extent: Apply the rule of nines (see BSA givenearlier) graded 0–100 on the front/back drawing.b. Intensity: consists of 6 items – erythema, oedema,excoriations, lichenification, oozing/crustsand dryness. Each item can be graded on ascale 0–3.Ashcroft et al. (1999); Ramsay andLawrence (1991); Exum et al. (1996)Kunz et al. (1997); Oranje et al. (2007);http://adserver.sante.univ-nantes.fr/Scorad.html(continued)

40 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 3.7 (continued)Tool Disease parameters Source material(Revised) Leeds AcneScore (1998)2. Subjective items include:a. Daily pruritusb. SleeplessnessBoth subjective items can be graded on a 10-cmvisual analogue scale.SCORAD scores: The maximum SCORADscore is 103. The maximum subjective score is 20.The maximum objective SCORAD score is 83(plus an additional 10 bonus points). Bonus pointsare given for severe disfiguring eczema (on faceand hands). Mild 25, mild to moderate 25–50and severe 50. There are criticisms of the toolincluding that it can be time consuming inclinical practice and that it has a bias for use withchildren (see Appendix 2).Pictorial grading system – a photographicassessment system with severity criteria as:1. Extent of inflammation2. Range and size of inflamed lesions3. Associated erythemaOverall assessment is based predominantly onthe number of inflamed lesions and theirinflammatory intensity.The published photos demonstrate the extensiverange of facial acne grades of increasing severityfrom 1 (least severe) to 12 (most severe).Different parts of the body are used, such as face,chest and back. The system is not suitable forthose with non-inflamed acne or with highlylocalised acne or those with sporadic andasymmetrical large nodular lesions. Most patientshave a combination of inflamed and non-inflamedlesions; the grading system focuses on inflamedlesions.O’Brien et al. (1998) which builds onBurke and Cunliffe (1984)Disease-related quality of lifeThe quality of life impact of skin conditionscan be considerable. This factor needs to betaken into account when assessing patient’sneed and their response to treatment. The psychologicaland social impact of chronic skinconditions has been found to be of significance(Rapp et al., 1999), especially when comparedto other medical diseases. Irrespective ofdisease severity, the quality of life impact ofmany chronic skin diseases can be major. Assuch, it is necessary to assess disease-relatedquality of life effectively using valid tools(Chen, 2007). Due to the significance of thisarea, it is addressed in detail in Chapter 6, inan examination of the psychological and socialimpact of skin disease and treatment.

Assessment and planning care 41Technological aidsA range of technological and other diagnosticaids are available. Those listed below are typicallyused in clinical practice.DermatoscopyIt is also known as dermoscopy. This techniquerefers to the examination of the skinusing skin surface microscopy. A dermatoscope(or dermoscope) is a device used for theexamination of cutaneous lesions. It has ahand-held device with a magnifier with eithercross-polarized or non-polarized light or a liquidmedium of oil between the instrument andthe skin to illuminate a lesion without glarefrom reflected light. The device is useful forexamining pigmented lesions such as naeviand potential malignant lesions such asmelanomas. There are specific dermoscopicpatterns that aid in the diagnosis of the followingpigmented skin lesions such as melanomas,moles (benign melanocytic naevi),freckles (lentigos), atypical naevi, seborrhoeickeratosis and pigmented basal cell carcinomas.Evidence suggests that while dermatoscopyimproves the diagnostic accuracy formelanoma compared to the unaided eye, itrequires sufficient training and is not recommendedfor untrained users (Kittler et al.,2002).Wood’s lightWood’s light is a lamp emitting long-waveUVA used to examine pigmentary changesin the skin and fluorescent infections. Thisultraviolet light source is used to screenfor the fungal infection, tinea capitis; however,only certain species fluoresce (green)(Microsporum canis and Μ. audouinii). Otheruses include highlighting patches of pityriasisversicolor caused by Pityrosorum yeast whichfluoresces yellow; erythrasma, a bacterialinfection affecting the skin folds, caused byCorynebacterium fluoresces green and vitiligowhich delineates patches which can be otherwisemissed.MycologyMycology can be used to identify superficialfungal infections including yeasts (candidiasis andpityriasis versicolor), dermatophytes (ringworm/tinea – tinea unguium) or moulds (e.g. Scopulariopsis)using scales scraped from the edge of ascaly lesion, nails using a blunt instrument suchas blunt scalpel blade or blunt edge of a stitchcutter. Scrapings of scale should be taken fromthe leading edge of the rash (as this is whereactive spores are most likely to be found)after the skin has been cleaned with alcohol, suchas surgical spirit or 70% alcohol. This minimisescontamination and is an aid to microscopy ifgreasy ointments or powders have been applied.Samples can be collected on kits providing blackpaper envelopes (e.g. Dermapak), which can beeasily transferred to the lab. It is essential to havean adequate sample and provide full clinicaldetails if the test is to be successful; whilst the precisequantity is difficult to quantify, as a generalrule it is worth including as much material as possibleso that full laboratory investigations can becarried out. It is always useful to have enoughskin or nail to repeat the culture if necessary.Sample the discoloured, dystrophic or brittle partsof the nail only, gently digging as far back as possiblefrom the distal part of the nail. For dermatophyteinfections, samples should be taken fromthe distal nail and from debris under the nail (subungualdebris). For superficial onychomycosis, thescraping should be from the nail surface and forCandida infections (e.g. a chronic paronychia) aswab should be taken from the proximal nailfold.Hair can be plucked from the affected areawith forceps; the infected hairs come out easily.The scalp may then be scraped with a blunt scalpel.Preferably, the sample should include hairstubs, the contents of plugged follicles and skinscales. Hair cut with a scissors is unsatisfactoryas the focus of infection is usually below or nearthe surface of the scalp.BiopsyWhere diagnosis is unclear but there is a differentialdiagnosis, an ellipse of skin can be taken

42 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsthrough the edge of a lesion. There is a need toensure that normal and abnormal skin (epidermis,dermis and fat) are included in the sample.Incisional, excisional and punch biopsies maybe taken. Punch biopsies provide only limitedsample, which may be inadequate for histologicalexamination. Typically, the punch biopsyincludes the full thickness skin and subcutaneousfat in the diagnosis of skin diseases.A round-shaped knife ranging in size from1–8 mm is taken. The smaller size punch (1 mm)helps to minimise bleeding and assists inthe vhealing of the wound without stitching. Todiagnose many inflammatory skin conditions,the common punch size used is the 3.5- or 4-mmpunch.BacteriologyThe source of bacteria can be determined byswabbing a fluid sample pustules, vesicles, erosionsand ulcers.Patch testingIt is a technique used to diagnose contact allergicdermatitis based on the principle of delayedhypersensitivity (an immune response). Evidenceof contact allergy is derived from a patient history(such as occupation), clinical examinationand patch testing. The aim of the patch test is toascertain allergic contact dermatitis by aiming toreproduce a rash on a small controlled area ofskin using standardised batches or trays of allergens(termed batteries) or those commonly usedat work or home. Standard batteries of substances(now often pre-prepared) are comprisedof patches made up of Finn chambers andhypoallergenic tape that are applied to thepatient’s upper back; they should incorporateprobable (standard battery) and possible substances(e.g. occupational specific) based on theirhistory. The results are read at two stages,48 hours and 72 hours; this timing sequence isrelated to the type IV hypersensitivity reaction,which is a delayed immune response. Care isneeded to avoid misleading results from contactirritants that are distinct from hypersensitivityreactions. Differentiation is not always easy,however, the use of standard allergens andrigorous technique are required. A key referencesource is a book on contact and occupationaldermatology by Marks et al. (2002). Furtherdetails and sources are given in Chapter 9.Planning careA considerable amount of data is collectedthrough the process of history taking and examination;however, the key outcome needs tobe an informed clinical decision regarding thepatient’s need for nursing, medical support anda plan for intervention. Clinical judgements aremade not only on information gathering, bothclinical and about the person and their socialcontext, but also account needs to be taken ofother factors, such as the patient’s own beliefsand priorities and the resources available tointervene effectively. Chapter 7 provides detailsof how to help patients to participate in decisionregarding their treatment regimen and how touse this optimally. Here brief reference is madeto the knowledge that informs clinical judgementsand a brief outline of the key theoriesthat describe and explain how clinical decisionsare made. These are intended to raise awarenessof the complexity of the decision-making processand what elements need to be consideredwhen trying to formulate effective clinical judgements.Finally, the section briefly highlightsissues of prioritisation in dermatology care andwhich ‘red flag’ skin conditions require a rapidresponse to minimise patient risk.Knowledge sources informingclinical judgementClinical judgements underpinning care planningwill draw on the different types of knowledgeavailable. This includes empirical, aesthetic,ethical, personal and practical (Titchen andErsser, 2001).Empirical knowledge refers to scientific, technicalor factual knowledge. This embraces researchevidence including that from a systematic reviewto inform treatment choices or the selection of

Assessment and planning care 43more effective methods to provide patient education.It also includes theoretical knowledge, suchas those regarding the pharmacological action ofdrugs, which may influence judgements aboutthe effective drug administration and, for example,ways to improve the absorption of a topicalmedication. Empirical knowledge is fundamentalto the assessment process in which formalisedknowledge has been categorised to aid systematicclinical assessment of the skin. Such knowledgeprovides the rational basis for explaining diseaseand its progression through, say, genetic, immunologicalor wider biological or pathological principles.Similarly, the behavioural sciences mayexplain social withdrawal due to poor self-esteem,how stress and anxiety may provoke a flare of achronic skin condition or explain the inability of aperson to cope with their self-management regime.Personal knowledge or knowledge of self hasbeen highlighted earlier in the discussion of effectiveconsultation skills. Awareness is required ofone’s own individual perceptions, prejudices andbias shaped by own professional and personalhistory. These factors can lead to precipitantjudgements on assessment and patient care.Aesthetic knowledge refers to that knowledgethat relies on an individualised appraisal of aunique situation – searching for patterns in thesituation. This is based on how experienced cliniciansformulate intuitive hunches on clinicalsituations and know how to mediate betweenempirical, practical and personal knowledgein the complex world of professional practice,using all the senses (Eisner, 1985; Titchen andErsser, 2001). Experience can of course providea template to aid recognition of similar assessmentor treatment situations (such as the earlyrecognition of infected atopic eczema) but thiscan also close off options for consideration. Inthe dermatological field, with the considerablenumber of dermatological diagnoses, it is probablethat clinicians will typically gravitate to thecommon diagnostic groupings discussed earlierin this chapter. Intuitive impressions can beverified against empirical knowledge to betterinform and explain clinical judgements.Practical knowledge or ‘know how’ embracesskills such as those of a consultation, providingeffective dressing or bandaging techniques. Hereit is important to assess patient and carer orparental skills to manage their condition or thatof their family member. One example wouldinvolve assessing if the patient is correctly utilisingthe appropriate topical medications andfinding useful ways of supporting the person witha skin condition. Specifically, it is often necessaryto assess both one’s own and the patient’s insightinto their self-management and which knowledgeand skills need to be developed.Concepts and theories of clinicaldecision-makingA key concept in decision-making is that of heuristics;these are rules of thumb or strategies thatassist in reasoning (Fonteyn and Ritter, 2008)and assist the processing of large amounts ofdata. These devices are important to clinicians,but are often taken for granted by those withexperience. Familiarity with heuristics can enablehealth professionals to gain awareness of howthese factors may influence their clinical judgements.Short cuts are developed with the processingof irrelevant data when formulating clinicaljudgements. Much of the time clinicians employthose heuristics most readily available in theirmind, although these can introduce bias; forexample, based on case examples from clinicalexperience which may or may not be relevant,with the individual being either representative ornot of the cases typically seen. This may apply toinitial clinical assessments or the evaluation ofdermatological treatments. Anchoring heuristicsare cognitive reference points or anchors, whichcan guide decisions. In dermatology, such devicesare important in formulating assessment or diagnosticjudgements about lesions. The classificationsystems described earlier in this chapterprovide such heuristic aids to the pattern recognitionof lesions and rashes.One theory of reasoning, which gives an insightinto the explanation of how clinical judgementsare formed, is the Hypothetico-deductive theory.This is based on the work of Elstein et al. (1978),with the key processes being cue acquisition (suchas a raised erythematous scaly plaque), hypothesisgeneration and cue interpretation (chronic plaque

44 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalspsoriasis) and hypothesis evaluation – that is,reviewing how well this fits with the clinical examinationof the individual (Carnevali and Thomas,1993). Such work is recognised to have relevanceto nursing (Tanner et al., 1987).Dermatological ‘red flag’ conditionsNurses working in any clinical setting require theskills to identify which skin conditions requireimmediate emergency referral or a response byother practitioners with appropriate advancepractice skills and the relevant scope of practice.Some of the key ‘red flag’ conditions, whichrequire prompt medical referral, are listed below:■■■■■■■■Viral rashes if systemically unwellAny rash that is purpuric in natureAny rash associated with either temperature,multi-lymphadenitis headaches or stiffnessof neckInsect bites or stings that have a significantarea of cellulitis or signs of vascular trackingIf the swelling from insect bites or stingscompromises the patient’s airway (to theface or neck)Any sign of pharyngeal/facial swelling, difficultyin breathing or anaphylactic reactionShingles: herpes zosterRaised skin lesions that show signs of infectionAcute dermatological situations which require arapid treatment response include adverse drugreactions (e.g. toxic epidermal necrosis), herpessimplex affecting the eye, erythrodermic psoriasis– which is a very severe skin condition wherethere is a risk of shock and death and blisteringdisorders (e.g. epidermolysis bullosa) and wherethere is a significant disruption to the skin barrier(see Chapter 13).InterventionA key element of the care planning process isto formulate decisions regarding the appropriatenessof treatment. As well as workingwithin multi-professional teams and contributingto such decisions, nurses will be makingsome treatment choices in a growing numberof countries with the appropriate nurse prescribingqualification or professional preparation.Each chapter, within the specific clinicalarea or condition discussed, will address issuesof treatment, but as an overview, a summary isgiven here in Table 3.8 categorising the maintreatment regimens commonly used within thedermatological field.Treatment protocols and guidelines tend tostage therapy in accordance with the severityof disease and the patients response over time;assessment of the patient’s response at eachstage is required. For example, in the case ofpsoriasis, patients are likely to commence withtopical therapy and be supported in self-managementwherever possible. This may proceedto phototherapy or a combination of lighttherapy. For those with more severe disease,they may progress to systemic/oral therapy andthereafter possibly onto biological therapy.Table 3.8 Categories of common dermatologicaltreatments.1. Pharmacologicala. Topicals: emollient (focus Chapter 5), tars,dithranol, topical immune-modulators, steroids,vitamin D analogues, retinoids, keratolytic agents,antibiotics, antifungal and antiviral drugs.b. Systemic: immunosuppressive agents/biological therapies, antibiotics and antifungals,retinoids, steroids, antiviral agents and antihistamines.2. Phototherapy: UV, including narrow band (A and B),photodynamic therapy3. Surgical, cryotherapy, laser: Skin biopsy (punch, shave,incisional biopsy and excision), curettage and cautery,skin grafting, Mohs microscopically controlled excisionand cryotherapy (liquid nitrogen). Laser therapy:quasi-continuous wave and pulsed.4. Psychological and educational: (details given inChapter 7)5. Iontophoresis (for hyperhidrosis, excessive sweating)6. Bandages and dressings

Assessment and planning care 45Such progression would require assessment notonly in changes in disease severity but alsoperhaps in disease-related quality of life andthe patent’s self-management ability, in relationto topical therapy.Phototherapy assessment requires a systematicassessment of the patient’s skin type andprevious history of UV exposure and responseto inform the assessment of a suitable doseregimen. The response to phototherapy needsto be assessed, both in terms of the diseaseseverity and adverse effects, such as erythemaand dryness of skin. The individual’s skinresponse to UVB depends on their skin phototype,prior exposure to sunlight or othersource of UV and the presence of photosensitivity.Typically for UVB therapy, the minimalerythema dose (MED) is measured; these varywidely within each skin type. A template isapplied to a non-exposed area, such as thevolar surface of the arm; test sites are outlinedwith a skin marker so that they can be identified.The response is measured 24 h later. TheMED is the lowest dose that produces pinkerythema with distinct borders.The use of systemic therapy requires a complexmonitoring regimen not only to determinesuitability for treatment (to meet guidelinerequirements and patient protection, e.g. pregnancy)to monitor therapeutic effect, but alsoto assess for adverse effects in order to managerisk from cytotoxic agents. An increasingnumber of nurses are involved in monitoringpatients on such therapy. For example, methotrexateuse requires liver and renal monitoring,pulmonary review and a full bloodcount (Wakelin, 2002). Biologic monitoringis complex. A growing number of nurses areplaying a key role in the monitoring of bothtreatments, shorter- and longer-term response,especially to pick up any adverse effects.Short-term monitoring will involve monitoringfor infusion reactions with TNF inhibitors(e.g. Infliximab) such as hypotension,dyspnoea and urticaria (anaphylaxis). Adverseeffects include headaches, gastrointestinalupsets and chills. Longer-term monitoringwill involve the use of PASI and a review ofrisk such as infection (hepatitis B reactivation,tuberculosis, hepatotoxicity and malignancy).For further details see Chapter 8.EvaluationStructured assessment tools may be used withinclinical practice as well as in research evaluation.Specifically they are helpful as treatmentor nursing care evaluation tools to monitor theprogress of therapy or intervention. One suchexample of evaluation is the use of the PASIscore. A 75% improvement (PASI75) is wellestablished as a clinically meaningful endpointfor trials but PASI50 (50% improvement) isalso considered by some to be a clinically validendpoint. Common clinical guidelines, such asthose for biological therapy for psoriasis, nowincorporate PASI parameters to specify the levelof disease severity required to permit treatment(Smith et al., 2005; National Institute forHealth and Clinical Excellence [NICE], 2008).Consideration is required of the timing of theevaluation measurement; for example, if applyingtar, there will be a slow response to treatmentover a period of weeks. Both healthprofessionals and patients need to give recognitionof the duration over which interventionsare typically effective, since patients may abandontreatments, which they believe are notworking. Research evidence suggests patientsmay use timing of the treatment effect as a criterionfor judging the effectiveness of their therapyin psoriasis care (Ersser et al., 2002).Clinicians need to take account of the criteriathat patients use in evaluating treatment regimens.Premature evaluative measurements mayprovide a misleading picture of the effectivenessof a particular therapy; therefore, there is aneed to consider the evidence underlying theduration of treatments. Practitioners also needto be mindful of the role standardised tools play(see e.g. Table 3.7) as measures at key endpointsin the research evaluation of existing or newtherapies; this will be useful when interpretingresearch results within clinical papers andunderstanding the way in which evidence mayinform the clinical guidelines used by nurses.

46 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsConclusionThis chapter has highlighted the significance ofthe assessment and planning process within dermatologicalcare. Emphasis has been placed noton medical diagnosis, albeit important, butrather on the conceptualisation, description andcategorisation of normal skin and then bycontrast diseased skin through reference to thelesions and rashes commonly seen, to aid communicationbetween health professionals andthe patient. The process of assessment has beenoutlined and an illustration of the range of questionnaireand technological tools use to collectdata. Then we have outlined the importance ofeffectively using data collected to inform clinicaldecisions and the planning and evaluation process.Finally, an outline has been given of commondermatological interventions used tomanage and treating skin conditions and theirsequelae. This chapter has set out the nature ofdermatological and health-related needs andhow these are assessed and subsequent careplanned; these issues are then illustrated anddiscussed throughout the book, mainly focusingon common dermatological problems and theireffective management.ReferencesAlaluf, S., D. Atkins et al. (2002). Ethnicvariation in melanin content and compositionin photoexposed and photoprotected humanskin. Pigment Cell Research, 15(2): 112–118.Ashcroft, D.M., A. Li Wan Po et al. (1999).Clinical measures of disease severity andoutcome in psoriasis: A critical appraisal oftheir quality. British Journal of Dermatology,141: 185–191.Ashton, R. and B. Leppard (2005). DifferentialDiagnosis in Dermatology. Abingdon, Oxon:Radcliffe Publishing Ltd.Burke, B.M. and W.J. Cunliffe (1984). Theassessment of acne vulgaris – the Leedstechnique. British Journal of Dermatology,111(1): 83–92.Carnevali, D.L. and M.D. Thomas (1993).Diagnostic Reasoning and TreatmentDecision Making in Nursing. Hagerstown,Maryland: Lippincott Williams & Wilkins.Chen, S.C. (2007). Dermatology quality of lifeinstruments: Sorting out the quagmire. Journalof Investigative Dermatology, 127: 2695–2696.Eisner, E. (1985). The Art of EducationalEvaluation: A Personal View. London:Flamer Press.Elstein, A.S., L.S. Shulman et al. (1978).Medical Problem Solving: An Analysis ofClinical Reasoning. Cambridge, MA: HarvardUniversity Press.Ersser, S. (1997). Nursing as a TherapeuticActivity: An Ethnography. Aldershot:Avebury Press.Ersser, S.J., H. Surridge et al. (2002). Whatcriteria do patients use when judging theeffectiveness of psoriasis management?Journal of Evaluation in Clinical Practice,8(4): 367–376.Exum, M.L., S.R. Rapp et al. (1996).Measuring severity of psoriasis. Journal ofDermatological Treatments, 7: 119–124.Fawcett, R.S., S. Linford et al. (2004). Nailabnormalities: clues to systemic disease.American Family Physician, 69(6):1417–1424.Fonteyn, M.E. and B.J. Ritter (2008).Clinical reasoning. In: Higgs, J., Jones,M.A., Loftus, S., Christensen, N. (Eds),Nursing Clinical Reasoning in the HealthProfessions. Amsterdam: Elsevier ButterworthHeinemann.Gawkrodger, D. (1998). Racial influences onskin disease. In: Burns, D.A., Breathnach,S., Cox, N., Griffiths, C. (Eds), Rook’sTextbook of Dermatology. Oxford:Blackwell Science Ltd.Gordon, M. (1976). Nursing diagnoses and thediagnostic process. The American Journal ofNursing, 76(8): 1298–1300.Graham-Brown, R. and T. Burns (2006).Lecture Notes: Dermatology (9th edition).Oxford: Blackwell Science.Johannsen, L.L. (1998). Skin assessment anddiagnostic techniques. In: Hill. M.J. (Ed.),Dermatologic Nursing Essentials: A Core

Assessment and planning care 47Curriculum, pp. 17–31. Pitman, New Jersey:Anthony J. Jannetti, Inc.Kittler, H., H. Pehamberger et al. (2002).Diagnostic accuracy of dermoscopy. TheLancet Oncology, 3(3): 159–165.Kunz, B., A.P. Oranje et al. (1997). Clinicalvalidation and guidelines for the SCORADindex: Consensus report of the European TaskForce on Atopic Dermatitis. Dermatology,195(1): 10–19.Lawrence, C.M. and N.H. Cox (2002). PhysicalSigns in Dermatology. London: Mosby.Lawson, V., M.S. Lewis-Jones et al. (1998). Thefamily impact of childhood atopic dermatitis:The Dermatitis Family Impact Questionnaire.British Journal of Dermatology, 138(1):107–113.Leach, E.E., P.B. McClelland et al. (1996).Basic principles of photobiology andphotochemistry for nurse phototherapistsand phototechnicians. Dermatology Nursing,8(4): 235–241.Lehmann, H., K. Robinson et al. (2002). Acnetherapy: A methodologic review. Journal ofthe American Academy of Dermatology, 47:231–240.Mackie, R.M. (2003). Clinical Dermatology(5th edition). Oxford: Oxford University Press.Marks, J.G., V.A. DeLeo et al. (2002). Contactand Occupational Dermatology (3rd edition).London: Mosby.NANDA-International (2007). NursingDiagnoses: Definitions and Classification2007–2008. Philadelphia: NANDAInternational.National Institute for Health and ClinicalExcellence (NICE) (2008). Infliximab for theTreatment of Adults with Psoriasis. London:NICE.O’Brien, S.C., J.B. Lewis et al. (1998). TheLeeds revised acne grading system. Journal ofDermatological Treatments, 9(4): 215–220.Oranje, A., E. Glazenburg et al. (2007). Practicalissues on interpretation of scoring atopicdermatitis: The SCORAD index, objectiveSCORAD and the three-item severity score.British Journal of Dermatology, 157(4):645–648.Ramsay, B. and C.M. Lawrence (1991).Measurement of involved surface area inpatients with psoriasis. British Journal ofDermatology, 128: 69–74.Rapp, S.R., S.R. Feldman, M.L. Exum, A.B.Fleischer Jr, D.M. Reboussin (1999). Psoriasiscauses as much disability as other majormedical diseases. Journal of the AmericanAcademy of Dermatology, 41: 401–407.Smith, C.H., A.V. Anstey et al. (2005). BritishAssociation of Dermatologists guidelines foruse of biological interventions in psoriasis2005. British Journal of Dermatology,153(3): 486–497.Tanner, C.A., K.P. Padrick et al. (1987).Diagnostic reasoning strategies of nurses andnursing students. Nursing Research 36(6):358–363.Titchen, A. and S.J. Ersser (2001). The natureof professional craft knowledge. In: Higgs,J. Titchen, A. (Eds), Practice Knowledge andExpertise in the Health Professions. Oxford:Butterworth-Heinemann.Tortora, G. and B. Derrickson (2006). Principlesof Anatomy and Physiology (11th edition).New Jersey: John Wiley and Sons Inc.Wakelin, S.H. (2002). Systemic Drug Treatmentin Dermatology. London: Manson PublishingLtd.Williams, H.C. (1997). Dermatology: HealthCare Needs Assessment. Oxford: RadcliffeMedical Press.


Protecting the skin andpreventing breakdown4Steven J. ErsserIntroductionNurses spend considerable time protecting theskin and preventing its deterioration.The intricately designed structure and functionof the skin protects the body from a rangeof external physical and biological threats.Although barrier function is localised to thestratum corneum, protection is one of the primaryfunctions of the skin as an organ. Thisincludes defence against exposure to chemicals,irradiation, traumatic insult and microbiologicalthreats such as bacteria, viruses and fungi.Chapter 2 has outlined the details of the skin’sprotective structural features and protectivebiological features. This chapter considers theprocesses involved in vulnerable skin and outlinesthe key factors associated with disruptionof the skin barrier due to disease, biology andthe impact of external physical factors, includingtreatment effects. It also highlights specificinterventions for promoting skin barrier function,maintaining its integrity and preventingbarrier disruption and breakdown.The concept of skin vulnerabilityThe vulnerability of the skin reflects the susceptibilityof the skin barrier’s integrity and healthdue to the effects of a wide range of influencingfactors, not only biological but also psychologicaland social. It therefore reflects a broaderconcept of health needs assessment rather thansimply dermatological disease; this provides awider basis for understanding the wide rangeof skin care needs met by health professionals.Skin vulnerability may result from difficultiessuch as the lack of self-care managementskills, the influence of developmental factors(age and immaturity), stress and anxiety andthe impact of socio-economic factors such aspoverty and environmental factors, includingclimatic impact. The interplay of these factorscan disrupt barrier functions of the skin, leadingto breakdown, disease and further physical,psychological and social effects. The concept ofskin vulnerability directly relates to that of nursingdiagnosis (Chapter 3) that highlights thescope for nursing intervention.

50 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsWhat causes skin breakdown?In this section, we examine some of the keypathological and physical factors that maydirectly lead to skin breakdown. These includethe inflammatory response, pressure effects,poor perfusion, the effects of washing practiceson the skin and those arising from urinaryincontinence.InflammationInflammation is the body’s response to injury,which may be acute or chronic. Acute inflammationis the immediate defensive reaction of tissueto any injury, which may be caused by infection,chemicals or physical agents and involvespain, heat, redness and swelling (Martin andMcFerran, 2008). It has also been defined as aset of local cellular and vascular responses totissue damage or infection, which accelerates thedestruction and phagocytic removal of invadingorganisms and debris (McGeown, 2002). Thefundamental inflammatory process occurs inmany dermatological conditions, where there isthe key indicator of redness or erythema overthe area due to blood flow.Inflammation has a protective function byhelping to eliminate the cause of tissue damage,removing dead cells and maintaining stabilitywithin the internal physiological environment. Inthe case of a wound there may be also swelling;heat, pain and loss of function, with injury leadingto vasoconstriction of vessels at the marginsof the wound. Hyperaemia then occurs in whichthe blood vessels within the area dilate, increasinglocal blood flow and redness. The damagedcells release chemical mediators such as bradykinin,histamine and serotonin, which increasecapillary permeability, allowing the leakage offluid into the tissues, causing oedema and possiblypain. The loss of plasma proteins exerts anosmotic effect in the tissues slowing down theflow of blood in the dilated vessels. As part ofthe protective response, white blood cells, particularlyneutrophils, migrate from the vessels to theinflamed area attracted by the chemicals releasedby injured tissue cells and microorganisms.Antibodies within the exudate trigger neutrophilsand macrophages phagocytosing thesecells. Eventually fibrin builds up, with theinflamed area becoming sealed by the networkof fibrin threads, localising the damaged tissues(McGeown, 2002; Hinchliff et al., 2005).Inflammation is a common pathologicalprocess within dermatological disease. This isevident in many of the lesions and rashes, asoutlined in Chapter 3. The inflammatory dermatosesinclude common skin disease such as psoriasisand eczema; these are illustrated withinChapters 8 and 9.Dry skinDry skin or xerosis is a common feature of skindisease, which reflects disruption to the skin barrierand the undue loss of moisture from the skintissue. A list of common disease- or treatmentrelatedcauses of dry skin is given below:■■■■■■Atopic eczemaIchthyoses (inherited)PsoriasisLeprosyDrug induced (e.g. clofazimine given forleprosy)Phototherapy induced (e.g. PUVA therapy)Disease processes lead to water loss becausepathological or pharmacological effects willoften disrupt the structure and processesthat maintain the skin barrier integrity andretaining water within the dermis leading totransepidermal water loss (TEWL) and dehydrationof the skin. Skin dryness may greatlyvary in severity. It may occur without diseasethrough factors such as over-washing of theskin or exposure to harsh climatic conditions.Because of severe environmental conditions orthe presence of dermatological disease suchas eczema or ichthyosis, the skin barrier willbe impaired which will lead to dehydrationof the skin by evaporation, develops crackingand fissuring of the skin, which will in turnfurther impair the integrity and effectivenessof the skin barrier.

Protecting the skin and preventing breakdown 51Other external and intrinsic factors that causedry skin and affect the skin barrier includes thefollowing:■■■■Unsuitable skin hygiene, such as excessivewashing, use of soap, water saturation dueto undue soaking of the skin, rough skindrying technique, excessive routine skinwashing and lack of moisturisation;Environmental factors both at home andexternally including excessive UV exposure,centrally heated low humidity environmentsand use of air conditioning;Poor nutrition and inadequate hydration;Changes related to the maturity of the skin,with the risk of water loss from an immatureinfant’s skin – with its high surface area tovolume ratio and water loss from aged skindue to age-related changes in skin structure,such as the loss of sebum (see Chapter 2).Poor perfusion and disruptedmicrocirculation of the skinPoor perfusion of blood to the skin may resultfrom a range of pathological factors such ascardiovascular disease due to arteriosclerosisand heart failure, the effects of oedema andtrauma and the occlusion of blood vessels dueto pressure. For critically ill patients, the circulatoryfailure associated with hypovolemia andlow cardiac output is associated with redistributionof blood flow caused by increased vasoconstriction,which leads to a decrease in skinperfusion. Therefore, the degree of skin perfusionmay reflect the adequacy of global bloodflow. The clinical signs of poor skin perfusioninclude evidence of cold, pale, clammy andmottled skin.Oedema and lymphoedemaOedema and lymphoedema may disrupt themicrocirculation thereby impairing the skin barrier.Oedema may be caused by heart failure,nephrosis, inflammation, venous hypertension,lymphatic impairment due to cancer and relatedtherapy, filariasis, immobility and congenitaland traumatic factors (Ryan, 2008) Chronicoedema is a common problem with at least100,000 patients affected in the UK alone; it isalso poorly identified by health professionals(Moffatt et al., 2003). Chronic oedema is tissueswelling that remains over 3 months, which isnot relieved by elevation or diuretics. A usefulindicator is a positive Stemmer’s sign – the inabilityto pinch fold of skin at the base of secondtoe due to thickening. As a consequence thismay impair the skin barrier leading to associatedskin changes: these may include the following:dry flaky skin; hyperkeratosis – hard, scaly skin,development of skin creases around the toes andankles; increased subcutaneous tissue; fibrosisof the tissue and lymphangioma, where thereare blister-like bulging of dilated lymphatic vesselspapillomatosis, with a cobblestone effect onthe skin due to lymphangioma and fibrosis. Theskin may be further impaired due to the greatersubsequent risk of infection.Lymphoedema is an accumulation of lymphin the tissues, producing swelling; the legs aremost often affected, but arms and genitaliamay also be involved. It may be due to a congenitalabnormality of the lymphatic vessels, asin Milroy’s disease, congenital lymphoedema ofthe legs or result from obstruction (Martin andMcFerran, 2008).Lymphoedema for clinical problems otherthan cancer treatment is much more prevalentthan generally perceived, although the resourcesare mainly cancer service based.Skin problems seen in lymphoedema includethe following: (1) hyperkeratosis (an over proliferationof the keratin layer, (2) folliculitis, (3) fungalinfections, (4) ulceration, (5) venous eczema,(6) contact dermatitis, (7) lymphangiectasia (softfluid-filled projections caused by the dilatation oflymphatic vessels), (8) papillomatosis (firm raisedprojections of skin due to raised lymphatic vesselsand fibrosis), (9) lymphorrhoea (the leakageof lymph from the skin surface) and (10) cellulitis/erysipelas.PressureAn efficient skin barrier is dependent on anadequate perfusion of blood. The primary effectof pressure on the skin is to occlude capillaries

52 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsand thereby disrupt blood flow and the carriageof nutrients to the tissues. Pressure effects mayarise due to immobility, commonly bed rest orspending prolonged periods in a chair. Pressureeffects on the skin have been the subject ofextensive research.The European Pressure Ulcer Advisory Panel(EPUAP) website defines a pressure ulcer asan area of localised damage to the skin andunderlying tissue caused by pressure or shearand/or a combination of these (EPUAP, 2008).Nixon (2001) outlines the distinction betweenthe aetiology and pathology of pressure ulcers.Autoregulatory systems that affect blood flowduring and following pressure effects are highlyrelevant to pressure ulcer aetiology. Theseinclude the raising of capillary pressure to maintainflow, intermittent flow at subcritical pressuresand response to repetitive loading and thereactive hyperaemic response following partialor full occlusion. Such occlusion leads to anoxiaand a related accumulation of metabolites.Following pressure release, the large and rapidincrease in blood flow through the deprived tissuesis termed reactive hyperaemia. Key mechanismsinclude those that are myogenic andmetabolic, related to the metabolite release fromeither anoxic tissues or the lack of oxygen. Thedegree and duration of the hyperaemic responseis related to the duration of occlusion (Walmsleyand Wiles, 1990) and factors such as age (withthe elderly being very vulnerable), smoking, vascularor related disease (e.g. diabetes) and conditionssuch as end-stage renal failure and spinalcord injury. Another important factor is therepetitive loading of pressure, which operatesvia an active vasomotor response mechanism(Bader, 1990).The different types of pressure ulcer includethose related to epidermal or dermal necrosis,deep pressure ulcers with necrosis occurringwithin the subcutaneous tissues and full thicknesswounds of dry black eschar. The key pathologicalmechanisms include injury caused byabrupt reperfusion of the capillary bed followingocclusion of blood flow, damage to the vasculaturedue to forces such as shear and cell deatharising from prolonged direct occlusion of bloodvessels (Nixon, 2001).The effects of washing (skin hygiene)practices on the skinDespite the significant amount of time nursesspend washing patients, the effects of washingactivities on skin barrier function have receivedlimited scientific appraisal. The evidence wehave is largely based on the literature reviews,drawn from clinical observation, supported bylimited experimental (quasi) study evidence andexpert panel sources (Ersser et al., 2005).The use of very hot water may cause unnecessarydrying of the skin by removing skin oils andaccelerating water loss by evaporation (Gooch,1989). As an emulsifying agent, soap acts by dispersingone liquid into another immiscible liquidand so it suspends the oil or debris in water,aiding rinsing. Sodium lauryl sulphate is one ofthe most common synthetic surfactants foundin soaps and detergents (Kirsner and Froelich,1998). It is also a potent skin irritant, especiallyafter prolonged exposure (e.g. Held et al., 2001),which may bind to keratin and cause denaturationof cell membranes, leading to an irritantresponse. Surfactants can also cause allergiccontact dermatitis, but due to the high intensityeffect of many, it can be difficult to differentiatean allergic reaction from contact irritation duringpatch testing (Flyvholm, 1993). Non-ionicsurfactant, such as propylene glycol, is the leastirritating group of surfactants. Products such asbaby shampoo contain low- irritant, amphotericsurfactants, such as cocoamido-propyl betaine(Kirsner and Froelich, 1998).Other physico-chemical effects of soap maydisrupt the delicate skin barrier. Washing withsoap may remove the natural protective emollientsebum oil from the skin (Baillie and Arrowsmith,2001). Soaps and some cleansers may also raisethe alkalinity of the skin (Korting et al., 1987)and thereby negating the influence of the protectiveacid mantle (see Chapter 2). They may alsochange the balance of resident flora on the skin,leading to the proliferation or reduction of countsof common bacteria such as Propionibacteriumacnes or Staphylococcus aureus, respectively(Korting and Braun-Falco, 1996); this mayenhance the risk of skin colonisation and possibleinfection by pathogenic microorganisms.

Protecting the skin and preventing breakdown 53Skin that is not dried carefully after washingcan cause maceration and undue cooling. Themechanical and chemical drying of the skin canadversely affect barrier function, although theliterature on this subject is limited.The effects of urine and incontinenceon the skinThe effects of urinary incontinence on skin vulnerabilityare another neglected area of nursinginvestigation (Ersser et al., 2005). Despite thescale of the problem, the effects and preventionof urine exposure on skin barrier disruption hasreceived limited research attention. The prevalenceof urinary incontinence provides an indicationof the potential significance of the problem(Getliffe and Dolman, 2003). It is estimated that200 million people worldwide have significanturinary incontinence and many more with mildbladder problems (Abrams et al., 2002), with ahigh occurrence among people living in institutionalsettings. Obesity affects 20% of the populationin UK (National Audit Office, 2001). It isa major health problem in most affluent countriesand is likely to lead to skin vulnerabilitydue to the formation of skin folds. Children areanother vulnerable group; it is estimated that inthe UK 500,000 experience nocturnal enuresis(persistent bedwetting) (Department of Health,2000). Although incontinence may not of courseaccompany older age, an increased incidence ofmultiple disabilities in this group may contributeto reduced ability to maintain continence, makingthis group vulnerable to skin damage.The skin of an incontinent person will beexposed to regular contact with urine, sweatand possibly faeces. As such, the skin is vulnerableto chemical irritation by urine andphysical effects caused by wetness of the skinthat encourages maceration; these can disruptthe skin barrier and lead to breakdown.The decomposition of urinary urea by microorganismsrelease ammonia to form the alkali,ammonium hydroxide, thereby disrupting theacid mantle. Chemical irritation of the skin mayarise from both the rise in alkalinity and bacterialproliferation. Perineal dermatitis may arisefrom urine exposure, which is characterised byinflammation of the skin, and may include redness,tissue breakdown, oozing, crusting, itchingand pain (Brown and Sears, 1993; Gray, 2004)within the perineal area.Faecal incontinence may present even morerisk to skin integrity (Allman, 1986; Shannon andSkorga, 1989). It is more common in the generalpopulation than is often realised and the surveycited above suggests 5.7% of women and 6.2%of men over 40 years living in their own homesreport some degree of faecal incontinence (Perryet al., 2002). Overall, 1.4% of adults reportedmajor faecal incontinence (at least several timesa month) and 0.7% had disabling incontinencewith a major impact on their quality of life.Excess moisture can increase the friction coefficient,making the skin more vulnerable to breakdowndue to friction forces (Nach et al., 1981).This, coupled with frequent washing of theincontinent patient’s skin, can disrupt skin barrierfunction by removal of skin lipids and the accelerationof epidermal water loss (further examinationis given later). A number of studies reveal ageneral association between urinary incontinenceand pressure sores, but few demonstrate a causallink. For example, a study of nursing home residentsby Schnelle et al. (1997) demonstratedthat skin problems tend to occur in areas wherethere has been consistent excessive skin wetness(hydration) through urine exposure. These findingsare consistent with supporting experimentalevidence that skin exposed to urine due to infrequentpad change can increase the wetness of theskin; the increase in friction and abrasion predisposingit to breakdown (Fader et al., 2003).Prolonged exposure to water alone may causehydration dermatitis (Kligman, 1994; Tsai andMaibach, 1999) and prolonged occlusion of theskin (as within a continence product) may reduceskin barrier function (Fluhr et al., 1999) and significantlyraise microbial counts and pH (Alyet al., 1978; Faergemann et al., 1983).Consideration also needs to be given to theeffects of drying practices related to washingpractices. An excessively dry stratum corneumcan develop cracks and fissures and canbe as ineffective a barrier as an over-hydratedone (Tsai and Maibach, 1999). Dry and scaling

54 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsskin contributes to the risk of pressure ulcerdevelopment, although only limited evidence hasbeen found. Those with dry or scaling skin havebeen found to be at least 2.5 times more likelyto develop wounds from skin breakdown comparedto a matched control group (Gulralniket al., 1988), based on one of the largest studies(n 5, 193) examining predictors of pressure soresin the community (55–75 years). As a risk factor,dry skin is not reflected in pressure risk scales,which focus on the key role of moisture. Asideto dry and over-hydrated skin, some patients alsodevelop sore skin in which there is erythema dueto inflammatory effects and a damaged skin barrier.Again, the issue of sore skin is another areagiven scant attention in the literature.Other factors affecting skin breakdownMalignancy can affect the skin barrier whenthe pathological process leads to a breakdownin skin integrity, such as a malignant fungatingwound, which may include mycosis fungoides, atype of cutaneous T-cell lymphoma. Whilst suchproblems will require wound care, the effects ofcancer treatments can have implications for skincare. Iatrogenic effects or the effects of medicaltreatment on the skin such as radiotherapyeffects and adverse drug reactions (ADRs) arenow examined.RadiotherapyRadiotherapy may cause acute radiation dermatitis,with the reaction intensity dependingon the dose, the treated area and individualvariation (Tucker et al., 1984). Common effectson the skin include erythema, which resemblessevere sunburn, and peeling or desquamation;rarely it can lead to necrosis (Porock andKristJanson, 1999). Skin reactions tend to beshort lived; they are also uncomfortable forpatients, with accompanying itch and pain attimes (Campbell and Illingworth, 1992).Adverse drug reactionsAdverse drug reactions (ADRs) or side effectscan have a significant cutaneous effect, whichmay lead to a significant breakdown of skinintegrity. They can account for 5% of all hospitaladmissions in the UK and between 10%and 20% of hospital inpatients (The NationalPrescribing Centre, 1998) and hence can be acommon reason for dermatological contact withother hospital areas. Whilst a rash is a commonskin reaction, drug eruptions can be severe andlead to skin barrier breakdown (see Chapter 13for more details on drug reactions).The mechanisms of ADRs include anaphylacticreactions (type I), cytotoxic reactions (type II)and immune complex–mediated reactions (typeIII), in which combinations of some of thesemechanisms may occur (Mackie, 2003). Typicalcutaneous reaction patterns due to ADRs aresummarised in Table 4.1.In countries such as South Africa, whichhave high HIV-AIDS prevalence and so ahighly immuno-compromised population, someTable 4.1 Cutaneous reaction patterns due to ADRs.Reaction patternToxic erythemaErythema multiformeand Stevens–JohnsonsyndromeErythema nodosumErythrodermaVasculitis and purpuriceruptions or aggravationof psoriasisVery severe blisteringeruption (toxicepidermal necrolysis)PhotosensitivityAcneSLE-like syndromeExfoliative dermatitisSource: Based on Mackie (2003).Likely drugsAntibiotics, sulphonamides,barbiturates, anti-rheumaticsAntibiotics, sulphonamidesand anti-rheumaticsContraceptive pill,sulphonamidesAntibiotics andanti-rheumaticsPhenytoin, indomethacinSulphonamides, allopurinoland phenylbutazoneTetracyclines, phenothiazinesPhenytoinHydralazine, penicillin andsulphonamidesGold, isoniazid andphenylbutazone

Protecting the skin and preventing breakdown 55conditions such as severe blistering conditiontoxic epidermal necrolysis are much more common,which has a significant effect on skinbreakdown and perhaps a major challenge fornursing and medical care. Strong (1998) givesfurther details on dermatological emergenciesfrom a nursing perspective.Preventative practicesSkin washing and drying practicesThe earlier section on washing the skin highlightsthe importance of several factors in maintainingthe skin barrier; avoiding excessive useof soap and where possible using soap substitutesor cleansers, not using water that is toohot and minimising rough drying technique.For those with chronic skin conditions such aspsoriasis and eczema, emollients may be used assoap substitutes (see Chapter 5). For routine skincare for those requiring regular washing, suchas the incontinent patients, skin cleansers mayprovide an alternative means to maintain skinhygiene. They may reduce some of the adverseeffects of soap, due to their chemical composition,and help to maintain a pH level that minimisesbarrier disruption. Several studies havecompared the use and effect of skin cleanserswith soap and water use, but design weaknessesare common, such as small sample size, andhence conclusions are often unclear. For example,Whittingham (1998) compared the relativeeffectiveness of one of two cleansers (TripleCare, Smith & Nephew and Clinisan, Vernacare)with that of using soap and water on skin conditionamong a sample of highly dependent elderlypatients with some degree of incontinence.Other studies have compared the combineduse of cleansers with a barrier cream with theeffectiveness of soap and water, although againdesign weaknesses are common (e.g. Byerset al., 1995; Dealey, 1995) compared to skinwashing and cleansing regimens and their effecton skin integrity using a ‘multi-baseline crossoverdesign’, with soap and water as the baselinecontrol. Although a small study, repeatedobservations revealed statistically significant differencesbetween the regimens, and there was noclinically observable evidence of skin breakdown.Based on the transepidermal water loss (TEWL)and erythema measurements, the soap and waterregimen was the least efficient in promoting skinhealth. There were statistically significant differenceson TEWL measures between the soapand water control and the use of cleanser alone(p = 0.02), soap and barrier cream (p = 0.01) andcleanser plus barrier cream (p = 0.03). Soap alsoproduced a more alkaline skin (pH 7.5), but barrierfunction improved with the use of a barriercream and was even greater with the cleanser andcream regimen. As such, for use with vulnerableskin, the use of carefully selected cleansers andemollients should be considered (see Chapter 5).The capillary action of the towel wicks wateraway from the surface and various authorshave suggested drying the skin gently, patting itrather than rubbing to reduce frictional damage(Fiers, 1996). Unpublished preliminary observationsfrom the authors’ group would support thefact that a minimal rubbing drying technique,such as patting, may reduce frictional damage.Measurements of skin barrier function (includingTEWL) were significantly increased following asingle wash with towel drying by rubbing, themean pre-wash TEWL (±SEM) being 8 ± 0.12g/hm 2 increasing to 12.6 ± 0.52 g/hm 2 after a singlewash, representing a significant disruptionto skin barrier function (p < 0.01) (Ersser et al.,2005).Promoting skin hydrationThe principles of improving skin hydration aretwofold: firstly the need to promote the retentionof moisture (and prevent dehydration)and secondly to support the process of addingwater to the skin structure. Emollient therapy isa key technique for achieving both approachesby reducing water loss by moisturisation (occlusiveeffect), promoting water retention and helpingwater to penetrate directly into the skin, asin the application of creams. Emollient therapyis examined in detail in Chapter 5 and ina best practice review document (Ersser et al.,

56 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals2007). Even in situations and countries wherepharmaceutical emollients are scarce, the effectof safe oils on the skin barrier can be effective(Darmstadt et al., 2002).Details have been given on washing and dryingpractices to prevent or minimise water lossfrom the skin. In summary this includes minimisingsoap use and considering the use ofsoap substitutes, avoiding very hot water whichenhances evaporation and removes natural skinoils such as sebum, sealing the skin with emollientsafter soaking, drying to minimise traumato the skin barrier. Occlusive techniques are theother main techniques that enhance the hydrationof the skin and minimise trauma to the skinbarrier related to scratching.Wrapping or bandaging techniques involve aprocess of occluding the skin to promote skinhydration and skin protection. These techniquesmay be wet or dry, depending on the relativeneed for hydration and skin protection, respectively.Hydration is achieved by the applicationof liberal quantities of emollients under thewrapping, which may be a bandage or cottonclothing. Occlusion increases emollient absorption.Wraps can be very helpful for parents ofchildren with eczema who can be resistant totreatment in order to improve the quality of lifeand sleep (Goodyear and Harper, 2002). Thisrequires nursing support to ensure parents andthe child are need to be taught to prepare themapply the wraps suitably, maintain effectivenessand to minimise any adverse effects. Box 4.1outlines the principles of wrapping techniques;these apply to both adults and children requiringwrapping.There are various elements of the basic wetwrapping technique; the following describessome of the core elements which may be adaptedaccording to the need. Two layers of wrappingare used – tubular bandages, ordinary soft cottonclothing or designed commercial garmentssuch as Tubifast. A warm damp inner wrappinglayer (produced using comfortably hot water) isplaced over skin onto which an emollient andpossibly a topical treatment (e.g. steroid) hasbeen applied. Keep tight fitting to prevent fastcooling. The outer dry layer is placed over thewet layer. The frequency of application willBox 4.1 Principles of wrappingtechniques■■■■■■■Helps to interrupt the scratch – itchcycleMay reduce topical steroid use – wetgarments can help aid penetration oftopical treatmentActs as a mechanical barrier preventingfurther damage to the skinCools and soothes the skin as waterevaporatesPrevents emollients being wiped offand protects clothingMaintains hydrationReduces inflammation and allergenloaddepend if the condition is severe or not, if so theparents can wrap each day and night, then onceunder control apply approximately thrice perweek. Overnight use is particularly useful withthe utilisation of existing night clothing and theopportunity to ameliorate night-time scratching.Wet wraps can be used for children from 3months of age.Dry wraps – A single dry layer is applied overan emollient to aid the occlusive and protectiveeffect. As with wet wrapping, this can be appliedto the badly affected areas with either the tubularbandage or the Tubifast garments (e.g. vest,leggings or socks). The garments stretch easilyand are more comfortable to wear; they arewashable/reusable.Wraps can normally be used for children from3 months of age. These principles equally apply toadults requiring wrapping, due to either the needfor hydration or to alleviate the effects of damagingscratching behaviour. This process helps todisrupt the scratch–itch cycle, in which scratchingaggravates the pruritic experience and therebymay lead to further damage in a cyclic manner.Medicated paste bandages may also be usedunder medical supervision. These are used totreat conditions such as eczema that affect thelimbs and vary according to their constituent

Protecting the skin and preventing breakdown 57medication, including substances such as zincoxide, ichthammol and coal tar (both of whichalleviate pruritus). As well as acting as a barrierto prevent damage from scratching they canhave a cooling and soothing effect on pruriticskin, as well aiding the penetration and effectivenessof topical medications, as with other formsof occlusion. Guidance on how to apply pastebandages has been developed by the BDNG(British Dermatological Nursing Group, 2008).Application should be preceded by bathing anduse of a soap substitute and the application ofthe topical agent. The bandages are applied fromthe base of the limb, i.e. starting from the wristor the ankle upwards. There are two methodsillustrated in the BDNG ‘how to article’. (1) Cutand overlap method: The limb is then bandagedaround the limb through one and half turns creatingan overlap by half the width of the bandageeach time – it is then cut; this process is repeatedas the limb is ascended. (2) The second ‘pleatingmethod’ involves wrapping the bandage aroundthe limb and then folding back or pleating uponitself and then applying in the reverse direction,also overlapping by half the width of the bandage,avoiding pleats near bony prominences.Bandages are covered with a further outer cottontubular or self-adhesive bandage which preventsstaining of clothes and slippage. The final processinvolves checking that the bandage is not tootight and so the fingers and toes are moveableand perfused normally.Caution is needed when using wraps, whichmust be intimated to the patients or their carers.Careful parental teaching is thereforeneeded, which can be initially time consuming.Occlusion can intensify the activity of activetopical treatments such as steroids – alwaysuse the lowest strength required to bring conditionunder control. It is important not to usewet wraps if the skin is infected; as such thereis a need to monitor the skin – pulling backthe bandages to ensure skin has not got worse.Avoiding the use of occlusion is necessary since –the warmth and moisture favour the build upof microorganisms. Application should also beavoided if the child is unwell. It is advised notto cut holes for fingers or toes too small, asthis can lead to swelling in these areas if tight.Useful guidance on wet wrapping is providedby Goodyear et al. (1991), whilst evidence forthe efficacy and safety is usefully summarised byDevillers and Oranje (2006), although furtherresearch evaluation of these techniques and theiroptimal usage is still required.Maintaining skin integrityAlleviating pressureThe focus of pressure ulcer prevention remainsthe mitigation of the effects of immobilitydespite some uncertainty regarding the precisenature of pressure sore aetiology (Clark, 2001).Specifically, this requires reducing the time ofweight bearing of the body’s bony prominences,through repositioning or using support devices,such as air pressure alleviating mattresses. Thelatter may also reduce the magnitude of theforces applied during tissue loading. Guidelinesfrom EPUAP (2008) highlight the importanceof the following key preventative strategies (seeBox 4.2). The new guidelines from EPUAP andthe National Pressure Ulcer Advisory Panel(NPUAP) are due to be published soon (www.epuap.org and www.npuap.org, respectively).The Panel for the Prediction and preventionof Pressure Ulcers in Adults published by theAgency for Health Care Policy and Research(AHCPR) (1992) reflects guidance of US nationalimportance. They recommend that patient repositioningbe performed ‘at least every 2 hours’.Discussions on the issues related to preventionthrough patient turning are examined effectively(Clark, 2001). The EPUAP website in 2008 indicatedthat their own and the AHCPR guidelinesremain the current internationally recognisedones available, although they acknowledge theseneed updating.Support surfaces such as pressure-relievingbeds, mattresses and seat cushions may be used asaids to prevent pressure ulcers both at home andin institutions. The evaluation of pressure-relievingsupport surfaces has investigated such supportsystems through a rigorous trial (‘PRESSURE’)(Nixon et al., 2006) and a Cochrane review(McInnes et al., 2008). The PRESSURE trialundertaken for the Health Technology Assess ment

58 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 4.2 Key pressure ulcerprevention strategies based onEPUAP guidance (1998)(1) Systematic risk assessment, using toolscombined with clinical judgement,(2) Maintaining and improving tissue toleranceto pressure to prevent injuryby conducting skin assessment of thebony prominences and skin condition(dryness, cracking, erythema, maceration,fragility, heat and induration) andoptimising the skin’s condition (e.g.reducing excessive moisture),(3) Minimise friction and shear forcesthrough correct positioning and transferringtechniques,(4) Identify nutritionally compromisedindividuals through assessment andplan for nutritional support to meetindividual needs,(5) Improve the patient’s activity levelwhere possible,(6) Protect against the adverse effects ofexternal mechanical forces: pressure,friction and shear through frequentand correct repositioning and the useof suitable support surfaces, and(7) Education directed at health professionals,patients, family and caregivers(e.g. teach able patients to redistributeweight every 15 minutes).programme was a multicentre, randomised controlledparallel group trial. They found no differencebetween alternating pressure mattressreplacements and overlays in terms of thepatients developing new pressure ulcers (Nixonet al., 2006). However, alternating pressure mattressreplacements were found more likely to becost saving. It is suggested that patient preferencecan be supported without risk, if they prefer anoverlay to a replacement mattress. The reviewby McInnes et al. (2008) aimed to assess theeffectiveness of support surfaces in the preventionand treatment of pressure ulcers. They concludedthat higher specification foam mattresses shouldbe considered rather than standard hospital foammattresses. They propose that organisationsconsider the use of pressure relief for high-riskpatients in the operating theatre, as this is associatedwith a reduction in the post-operative incidenceof pressure ulcers. The review also suggeststhat the evaluation of seat cushions is limited.Assessing and limiting the effectsof incontinence on the skinIncontinence is identified as a risk factor in manypublished pressure ulcer assessment tools (Nortonet al., 1962; Gosnell, 1973; Waterlow, 1988).Tools such as the Braden Scale (Bergstrom et al.,1987a, b) specify the moisture factor, consideringsweat and or incontinence as possible sources.The literature includes analyses of the rigour bywhich risk can be predicted (e.g. Haalboom et al.,1999). The review by Cullum et al. (1995) indicatedthat such tools have been developed inan ad hoc fashion without the use of statisticalregression models to choose and weigh the factorsthat may predict development. As such, theirvalidity remains problematic. Morison (2001)argues that incontinence or moisture may not bea primary factor but rather an indicator of poorphysical condition, stating that it has not beenidentified by prospective cohort studies, whichidentify key diagnostic factors using multivariatestatistics. However, there are indications of theimportance of moisture in pressure ulcer risk fromsome studies (Haalboom et al., 1999). This studyrevealed that the incontinence factor increasedthe incidence of pressure ulcers by a factor of 6.2(Odds Ratio), although the wide 95% confidenceinterval (2.3–17) revealed the low precision of thepoint estimate.The EPUAP (1998) identified incontinenceand ‘moistness’ as key pressure ulcer risk factorand therefore as clinical issues to be managed.Halfens et al. (2000) examined the evidence tosupport the established Braden scale (Bergstromet al., 1987a, b); analysis revealed that onlyage and incontinence of urine and/or faeceswere related to the external criteria for risk of

Protecting the skin and preventing breakdown 59pressure sore (including non-blanchable oedemaand skin loss).Preventing and minimising iatrogenic effectsHealth professionals may adversely disrupt theskin barrier in a range of ways; these may includethrough poor washing practices, the impact ofADRs on the skin and a lack of adequate pressure-relievinginterventions. As washing practiceand pressure ulcer prevention are discussed elsewhere,here we will focus on the adverse effectsof drugs on the skin and their prevention.Preventing ADRsThe nature and effects of ADRs have beendescribed earlier. Central to prevention is familiaritywith the drugs commonly causing drugeruptions and risk factors such as medicationhistory or medical conditions such as an allergyhistory and renal or liver impairment that mayaffect elimination. Other risk factors includenew drugs and first doses and contraindicateddrugs, which are by definition those drugswhere risk of patient harm is high. Assessmentis therefore essential with a review of medicaland medication history, allergy and the natureof any prior ADRs.settings. Those affected may include peoplewith lymphatic filariasis, which affects up to40 million people (Global Alliance to EliminateLymphatic Filariasis [GAELF]). Vaqas and Ryanhighlighted the importance of ankle movementto improve lymph flow, limb elevation to reducevenous pressure in the lower limb and breathingexercises to support clearance of the centrallymphatics. The role of skin care has been highlighted– especially maintaining epidermal integritythrough careful washing of the skin and useof emollients to help maintain skin barrier integritywhich in turn will help to prevent bacterialpenetration. This is important given that recurrentinflammatory episodes are a common complicationof lymphoedema and correlate with itsgrade of severity (Pani and Srividya, 1995).Protecting the skin during radiotherapyThe consensus in the literature is that the severityof skin reactions can be reduced by washingthe skin with mild soap or a cleansing agent andmoisturising with a light moisturising creamor emollient (e.g. National Breast and OvarianCancer Centre, 2008). Mild soaps are typicallyconsidered those that are less irritant to the skinManaging lymphoedemaEvidence suggests that a combination of physicaltreatments are effective for managinglymphoedema (Ko et al., 1998), although there islimited evidence to identify which components aremost important. The key elements include compressionusing bandaging or garments, massage,exercise and skin care. The international consensusdocument on lymphoedema management providesan evidence-based guideline on effective servicemodels (Lymphoedema Framework, 2006). Theskin care component highlights the importanceof maintaining skin integrity and the care managementof skin problems to minimise the risk ofinfection. Whilst the principles are summarised inBox 4.3, the guidelines specify the details.Vaqas and Ryan (2003) examined the managementof lymphoedema in resource-poorBox 4.3 General principlesof skin care for lymphoedemamanagement.■■■■■Wash daily using pH neutral soap or asoap substitute and dry thoroughly.Ensure skin folds, if present, are cleanand dry.Monitor for affected and unaffectedskin for cuts, abrasions or insect bites,paying specific attention to any areasaffected by sensory neuropathy.Apply emollients.Avoid scented products.Source: Lymphoedema Framework (2006).

60 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsand have reduced levels of irritating additivessuch as perfumes. Furthermore, patients shouldalso use sunscreen or wear protective clothing,avoid irritants (such as deodorant, perfume,hair dye) and keep the skin folds dry. Trial evidencein the breast cancer context suggests thatwashing irradiated skin during radiotherapycan be undertaken as it is not associated withincreased skin toxicity (Roy et al., 2001). In akey study, Campbell and Illingworth (1992)found no statistically significant difference in theseverity reaction between those washing withwater alone and those using soap, although skinreactions were worse in patients who were notallowed to wash at all.A review indicates that two preparationsreduce the severity of skin reactions experiencedby patients, i.e. sucralfate cream and hyaluronicacid cream (Naylor and Mallett, 2001), however,these may are not now available throughthe standard formulary (BNF). Furthermore,it is suggested that some cream (non-steroidalwater in oil preparations) can limit the effectsof radiation. A paper by Leonardi et al. (2008)evaluated a cream containing hyaluronic acid(which is a major component of the extracellularmatrix of the skin) and shea butter. Theyfound a statistically significant difference withthe control vehicle on the severity of skin toxicity,burning and desquamation in favour of thecream, although the small number of patientsmay limit the study. Hyaluronic acid is the mostpowerful moisturising agent known because ofits significant hygroscopic properties that enableit to attract 1,000 times its weight in water. Sheabutter resembles sebum in its fatty acid compositionand as such can help to restore skin barrierfunction, by supporting the skin elasticity andturgidity (Abramovits and Boguniewicz, 2006).Well and MacBride (2003) gave an excellentsummary of radiation skin reactions and theirmanagement. They highlight that there is limiteddata depicting patients’ experiences of skinreactions and much conflicting evidence on theirprevention and management. The importance ofpatient information targeting at risk patients isalso emphasised on the risks of breakdown andself-care strategies to minimise problems. Thoseat high risk include people with greater UVsensitivity, smokers, those with heavier breastsor larger tumours.Nursing intervention to supportbehavioural change (prevention)in relation to sun exposureDespite the significance of skin cancer as a growinghealth issue, evidence indicates limited knowledgeand unsafe sun practices in the UK (Officeof National Statistics, 1999). Further research isrequired to promote and evaluate behaviouralchange to prevent cancer and promote earlydetection (National Cancer Research Institute,2005). The Cancer Research UK Sunsmart campaignaims to achieve this by ‘action … to informand empower patients so that they can play anactive role in decisions’, but there is limited discussionabout delivery models, other than UVawareness campaigns (Department of Health,2007). Review evidence of primary care preventionproposes caution when drawing from USand Australian strategies (Melia et al., 2000). TheRoyal College of Physicians’ (2007) guidelines onthe prevention of skin melanoma highlight theneed for sun avoidance and effective sunscreenand clothing use.The International Cancer Research Portfolio(International Cancer Research Funding Organisations,2008) highlights US research using aneducational preventive intervention with youngpeople. Although sun exposure in children is animportant preventable factor since risk developsin childhood (Armstrong and Kricker, 2001)through genetic mutation and learnt risk behaviour,educational intervention with this groupremains problematic since adolescents continueto report intentional sun exposure to geta tan (e.g. Melia et al., 2000; Cokkinides et al.,2002). The key risk factors for skin cancer arewell established (Gandini et al., 2005; SouthWest Public Health Observatory, 2008); thisincludes young adults’ frequent use of sun beds(Armstrong and Kricker, 2001). A review paperargues prevention is also valuable later in life,especially in people who have heavy exposureto solar radiation in childhood (Armstrong and

Protecting the skin and preventing breakdown 61Kricker, 2001). Also, achieving attitude and UVprotective behavioural change in adults, many ofwhom will be parents, may result in good practicebeing passed to children (e.g. parental UVrisk behaviour is a predictor of that by youngpeople; Cokkinides et al., 2002). However,adults have received little focused attention inpreventive studies.Using evidence of theory related to effectivebehaviour change is likely to maximise the effectivenessand efficiency of lifestyle interventions(Berwick et al., 2000; National Institute forHealth and Clinical Excellence, 2007). Relevanttheories include Bandura’s Construct of Selfefficacy(Bandura, 1977, 1996) and Theory ofPlanned Behaviour (Ajzen, 1991, 2001). Selfefficacyis derived from Bandura’s (1977, 1996)social learning theory, highlighting a person’sbelief and their capacity to undertake a healthbehaviour, such as to prevent skin cancer andengage in effective self-examination. A body ofresearch highlights self-efficacy as an importantpredictor of engagement in healthy behaviours(Havas et al., 1998; Rosal et al., 1998;Clark and Dodge, 1999). The theory of plannedbehaviour is the most widely applied model ofbeliefs, attitudes and intentions that precedeaction (Ajzen 2001; Connor and Sparks, 2005).Both theories are likely to bolster intentions andsustain action.Nurses are a substantial resource with apotential to deliver effective health education(Latter, 2000; Runciman et al., 2006). Evidencesuggests primary care nurses could play aneffective role in reducing the risks of cancerby promoting early detection and fast referral(Austoker, 1994; Oliveria et al., 2002). Studiesof nurse-led interventions to increase awarenessor change behaviour related to cancer havebeen successful (Koinberg et al., 2004; Sharpand Tischelman, 2005). However, most previousinitiatives have been applied in cancer contextsother than skin cancer prevention, with manyinvolving self-examination only (e.g. Oliveriaet al., 2002) and limited theoretical underpinning.A nurse-led teaching intervention, usingimages, can enhance patient skin self-examination(Oliveria et al., 2004); however, thisstudy did not incorporate the evaluation ofeducation to reduce risk behaviours. A goodexample of a self-examination guide is that providedby the Wessex Cancer Trust (Hancock,2007).A key challenge for nurse-led prevention isto establish how best to raise awareness aboutskin cancer but in particular change behaviour.A systematic review by Saraiya et al. (2004)argues for research focused on health outcome,patient behaviour and examination ofthe ‘role of the non-physician provider to helpidentify if counselling skills to change behaviourmight be better suited to providers withthe time and skills, such as a nurse’ (p. 444);however, there is little evidence of such studies.Also, resource-efficient models of servicedelivery are required for primary care–basedhealth promotion. One possibility for considerationis telephone consultation. Nurses havebeen found to increase patient self-efficacy intargeted telephone interventions with patients(Wong et al., 2005) with systematic reviewevidence finding them to be safe and acceptableto patients (Bunn et al., 2004).Details of key health education messagesrelated to skin cancer prevention are given inChapter 11.Nutrition to support skin integrityRequirements of the skin barrier/nutrients for a healthy skinThe effective structure and functioning ofhealthy skin is dependent on an adequate levelof nutrition. It is evident from the deficiency ofcertain essential nutrients that certain diseasesmay arise. This includes, for example, vitamindeficiency such as scurvy due to vitamin C deficiency,which can lead to bleeding gums, easybruising and sometimes purpura, and pellagra(including dermatitis) due to nicotinic acid(niacin or vitamin B 3 ) deficiency, which includesigns such as dermatitis to sun exposed sites,scaly erythema and hyperpigmentation (Mackie,2003). Another condition is kwashiorkor thatis due to protein malnutrition and leads to dry

62 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsskin, erythematatous eruption and dry brittlehair. Table 4.2 summarises the key nutrientsrelated to skin health, based on Allen (2000),Dealey (2005) and Patel (2005).Malnutrition remains a significant problemamong outpatients (Neelemaat et al., 2008) andindeed may occur when patients are hospitalised(O’Flynn et al., 2005). Other common forms ofmalnutrition, such as obesity, are responsiblefor changes in skin barrier function, sebaceousglands and sebum production, sweat glands,collagen structure and function, wound healingand the microcirculation and are implicatedin a wide spectrum of dermatological diseases(Yosipovitch et al., 2007).When the skin is under stress the demand fornutrients will alter and specific items play animportant role in countering disease, such as essentialfatty acids (EFA) in eczema and psoriasis andzinc in wound healing (Allen, 2000). Extensiveskin inflammation increases its requirements forenergy and fluid and for specific nutrients such asfolic acid and protein.Nutritional support is required for the healingof wounds (Dealey, 2005) and may help protectagainst pressure ulcer development and improveTable 4.2 Key nutrients related to skin health.Nutrient Relevant function Good sourcesCarbohydrateEssential fatty acids (EFAs)MineralsZincEnergy for fibroblast, macrophage,leucocyte function and collagen synthesisFormation of new cells (cell wallphospholipids), energy formation, skinbarrier functionEnzymatic activity – intermediary inmetabolism, cell proliferation andepithelisation, collagen synthesisWholegrain cereals, potatoes,wholemeal breadDairy products, vegetable oil, oilyfish, nutsMeat, wholegrain cereals, cheeseIron Collagen synthesis Meat, eggs, dried fruitCopper Collagen synthesis Shellfish, liver, meat, breadProteinCollagen synthesis (about a third of thebody’s protein), fibroblast proliferation,angiogenesis, immunityVitamin AMembrane stability, normal growth anddifferentiation of the epidermisVitamin B complex includingB 3 (niacin) Collagen cross-linking, Enzymatic activity –intermediary in metabolismB 2 (riboflavin)Deficiency can cause fissuring andinflammation around the lips/mouth andtongueAmino acid metabolismB 6 (pyridoxine)Meat, fish, eggs, cheese, pulses,wholegrain cerealsLeafy vegetables (broccoli, spinach),carrots, apricots, liverCereal grains, meat, nuts and somefruit and vegetablesVitamin CEnzymatic activity, collagen synthesis,blood vessel maintenance, immunityCitrus fruit and fresh vegetablesVitamin D Cell signalling, keratinocyte proliferation Solar irradiation of Vitamin D 3(cholecalciferol) in the skin and somefish (mackerel, tuna and salmon);Cheese, eggs, beef, liver

Protecting the skin and preventing breakdown 63the rate of healing (Houwing et al., 2003).However, a systematic review suggests that moreevidence is required to identify effective dietaryinterventions (Langer et al., 2003). Nutritionguidelines for pressure ulcers have been developed(Schols and de Jager-v d Ende, 2004).EczemaDry skinItchingPreventing skin damage by scratchingScratchingBreaking the scratch–itch cycle andbehavioural managementA fundamental management problem witheczema is the disruption of the skin barrier dueto scratching in response to itch. Itching evokesscratching that further damages the skin leadingto more itching, a vicious itch–scratch cycleis established (see Figure 4.1) and thereforebreaking this cycle is a primary clinical aim(Hagermark and Wahlgren, 1995).Behavioural management is a strategy that mayhelp manage damaging habit of the itch–scratchcycle. The key principle of classical conditioningviews learning as a behavioural response toitch may take place if it is paired with a positiveor aversive stimulus. Cognitive behaviouralapproaches focus on the ability and intention tochange behaviour to the benefit of the individualand others. Habit reversal is a well-establishedmethod of eliminating nervous habits and tics,whereby an alternative or competing behaviourwas adopted in place of the undesirable behaviour(Azrin and Nunn, 1973). The empirical baseemerged from the early studies of Azrin. Classicstudies include work on nervous habits in adolescents(Allen, 1998; Rapp et al., 1998); theseinclude small numbers of cases and the use ofdirect observation techniques.One the clearest accounts of habit reversalremains that by Bridgett et al. (1996) in London,based on the work of Melin, Noren and colleaguesin Uppsala Sweden, as cited previously(Noren, 1995). They advise that this does notrequire a trained behavioural therapist – and assuch this technique can be used by those thatare delivering dermatology care and could beapplied for all ages.Figure 4.1 The itch–scratch cycle.Miltenberger et al. (1998) provide an overviewof the elements of habit reversal and evidenceregarding its effectiveness. This paperhighlights the mechanisms responsible for itssuccess and its effectiveness in reducing nervoushabits, such as scratching, in a replicable way.Research over time has attempted to elucidatethe key elements of effectiveness. Miltenbergeret al. (1998) summarises these three componentsas follows, as relevant to the parent–childsituation.It comprises of three main elements: awarenessraising, introducing a competing response andmotivational training to maintain engagement.The book by Bridgett et al. (1996) is a useful anddetailed practical guide to supporting adults andchildren with atopic skin disease through habitreversal. The following outline on the nature oftraining is focused more on supporting the parentand the child, although of course the sameprinciples apply to adult patients.Awareness training (registration) is concernedwith demonstrating the occurrence of the habitand bringing it more closely to the child andparent’s attention. This involves helping themto describe the topography of the behaviour, i.e.identifying when it is about to occur and whatantecedent factors are most reliably predictingoccurrence. One practical way to implement thisis to ask parents to keep a scratch diary to recordepisodes of when their child scratches and anyinfluencing factor that seems to be implicated.The nurse or dermatologists can review this withthe parent and child to raise awareness of howtheir child is responding to the problem of itch.

64 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsThe next stage (competing response training)involves replacing the damaging behaviour with anew individualised pattern which does not lead todamage to the skin, with the following features:the new behaviour was opposite to the old habit,could be maintained for several minutes and wassocially acceptable. Alternative behaviours mayinclude clenching the fists, gently pinching theskin or patting it. The substitute behavioural maybe planned as a play activity for children, with abehavioural response linked to a story.Motivational training involves reviewingall ways in which the habit is inconvenient orembarrassing to the child and parent promptingthe child to use competing response and praisingand encouraging them when successful.They emphasise from clinical experience thathabit reversal in this application is only successfulwhen individualised and combined with aneffective topical treatment. Key to the successof the approach is the person being enabled tomanage their own condition. The approach canbe delivered as a group approach to improvecost-effectiveness, as illustrated by Ehlers et al.(1995); this could be adapted to the setting ofa nurse-led clinic. Increasingly, computer-basedor multimedia educational programmes willpromote behavioural treatment and aid in effectiveself-management through programmedinstruction. This represents an area where thereis further scope for development and evaluationresearch.ConclusionThis chapter has focused on the topic of universalrelevance to nurses and many other healthprofessionals, the need to protect the skin andprevent breakdown. The significance of theskin barrier has been highlighted, including theneed to support its structures and functions.The concept of skin vulnerability has beenintroduced – which conveys the need to understandboth biological and behavioural basis ofskin vulnerability as a platform for preventingand managing breakdown of the skin barrier;this we would argue is a fundamental nursingrole. The causes of skin breakdown have beenoutlined followed by the related approaches toits prevention, as the initial therapeutic priority.Attention has also been given to the role of theindividual in preventing breakdown, with anexamination of the strategies that can be usedfor the nurse to support appropriate behaviouralchange. Other therapeutic strategies havebeen outlined, such as the importance of nutritionalsupport – all of which is within the scopeof the nursing role – with opportunities for supportingcontributions from other members ofthe multidisciplinary team.ReferencesAbramovits, W. and M. Boguniewicz (2006).A multicenter, randomized, vehicle-controlledclinical study to examine the efficacy andsafety of MAS063DP (Atopiclair) in themanagement of mild to moderate atopicdermatitis in adults. Journal of Drugs inDermatology, 5(3): 236–244.Abrams, P., L. Cardozo, S. Khoury and A. Wein(Eds) (2002). Incontinence: Report of theSecond International Consultation onIncontinence, 1–3 July 2002. Paris: HealthPublications.Agency for Health Care Policy and Research(1992). Pressure Ulcers in Adults: Predictionand Prevention. A.S.C.P. Guidelines.Ajzen, I. (1991). The theory of plannedbehaviour. Organizational Behavior andHuman Decision Processes, 50: 179–211.Ajzen, I. (2001). Nature and operation ofattitudes. Annual Review of Psychology, 52:27–58.Allen, B.R. (2000). Skin, Hair and Nails.Human Nutrition, pp. 731–746. Edinburgh:Churchill Livingstone.Allen, K.D. (1998). The use of an enhancedsimplified habit-reversal procedure toreduce disruptive outbursts during athleticperformance. Journal of Applied BehavioralAnalysis, 31(3): 489–492.

Protecting the skin and preventing breakdown 65Allman, R.M. (1986). Pressure sores amonghospitalized patients. Annals of InternalMedicine, 105: 337–342.Aly, R., C. Shirley et al. (1978). Effect ofprolonged occlusion on the microbialflora, pH, carbon dioxide andtransepidermal water loss on human skin.Journal of Investigative Dermatology, 71(6):378–381.Armstrong, B.K. and A. Kricker (2001). Theepidemiology of UV induced skin cancer.Journal of Photochemistry and PhotobiologyB, Biology, 63(1–3): 8–18.Austoker, J. (1994). Melanoma: Preventionand early diagnosis. British Medical Journal,308(3944): 1682–1686.Azrin, K.D. and R.G. Nunn (1973). Habitreversal:A method of eliminating nervoushabits and tics. Behaviour Research andTherapy, 11(4): 19–28.Bader, D.L. (1990). The recovery characteristicsof soft tissues following repeated loading.Journal of Rehabilitation Research andDevelopment, 27(2): 141–150.Baillie, L. and V. Arrowsmith (2001). MeetingElimination Needs. Developing PracticalNursing Skills. London: Hodder Arnold.Bandura, A. (1977). Social Learning Theory.Englewood Cliffs, New Jersey: Prentice Hall.Bandura, A. (1996). Social Foundations ofThought and Action: A Social CognitiveTheory. Englewood Cliffs, New Jersey:Prentice Hall.BDNG (British Dermatological Nursing Group)(2008). How to apply a paste bandage, fromwww.bdng.org.uk/news/patients/How_to_Apply_Paste_BandagesBDNG.pdf.Bergstrom, N., B.J. Baden et al. (1987a). TheBraden scale for predicting pressure sore risk.Nursing Research 36: 205–210.Bergstrom, N., P.J. Demuth et al. (1987b).A clinical trial of the Braden scale forpredicting pressure sore risk. Nursing Clinicsin North America 22(2): 417–428.Berwick M, Oliveria S, Luo ST, Headley A,Bolognia JL.Berwick, M., S. Oliveria, S.T. Luo, A. Headleyand J.L. Bolognia (2000). A pilot study usingnurse education as an intervention to increaseskin self-examination for melanoma. Journalof Cancer Education, 15(1): 38–40.Bridgett, C., P. Noren et al. (1996). AtopicSkin Disease: A Manual for Practitioners.Petersfiled: Wrightson Biomedical PublishingLimited.Brown, D.S. and M. Sears (1993). Perinealdermatitis a conceptual framework. Ostomy/Wound Management, 39(7): 20–22, 24–25.Bunn, F., G. Byrne et al. (2004). Telephoneconsultation and triage: Effects on healthcare use and patient satisfaction. CochraneDatabase of Systematic Reviews, 18(4):CD004180.Byers, P.H., P.A. Ryan et al. (1995). Effectsof incontinence care cleansing regimens onskin integrity. Journal of Wound OstomyContinence Nursing, 4: 187–192.Campbell, I.R. and M.H. Illingworth (1992).Can patients wash during radiotherapy to thebreast or chest wall? A randomised controlledtrial. Clinical Oncology (Royal College ofRadiologists), 4: 78–82.Clark, M. (2001). Pressure Ulcer Prevention.The Prevention and Treatment of PressureUlcers. Edinburgh, Mosby: M. J. Morison.Clark, J. and N. Dodge (1999). Exploring selfefficacyas a predictor of disease management.Health Education and Behavior, 26: 72–89.Cokkinides, V.E., M.A. Weinstock, M.C.O’Connell and M.J. Thun (2002). Use ofindoor tanning sunlamps by US youth, ages11–18 years, and by their parent or guardiancaregivers: Prevalence and correlates.Pediatrics, 109(6): 1124–1130.Connor, M. and P. Sparks (2005). Theory ofplanned behaviour and health behaviour.In: Connor, M., Sparks, P. (Eds), PredictingHealth Behaviour: Health and Practice withSocial Cognition Models. Maidenhead: OpenUniversity.Cullum, N., J.J. Deeks et al. (1995). Preventingand treating pressure sores. Quality in HealthCare, 4(4): 289–297.Darmstadt, G.L., M. Mao-Qiang et al. (2002).Impact of tropical oils on the skin barrier:Possible implications for neonatal health in

66 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsdeveloping countries. Acta Paediatrica, 91(5):546–554.Dealey, C. (1995). Pressure sores andincontinence a study evaluating the use oftopical agents in skin care. Journal of WoundCare, 3: 103–105.Dealey, C. (2005). The Care of Wounds: A Guidefor Nurses. Oxford: Blackwell Publishing.Department of Health (2000). Good Practice inContinence Services. London: Department ofHealth.Department of Health (2007). What the CancerReform Strategy means to Patients. London:Crown.Devillers, A.C. and A.P. Oranje (2006).Efficacy & safety of wet wrap dressings as anintervention treatment in children with severeand /or refractory atopic dermatitis: A criticalreview of the literature. British Journal ofDermatology, 154: 579–585.Ehlers, A., U. Gieler et al. (1995). Treatmentof atopic dermatitis: A comparison ofpsychological and dermatological approachesto relapse prevention. Journal of Consultingand Clinical Psychology, 63(4): 624–635.Ersser, S.J., K. Getliffe et al. (2005). A criticalreview of the inter-relationship between skinvulnerability and urinary incontinence andrelated nursing intervention. InternationalJournal of Nursing Studies, 42(7): 823–835.Ersser, S., S. Macguire et al. (2007). BestPractice in Emollient therapy: A Statementfor Health Care Professionals. Aberdeen:A supplement of Dermatological Nursing.European Pressure Ulcer Advisory Panel(EPUAP) (1998). Pressure Ulcer PreventionGuidelines. Retrieved 23 April 2009 fromhttp://www.epuap.org/glprevention.html.European Pressure Ulcer AdvisoryPanel (EPUAP) (2008). Pressure UlcerClassification. Retrieved 2008 fromhttp://www.puclas.ugent.be/puclas/e/page3480.html.Fader, M., S. Clarke-O’Neill et al. (2003).Management of night-time urinaryincontinence in residential settings for olderpeople an investigation into the effects ofdifferent pad changing regimes on skin health.Journal of Clinical Nursing, 12: 374–386.Faergemann, J., R. Aly et al. (1983). Skinocclusion effect on Pityrosporum orbiculare,skin PCO2, pH, transepidermal waterloss, and water content. Archives ofDermatological Research, 6: 383–387.Fiers, S.A. (1996). Breaking the cycle: Theetiology of incontinence dermatitis andevaluating and using skin care products.Ostomy/Wound Management, 42(3): 32–34,36, 38–40.Fluhr, J. W., S. Lazzerini et al. (1999). Effectsof prolonged occlusion on stratum corneumbarrier function and water holding capacity.Skin Pharmacology and Applied SkinPhysiology, 4: 193–198.Flyvholm, M.A. (1993). Contact allergens inregistered agents for industrial and householduse. British Journal of Industrial Medicine,50: 1043–1050.Gandini, S., F. Sera et al. (2005). Meta-analysisof risk factors for cutaneous melanoma:III. Family history, actinic damage andphenotypic factors. European Journal ofCancer, 41(14): 2040–2059.Getliffe, K. and M. Dolman (2003). PromotingContinence: A Clinical and ResearchResource. Edinburgh: Elsevier Science.Global Alliance to Eliminate LymphaticFilariasis (GAELF). Retrieved 7 May 2009from http://www.filariasis.org/.Gooch, J. (1989). Skin hygiene. TheProfessional Nurse, 5(1): 13–18.Goodyear, H.M. and J.I. Harper (2002). Wetwrap dressings for eczema: An effectivetreatment but not to be misused. BritishJournal of Dermatology, 146(1): 159.Goodyear, H.M., K. Spowart et al. (1991).‘Wet-wrap’ dressings for the treatment ofatopic eczema in children. British Journal ofDermatology, 125(6): 604.Gosnell, P.J. (1973). Assessment tool to identifypressure sores. Nursing Research 22: 55–59.Gray, M. (2004). Preventing and managingperineal dermatitis: A shared goal for woundand continence care. Journal of Wound,Ostomy and Continence Nursing, 3(1):S2–S11.Gulralnik, J.M., T.B. Harris et al. (1988).Occurrence and predictors of pressure

Protecting the skin and preventing breakdown 67sores in the national health and nutritionexamination survey follow-up. Journal ofAmerican Geriatrics Society, 36: 807–812.Haalboom, J.R., J. den Boer et al. (1999). Riskassessmenttools in the prevention of pressureulcers. Ostomy/Wound Management, 45(2):20–26, 28, 30–34.Hagermark, O. and C.F. Wahlgren (1995).Treatment of itch. Seminars in Dermatology,14(4): 320–325.Halfens, R.J.G., R.M. Achterberg et al. (2000).Validity and reliability of the Braden scale andthe influence of other risk factors: A multicentreprospective study. InternationalJournal of Nursing Studies, 37: 313–319.Hancock, D. (2007). How to Check YourSkin for Skin Cancer: Skin Examination.Southampton: Wessex Cancer Trust.Havas, S., K. Treimen et al. (1998). Factorsassociated with fruit and vegetableconsumption among women participatingin WIC. Journal of American DieteticAssociation, 98: 1141–1148.Held, E., H. Lund et al. (2001). Effects ofdifferent moisturizers on SLS-irritated humanskin. Contact Dermatitis, 44: 229–234.Hinchliff, S.M., S.E. Montague et al. (2005).Physiology for Nursing Practice. Oxford:Bailliere Tindall.Houwing, R., M. Rozendaal et al. (2003).A randomised, double-blind assessment of theeffect of nutritional supplementation on theprevention of pressure ulcers in hip-fracturepatients. Clinical Nutrition, 22(4): 401–405.International Cancer Research FundingOrganisations (2008). International CancerResearch Portfolio. From http://www.cancerportfolio.org/index.jsp.Kirsner, R.S. and C.W. Froelich (1998).Soap and detergents understanding theircomposition and effect. Ostomy/WoundManagement, 44(3A Suppl.): 62s–70s.Kligman, A. (1994). Hydration injury to humanskin. In: Elsner, P., Berardesca, E., Mailbach, H.(Eds), Bioengineering of the Skin: Water andthe Stratum Corneum. Boca Raton: CRC Press.Ko, D.S.C., R. Lerner et al. (1998). Effectivetreatment of lymphoedema of the extremities.Archives of Surgery, 133: 452–458.Koinberg, I.L., B. Fridlund et al. (2004). Nurseledfollow-up on demand or by a physicianafter breast cancer surgery: A randomisedstudy. European Journal of OncologyNursing, 8: 109–117.Korting, H., M. Kober et al. (1987). Influenceof repeated washings with soap and syntheticdetergents on pH and resident flora of theskin of forehead and forearm. Acta Dermato-Venerologica, 67: 41–47.Korting, H.C. and O. Braun-Falco (1996).The effect of detergents on skin pH and itsconsequences. Clinics in Dermatology, 14:23–27.Langer, G., G. Schloemer et al. (2003)Nutritional interventions for preventing andtreating pressure ulcers. Cochrane Databaseof Systematic Reviews, 4: CD003216 (DOI:10.1002/14651858).Latter, S., P. Yerrell, J. Rycroft-Malone andD. Shaw (2000). Nursing, medicationeducation and the new policy agenda: Theevidence base. International Journal ofNursing Studies, 37(6): 469–479.Leonardi, M.C., S. Gariboldi et al. (2008).A double-blind, randomised, vehicle-controlledclinical study to evaluate the efficacy ofMAS065D in limiting the effects of radiationon the skin: Interim analysis. EuropeanJournal of Dermatology, 18(3): 317.Lymphoedema Framework (2006). Best Practicefor the Management of Lymphoedema.International Consensus. London: MEP Ltd.Mackie, R.M. (2003). Clinical Dermatology(5th edition). Oxford: Oxford University Press.Martin, E. and T. McFerran (2008).A Dictionary of Nursing. Aylesbury, England:Aylesbury Market House Books Ltd.McGeown, J.G. (2002). Physiology. Edinburgh:Churchill Livingstone.McInnes, E., S.E.M. Bell-Syer et al. (2008)Support surfaces for pressure ulcerprevention. Cochrane Database ofSystematic Reviews, 4: CD001735 (DOI:10.1002/14651858).Melia, J., L. Pendrey et al. (2000). Evaluation ofprimary prevention initiatives for skin cancer:A review from a UK perspective. BritishJournal of Dermatology, 143: 701–708.

68 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsMiltenberger, R.G., R.W. Fuqua et al. (1998).Applying behaviour analysis to clinicalproblems: Review and analysis of habitreversal. Journal of Applied BehaviourAnalysis, 31(3): 447–469.Moffatt, C.J., P.J. Franks et al. (2003).Lymphoedema: An underestimated healthproblem. QJM, 96(10): 731–738.Morison, M.J., Ed. (2001). The Prevention andTreatment of Pressure Ulcers. Edinburgh:Mosby.Nach, S., J. Close et al. (1981). Skin frictioncoefficient changes induced by skin hydrationand emollient application and correlationwith perceived skin feel. Journal of theSociety of Cosmetic Chemists, 32: 5565.National Audit Office (2001). Tackling Obesityin England. London: The Stationery Office.National Breast and Ovarian Cancer Centre(2008). Skin Care during Radiotherapy.Australia: NBOCC.National Cancer Research Institute (2005).Strategic Plan 2005–2008. London, NCRI.National Institute for Health and ClinicalExcellence (2007). The Most Appropriatemeans of Generic and Specific Interventionsto Support Attitude and Behaviour Change atPopulation and Community Levels. London:NICE.Naylor, W. and J. Mallett (2001). Managementof acute radiotherapy induced skin reactions:A literature review. European Journal ofOncology Nursing, 5: 221–233.Neelemaat, F., H.M. Kruizenga et al. (2008).Screening malnutrition in hospital outpatients.Can the SNAQ malnutrition screening toolalso be applied to this population? ClinicalNutrition, 27(3): 439–446.Nixon, J. (2001). The pathophysiology andaetiology of pressure ulcers. In: Morison,M.J. (Ed.), The Prevention and Treatment ofPressure Ulcers. Edinburgh: Mosby.Nixon, J., E.A. Nelson et al. (2006). Pressurerelieving support surfaces: A randomisedevaluation. Health Technology Assessment,10(22): iii.Noren, P. (1995). Habit reversal – a turning pointin the treatment of atopic dermatitis. Clinicaland Experimental Dermatology, 20(1): 2–5.Norton, D., R. McLaren et al. (1962). AnInvestigation of Geriatric Nursing Problemsin Hospital. Edinburgh, Churchill Livingstone.O’Flynn, J., H. Peake et al. (2005). Theprevalence of malnutrition in hospitals can bereduced: The results from three consecutivecross-sectional studies. Clinical Nutrition,24(6): 1078–1088.Office of National Statistics (1999). Attitudes toprotecting self from sun exposure: By gender.Social Trends 32. From http://www.statistics.gov.uk/StatBase/ssdataset.asp?vlnk=5238&Pos=3&ColRank=2&Rank=272.Oliveria, S.A., J.F. Altman et al. (2002). Use ofnonphysician health care providers for skincancer screening in the primary care setting.Preventive Medicine 34(3): 374–379.Oliveria, S.A., S.W. Dusza et al. (2004). Patientadherence to skin self-examination – Effectof nurse intervention with photographs.American Journal of Preventive Medicine,26(2): 152–155.Pani, S.P. and A. Srividya (1995). Clinicalmanifestations of bancroftian filariasis withspecial reference to lymphoedema grading.Indian Journal of Medical Research, 102:114–118.Patel, G.K. (2005). The role of nutrition in themanagement of lower extremity wounds.The Journal of Lower Extremity Wounds,4(1): 12–22.Perry, S., C. Shaw et al. (2002). The prevalenceof faecal incontinence in adults aged 40 yearsor more living in the community. Gut, 50(4):480–484.Porock, S. and L. KristJanson (1999). Skinreactions during radiotherapy for breastcancer: The use and impact of topical agentsand dressings. European Journal of CancerCare, 8(3): 143–153.Rapp, J., R.G. Miltenberger et al. (1998).Simplified habit reversal treatment for chronichair pulling in three adolescents: A clinicalapplication with direct observation. Journalof Applied Behavior Analysis, 31: 299–302.Rosal, M.C., J.K. Ockene et al. (1998).Coronary Artery Smoking InterventionStudy (CASIS): 5 year follow up. HealthPsychology, 1(7): 476–478.

Protecting the skin and preventing breakdown 69Roy, I., A. Fortin et al. (2001). The impactof skin washing with water and soapduring breast irradiation: A randomizedstudy. Radiotherapy and Oncology, 58(3):333–339.Royal College of Physicians (2007). ThePrevention, Diagnosis, Referral andManagement of Melanoma of the Skin:Concise Guidance to Good Practice.Number 7 Clinical Standards: Royal Collegeof Physicians and British Association ofDermatologists. London: Royal College ofPhysicians.Runciman, P., H. Watson et al. (2006).Community nurses’ health promotion workwith older people. Journal of AdvancedNursing, 55(1): 46–57.Ryan, T.J. (2008). Healthy Skin for All:A Multi-faceted Approach. Oxford:Parchment Press.Saraiya, M., K. Glanz et al. (2004).Interventions to prevent skin cancer byreducing exposure to ultraviolet radiation:A systematic review. American Journal ofPreventive Medicine, 27(5): 422–466.Schnelle, J.F., G.M. Adamson et al. (1997). Skindisorders and moisture in incontinent nursinghome residents intervention implications.Journal of American Geriatrics Society, 45:1182–1188.Schols, J.M.G.A. and M.A. de Jager-v d Ende(2004). Nutritional intervention in pressureulcer guidelines: An inventory. Nutrition,20(6): 548–553.Shannon, M.L. and P. Skorga (1989). Pressureulcer prevalence in two general hospitals.Decubitus, 2(4): 38–43.Sharp, L. and C. Tischelman (2005). Smokingcessation for patients with head and neckcancer. Cancer Nursing, 28(3): 226–235.South West Public Health Observatory (2008).Factsheet No 2: Malignant Melanoma inthe South West. ICD-10: C43, 15 September2005 (date created) from http://www.swpho.nhs.uk/.Strong, D. (1998). Dermatologic Emergencies.Dermatologic Nursing Essentials: A CoreCurriculum. New Jersey: Anthony J. Jannetti.The National Prescribing Centre (1998).MeReC bulletin. Prescribing new drugs ingeneral practice. Liverpool, 9: 21–24.Tsai, T.F. and H.I. Maibach (1999). Howirritant is water? An overview. ContactDermatitis, 41: 311–314.Tucker, S., I. Turesson et al. (1984). Evidence ofindividual differences in the radiosensitivity ofhuman skin. International Journal of RadiationOncology Biology Physics, 10: 607–618.Vaqas, B. and T.J. Ryan (2003). Lymphoedema:Pathophysiology and management inresource-poor settings – relevance forlymphatic filariasis control programmes.Filiaria Journal, 2: 4.Walmsley, D. and P.G. Wiles (1990). Reactivehyperemia in the skin of the human footmeasured by laser doppler flowmetry – effectsof duration of ischemia and local heating.International Journal of Microcirculation –Clinical and Experimental, 9(4): 345–355.Waterlow, J. (1988). The Waterlow card forthe prevention and management of pressuresores: Towards a patient policy. Care Scienceand Practice, 6(1): 8–12.Well, M. and S. MacBride (2003). Radiationskin reactions. In: Faithfull, S., Wells, M.(Eds), Supportive Care in Radiotherapy, pp.135–159. Edinburgh: Churchill Livingstone.Whittingham, K. (1998). Cleansing regimensfor continence care. Professional Nurse, 3:167–172.Wong, K., F.K. Wong et al. (2005). Effectsof nurse-initiated telephone follow-up onself-efficacy among patients with chronicobstructive pulmonary disease. Journal ofAdvanced Nursing, 49(2): 210–222.Yosipovitch, G., A. DeVore et al. (2007).Obesity and the skin: Skin physiology andskin manifestations of obesity. Journal of theAmerican Academy of Dermatology, 56(6):901–916.


5EmollientsRebecca PenzerIntroductionThroughout human history it is possible tofind references to the use of emollients. AncientEgyptians used sesame, almond and olive oilsto anoint their skin and to care for the wigsthat were fashionable at the time. Natural oilswere also used to perfume these. Cleopatrafamously bathed in asses’ milk believing that itwould be good for her skin. Lanolin, extractedfrom sheep wool, was widely used as an emollientin medieval Europe. In 1872 a patent wasfiled for ‘Vaseline’, a product which 140 yearslater is still immensely successful. Today thereare a myriad of cosmetic emollients available,all making various claims towards creatingor maintaining youthful looks in the user. Thechoice of medicinal emollients is also extensive.The British National Formulary lists at least 34topical emollient products (this does not includethe bath oils), which can make selecting a suitableproduct something of a challenge (BritishMedical Association and Royal PharmaceuticalSociety of Great Britain, 2007) (see Appendix 3for list of emollients). This chapter will explorewhat emollients are and how they work, itwill also provide some practical guidance forselecting and using emollients to ensure thatthey are being used to best therapeutic effect.DefinitionA standard definition for emollients is notwidely available, although they are commonlyreferred to as substances that ‘…reduce thesigns and symptoms of dry, scaly skin, makingthe rough surface soft and smooth’ (Kligman,2000). This definition does not, perhaps, dojustice to the complex nature of emollients. Notonly are modern day formulations complex, buttheir effects are numerous and generally notentirely understood (Marks, 2001). Their usefulnessis well recognised by those who work inthe field of dermatology; however, there is littlegood science to back up how they should beused, although increasingly scientific attention isbeing given to how they work.Often the words moisturiser and emollientare used synonymously. The British NationalFormulary makes no distinction between thetwo. However, some sources do differentiatebetween an emollient and a moisturiser; thesedifferences are discussed here.

72 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsThe New Zealand online dermatology resource,Dermnet NZ, refers to an emollient as a substancethat softens the skin and a moisturiser as onewhich adds moisture (www.dermnet.nz). Voegeli(2007) suggests that the following distinctionsshould be made:■■Emollients are lipids that occlude the skinsurface thus preventing water loss from thestratum corneum.Moisturisers are lipid emulsions that activelyhydrate the skin by the application of ahumectant to the skin surface (often glycolor urea). Humectants are water loving anddraw water from the dermis into the epidermisthus hydrating it.It is worth noting that some products haveemollient properties only and some have bothemollient and moisturising properties. In thisbook, the word emollient will be used to refer toproducts that soften the skin by increasing thelevel of moisture in the stratum corneum, i.e. anemollient moisturises the skin. The mechanismsfor this are discussed later in this chapter.Constituents of emollientsEmollient products are composed of a variety ofconstituent substances. Broadly speaking thesecan be divided into active ingredients and excipients.Active ingredients are those ingredients thatexert a therapeutic benefit. Excipients can bedescribed as the ingredients that allow the productto be effective but have no direct therapeuticbenefit themselves. They will include preservativesand emulsifiers. Manufacturers are obligedto list the active ingredients and excipients oftheir products. It is worth noting that this listingdoes not always highlight the potential sensitiserswithin a product. For example, emulsifying waxcontains cetostearyl alcohol which is a potentialsensitiser. On products, only emulsifying waxwill be listed. In general the British NationalFormulary will highlight when a product has apotential sensitiser in it. Other common constituentsand their purpose are listed in Table 5.1.Emollients will always have some level of lipidin them. Lipid is a broad term used to describedifferent types of waxes, oils and fats (Marks,2001). Oils are the most common lipids foundin emollient products; these include vegetableoils such as sunflower oil, mineral oils such aspetrolatum or synthetic man-made oils such aspolysiloxane. The only animal fat that is regularlyused is lanolin.Lanolin (also known as a wool alcohol or awool wax) is extracted from sheep’s wool. It isexcreted by the sheep’s sebaceous glands andkeeps the fleece soft whilst also protecting itfrom the elements. Historically, it has a reputationfor being highly allergenic. Whilst this mayhave been of some concern in the past, modernextraction and purification methods mean thatlanolin has a very low incidence of sensitisationand should not be considered a common allergen(Stone, 2000; British Medical Associationand Royal Pharmaceutical Society of GreatBritain, 2007).There is evidence to show that lanolin isan effective emollient. This is summarised byHarris and Hoppe (2000) who report a numberof studies. These suggested that lanolin:■■■■■Reduces transepidermal water loss in xeroticskin and has long-term effects (up to 14 daysafter 21 days of application);Restores barrier function in normal skin thathas been perturbed by acetone;Can act as a barrier to virus particles andirritants;Increases the rate of re-epithelisation;Decreases levels of skin roughness for up to8 hours after application (Harris and Hoppe,2000).Lipids may be mixed with differing amounts ofwater to produce the various consistencies ofemollient. The absolute quantity of water andthe amount relative to the level of lipid presentwill affect the consistency and efficacy of theproduct. Therefore, products with high lipidcontent (and no water) will tend to be greasyand heavy whilst those with low lipid content(and high levels of water) will be less greasyand lighter. Most cosmetic emollients (usually

Emollients 73Table 5.1 Potential sensitisers as listed in BNF and found as excipients in emollients.ExcipientPropertyBenzyl alcoholButylated hydroxyanisoleButylated hydroxytolueneCetostearyl alcohol (including cetyl and stearyl alcohol)ChlorocresolEdetic acid (EDTA)FragrancesHydroxybenzoates (parabens)ImidureaIsopropyl palmitateN-(3-Chloroallyl)hexaminium chloride (quaternium 15)PolysorbatesSodium metabisulphitePropylene glycolWool fat and related substances including lanolin (notgenerally thought of as excipient, but rather an activeingredient)Sorbic acidPreservativePreservativeHas moisturising properties(and emulsifying properties)PreservativeImproves product stabilitytowards the airTo make a product smellpleasant or to maskunpleasant odoursPreservativePreservativeThickening agentPreservativeEmulsifierPreservativeHumectant, preservative andstabiliserEmollientPreservativelotions) have a high water content, whichensures that they sink into the skin quicklywithout leaving greasy traces. However theyare less effective at retaining water in the skinthan their greasier counterparts, creams andointments.Potential side effectsEmollients are commonly thought to have fewside effects and it is true that generally patientscan use these products without fear of unwantedoutcomes. However, there are some factors thatit is important to be aware of.Contact dermatitisContact dermatitis is the term given to adverseinflammatory changes that occur in the skinwhen it comes into contact with certain products.Patients will sometimes complain of transientstinging or discomfort when a product isapplied. This is not unusual and may be causedby the application of a substance to inflamedand broken skin rather than by any true sensitivity.This cannot be described as a true contactdermatitis. However, if the discomfort is morethan just transient it may represent a true contactdermatitis; in other words, the patient isexperiencing an irritant or allergic reaction tosome ingredient within the product.

74 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsAn allergic contact dermatitis is an immunemediatedresponse to a product; once the patienthas been sensitised they will react to the producteven if they come into contact with only a smallamount of it. The severity of the reaction mayincrease if exposure to the allergen is increased.The reaction may be immediate or can bedelayed for 48–96 hours after the contact (Nicolet al., 1995). An immediate response is knownas a Type 1 or an IgE-mediated response. It canbe mild or in severe cases the individual may gointo anaphylactic shock. A delayed response isknown as a Type 4 or T-cell-mediated response.In contrast an irritant contact dermatitis is anon-immune-mediated reaction where the skinreacts immediately or within hours. The adverseresponse can occur after a period of cumulativeuse, e.g. after frequent hand washing. Inthis instance no response is seen initially, butrepeated use of a product causes inflammation.Alternatively, an irritant contact response canoccur immediately after contact with a substance.If a contact dermatitis is suspected, patch testingmay be an appropriate way to investigate theprecise cause of the inflammation (see Chapter 9for further details on patch testing). Whilst thisprocess may be able to determine the nature ofthe allergen or irritant, it may then be almostimpossible to determine whether it is present incommercial preparations.It is most common for the excipients to actas sensitisers rather than the active ingredientsthemselves. Common irritants/allergens includeperfumes and preservatives (de Groot, 2000). Itis thought that for around 1% of the population,fragrances act as sensitisers and that for thosewith eczema this percentage increases to around14% (de Groot, 2000). It is good practice, therefore,to recommend that people with sensitiveskin use products that are truly fragrance free. Itcan be difficult to find absolutely fragrance-freeproducts as many contain masking fragrances.Most prescribable products in the UK are fragrancefree.In order to reduce the impact of any potentialadverse reactions when applying emollients,patients should be advised to apply a small ‘testpatch’ to an area of their body (the inner armis a good place to use). This should be left for48 hours; if no adverse reaction is seen, the productis most likely to be safe to use extensively.Another issue when considering potentialadverse effects of emollients is the importanceof using the product correctly, both the correctamount and in the correct way. For examplea product that is used extensively in a waythat it was not designed for, is aqueous cream.Originally designed as a wash product (i.e. tobe applied to the skin as a soap substitute andthen washed off), it has become a commonlyused leave-on emollient. For many people thisdoes not create any problems, although it is nota particularly effective emollient for those withdry skin. However, Cork et al. carried out anaudit which showed that when aqueous creamwas used as a leave-on product for children witheczema, it caused a significantly higher level ofstinging and discomfort than other emollientproducts (Cork et al., 2003). Interestingly, thesame audit showed that when aqueous creamwas used as a wash product, it did not causethe same level of adverse reactions, and was anacceptable product. This audit emphasises theimportance of using products in the way thatthey were designed for; this will help reduceadverse reactions.Adverse effects caused by the occlusivenature of emollientsGreasy topical emollients can result in painfulpustules caused by the blockage and consequentinfection of the hair follicle; this is known as folliculitis.This can usually be avoided by correctapplication of emollients, i.e. in the direction ofthe lie of the hair. Changing the emollient to alighter, less greasy one may be enough to resolvethe problem; if not it may be necessary to stopemollient application for a time until the folliculitisresolves. Occasionally, topical or even oralantibiotics may be needed. If there is a high bacterialload on the skin caused by poor hygiene,folliculitis may be more likely if an occlusiveemollient is applied. This will be aggravatedfurther by hot, humid climatic conditions.In dry, hot environments occlusive emollientsmay reduce heat loss through the skin. The lipids

Emollients 75act as an insulator decreasing evaporation fromthe skin and thus affecting thermoregulation.This may be particularly important in small childrenwho have a high surface area to volumeratio. In an adult or older child, thick occlusiveemollients may feel very uncomfortable inhot weather. So choosing a lighter, less greasyemollient is preferable.Other safety concernsEmollients of all types, but particularly bath oilsand soap substitutes, can make the skin and thebath or shower feel slippery. Caution needs tobe taken especially with vulnerable groups likebabies and older people to prevent accidents.Another potential safety concern involves theflammability of paraffin-based emollients whenthey are soaked into a fabric. Thus dressings orclothing that have absorbed quantities of emollientsthat are primarily paraffin based (whichincludes most ointments) are at risk of catchingfire if they come into contact with a nakedflame. Patients should be advised not to smokeor come into contact with any type of flame ifthey are wearing paraffin-soaked garments orbandages (British Medical Association and RoyalPharmaceutical Society of Great Britain, 2007).Emollient formulationsIn order to ensure the maximum impact ofemollients, it has become common practice touse them at every stage of the skin-care process.This means that there are emollient cleansers,emollient bath additives and topical emollientswhich are left on the skin (Holden et al., 2002).These three elements are often collectivelyreferred to as ‘total emollient therapy’. Thissection will give an overview of the availableemollient formulations.Bath additivesThese are liquid, lipid products usually basedon liquid paraffin but may be formulated usingvegetable oils such as soya. When added towater, they are dispersible and therefore appropriatefor use within washing water. Their primaryaim is to form a thin layer of oil over thesurface of the skin thus helping to rehydrate it.Most will also cleanse the skin thus removingthe need for further skin cleansing products.Method of applicationA quantity, as identified by the manufacturer,should be added to the wash water and thewater then agitated to ensure the product isdispersed properly. Some bath additives canbe used directly onto the skin in the shower,although clearly it is much harder to measurethe amount used. This may be important in thecase of an antibacterial bath product as it maybe irritant if overused. There is little independentresearch evidence that proves the therapeuticbenefit of bath emollients (Drugs andTherapeutics Bulletin, 2007); however, patientsmay find them helpful and some companyfundedresearch does suggest they are beneficial(Bettzuege-Pfaff and Melzer, 2005).Many of the greasier ointment emollients (e.g.emulsifying ointment) can also be added to bathwater. They must first be dissolved in hot waterand then added to a bath of normal temperaturewater. It may not disperse as well as a tradename bath additive but there is no evidence tosuggest it is any more or less effective.Most bath additive products will make thebath and the person who has been immersed inthem, slippery.Skin cleansersFor most people with dry skin conditions andcertainly for those who have eczema, using soapis not recommended. Soap works by removingnatural oils from the skin and with those oils gothe debris that builds up on the skin over a day.This will cause those with a dry skin to becomeeven drier. Therefore, skin cleansers should beused instead of soap. Rather than stripping theskin off their natural oils, skin cleansers (alsoknown as soap substitutes) help to trap moisturein the skin, whilst removing the surface dirt.

76 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsMethod of applicationAs mentioned earlier, many of the bath additiveproducts can be used as skin cleansers. However,proprietary substances like aqueous cream andemulsifying ointment can also be used as soapsubstitutes. They should be applied to the skinusing the hand or a washcloth and then rinsedoff.Whilst cleansing the skin there are certainpractices that should be avoided:(1) Using soaps and bubble baths as they removenatural oils from the skin;(2) Soaking for prolonged periods (over 15minutes) in the bath as the skin can becomewaterlogged and this will effect the barrierfunction;(3) Excessively hot water in the bath as this willincrease the level of moisture lost from theskin;(4) Vigorous drying and rubbing of the skinafter a bath as this too will compromise theskin barrier function and may also make theskin more irritated.Leave-on topical emollientsAs the name suggests ‘leave on topical emollients’are ones that are applied to the skin andleft in place, not washed off.LotionsLotions have a high level of water in themand are therefore easy to use. They are readilyabsorbed into the skin and do not leave it feelinggreasy. Because of these features most cosmeticemollients fall into this category. They are not,however, very effective for those with a dry skincondition. Some products in certain conditions(hot, dry weather) may actually dry the skin asthe high level of water in the product evaporatesoff the skin taking natural moisture with it andthus making the skin even drier.CreamsCreams are a mixture of water in lipid, generallythere is more lipid than water. These productsabsorb into the skin relatively quickly, but arethicker and greasier than lotions. The water andlipid combination of both creams and lotionscreates a number of challenges with regards tomaintaining a stable product. Emulsifiers haveto be added to ensure that the lipid and wateremulsion stay together and preservatives areneeded to prevent bacterial contamination.OintmentsOintments fall at the very greasy end of theemollient continuum. They do not contain anywater and therefore there is no need to addpreservatives. This does not necessarily meanthat there are no potential sensitisers in ointmentsas there may be other ingredients addedto stabilise or enhance the effectiveness of theproduct. Preservatives are not needed in lipidonlyproducts (i.e. ointments) as there is nomedium for bacterial growth. Therefore, whilstthese are the heaviest, greasiest emollient products,they are the ones that are least likely tocause sensitisation. The consistency of ointmentsis affected by ambient temperature. Warmth willsoften ointments, which may appear quite hardand unpliable whilst in the pot.SpraysEmollient sprays contain lipids such as white softparaffin, liquid paraffin and fractionated coconutoil. Propellants, for example butane and isobutene,are added to ensure that the emollient isejected from the can in a spray format over theskin. Some spray emollients use a ‘bag in a can’technology. This means that the spray can beeffectively sprayed at any angle and that the emollientis kept totally separate from the propellant.Gel emollientsThese are oil and water products; however, theway that they are emulsified is different fromnormal creams and lotions. The carbomer gellingagent holds the oil and water togetherwhilst it is in the bottle (and gives the productits typical ‘jelly-like wobble’); however, when itis applied to the skin, the gelling agent dissolvesand allows the oil and water to separate. Thishas the impact of allowing the oil to stay on the

Emollients 77skin longer and not to be vulnerable to beingwashed away.Method of applicationThere does not seem to be a scientific word forthe science of topical emollient application. Thisis reflected in the fact that the literature is virtuallydevoid of any experimental data about howtopical emollients should be applied to the skin toachieve maximum therapeutic effect. Indeed thereare significant questions over such basic questionsas ‘Do medicinal bath oils offer any benefit?’‘Which should be applied first to the skin, atopical emollient or a topical steroid?’ Thus muchof the practice in relation to emollient use is basedupon ‘custom and practice’ and deriving appropriatetechniques from first principles.When considering methods of emollientapplication, there are five questions for whichit would be useful to have answers, in order toguide practice. These are:■■■■■How much topical emollient to apply?How frequently to apply the topicalemollient?When to apply the topical emollient – whichincludes when to apply it in relation to othertopical medicines?How to physically apply the topicalemollient?Where to apply the topical emollient?Literature reviews reveal that there is preciouslittle scientific evidence to guide practice in anyof these areas (Penzer, 2005; Ersser et al., 2007),which means that guidance offered in textbooksand journals is based on clinical practice andexperience.The other factor that should be taken intoaccount when prescribing emollients is thatpatients with dry skin conditions have to ‘wear’their treatments. How it feels on their skin,how easy it is to apply and whether there is asmell associated with it, all impact on whethersomeone will use the emollient or not. No singleemollient will suit everyone, and there isno doubt that patients need to experimentwith different types of emollients before theysettle on one or two that suit them (All PartyParliamentary Group on Skin, 2006). Becausethe skin can feel different depending on climate,it is possible that individuals may need alternativeemollients at different times of the year. Forexample, in winter, a heavy greasy emollientmay feel fine, but in the summer months somethinglighter might be preferable.How much topical emollient to apply?Unlike the prescription of oral medications,the prescription of topical emollients is byits nature an inexact science. The amount ofemollient that a person needs in order to gainmaximum therapeutic benefit will depend onthe extent of their dry skin (in terms of boththe area affected and level of dryness) andtheir size, e.g. an adult will require more thana child and a large adult more than a smallerone. This means that judgements must be madeby the health care professional as to the likelyquantity required and clear instructions givento the patient to this effect. What is not acceptableis to expect the patient to follow a generalinstruction like ‘apply liberally’ as this may beinterpreted in any number of ways.Guidance for the correct amounts of emollientscan be found in the British NationalFormulary (British Medical Association andRoyal Pharmaceutical Society of Great Britain,2007) and are laid out in Table 5.2. Othersuggested quantities are provided by BrittonTable 5.2 Recommendation for quantities of emollients foran adult over a period of 2 weeks.Creams andointments (g)Lotions (ml)Face 15–30 100 mlBoth hands 25–50 200 mlScalp 50–100 200 mlBoth arms or both legs 100–200 200 mlTrunk 400 500 mlGroins and genitalia 15–25 100 ml

78 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 5.1 Amounts of emollientmeasured in spoonfulsA formal topical regime of emollientwould be, for example, 10 g to each of thefollowing areas:Each armThe chestThe abdomenEach thighEach shinUpper backLower back2 g to the face10 g is the equivalent of a desert spoonful.If someone is less dry, the same ratiosshould be used by 5 g (a teaspoon) per areaor 20 g (a tablespoon) per area if more dry.who gives three possible regimes as guidance(Britton, 2003) (see Box 5.1). This is particularlyhelpful when explaining to patients as itmay be easier for them to understand measuressuch as spoonfuls rather than grams or millilitres.Custom and practice has become thatan adult with a dry skin condition should usearound 500 g of topical emollient a week and achild should get through 250 g per week. Thisis only guidance and really only serves to ensurethat patients with dry skin conditions are notprescribed quantities less than 500 g (unless it isfor the convenience of having a smaller quantityto carry around.)How frequently to apply emollients?The usual advice for patients with a dry skincondition is to apply a topical emollient at leasttwice daily. Better advice is to apply emollientsto the skin whenever it gets dry, which in realitymay be every 2 hours. This is likely to beimpractical for most people, so the patientneeds to be able to experiment with emollientsto find the one that suits them best and hydratesthe skin most effectively without too manycompromises in terms of impact on quality oflife. It is generally thought that greasier emollientsare effective for a longer period of timethan creams and gels, but this will depend tosome extent on the individual.When to apply emollients?It is generally agreed that an optimal time toapply emollients is after a bath. This helps totrap water into the stratum corneum and thewarmth of the skin makes applying emollientseasier. The trapping of moisture in the skin canbe enhanced if the skin is left slightly damp afterwashing. Whilst it is important that flexures arewell dried, to prevent intertrigo, the rest of theskin can be left slightly moist and emollientsthen applied. This process of ‘soaking andsealing’ moisture into the skin is key in helpingrehydrate the skin (Nicol and Boguniewicz,2008). To reduce the likelihood of the skinbecoming very dry overnight, it is always advisableto apply emollient just before going to bed.There is considerable debate about when toapply emollients in relation to other topical products,particularly topical steroids which are usedfor patients who have eczema. It is agreed thatemollients are of key importance in the treatmentof eczema (Akdis et al., 2006); the debatecentres around when they should be applied. Anumber of authors have shown that use of emollientsappears to reduce the amount of topicalsteroid needed to control eczema (Watsky et al.,1992; Lucky et al., 1997; Hanifin et al., 1998;Grimalt et al., 2007). However, these are in noway universally accepted findings. Using biologicalprinciples, some would argue that applyingan emollient prior to a steroid may reduce itsefficacy. The argument used is that the emollientsaturates the layers of the stratum corneumpreventing effective penetration of the topicalsteroid to the deeper layers and therefore reducingits efficacy. Currently no robust clinical dataexists to support or disprove this point.Where does this leave the practitioner who iscaring for someone with eczema who is usingemollients and topical steroids? If an emollientis applied prior to a steroid, considerationshould be given to how long it is given to ‘soak’

Emollients 79into the skin before a steroid is applied. Thetiming will vary, but it is generally acceptedthat the skin should be tacky but not slippery.Around 30 minutes is usually long enough forthis to have happened, but may need to be upto an hour. Similar thoughts should be givento the circumstances around applying a steroidbefore an emollient. If a steroid is not allowedto sink in properly concerns around diluting theeffect of the steroid or smearing onto parts ofthe body where it is not required may be valid,although Smoker could not find any evidenceto back up these concerns (Smoker, 2007). Ifocclusion is to be applied over topical treatmentsallowing a time period to elapse may beless important. In the case of wet wrapping forexample, applying topical steroid to the areasthat need it and then applying emollient elsewhereis a sensible approach (see Chapter 9 forfurther detail).In other disease areas like psoriasis, the evidenceis even weaker as to the order in whichto apply treatments. One unpublished experimentreported by Finlay suggested that the useof emollient improved outcomes for patientstreated with dithranol (Finlay, 1997). Whilst itis generally accepted that emollients are helpfuladjuvants for the treatment of psoriasis(National Institute for Clinical Excellence, 2001;Hall, 2003), their exact use is hardly explored atall in the literature (Penzer, 2005).In conclusion, all it is possible to say categoricallyis that the lack of evidence in this fieldmakes definitive recommendations for practicein this area difficult. The general principles thatshould guide practice include:(a) Applying active topical medications (e.g. steroids)to well-moisturized skin, is generallypreferable than applying them to dry skin;(b) Around 30 minutes should elapse betweenapplying an emollient and an active topicalmedication. The exact time period willdepend upon how dry the skin is and howgreasy the emollient;(c) If both emollient and topical steroid have togo on at the same time, applying the steroidto the inflamed areas and the emollienteverywhere else is acceptable;(d) If products are being applied under occlusivebandages or dressings, it is probably lessimportant for there to be a gap between theactive topical medication and the emollient.How to apply emollients?The literature in general agrees that emollientsshould be applied using a gentle strokingmotion following the lie of the hair on the body.This said, no specific scientific evidence couldbe found to back this up. The rationale for thisis based on a biological principle that rubbingthe skin with a greasy emollient could lead toan irritated or blocked hair follicle and theresulting folliculitis (see the section on potentialside effects). The only possible exception tothis is when an emollient is being used as partof another therapeutic process, e.g. lymphaticdrainage massage. In these instances, goingagainst the lie of the hair may be necessary; itis generally recommended to use a lighter, lessgreasy emollient in this case as these are lesslikely to adversely affect the hair follicle.Most cream emollients now come in pumpdispensers, which makes their use much morestraightforward. It also prevents potential contaminationcaused by the introduction of debris(especially skin scales) when a hand is put intoa pot. If a pump dispenser is not available,emollient should be taken out of a pot usinga clean spoon or a spatula. Individuals shouldbe encouraged not to share pots to maintaininfection control.Where to apply the emollient?Whilst the answer to this may seem obvious,it is always worth clarifying with patients thatemollient can be applied all over the skin withoutany adverse side effects. If the dry skin isvery localized, then application to just thoseareas may be acceptable, but often dry skinis diffuse and a general all over application isrecommended.There is a lot to remember to tell a patientabout using emollients. Box 5.2 is a checklistto act as an aide memoir to make sure that everythingis covered. The order the list is writtenin here may not suit you or your patient; as

80 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 5.2 Aide memoir fordiscussing emollient use withpatients(1) Why emollients are important and howthey work?(2) How much to use (described in a waythat the patient can understand, butspoonfuls may be helpful)?(3) When to apply an emollient and inparticular emphasise the importance ofapplying after bathing?(4) Where to apply the emollient?(5) How to apply the emollient?(6) When to apply emollients in relationto the other topical treatments that theyare using?(7) Health and safety issues;(8) Which emollient they will use andwhether they need more than one fordifferent times of the day?long as everything is covered (and makes senseto the patient) the order is not that important.Appendix 3 might be helpful as it lists availableemollients in Britain.How emollients work?The science of emollient therapy is constantlydeveloping. This reflects an increased understandingof what happens at a cellular levelwhen an individual experiences dry skin or a dryskin condition. For an in-depth look at emollients,their chemistry and function, Loden andMaibach’s book provides an excellent, detailedoverview (Loden and Maibach, 2000).Skin becomes dry for two main reasons:(a) Natural moisture from within the stratumcorneum is lost due to barrier dysfunction.(b) The natural moisturising lipids that arenormally found within the skin are for somereason deficient.The level of water in the epidermis is greater atthe interface with the dermis and is least in thestratum corneum. The natural lipids (mainlyceramides) which are found in the intercellularspaces of the epidermis impede the movement ofthe water from the deeper layers to the stratumcorneum. When there is a deficiency of thesenatural lipids, the movement of water is lesseffectively impeded and therefore more readilylost from the surface of the skin.Because the outer layer of the stratum corneumcontains only approximately 10% water,any reduction in this quantity causes the skinto loose its flexibility (Marks, 2001). Whenwater is lost from the stratum corneum, thecorneocytes become shrivelled, shrink and gapsin between them develop. These gaps allow furthermoisture and natural lipid to ‘escape’ leadingto even drier skin. The analogy that is oftenused is a brick wall. The corneocytes are the‘bricks’ which in normal skin are held togetherwith ‘cement’, i.e. the natural lipids. As soon aseither the ‘bricks’ or ‘cement’ are compromised,the impermeable, smooth structure of the skinis affected and it becomes dry. It feels rough,often sore and itchy. More detail is given abouthow dry skin manifests itself in specific dryskin conditions in Chapters 8 (psoriasis) and 9(eczema).Desquamation, the loss of skin cells fromthe surface of the skin, is also thought to bean important factor in skin dryness. Normallycorneocytes are shed from the skin surface singly.At the correct point in time (i.e. at the skinsurface), they lose the binding forces that holdthem together and shed in such a manner thatis not visible to the naked eye. However, in dryscaly conditions, the corneocytes ‘stick’ togetherand shed in a way that is visible to the nakedeye. Emollients seem to correct this problem.One suggested mechanism is that water trappedin the skin by emollients activates an enzymewhich breaks the desmosomal contacts thatkeep corneocytes stuck to one another (Marks,2001). In doing this, corneocytes are shednormally again.In order to increase the level of water in theskin, emollients exert an occlusive or humectanteffect, or both depending on their constituents.

Emollients 81Occlusive effect of emollientsLipids have an occlusive effect, trapping naturalmoisture into the skin by mimicking therole played by sebum. Transepidermal waterloss is reduced particularly when greasy emollientswith a high level of lipid, for exampleliquid paraffin, are used (Rawlings et al.,2004).Humectant effects of emollientsHumectants are substances which attract water.The dermis has a high level of water in it (70%of the dermis is water). Thus when humectantsubstances such as urea and glycerine areadded to emollients and then applied to theskin, they attract water from the dermis intothe epidermis thus helping to rehydrate it. Inthis way, they mimic the role of natural moisturisingfactor (NMF). NMF is comprised of agroup of humectant substances (e.g. pyrrolidonecarboxylic acid) which occur naturally withinthe upper epidermis. Because of its water-lovingproperties, NMF is responsible for maintainingwater in this part of the epidermis (Marks,2001). An emollient containing humectants canonly be effective if it also contains an occlusivesubstance such as soft paraffin. Withoutthis the water drawn into the epidermiswould not be trapped there and would be losttransepidermally.Although not particularly well understood,it does appear to be the case that emollientshave an antimitotic, anti-inflammatory andantipruritic properties.Antimitotic effects of emollientsAn experimental study on mice whose skinhad been stimulated through tape strippingshowed that application of emollient decreasedthe mitotic activity in the epidermis (Treeand Marks, 1975). The authors suggestedthis may have been due to either repair of thebarrier function of the skin or a reduction inprostaglandin synthesis which is caused by useof emollients high in petrolatum.Anti-inflammatory effects of emollientsStudies in the field of eczema have shownthat even minor damage to the skin (throughscratching) can cause the release of powerfulinflammatory agents such as IL-1α. Wood et al.showed that by occluding tape stripped skin withpolythene, release of IL-1α could be prevented(Wood et al., 1996) and Cork speculated thatthis action is replicated when a layer of occlusiveemollient is applied to the skin (Cork, 1997).On a practical note, it is worth noting thatthe physical motion of applying the emollientcan make the skin look more inflamed. Twomechanisms are possible. Firstly, whilst vigorousrubbing in of emollients is to be avoided, thevery process of emollient application can increaseblood flow to the skin surface which mimics theappearance of inflammation. Secondly, if the skinis scaly this will cover up the underlying inflammationand make the skin look a duskier colour.As an emollient will help to reduce the level ofscale, it may, in turn, make the skin look moreinflamed when it is applied to the skin. Patientsshould be reassured in both instances that theemollient is not causing further inflammation.Antipruritic effects of emollientsExperience shows that applying emollients todry, itchy skin usually provides some transientrelief (even those without specific antipruriticagents in them). Emollients containing high levelsof water may be more relieving as there is acooling effect caused by water from the productevaporating from the skin.Effects of added active ingredientsto emollientsA number of different effects can be created byadding further substances to a basic emollientbase.Anti-infective agents: Whilst independentevidence for the impact of anti-infectiveagents is hard to come by, it would appearthat these products do reduce the bacterial

82 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsload on the skin which can be very helpfulfor people who suffer recurrent infectiveepisodes of their skin, e.g. those with atopiceczema. Examples of the anti-infectiveingredients are chlorhexidine hydrochlorideand benzylkonium chloride.Antipruritic agents: Lauromacrogols have anantipruritic effect which, whilst not entirelyunderstood, probably work by inhibitingthe transmission of itch sensations throughthe unmyelinated C fibres. They also actas an anaesthetic when applied to mucousmembranes or bruised skin (Bettzuege-Pfaffand Melzer, 2005).Descaling agents: An example of these issalicylic acid which is used to break downhyperkeratotic skin and thus remove thebuild up of scale.Considerations that will effect howpatients use emollientsEncouraging patients to concord with treatmentis a key role for nurses; the concept of concordanceis examined in some depth in Chapter 7.With regards to emollient use, one of the keyconsiderations is the usability of the product.The Skin Care Campaign reminds us thatpatients have to ‘wear’ topical products and thisis of course true for emollients. Products that suitone person will not suit another and so choice iskey to successful selection and subsequent use.‘Psychorheology’ is the name given to the studyof the response an individual has to the applicationof a topical product (Marks, 2001).In practical terms, the best way to get patientsto use emollients is to provide them with anumber of samples that they can go away andtry before getting large quantities prescribed.To make this a reality, a team approach withthe pharmacy department or advisor within theworkplace is essential. Consideration needs to begiven to workplace policies on getting free samplesfrom the pharmaceutical industry and ongiving non-prescribed items to patients. Havingemollient formularies within a workplace helpsin the process of establishing the emollientswhich can be given out as samples.Patient choice of emollient might be affectedby something related to the product, the environmentor themselves. Each of these areconsidered in turn.The productA common concern for patients is the consistencyof the product, how greasy it is and how itsmoothes onto the skin. This is not as simple assaying people do not like greasy products anddo like creamy ones, because this is simply notthe case. The product needs to be easy to applyto the skin and not to sting. Although mostpharmaceutical products have no fragrance addedto them, some do have a slight aroma. Indeed, it isprobably because there is no fragrance to ‘mask’the smells of the ingredients that people complain.Smell is a very personal issue. So, if someone doesnot like the smell of a product (even if it doesnot appear to have a smell) it is important thatanother product is tried. The physical presentationof a product may also have a bearing, e.g. apump dispenser may be much easier than havingto scoop a product out of a pot.The environmentOne of the major environmental factors that canimpact on and individual’s choice of emollient isthe ambient temperature. Thick greasy emollientscan also act as insulators and in hot weather maybe too uncomfortable to use. It is also true thatwhen the atmosphere is dry, the skin is morelikely to become dry as there is less natural moisturein the air. Windy conditions can have a similareffect. Thus in hot conditions a lighter creammight be preferred whereas in cold, dry, windyconditions an ointment might be more suitable.The personThe condition of an individual’s skin willimpact on the type of emollient that they mayfeel able to use. If the skin is very dry, a greasy

Emollients 83ointment may feel most comfortable; if it isonly moderately dry, a cream might be moreappropriate. What a person does on a day-todaybasis will also make a difference; someonewho is at work in smart clothing is unlikely towant to put on greasy emollients prior to gettingdressed, but the same person may well bewilling to use the greasier products under theirpyjamas before going to bed. A greasy productmay be fine on the feet where it can be coveredup with socks and shoes, but totally unbearableon the face.To get the most out of emollients, healthcare professionals need to engage in a conversationwith their patients ascertaining as muchinformation on the above as possible. It is notas straightforward as thinking ‘very dry skin,needs very greasy emollients’. Therapeuticallythis may be the best decision to make, but inreality, if a patient does not like the product, itwill stay in the pot where it has no therapeuticbenefit at all!ConclusionEmollients are vital therapeutic products in thefield of dermatology. They are not just simple inertproducts, but complicated mixtures of carefullyformulated compounds with a range of impactson the skin. Whilst the knowledge relating to howemollients work on the skin is increasing, andthere is a significant body of scientific knowledgein relation to this, there is an enormous scarcity ofexperimental data to inform how emollients arephysically used. This leaves practitioners to makedecisions based on first principles and custom andpractice. This is a field that would benefit fromfurther research to ensure that emollients are usedto maximum effect.ReferencesAkdis, C., M. Akdis et al. (2006). Diagnosisand treatment of atopic dermatitis in childrenand adults: European Academy of Allergyand Clinical Immunology/American Academyof Allergy, Asthma and Immunology/PRACTALL Consensus Report. Allergy,61(8): 969–987.All Party Parliamentary Group on Skin (2006).Report on the enquiry into the adequacy andequity of dermatology services in the UnitedKingdom. London: APPGS.Bettzuege-Pfaff, B. and A. Melzer (2005).Treating dry skin and pruritus with a bathoil containing soya oil and lauromacragols.Current Medical Research and Opinion,21(11): 173501739.British Medical Association and RoyalPharmaceutical Society of Great Britain (2007).British National Formulary 54. Retrieved7/01/08, 2007, from www.bnf.org.Britton, J. (2003). The use of emollientsand their correct application. Journal ofCommunity Nursing, 17(9): 22–25.Cork, M.J. (1997). The importance of skinbarrier function. Journal of DermatologicalTreatment, 8: s7–s13.Cork, M.J., J. Timmins et al. (2003). Anaudit of adverse drug reactions to aqueouscream in children with atopic eczema.The Pharmaceutical Journal, 271: 747–748.de Groot, A. (2000). Sensitizing substances. In:Loden, M., Maibach, H. (Eds), Dry Skin andMoisturizers. Boca Raton: CRC Press.Drugs and Therapeutics Bulletin (2007). Bathemollients for atopic eczema: Why use them?Drugs and Therapeutics Bulletin, 45(10):73–75.Ersser, S., S. Maguire et al. (2007). A BestPractice Statement for Emollient Therapy.Retrieved 7 January 2008, from www.dermatology-uk.com/educational_projects.shtml.Finlay, A.Y. (1997). Emollients as adjuvanttherapy for psoriasis. Journal ofDermatological Treatment, 8: s25–s27.Grimalt, R., U. Mengeaud et al. (2007). Thesteroid sparing effect of emollient therapy ininfants with atopic dermatitis: A randomisedcontrolled study. Dermatology, 214(1): 61–67.Hall, M. (2003). Target skin. In: Kirkness, B.(Ed.). London: The Association of the BritishPharmaceutical Industry.

84 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsHanifin, J., A. Herbert et al. (1998). Effects ofa low potency corticosteroid lotion plus amoisturizing regimen in the treatment of atopicdermatitis. Current Therapeutic ResearchClinical and Experimental, 59(4): 227–233.Harris, I. and U. Hoppe (2000). Lanolins. In:Loden, M., Maibach, H. (Eds), Dry Skin andMoisturizers – Chemistry and Function. BocaRaton: CRC Press.Holden, C., J. English et al. (2002). Advisedbest practice for the use of emollients ineczema and other dry skin conditions.Journal of Dermatological Treatment, 13(3):103–106.Kligman, A.M. (2000). Introduction. In:Loden, M., Maibach, H. (Eds), Dry Skin andMoisturizers: Chemistry and Function. BocaRaton: CRC Press.Loden, M. and H. Maibach, Eds (2000).Dry skin and moisturizers: Chemistry andfunction. Boca Raton, CRC Press.Lucky, A.W., A.D. Leach et al. (1997). Useof an emollient as a steroid-sparing agentin the treatment of mild to moderateatopic dermatitis in children. PaediatricDermatology, 14(4): 321–324.Marks, R. (2001). Sophisticated Emollients.Stuttgart: Thieme.National Institute for Clinical Excellence(2001). Referral Advice: A Guide toAppropriate Referral from General toSpecialist Services. London: NICE.Nicol, N. and M. Boguniewicz (2008).Successful strategies in atopic dermatitismanagement. Dermatology Nursing,Oct(Suppl): 3–18.Nicol, N., A. Ruszkowski et al. (1995). Contactdermatitis and the role of patch testing in itsdiagnosis and management. DermatologyNursing, Feb(Suppl): 5–27.Penzer, R. (2005). What advice do nurses workingwith adult patients with moderate plaquepsoriasis give on the use of topical emollients?Dermatological Nursing, 4(4): 21–22.Rawlings, A.V., D.A. Canestrari et al. (2004).Moisturizer technology versus clinicalperformance. Dermatologic Therapy,17(Suppl 1): 49–56.Smoker, A. (2007). Topical steroid oremollient – Which one do you apply first?An investigation into the sequencing oftopical steroid and emollient applicationand the most clinically effective method ofapplication. University of Southampton.Stone, L. (2000). Medilan: A hypoallergeniclanolin for emollient therapy. British Journalof Nursing, 9(1): 54–57.Tree, S. and R. Marks (1975). An explanationfor the ‘placebo’ effect of bland ointmentbases. British Journal of Dermatology, 92:195–198.Voegeli, D. (2007). Factors that exacerbate skinbreakdown and ulceration. In: Pownell, M.(Ed.), Skin Breakdown – The Silent Epidemic,pp. 17–22. Hull: The Smith and NephewFoundation.Watsky, K.L., L. Freije et al. (1992). Waterin-oilemollients as steroid-sparing adjunctivetherapy in the treatment of psoriasis. Cutis,50: 383–386.Wood, L., P. Elias et al. (1996). Barrierdisruption stimulate interleukin-1 alphaexpression and release from a pre-formedpool in murine epidermis. Journal ofInvestigative Dermatology, 106(3):397–403.

6Psychological and socialaspects of skin careRebecca PenzerIntroductionThis chapter seeks to explore the issues aroundthe psychological and social impacts of skindisease. Often these two concepts get groupedtogether and psychosocial issues are discussedwith no distinction being made. This is a temptingapproach as there are many overlaps; however,here they will be considered as two sides ofthe same coin. The psychological aspect refersto issues related to the mind, about how theindividual copes with their surroundings andexperiences. The social aspect is about how theindividual interacts with other people and howthey feel to be part of human society.The interplay between the skin and the mindand individuals and their communities, is notin any way a new concept. Indeed, the nursingliterature has made mention of it years beforemore scientific work examined the nature of therelationship between the brain and the skin. Inan attempt to understand this relationship, thischapter will look at the pathophysiologicalchanges that affect both the brain and the skin inwhat has become known as the brain–skin axis.Once these are understood, it is then helpful togain some insight into the coping mechanismsthat people employ to enable them to live withchronic skin conditions. At the same time, it isimportant to bear in mind that some peoplestruggle to cope and as such, the chapter willlook at some nursing interventions that canimprove mental well-being and the ability tocope with adverse health experiences.Mention will be made of mental illness, however,the focus of the chapter is on promotingmental health well-being and knowing when torefer on if a mental disorder is suspected.The chapter starts with consideration of thesocial impacts of skin disease and particularlythe social pressure that individuals with skindisorders experience on a day-to-day basis.Social impactsHistorical contextSkin disease throughout history has been associatedwith contagion and dirt. This is at leastpartially due to the fact that many contagiousdiseases had skin manifestations (e.g. the plague)so that the relationship between some skin rashesand infectivity were indeed real. It is also thought

86 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsthat the natural human response of scratchinghas evolved to ensure that humans are madeaware when something unpleasant is on theirskin and the scratching is a way of getting rid ofit. These two facts seem to be deeply buriedwithin the human psyche. Thus it remains a commonreaction to recoil from someone who has avisible skin condition and someone who scratchesmay be viewed as somehow dirty or unclean.Indeed this almost instinctive response to skindisease is very often totally out of proportion tothe objective manifestation of the condition. Themedia and entertainment industry seem to playon this deeply held ‘fear’ making the ‘bad guys’in films appear with facial defects such as acnescars or severe burns, thus reinforcing our instinctthat ‘bad’ skin equals evil and thereby of coursethat ‘beautiful’ skin equals good.■■■■sensitivity to others’ attitudesguilt and shamesecretivenesspositive attitudesIn this study, different people had these experiencesto different levels; however, the singlefactor that was most likely to predict for feelingsof stigma and despair was bleeding skin.Whilst stigma may be thought of as a socialconstruct, feelings of stigmatisation can havesignificant impact on psychological well-being.It was shown that a group of psoriasis patientswho had felt stigmatised by people deliberatelyavoiding touching them, had significantly higherdepression scores than a group with similar levelof disease who did not feel stigmatised (Guptaet al., 1998).StigmaAs a consequence, people with chronic skindiseases such as acne, eczema or psoriasis maysuffer ridicule and rejection. Even if thisresponse is anticipated rather than real, an individualmay choose to avoid social interactionsor avoid certain activities to ensure that they donot have to face unpleasantness from others(Hong et al., 2008). Individuals may describethemselves as being stigmatised by their condition,where stigma can be described as a ‘connotationof disgrace associated with certainthing’(Allen, 2000). As this definition highlights,people with skin disease often associate it toissues of morality, in other words, there is somelevel of (perceived) disgrace associated with it.This may in part be due to religious teachingsemphasising the impor tance of cleanliness andbecause of skin diseases’ association with dirt itbecomes associated with Godlessness.A study looking at feelings of stigmatisationin patients with psoriasis noted six differentdimensions of stigma experience, many of whichecho what has already been stated (Ginsburg &Link, 1989). Those dimensions were:■■anticipation of rejectionfeeling of being flawedDisability and impairmentThese words are sometimes used in relation toskin disease particularly to express a level ofimpact that the condition has on a person. Someof the outcome measures used to document thelevel of impact of the disease are expressed as adisability index, e.g. the Psoriasis DisabilityIndex. The term ‘disability’ is an emotive wordand different models view it in very differentways. For example, the medical model woulddefine disability as a lack of ability as comparedto a standard or norm. It may involve a physical,cognitive or intellectual impairment, mentaldisorder, or various types of chronic disease.This definition focuses on what the individualcannot do because of something that societymight consider an impairment (Open University,2006). A social model of disability takes a verydifferent view labelling disability as a disadvantageor restriction on doing things that is thefault of society and the way that it is run. Thusthe focus is on the way that society is set up andas such people become disabled because of thelack of preparedness of the society, rather thanany personal intrinsic factor. (Open University,2006) When considering the disability caused byskin disease, this definition is helpful as it is sooften the responses from society at large that

Psychological and social aspects of skin care 87creates a disability for the individual sufferer.An impairment (that may have once beenreferred to as a handicap) is when a person hasan injury or an illness for a long time that makesthem different from other people. Impairmentdoes not cause disability.A piece of research carried out by Jowett andRyan in 1985 looked at what they then labelledthe handicapping impact of skin disease. Thiswas early work looking at not only the physical,but also psychological and social burden of skindisease. Whilst the term handicap may no longerbe used, this work clearly outlined how significanta range of skin conditions were on peoples’psychological and social well-being (Jowett &Ryan, 1985).Body imageBody image can be described as a subjectiveconcept of one’s physical appearance based onself-observation and the reaction of others.Thus the image that individuals form of themselveshas two parts to it, firstly how they seethemselves and equally important how they perceiveothers reacting to them. When discussingbody image, people are said to have a good or apoor body image, which in effect refers to thelevel of contentment that someone has withtheir body. Perception of body image is not necessarilyrelated to the reality of what is before aperson, for example someone with what outwardlywould seem like a ‘normal’ body, mayhave a poor body image. Papadopoulus and Bor(1999) suggest a list of behaviours that thosewith poor body image might exhibit. Thusthose with poor body image might:■■■■■Edit social experiences to reinforce existingnegative perceptions of themselves;View their bodies only as aesthetic objects;Minimise other positive aspects of theirappearance;Have a heightened sense of body awareness;Comply with narrow social standards interms of what is attractive.(Papadopoulus & Bor, 1999)What do these points mean with regard tosomeone with a skin condition? Editing socialexperiences means that an individual will chooseto remember the unpleasant things that happento them which in turn reinforce their beliefsabout themselves. For example, someone withacne will remember how someone stared atthem because this reinforces their belief thattheir acne is incredibly noticeable and ugly.They will not remember the pleasant instanceswhere people smile and say hello. When someonehas a skin disease they are likely to havea heightened sense of body awareness. Everyday they are reminded of how their body is not‘working’ for them because they have to treatit with creams, because it feels itchy or sore orbecause they have to display it to a health careprofessional. When parts of the skin are felt tobe uncomfortable and unattractive, it is easyto forget or ignore the other parts of the bodywhich are still normal, working well and attractive.All these factors can help to create a poorbody image.Social pressuresIn a review article, Hong et al. (2008) outlinesthe many pressures that people with chronicdiseases, such as eczema and psoriasis, experience.For many, family relationships areaffected with families reporting that they tooare negatively affected by the conditions. Foradults, sexual functioning is affected with significantnumbers reporting decreased sexualdesire.Economic pressuresEconomic burden can be considered in anumber of different ways. Firstly, there is a burdento the health service in terms of the amountthat it costs to provide the direct care topatients. 1994 figures suggested that the costswere around 2% of the total NHS budget(Williams, 1997). New drugs (particularly thebiologics) and increased levels of skin cancerare likely to mean that this figure has increased;

88 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 6.1 Possible personal costs of a skin disease.ModificationEnvironmentalmodificationsparticularly forpatients witheczemaExtra washingof clothesand beddingdue to greasytreatmentsAttempts tofind ‘magiccure’Personal costs• Changing curtains for blinds• Changing carpets for hard flooring• Cotton clothing/special clothing• Water softener• Extra cleaning• Special mattress and bedding covers• Increased water usage• Increased energy usage (electricity)• Increased washing detergent• Need to replace washing machinemore frequently• Money and emotion wasted onunproven and potentially dangeroustreatmentspsoriasis and severe acne as conditions thatwould make a person permanently unsuitablefor entry into the services. There is also a veryreal direct cost to patients with skin disease interms of what they need to do to manage theircondition. Thus, unless the individual is eligiblefor free prescriptions, costs of these can be veryhigh especially as often 2, 3 or even more itemsare required. It is sometimes cheaper forindividuals to buy a season ticket, where theypay a lump sum up front and then receive freeprescriptions regardless of the number theyneed. In England, details can be found at www.nhsbsa.nhs.uk/1127.aspx and in Scotland atwww.psd.scot.nhs.uk/doctors/prepaymentcertificates.html.However, the costs do not stopat prescriptions. Table 6.1 shows some of theother additional costs that someone with skindisease may incur.however, they may have been offset by decre asesin the amount of care provided on an in-patientbasis. Secondly, there is an economic burden tosociety as a whole, as people with skin diseasehave to take time off work and are thereforeunproductive. Williams sites that skin diseasewas one of the most common reasons forclaiming injury and disablement benefit inthe period 1977–1983. Finally, the personaleconomic burden has not been evaluatedin terms of cost. However, a US study foundthat around 10% of people believed that theirskin condition was a handicap to them whileworking or doing housework (Johnson &Jones, 1985). The economic impact of eczemais discussed in Chapter 9.For some, the social stigma felt because oftheir skin disease prevents them from applyingfor jobs, and anecdotal reports from patientsmake it clear that it can be difficult to get jobsthat involve face-to-face contact with membersof the public. Whilst potential employers shouldnot discriminate against employees becauseof their skin disease, there are still someinstances where employment may be preventedbecause of the condition. For example, theBritish Armed Forces list chronic eczema, severePsychological impactThere are many issues to consider when lookingat the psychological impact of skin disease. Thissection will begin by looking at some of themost recent thinking on the physical responsesto stress that have an impact on the brain andthe skin.Brain–skin axisThere is varying degrees of evidence to supportthe relationship between stress and skin disease.For psoriasis and atopic eczema that evidence iswell-established, it is less well so for urticaria,herpes simplex virus and vitiligo and only a weakassociation exists for lichen planus, pemphigusvulgaris and acne (Pavlovsky & Friedman,2007). Whilst there is still much research neededto untangle the mechanisms that link the brainand skin with associated stress, current opinionsuggests that there are three areas of interest: thehypothalamic–pituitary–adrenal axis (HPA), theperipheral nervous system (PNS) and biologicalbarriers. The skin appears to have a dual role

Psychological and social aspects of skin care 89in relation to its response to stress. It is a targetfor key stress mediators (such as corticotrophinreleasing hormone, adrenocorticotrophichormone, cortisol, catecholamines, prolactin,substance P and nerve growth factor) but alsoa key source of these mediators of the stressresponse (Arck et al., 2006).Hypothalamus–pituitary–adrenal axisThe interplay between these three glandsdescribes the classic stress response. Followingexperience of a stressor, the hypothalamusreleases corticotrophin-releasing hormone, thisacts on the pituitary gland to release adrenocorticotrophichormone which finally inducesthe adrenal gland to produce cortisol. It isthought that cortisol protects the body understress, although the mechanism is not clear,and it has a well-known anti-inflammatoryeffect. What appears to happen in some chronicinflammatory disorders (particularly psoriasisand eczema) is that there is a muted HPAresponse with cortisol levels that are lower thanthose seen in a general population. Richardset al. (2005) demonstrated that patients withpsoriasis had lower levels of serum cortisol followingan experimentally induced emotionalstress, than controls. More significantly, thosewho rated their psoriasis as stress-responsivehad even lower serum cortisol levels than thosewho did not rate so. Thus psoriasis patients donot seem to show an appropriate response ofthe HPA axis (Richards et al., 2005). As a resultof this reduced HPA reactivity, the body is notprotected by the release of cortisol in responseto stress.Peripheral nervous system (PNS)The PNS is all nervous tissue other than thebrain and the spinal column (which are knownas the central nervous system). Part of the PNSis not under voluntary control and as such islabelled the autonomic nervous system (ANS).The ANS can be divided further into the parasympatheticand sympathetic nervous systems.The parasympathetic system maintains the bodyin a normal resting state. Stimulation of thesympathetic nervous system occurs during timesof stress. At a gross physiological level there area number of changes that happen to the body inorder to deal with that stress. These responsesare based upon an innate ‘flight or fight’response that were useful when stressors werelarge dangerous animals, threatening life andlimb. Whilst humans rarely run away literally,or fight the stressors in their lives, the biologicalresponses still prepare us to be able to do so(see Table 6.2).Table 6.2 Changes in the sympathetic nervous system inresponse to stress.Target organBrainCirculatory systemLungsGutLiverBladder and bowelSexual organsSympathetic effectBecomes alert and focused inorder to prepare for findingsafetyHeart beats fasterBlood flow diverted to musclesready for activityBlood flow away from skinleading to pallor (classic lookof fear)Blood clotting ability increases,preparing for possible injuryAirways open up allowing forincreased oxygenationRate of breathing increasesLess activity in digestionVomiting may occurConstriction leads to feelingof butterflies or knot in thestomachReleases more sugar and bloodsugar levels go up in order toprovide more energyTend to be more irritable withdecreased bladder capacity.May lead to involuntaryemptying of eitherErectile dysfunction in menLoss of lubrication in women

90 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBesides the more familiar role of the sympatheticnervous system in relation to stress, it alsohas a crucial immune-related role to play throughthe release of catecholamines. These appear tostimulate stress-induced lymphocytosis andlead to particular changes in lymphocyte trafficking,circulation, proliferation and cytokineproduction. Another neurohormone whichhas a crucial role to play is nerve growth factor(NGF), which is a potent immunomodulator,aiding cell communications and facilitatingmonocyte/ macrophage migration through vascularendothelium (Arck et al., 2006). NGFmodulates the synthesis of substance P whichprobably has a role in the activation of mastcells to secrete specific cytokines, chemokinesand tumour necrosis factor α (Pavlovsky &Friedman, 2007).Biological barriersStudies in both human and animal models suggestthat psychological stress has a direct impacton skin barrier and the ability for it to repair. Astudy looking at two groups of women whowere put under psychological stress in a laboratory,one group through interview stress andanother through sleep deprivation, both experienceda delay in barrier function recovery(Altemus et al., 2001). Further work on mousemodels suggest that this occurs because psychologicalstress leads to decreased epidermal proliferation,decreased epidermal differentiation anddecreased the density and size of corneodesmosomes.Decreased production of lamellar bodiesand decreased secretion from them leads to alower level of natural lipid in the skin that affectsbarrier function (Choi et al., 2005).CopingInternal factorsThe internal factors related to coping with achronic skin disease are those personal skills andabilities that an individual has to manage theircondition. The intrinsic capability of somebodyto cope with a stressful situation is complex andwill be influenced by previous experience andinherited tendencies. The relative importance ofnurture and nature is not going to be debatedhere, instead attention is drawn to the importanceof self-efficacy. Self-efficacy is defined as:‘an individuals’ belief in their capacity to successfullyexecute a health related behaviour’(Bandura, 1997). This concept is discussed ingreater depth in Chapter 7 with a particularemphasis on improving self-efficacy in order tohelp people make the most of their treatments.However, in a more general capacity, if an individualhas belief in their ability to manage theircondition effectively, they are likely to feel moreinclined to cope.External factorsTypology of the diseaseOne of the factors that patients report as beinghard to cope with about skin disease is itsunpredictable nature. The typology of a diseaserelates to its nature, onset, course and appearance,thus a condition may be progressive, episodicor acute. A progressive disease follows awell-documented course and although the timingsof the progression may not be entirely predictable,there are key indicators which allowan understanding of where the disease hasprogressed to. Mycosis fungoides is an exampleof a progressive condition. As explored inChapter 13, a biopsy can determine the stage ofthe disease, which will then determine its subsequentprogression.An acute condition in this instance is usedto describe a one off-event that occurs as aresponse to an external agent, e.g. a drug reaction.Although the response may be extremelyunpleasant and may occur again if the individualis exposed to the offending drug, it is veryclear what has caused the problem and how itmay be avoided in the future.Episodic conditions are, as their name implies,unpredictable, appearing for a time and thengoing away again. Most chronic skin conditionsexplored in this book belong in the episodic category.Psoriasis, eczema, urticaria and vitiligoare all examples of skin diseases that often seemto worsen for no apparent reason and may gointo remission similarly for no apparent reason.

Psychological and social aspects of skin care 91The seemingly random nature of these conditionscan make it very difficult to cope with asit is impossible to plan for special events to takeplace in periods of remission, as these cannot bepredicted. Clearly, treatments can improve thelikelihood of remission occurring, but patientswill report that treatments that have onceworked are no longer doing so, adding to thestress incurred by an episodic condition.It is helpful to turn to documented patientexperience to really begin to understand, howthis episodic nature can impact on the psychologicalwell-being of an individual (Kennaway,2008). Here, Guy Kennaway describes theappearance of psoriasis on his face.‘The stuff on my face was quick to establishitself in my life, providing a commentary onall my activities. Some things I did, like drinkheavy red wine and party late into the night, itdisapproved of, and it would be waiting in themorning to reprove me at its most blotchy. Butit wasn’t just a party-pooping bore. Anotherlong night on the Scotch could result in a clearcomplexion the next day. Above all it wasn’tpredictable although I never gave up trying tosecond-guess it. It seemed to have a preferencefor some of my friends over others, appearingall over my face and neck, bright red almostpulsating with rage, in the pub with some andthen calmly disappearing entirely with thedeparture – or arrival of others.’ (p. 6)TreatmentWhilst treatments may physically improve theskin condition, the process of using them can initself make the condition difficult to cope with.Topical treatments may be greasy, smelly, mayirritate the skin or change its colour. Systemictherapies bring their own stressors with them.For example, light therapy requires frequenttrips to the hospital and methotrexate regularblood tests along with the life-style change ofnot consuming alcohol. Unlike many chronicconditions where the behaviour change mayinvolve taking an oral drug regularly, skin diseasesrequire a commitment to ongoing applicationof topical treatments for an indeterminatelength of time. Many patients cite the time elementas a major negative impact that influenceshow they cope with their disease. Washing andgetting dressed are not straight forward activitiesthat take half an hour, applying of emollientsand other topical products may take overan hour and may need to be done at least twicea day.DiscomfortSkin that is affected by disease can be physicallyuncomfortable in a number of ways, but mostcommonly, patients will describe itch, soreness,tightness and pain.Itch is associated with a number of skin conditionsparticularly eczema and urticaria andperhaps to a lesser extent psoriasis. It is thoughtto be the most common symptom of dermatologicdisease (Gupta et al., 1994). It causesextreme discomfort and patients will often saythey would rather have pain than live with itch.Indeed some will scratch themselves raw inorder to experience soreness rather than itch. Ithas been rated second only to disfigurement as asource of patient distress for those with pruriticdermatoses (Gilchrest, 1982). Skin disease oftenprovides the sufferer with a constant reminderof its presence, as humans ‘wear’ their skin it isimpossible to escape from it. Whilst techniquesfor managing pain have improved over time,there is still relatively little development of novelways of treating itch.Mental health well-beingWhilst it is important to acknowledge the roleof stress and coping on the experience of a skindisease, perhaps the most important focus fornurses is on enhancing the mental health wellbeingof their patients in order to help themcope with the stress of life. It is clear from allthat has gone before in this chapter that stresscan lead to a flare up or deterioration of chronicskin conditions. Whilst the mechanisms for thisare complex and only partly understood, itwould seem that for many conditions it is anirrefutable truth. What is also the case is thatexperiencing a skin condition is stressful initself. Thus, intervening to improve mentalhealth may improve the physical state of the

92 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsskin by reducing the physiological stressresponses and also by improving an individual’sability to cope with stressful events in their lives.In this way a therapeutic objective is to breakthis vicious circle (see Figure 6.1).Mental health can be viewed on a spectrum,which does not have any absolutes associatedwith it. For example, an individual may have atendency towards being anxious, but not havean anxiety disorder. Helping that individualto cope better with their anxiety would, in alllikelihood help to improve their mental healthwell-being and may in turn help them to copebetter with their skin disease. An individual canbe said to have a mental health disorder whentheir mental state interferes with their daily living.The World Health Organisation (WHO)describes it thus: ‘Mental disorders comprise abroad range of problems, with different symptoms.However, they are generally characterisedby some combination of abnormal thoughts,emotions, behaviour and relationships withothers.’ (WHO, 2009)Thus, anxiety is a normal emotion that wefeel when we are asked to do something thatis outside our ‘comfort zone’. But an anxietydisorder includes a range of responses whichbecome problematic. For example, most peopledo not enjoy being sick, but for some it becomesa phobia known as emetophobia. Most peoplewill go through rituals of checking keys andlocking windows when they leave the house;however, someone with obsessive compulsivedisorder will go through elaborate, repetitivebehaviours that make leaving the house difficultand time consuming.Skin manifestations of mental disordersAlong the spectrum of mental disorders, thereare some conditions that manifest themselvesthrough the skin, and are reflections of truemental health issues. It can be very difficult tohelp these patients as they are often adamantthat their skin lesions are true dermatologicalconditions rather than self-induced.Trichotillomania describes hair pulling, whichresults in fractured hair and bald patches. Thismay be as a result of a habit or tic which theindividual needs pointing out to them and maybe relatively easy to stop. However, it may alsobe as a result of some underlying psychopathologypossibly related to anxiety.Patients may deliberately inflict damage totheir skin and then consciously try to deceiveabout the real nature of the lesions—this could bethought of as a form of cutaneous Munchausensyndrome. Those who have true dermatitis artefactaare seemingly unaware of the true nature oftheir lesions. The lesions in both instances mayseem peculiar and not appear like any ‘normal’pathological process; however, in some cases,the patient may recreate the symptoms of a previouslyexperience condition. This is a form ofself-harm and may be as a result of stressful oranxiety provoking experiences that are occurringin the individual’s lives. Referral to a clinicalpsychologist will be helpful, as they may be ableto help the person resolve the experiences leadingto the self-harming behaviour.Delusional parasitosis is extremely difficult totreat as the patient is absolutely convinced thatthey are infested with insects or worms. They mayendeavour to produce ‘evidence’ of such infestationby digging debris out from under their skin.StressNursing interventionsSkin diseaseFigure 6.1 Vicious circle of stress and skin disease.In this section, the role of the nurse will be considered.The overall objective of the nursingintervention is to provide support to patientswho have skin disease, in order to enhance theirmental health and thus enable them to cope withtheir condition as effectively as possible. Nurseswill already have a significant skill-set that they

Psychological and social aspects of skin care 93can draw on to achieve this, what is outlinedhere are ways to develop these skills further.This should not be mistaken as an attempt totrain people into being therapists with specificabilities. Instead, communication skills will bediscussed along with some techniques used incognitive behavioural therapy (CBT). These canbe incorporated into developing a set of professionalcompetencies relevant to the area of work.Should a patients needs go beyond the nurseslevel of competency, referral on to other practitionerse.g. a clinical psychologist, should alwaysbe considered. A further exploration of the therapeuticconsultation is discussed in Chapter 7.Active listeningIt is easy to assume that listening is a skill thatcan be done without thinking; however, it is ofcourse possible to listen without hearing, eitherthe words or their meaning. Depending onwhich studies are considered, only 25–50% ofwhat is heard is actually remembered. Effectivecommunication between two people can onlyexist when the person receiving the messagereceives and interprets it in the way that the persondoing the sending intended. The likelihoodof this occurring is increased if the receiver isengaged in active listening. In other words, theirattitude presumes that the person they are listeningto is important to them and that they acceptthe following to be true about that person:■■■■what they thinkwhat they needhow they feelwhat they wantActive listening has many benefits as it lendsitself to developing trust between two people andin turn enhancing the likelihood of arriving athelpful solutions. As well as being a useful skillto have in terms of helping patients, it can beused effectively to resolve conflict and enhanceproductivity in other work-related situations.Active listening is by definition active, it cannotbe carried out in a passive way, therefore, priorto using active listening skills some preparation isBox 6.1 Setting the environmentfor active listening■■■■Minimise intrusions or interruptionseither from loud noises, telephones orsomeone in person;Room temperature should be neithertoo hot nor too cold;Avoid creating a barrier by the way thedesk and chairs are arranged. Sittingfacing the patient, but at an anglerather than directly, is best;Seating should be comfortable.needed both of the listener and the environment.Box 6.1 shows some of the environmental factorswhich need to be taken into consideration.When first meeting the patient ensure that theyare greeted warmly and that introductions aregiven. Active listening will be taking place indifferent clinical settings, e.g. a ward environmentor a clinic. Wherever it occurs, the principlesaround establishing the right environment remainthe same. At the beginning, it is important thatthey know the amount of time available and thepurpose of the discussion. These may seem likeobvious things to explain, but it is worth ensuringthat both parties agree the same reason formeeting to prevent misunderstanding. When thepatient knows how much time they have got, itmeans they stop worrying about external factorsand prioritise the questions they want to ask,without feeling rushed at the end when the consultationis brought to a close. Once the patient issettled, they need to be given the opportunity tobe listened to in a non-judgemental, non-criticalmanner. Further acknowledgement of what isbeing said can be given by leaning forward,nodding and responding with appropriate facialexpressions, i.e. those that match the patients’feelings. Responses and questions should be pacedso as to encourage further disclosure. Finally, thepatient will feel listened to and understood, if yousummarise and paraphrase what they have said.The body language that is adopted duringactive listening is also a vital component of its

94 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalssuccess. The listener must have an open postureand maintain eye contact with the speaker. Whencommunicating, the words are not necessarilythe most important part of the communication.Classic studies carried out by Albert Mehrabianin the 1960s suggested that 7.8% of the impactis through the words and what is actually said,38% is the tone of the voice, pitch and the waythe message sounds and 55% of the impact ofa communication is through the movement ofthe body, facial expressions and hand gestures(Mehrabian & Ferris, 1967; Mehrabian &Wiener, 1967). These studies have been criticisedmethodologically, but the important findingsemphasise two key things. Firstly there are threeelements of face-to-face communication (words,tone and body language) and tone and body languageare particularly important for expressingfeelings and attitude. Secondly when words andbody language disagree, it is the body languagethat is believed. SOLER is a useful mnemonic toact as a reminder of good body language:Squarely face the personOpen your postureLean towards the speakerEye contact maintainedRelax while attendingActive listening in a clinical situation will havesome slightly different features from active listeningwithin a counselling or mediation situation.In these scenarios, an active listener isexpected not to give advice, or try and solve theother person’s problems for them. However, in aclinical situation, the reason that an individualhas come to see a nurse will be to receive adviceand support. Thus advice giving is permissible.However, often individuals with chronic skinconditions have considerable experience of howto manage their condition, and the giving ofadvice must be in the context of listening to andunderstanding how they currently manage andwhat their priorities for treatment are.Barriers to active listeningThere will always be barriers to active listeningsome of which it may be possible to change,others whilst important to be aware of, may notbe amenable to change. In a clinical situation,time is likely to be at a premium and it may notbe possible to have the ideal amount of it with apatient to cover all the issues. If this is the case,it needs to be acknowledged and arrangementsmade to see the patient again. Some of the thingslisted in the table on environmental factors mayalso create barriers to effective communication,but these should be possible to change. Issuesthat are harder to change are the internal barriersthat we all have due to our own experiencesand background. These may lead us to hear whatwe want to hear rather than what is being said.On a simple level if there are concerns in ourminds, for example the pressures of other thingsthat need doing, it may be difficult to be focusedenough to engage in active listening. It is particularlyimportant to acknowledge the impactof emotions on our listening especially when thetopics are ones that touch ‘hot buttons’. ‘Hotbuttons’ can be described as topics that have aparticular emotional resonance and make activelistening difficult or even impossible. An examplemay be if a patient is talking about bereavementand the listener has recently experienced such circumstancesthemselves, this may trigger a wholerange of emotions that are difficult to control.The impact of active listening on the listenershould also be considered. The process is morelikely to expose them to higher levels of emotionalenergy from the patient and this couldmake coping with the daily pressures of confrontingpatient difficulties, harder. In orderto deal with this, it is important to ensurethat adequate training is in place and that supervisionis available to support the health careprofessional.Consciously incorporating active listeninginto consultations with patients will make themmore effective from two perspectives. Firstly,it is more likely that psychological difficultieswill be expressed by the patients, and secondly,a thorough assessment of the patient’s physicalproblems and how they want to resolve them,will be possible. Table 6.3 summarises sometechniques that might be useful when engaged inactive listening. The next section considers theassessment process.

Psychological and social aspects of skin care 95Table 6.3 Techniques to promote active listening.Action What is it What is its purpose CommentsParaphrasingRestating a message,usually with fewer wordsTo test the understanding of whathas been heardTo communicate that the listeneris trying to understand what isbeing saidThe listener should try andunderstand:(a) what is the speaker’s thinkingmessage(b) what is the speaker’s feelingmessageFor example, the listener could say:‘I’m confused, let me try to state whatI think you are trying to say’ClarifyingThe process of bringingvague communicationsinto sharper focusTo ensure the listener has notmisinterpreted what the speakerhas saidTo get more informationTo give and receive feedbackTo check out the listener’sperceptionsPerceptioncheckingThe listener asks thespeaker to verify theformer’s perceptions of theconversationThe listener pulls together,organises and integratesthe main aspects of thedialogueFor example, the listener could say‘You said that you are fed up with havingswollen legs, but the stockings youhave to wear are too uncomfortable’It is important to pay attention tothe various themes touched uponand emotional overtones, puttingkey ideas and feelings into broadstatements. No new informationshould be introducedEmpathy should not be confused withsympathy. Empathy is ‘I hear what youare saying’ while sympathy is ‘I shareyour feelings’. Sympathy immediatelymeans an emotional involvement withthe speaker which is best avoided.SummarisingTo provide a sense of movementand achievementTo establish a basis for furtherdiscussionEmpathyReflection of content andfeelingFor the listener to show understandingof the speaker’sexperienceThis allows the speaker to evaluatetheir own feelings having heardthem expressed by someone elseAssessing psychological needsDuring consultation, there needs to be a focuson assessing the physical and psychologicalneeds of the patient. Although it is unlikely thatthese two areas of someone’s life will neatlybe assessed independently of one another, inthis section some specific techniques to assesspsychological needs through active listening willbe considered.Using the five ‘W’s is a useful way of thoroughlyexploring the impact that a psychological problemis laden with. Consider the following scenario:A patient with vitiligo comes to see you.They are expressing feelings of anxiety aboutgoing out to the shops because they feelthey are being stared at, because of the depigmentedpatches affecting their arms. Usingthe five ‘W’s, the following might be explored(see Box 6.2).This assessment can be further refined by gettingthe patient to say how often the problem occurs,the intensity of the level of anxiety (on a scaleof 0–8), the number of times it occurs and howlong it lasts for.Cognitive behavioural therapy (CBT)What is CBT?As the name suggests, CBT is a form of therapythat aims to change thoughts and behaviours inorder to improve mental health well-being. It isknown as a talking therapy that focuses on the‘here and now’ rather than trying to make links

96 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 6.2 An example of using thefive ‘W’s to assess psychologicalneed1. What is the problem?That I have vitiligo and that I get veryanxious because of it.2. Where does the problem occur?On my arms.3. When does the problem occur?Only when I am by myself doing theshopping, I don’t get so anxious if thereis someone with me.4. Why does the problem occur, thefeared consequences?I hate being stared at and I am scaredthat someone will say something rudeto me and I won’t know what to say orthat they will refuse to serve me.5. With whom is the problem better orworse?The problem is significantly worse ifI by myself and/or am with people thatI don’t know, if I have a friend with meI don’t feel anywhere near as anxious.between current problems and the past. Its basictenet is that by changing thought and behaviouralpatterns, a powerful effect may be seen ona person’s emotions. By identifying and analysingcounterproductive thoughts and behaviours, anindividual can be helped to alleviate feelings ofanxiety and depression. CBT is seen as a collaborativerelationship between therapist and patientand is most effective with motivated people whowant to help themselves feel better (Beck, 1995).It is most successfully used in cases of depression,anxiety, obsessive/compulsive disorder andpost-traumatic stress disorders. It is the therapyof preference in many of these instances becauseit has good scientific evidence to back up its efficacy,unlike many of the other talking therapies.It is recommended in the National Institute forHealth and Clinical Excellence guidelines thatpertain to mental disorders such as anxiety,(National Institute for Health and ClinicalExcellence, 2007).Using CBT skillsTo practise as a CBT practitioner requires prolongedtraining; however, some understandingof the fundamental principles of the therapycan be useful when using active listening skillswithin a consultation situation.In essence, CBT works through making sense ofproblems which at the time seem overwhelming toan individual. Thus, an individual will respond toa situation by having thoughts, emotions, physicalfeelings and actions. All these various componentswill have an effect on one another, e.g.how someone thinks about a problem will affecthow they feel about it emotionally and physically.Helping an individual to pass through a processof appraisal is a useful place to start. Within thecontext of CBT, this involves appraising the personalmeaning and significance of an event andthen appraising the capacity of an individual tocope with the event. For each situation, there arehelpful and unhelpful ways of responding (seeBox 6.3 for an example).Persistently having negative thoughts about situationsleads to uncomfortable feelings, includingrejection and sadness, as well as unhelpfulbehaviour, such as not returning to the gym.Helping patients involves reframing their experiences,so that rather than producing unhelpfulemotions the individual feels more comfortablein specific situations. This may simply involvedrawing the person’s attention to the fact thatthey view situations negatively and help them toview things more positively. It may be easier forpeople to do this if they understand the directconnection between thoughts and feelings, i.e.having more positive thoughts is more likely tolead to more positive feelings.As part of this process, it is useful to helppatients to learn that physical/bodily feelingscan be changed. This can be done through deepbreathing exercises or progressive muscle relaxationachieved by consciously tensing and relaxingmuscles. Slow deep breathing is one of the quickestways to counteract the effects of the sympatheticnervous system which stimulates the ‘flight

Psychological and social aspects of skin care 97Box 6.3 Helpful and unhelpfulways of responding to a situationA young professional man with eczemaon his face tells you that he was at thegym and the young female instructor whohad been friendly and spent half an hourwith him before, barely acknowledged hispresence.An unhelpful cycle would be:AppraisalShe ignored me because I have eczema onmy faceThoughtI hate my eczemaEmotionFeelings of rejection and sadnessBehaviourNot going back to the gymA helpful cycle would be:AppraisalShe ignored me because she is very busyThoughtI will come when the gym is less busyEmotionFeelings of hope and expectationBehaviourGoing back to the gym at a less busy timeor fight’ response. When fear or stress takes over,breathing tends to be shallow and limited tothe chest. Deep breaths which fill the lungs andexpand the abdomen will invoke a greater feelingof well-being and relaxation. Yoga and T’aiChi use slow, steady breathing and movement tosupport a steady central nervous system response(Pick, 2009).Changing people’s habitual responses to a situationtakes time and as has already been mentioned,it requires the patient to be motivatedtowards those changes. For those with skin disease,there is the added challenge of coping withthe physical discomfort of the problem. Butusing some of these CBT principles may help toreduce the level of psychological anxiety associatedwith the conditions.In summary, particular focus should be paidto three key areas:(1) Helping patients to cope with their diseaseby providing information about it and howto treat it effectively;(2) Promoting relaxation and anxiety management,using some of the techniques discussedhere;(3) Using appraisal to work with patients todevelop helpful rather than unhelpful patternsof thought.A programme that used all three of these elementssuccessfully showed that people whoenrolled showed significantly greater improvementsin disease severity, anxiety, depression,psoriasis-related stress and disability, than thosewho just had conventional treatment (Fortuneet al., 2002).Measuring impact of skin diseaseThere are a number of ways by which it is possibleto measure the impact that skin disease hason the individual. One way of doing this is toconsider disease severity, which assumes that themore severe the disease, the more impact it willhave on the patient’s life. Some disease severityscores are illustrated in the Appendices of thebook. It is also possible to use well-establishedinventories to assess specific aspects of mentalhealth, for example the Beck Anxiety Inventoryor the Penn State Worry Questionnaire, althoughspecific training may be needed to use theseeffectively. There are also a number of dermatology-specificmeasures, many of which focus onthe concept of quality of life, but others assessthe level of disability that is caused by a specificcondition.Put simply, quality of life can be defined asthe person’s ability to enjoy normal life activitieswhich can include health, personal relationships,environment, quality of working life, social lifeand leisure time. In dermatology, quality of lifeis used to measure the impact of a combined

98 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalseffect of psychological and social impacts. Theymay be used to assess the level of impact thata condition has on the individual at the startof a treatment episode and then re-employedas treatment progresses, to see how effectivethat treatment has been in improving qualityof life. A British Association of Dermatologists(BAD) survey showed, however, that in outpatientnotes, only 5% had a quality of life index‘always recorded’ or ‘well recorded’ going downto 3% when inpatient notes were considered(Eedy et al., 2008).Quality of life measures in dermatology are ofparticular importance because disease severity isnot always directly related to the level of impactthat the disease has on the individual (Honet al., 2006). Thus, someone with severe diseasemay have a relatively good quality of life,while someone with mild or moderate disease, adreadful quality of life. Assumptions cannot bemade dependent on disease severity. What hasalso been shown is that health care professionals’perceptions (in this case, doctors) of treatmentefficacy and clearance were perceived in avery different way from that of patients (Ersseret al., 2002). Specifically, patients tended to talkabout resolution of symptoms whereas doctorswere more interested in disease clearance.Richards et al. (2004) showed that dermatologistswere poor at assessing the psychologicaldistress experienced by patients with psoriasis,and even when this was noted generally nothingwas done about it.What these two studies along with the BADsurvey describe, is that health care professionalsoften assume that they understand how a skindisease impacts on an individual. These assumptionsare not always be correct and it is thereforeessential to have objective measures availableto help with the assessment of the impact thata skin disease has. Quality of life measurementis one that is commonly used, however, as theexamples below show there are other validatedtools which help health care professionals tounderstand the impact of a skin disease.There are a number of different quality of lifeindices for patients with dermatological conditions.Some of these are disease-specific whilesome are generic. Here the most commonlyused generic score for both adults and childrenis examined in more detail along with a diseasespecificscore for psoriasis and one for acne. Theadvantage of using the quality of life scores thatare outlined here is that they have been tested forreliability and validity, i.e. they will consistentlymeasure what they set out to measure.Dermatology Life Quality Index (DLQI)This is probably the most well-established andcommonly used quality of life tool in Britishdermatology, it has the advantage of being relativelyshort and therefore practical to use withinthe clinical environment. It has been translatedinto a number of languages. It is completed bythe patient on their own and they are asked toanswer all questions bearing in mind how theyhave felt over the last week. The responseseither ‘very much’, ‘a lot’, ‘a little’ or ‘not atall’ are then scored with points of 3, 2, 1 and0 respectively (Finlay & Khan, 1994). Whentotalled up the scores are interpreted as follows(see Box 6.4):However, what is also useful about this scoreis that it enables the practitioner to get a sensefor how certain areas of the individual’s life aremost affected. This is because the questions canbe grouped into themes (see Box 6.5).Once the score has been completed it becomesa useful part of the assessment process and canguide questioning around the areas that seem tobe most affected in the patient’s life. The toolwith related guidance is available at www.dermatology.org.ukand can be used free of chargein clinical situations.Box 6.4 Interpreting DLQI scores0–1: no effect at all on the patient’s life2–5: small effect on the patient’s life6–10: moderate effect on the patient’s life11–20: very large effect on the patient’slife21–30: extremely large effect on thepatient’s life

Psychological and social aspects of skin care 99Box 6.5 Break down of the DLQIscoreQuestions 1 and 2 relate to symptoms andfeelings with a maximum score of 6Questions 3 and 4 relate to daily activitieswith a maximum score of 6Questions 5 and 6 relate to leisure with amaximum score of 6Question 7 relates to work and schoolwith a maximum score of 3Question 8 and 9 relate to personal relationshipswith a maximum score of 6Question 10 relates to treatment with amaximum score of 3Box 6.6 Break down of CDLQIscoreQuestions 1 and 2 relate to symptoms andfeelings with a maximum score of 6Questions 4, 5 and 6 relate to leisure witha maximum score of 9Question 7 relates to school and holidayswith a maximum score of 3Question 3 and 8 relate to personal relationshipswith a maximum score of 6Question 9 relates to sleep with a maximumscore of 3Question 10 relates to treatment with amaximum score of 3Children’s Dermatology Life Quality Index(CDLQI)This score is in many ways similar to the DLQI,but it is designed for use in children, i.e. thosebetween the ages of 5 and 16. It is available inboth text and cartoon versions, and can be completedby the child with the help of their parent orguardian. The scoring is slightly different from theDLQI in that the score is expressed as a percentageof the total score of 30, the higher the score, themore affected is the quality of life (Lewis-Jones &Finlay, 1995). An Infant DLQI is also availablefor completion by parents or carers, devised bythe same authors (Lewis-Jones et al., 2001).Once again, more detailed analysis of thescoring can be gained by looking at the themes(see Box 6.6)The CDLQI assessment tool is available atwww.dermatology.org.uk and can be used free ofcharge in clinical situations. Further discussion isgiven in Chapter 9.Family Dermatology Life Quality IndexThis score is to be used on adults over the age of16 and aims to represent the impact that havinga family member with a skin disease has on anindividual (Basra et al., 2007). It uses the samebasic structure as the DLQI and the CDLQI andis available at the same website.Salford Psoriasis Index (SPI)This score is a composite tool and is not calleda quality of life score; however, it does includeconsideration of the psychological impact. Theindex is divided into three sections. Firstly, thePsoriasis Area Severity Index (PASI) is completed(see Chapter 3 and Appendix 1). Oncea score is reached, it is then given a SPI scoreas per Table 6.4. Secondly, the psychologicalimpact is measured by asking the patient tomark on a visual analogue score. The patient isasked ‘about the extent to which they perceivethat their psoriasis is affecting their day-to-daylife at the time of the assessment’. The score isfrom 0 to 10 with 0 being not at all affectedand 10 being completely affected (Kirby et al.,2000). The third and final section of the Indexis calculated according to how much treatmentthe patient has undergone (see Box 6.7).Once each individual score has been calculated,the total score is then expressed as a ratio.The first number represents the SPI, the secondpsychological impact and the third the amountof treatment received. Therefore, a ratio of 1:1:0shows that the individual has very little psoriasis,which is having a minimal psychologicalimpact with no systemic treatment or hospitaladmissions. A ratio of 10:10:6 shows very severepsoriasis which is having a major psychological

100 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 6.4 SPI scores inrelation to PASI scores.PASISPI extent0 00.1–3 13.1–5 25.1–8 38.1–11 411.1–14 514.1–18 618.1–23 723.1–29 829.1–36 936 10Box 6.7 Points for the amount oftreatment received1 point for each individual systemic treatmentincluding PUVA (Psoralen plus ultravioletlight A).1 extra point for each treatment receivedfor > one year.1 extra point if patient has received > 200treatments or > 1000J/cm² of PUVA.1 point for every hospital admission forthe treatment of psoriasis.1 point for every episode of erythema.impact and there is a significant history of systemictreatments and/or hospital admissions.The Cardiff Acne Disability IndexThis short questionnaire of five questions asksteenagers and young adults to rate the impact thattheir acne is having on them on a scale of 0–3, thetotal maximum score being 15. This is a quickand practical tool that can be given to a patientto complete in clinic and then used as a basis fordiscussion about the impact of the disease as wellas being used as a tool to monitor the effectivenessof treatment (Motley & Finlay, 1992).This tool is available at www.dermatology.org.uk and can be used free of charge in clinicalsituations.ConclusionThis chapter has sought to explore the socialand psychological aspects of skin care. It hasdone this by considering how society can influenceindividuals and how they feel about theirskin condition. The influence of the brain on theskin and how experiencing a skin disease affectshuman psychology has also been explored.Whilst lip service may be given to the psychologicalimpact of skin disease, the services and skillsare often not in place to help patients in improvingtheir mental well-being. Nurses have a significantrole to play here by refining and using skillsthat they already have. Various tools are availableto assess the psychological and social impact ofskin disease; these notably include dermatologyspecificand some age-specific measures that canbe employed in clinical practice.ReferencesAllen, R., Ed. (2000). The New PenguinDictionary. London: Penguin Book.Altemus, M., B. Rao et al. (2001). Stressinduced changes in skin barrier functionin healthy women. Journal of InvestigativeDermatology, 117(2): 309–317.Arck, P., A. Slominski et al. (2006).Neuroimmunology of stress: Skin takes centrestage. Journal of Investigative Dermatology,126: 1697–1704.Bandura, A. (1997). Self-Efficacy: The Exerciseof Control. New York: Freeman Press.Basra, M., R. Su-Ho et al. (2007). FamilyDermatology Life Quality Index: Measuringthe secondary impact of skin disease. BritishJournal of Dermatology, 156(3): 528–538.

Psychological and social aspects of skin care 101Beck, J. (1995). Cognitive Therapy: Basics andBeyond. New York: The Guild Press.Choi, E., B. Brown et al. (2005). Mechanismsby which psychologic stress alters cutaneouspermeability barrier homeostasis and stratumcorneum integrity. Journal of InvestigativeDermatology, 124(3): 587–595.Eedy, D., S. Burge et al. (2008). An audit ofthe provision of dermatology services insecondary care in the UK with a focus onthe care of people with psoriasis. The BritishAssociation of Dermatologists and The RoyalCollege of Physicians, London.Ersser, S., H. Surridge et al. (2002). Whatcriteria do patients use when judging theeffectiveness of psoriasis treatment. Journalof Evaluation in Clinical Practice, 8(4):367–376.Finlay, A. and G. Khan (1994). DermatologyLife Quality Index (DLQI) – a simplepractical measure for routine clinical use.Clinical and Experimental Dermatology,19(3): 210–216.Fortune, D., H. Richards et al. (2002). Acognitive-behavioural symptom managementprogramme as an adjunct in psoriasis therapy.British Journal of Dermatology, 146(3): 458.Gilchrest, B. (1982). Pruritus: Pathogenesis,therapy and significance in systemic diseasestates. Archives of Internal Medicine, 142:101–105.Ginsburg, I. and B. Link (1989). Feelings ofstigmatization in patients with psoriasis.International Journal of Dermatology, 20(1):53–63.Gupta, M., A. Gupta et al. (1994). Depressionmodulate pruritus perception: A study ofpruritus in psoriasis atopic dermatitis andchronic ideopathic urticaria. PsychosomaticMedicine, 56: 36–40.Gupta, M., A. Gupta et al. (1998). Perceiveddeprivation of social touch in psoriasis isassociated with greater psychologic morbidity:An index of the stigma experience indermatologic disorders. Cutis, 61(6): 339–342.Hon, K., W. Kam et al. (2006). CDLQI,SCORAD and NESS: Are they correlated?Quality of Life Research, 15(10):1551–1558.Hong, J., B. Koo et al. (2008). The psychosocialand occupational impact of chronic skindisease. Dermatologic Therapy, 21: 54–59.Johnson, M. and J. Jones (1985). Prevalence ofdermatologic disease in the United States: Areview of the national health and nutritionexamination survey, 1971–74. AmericanJournal of Industrial Medicine, 8(4–5):451–460.Jowett, S. and T. Ryan (1985). Skin diseaseand handicap: An analysis of the impact ofskin conditions. Social Science and Medicine,20(4): 425–429.Kennaway, G. (2008). Sunbathing Naked.Edinburgh: Canongate.Kirby, B., D. Fortune et al. (2000). TheSalford Psoriasis Index: An holistic measureof psoriasis severity. British Journal ofDermatology, 142(4): 728–732.Lewis-Jones, M. and A. Finlay (1995). TheChildren’s Dermatology Life Quality Index(CDLQI): Initial validation and practicaluse. British Journal of Dermatology, 132(6):942–949.Lewis-Jones, M., A. Finlay et al. (2001). TheInfants’ Dermatology Quality of Life Index.British Journal of Dermatology, 144(1):104–110.Mehrabian, A. and S. Ferris (1967). Inferenceof attitudes from non-verbal communicationin two channels. Journal of ConsultingPsychology, 31(3): 248–252.Mehrabian, A. and M. Wiener (1967).Decoding of inconsistent communications.Journal of Personality and Social Psychology,6(1): 109–114.Motley, R. and A. Finlay (1992). Practical use ofa disability index in the routine managementof acne. Clinical and ExperimentalDermatology, 17(1): 1–3.National Institute for Health and ClinicalExcellence (2007). Anxiety: anxiety (panicdisorder with or without agoraphobia, andgeneralised anxiety disorder): Managementof anxiety in adults in primary, secondaryand community care. London: NICE OpenUniversity (2006) Models of disability,Retrieved 3rd December 2009, http://www.open.ac.uk/inclusiveteaching/pages/

102 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsunderstanding-and-awareness/models-ofdisability.php.Papadopoulus, L. and R. Bor (1999). OpenUniversity (2006). Psychological Approachesto Dermatology. London: Wiley.Pavlovsky, L. and A. Friedman (2007).Pathogenesis of stress-associated skindisorders: Exploring the brain–skin axis.Current Problems in Dermatology, 35:136–145.Pick, M. (2009). Deep Breathing – The TrulyEssential Exercise. Retrieved 17 April 2009,from http://www.womentowomen.com/fatigueandstress/deepbreathing.aspx.Richards, H., D. Fortune et al. (2004).Detection of psychological distress in patientswith psoriasis: Low consensus betweendermatologist and patient. British Journal ofDermatology, 151: 1227–1233.Richards, H., D. Ray et al. (2005). Response ofthe hypothalamic–pituitary–adrenal axis topsychological stress in patients with psoriasis.British Journal of Dermatology, 153:1114–1120.Williams, H.C. (1997). Dermatology HealthCare Needs Assessment. Oxford: RadcliffeMedical Press.World Health Organisation (2009).Mental Disorder. Retrieved 15April 2009, from http://www.who.int/topics/mental_disorders/en/.

7Helping patients make themost of their treatmentSteven J. ErsserIntroductionA key challenge for people living with chronicskin conditions is the need to ensure that theyuse their treatment to optimal effect. Despitethe efforts to determine the effective treatmentplan, a crucial concern is how the individualinterprets and engages with the plan, since thereare multiple factors that may interfere with theirability to utilise the treatment in an effectiveway. Treatment effectiveness depends not onlyon having evidence of beneficial treatments andmaking discerning clinical judgements but alsoon the patient’s interpretation of the treatmentplan, their motivation and understanding of itand how in practice they apply it to their lifestyle.Therefore, effective treatment fundamentallydepends on people taking an active role inlearning about their therapy and knowing howto utilise it correctly. This chapter focuses onways of supporting patients to self-manage theircondition effectively through playing an activerole in treatment decisions and application.Dermatologists have been accused ofthinking that they are the only people whoknow about skin diseases and that they arethe only people sufficiently qualified to treatthem. How true is this, and is it likely thatdermatologists are going to be the majorsources of advice on dermatological mattersin the new millennium? (Prof. Robin Marks,University of Melbourne/Former President,International League of DermatologicalSocieties; Marks (2000))Self-management and patient supportThe management of a chronic illness requiresa number of factors to sustain effective healthbehaviour; this includes knowledge, skills andconfidence in managing a condition long term.These areas require education and psychologicalsupport that is systematically assessed andplanned. A key aspect of this support is emotionalsupport to help individuals to cope withtheir long-term condition and their treatmentregimens and recognition of their impact ontheir lifestyle. Awareness is also needed of specificissues that may affect some people, suchas low self-esteem, poor motivation and a lackof social confidence. Educational and support

104 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsneeds reflect aspects of the person’s care that canbe unmet or poorly met because their managementis not necessarily systematically plannedfor in the same way as treatment regimens.Chronic illness management relies on a personchanging their health behaviour, and specificallyadaptive self-management, which inturn requires the patient to understand theircondition and treatment to maintain health andimprove their quality of life. Professional supportis required to achieve this. An editorial inthe British Medical Journal (Bodenheimer et al.,2005) has highlighted the potential key role ofNurses as leaders in chronic care, reflecting theneed to combine treatment with education andsupport, which nurses are well placed to provide.People living with long-term conditions arehigh demand users of health services. There is astrong policy context urging the need to addressthe needs of this group, improve chronic diseasemanagement through helping to improve selfcareand the individual’s contribution to theircare (Department of Health, 2004, 2005a, b).Therefore, a key challenge for the majority livingwith chronic conditions is to engage in effectiveself-management and self-care support. TheDepartment of Health (2005a) highlighted thedifferent levels of need for this group to whichthe service needed to respond (Figure 7.1). Forthose living with long-term conditions that areat high risk of deterioration, disease managementis required to reduce risk, maintain healthand reduce the need for hospital admission.A key target group are those living with complexconditions. This includes patients with multipleconditions, such as a person with psoriasis whoalso has active psoriatic arthropathy and otherchronic conditions, e.g. diabetes. Interventionto maintain and promote the health of peopleliving with long-term conditions requires afoundation of support to ensure that they caneffectively do self-management.If people with chronic conditions are to beexpected to engage in a degree of self-management,it is necessary to be clear about theexpectations of the person and their carers.This provides the basis for instigating an effectiveplan of care and treatment and determiningwhere support is needed to prepare the personLevel 3Patients withhighly complexconditionsCase managementLevel 2High-risk patientsDisease/Care managementLevel 170–80% of patients with long-term conditionsSelf-Care support/managementHealth promotionFigure 7.1 Levels of need for people with long-termconditions. (Source: Department of Health, 2005a.Reproduced under the terms of the Click-Use licence.)and their family. It will also reflect where thereare unmet or poorly met educational and supportneeds and then, where intervention is required,when there are limits to self-management orthe process of self-care fails.Table 7.1 illustrates some of the complexity ofhelping patients to use their treatment optimallyand the educational and support challenges forhealth professionals. These areas of health careneed present nurses and other health professionalswith significant therapeutic opportunitiesto enable or empower the person and theirfamily to engage actively in self-management.Each area of knowledge and skill also requiresa degree of confidence for the person trying toapply these.Educational and support needs are both commonand individual. As such, rigorous patientsurveys can provide an indication of patternsof need that practitioners can plan to address(Krueger et al., 2001; Beresford, 2002). Theseneeds are reflected in Table 7.1. They convey aneed to understand their condition, those factorsthat adversely affect and improve it and theirtreatment. Dissatisfaction with the effectivenessof treatments is a theme running through thefindings. This has been validated through recentqualitative evidence, reflecting self-managementneeds (Ersser and Cowdell, 2009).

Helping patients make the most of their treatment 105Table 7.1 An illustration of common areas educational and psychological needs supporting self-management for those withchronic skin conditions.Self-management competence Knowledge required Skill requiredManaging symptomsCommunicate effectively withhealth professionalsManaging medicationUnderstanding and beliefsabout their conditionSymptoms and their triggersTreatment beliefs andunderstandingUnderstanding and beliefsabout their conditionTreatment beliefs andunderstandingTreatment choicesTreatment beliefs andunderstandingEffectively judge whent reatment is not workingRecognising and reportingcommon side-effectsEffective applications of topical treatmentsAdapting treatment to change in conditionWays of adapting their treatment to their lifestyle,whilst maintaining effectivenessExercising treatment choices adapted topreferences/lifestyleAdapting treatment to changes in their condition(e.g. during acute episodes of a chronic skincondition)Judging the limits of self-management and when toseek helpThe ability to recognise common side-effects isimportant where patients are using or changingtreatments on a long-term basisEducational resources and strategiesIt is important to maintain awareness of therange of educational resources available for supportingthose living with chronic conditions andtheir quality. Some key sources are illustrated inTable 7.2.The task of identifying reliable informationsources of quality information is a challenge forpatients who can become bombarded with informationsources. This may include sources such asinternet sites originating from patients, voluntarygroups and health professionals as structured educationalinformation of widely varying quality tosocial networking exchange. A systematic reviewof studies reviewing health-related websites foundthat 70% concluded that quality of informationwas a problem (Eysenbach and Till, 2001).Information also comes in the form of pamphletsfrom charities and industry, articles in magazines,the media and friends and family. Indeed,Surridge’s ongoing study (Surridge, 2005) highlightedthe complexity of the process by whichparents need to establish whether the source ofinformation is reliable and beneficial or not inhelping them to manage their child’s eczema.On account of the high volumes of educationalmaterial of variable quality, careful attentionis needed to the ways in which patients areguided to information sources and how best toutilise resources. This should be based upon anassessment of their educational needs, preferredmethods of learning and the means of access(e.g. internet) and the level and complexity ofinformation required. Indiscriminate handingout of generic information leaflets is invariablyineffective and may well be misleading since itmay lack necessary modification for the individual.There is a need to assess the effectivenessof the source material given and evaluate it aspart of a package of care. This may be done infollow-up clinics or possibly telephone consultationsto review learning, remaining areas of helpneeded and changing educational needs.Educational opportunities need to be plannedand tailored to individuals; however, consideration

106 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 7.2 Educational resources related to managingchronic skin care: examples.WebsitesPrintedmaterialsAudiovisualmaterialsDermatology professionals: BritishAssociation of Dermatologistsinformation sheets www.bad.org.uk/public/leaflets/Dermatology sites (advanced): www.dermnet.org.nz/Generic sites: NHS Direct www.nhsdirect.nhs.uk/Condition specific sites:National Eczema Society*: www.eczema.org/abouteczema.htmlPsoriasis Association*: www.psoriasisassociation.org.uk/National Psoriasis Foundation: www.psoriasis.org/home/Ichthyosis: www.ichthyosis.org.uk/Dermatology professionals: AmericanAcademy of Dermatology: www.aad.org/forms/pamphlets/default.aspxPatient groups: materials can be orderedfrom many organisations (see above *)Pharmaceutical companies: thesemake some materials and so may havecommercial influences; as such, theserequire careful review before use.However, useful unbiased resourcescan still be found, e.g. Dermol producesome useful tear off pads depicting andexplaining the maintenance of the skinbarrier using emollients.These are limited. Again, pharmaceuticalcompanies make some materials and somay have commercial influences.Podcasts – these are under-developedat present; however, they are likely toexpand: e.g. now available from thePsoriasis Association: www.psoriasisassociation.org.uk/(November 2008)needs to be given to common learning needs thatcan be efficiently delivered in a group context.This can provide the added benefit of groupsupport and vicarious learning from others andhow they adapt to their condition and treatment.Group support and learning may apply toadults with a chronic skin condition, teenagerswith severe acne and those with special needs,such as people living with psoriatic arthropathyor to carers, including parents of children witheczema. To ensure time is used efficiently, learningneeds should be identified. Educational aidsrequire consideration, such as the appropriate useof a DVD, discussion time and time for practicaldemonstrations and for questions.Systematic methods of education and psychologicalsupport have received limited attentionin dermatology, although there are a growingnumber of studies developing and testing interventionsto support the management of specificdermatology conditions – some of which aresubject to systematic reviews. One such exampleis a Cochrane review of psychological andeducational interventions to manage childhoodatopic eczema (Ersser et al., 2007). For the purposesof this chapter, the findings will be brieflysummarised related to educational intervention.Following a highly systematic search of the literatureand the exclusion of studies which failedto meet quality criteria for effective randomisedcontrolled trial (RCT) methodology, only foureducational studies met the inclusion criteria.RCTs’ meeting the inclusion criteria included:Chinn et al. (2002); Niebel et al. (2000); Staabet al. (2002) and Staab et al. (2006). In eachcase, the intervention was an adjunct to conventionaltherapy, not a substitute for it. It was notpossible to synthesise the data due to the variationin the type of data available (heterogeneity).However, it was possible to provide an extensivecritical appraisal of the included studies.In summary, the studies by Niebel et al.(2000) and Staab et al. (2002, 2006) identifiedthat education can lead to an improvementin clinical severity and in parental quality of life(Staab et al., 2006), but only marginal improvementwas seen in the latter within the study ofChinn et al. (2002). In each case, a systematicapproach to education was implemented usingone of two models of service delivery: (1) eczemaschools – multi-disciplinary approach (more typicalin Germany) and (2) nurse-led clinics (moretypical in the UK). Each of the four educationalstudies was directed towards parental education.It was observed in the Cochrane review thatthe Eczema School model was more resourceintensivecompared to the nurse-led clinic model(Ersser et al., 2007), although no comparative

Helping patients make the most of their treatment 107studies have been undertaken as yet of theirrelative effectiveness. Delivery of education wasdemonstrated in both hospital outpatient settings(Niebel and Staab studies) and in primary care(Chinn) and with and without the use of technology.For example, Niebel’s study revealed thatvideo-assisted education was more effective inimproving severity than direct education and thecontrol (discussion) (p < 0.001). The most rigorousstudy found to date was that of Staab et al.(2006), which evaluated long-term outcomes.This found significant improvements in bothdisease severity (3 months to 7 years, p 0.0002;8–12 years, p 0.003; 13–18 years, p 0.0001)and parental quality of life (3 months to 7 years,p 0.0001; 8–12 years, p 0.002), for childrenwith atopic eczema.Chapter 4 outlines specific methods of psychologicalintervention which have an educationalbasis, such as the use of behaviouralmanagement (habit reversal) to manage problematicsymptoms, for those living with eczema.Theory supporting effectiveintervention: Social learning theoryand the self-efficacy concept(There is a need to) ‘…increase an individual’sconfidence and belief to take control over theirlife’. (Department of Health 2002, p. 25: ExpertPatient Programme)Supporting effective self-management canbe a complex process for the patient and theirfamily. The person living with a chronic conditionneeds to have confidence in their abilityto exercise self-management. Self-efficacy is animportant and related concept which is similarto but distinct from that of confidence. It maybe regarded as a key motivational force whichhealth professionals need to support. Self-efficacyis defined as: ‘an individual’s belief in theircapacity to successfully execute a health relatedbehaviour’ (Bandura, 1977, 1989). It reflects apositive perception or belief set. The conceptis based on Albert Bandura’s Social LearningTheory (Bandura, 1977, 1997) which indicatesthat people learn by observing the behaviour ofothers within a social context. Furthermore, theyare more likely to engage in certain behaviourswhen they believe they are capable of carryingthem out successfully; i.e. when they have highself-efficacy. Belief in one’s efficacy to exercisecontrol is viewed by Bandura as a commonpathway through which psychosocial influencesaffect health functioning. Self-efficacy reflects adegree of mastery or control achieved throughthe development of behavioural or cognitiveskills, social skills, life knowledge and skills,all of which are directly relevant to managing achronic skin condition.So much of chronic illness management isabout behavioural adaptation to ensure that lifestyleis adapted to enduring illness, with peoplemanaging their illness in the context of their dailylives. Its application has been seen in work with awide range of groups living with long-term conditions,including those with diabetes mellitus(Shortridge-Baggett and van der Bijl, 1996; Shui,2006) and end-stage renal disease (Tsay, 2003).Self-efficacy is directly relevant to a person’sagency; this refers to their capacity to makechoices and to bring about actions and influencesarising from these choices, which are a keyfacet of such adaptation. However, it is importantto note that learning may or may not resultin behavioural change. For example, a personmay be taught to apply their topical treatments;however, they may not have the confidence toapply them or, say, the skill to effectively applya wrapping bandage. It is fundamental for achange of behaviour for the person, or indeedthe carer, to have sufficient degree of self-beliefby the person in their capacity to act, as wellas knowledge, skill and indeed motivation.Enhancing a person’s capacity to make choices isfundamental to helping them adapt to and effectivelyself-manage with a chronic illness; as such,this is a fundamental area of facilitative competencethat requires development. Self-efficacy isa significant quality for those living with chronicskin conditions because it has been demonstratedto be important to a health-promoting lifestyle(Gillis, 1993). Self-efficacy is recognised as a keybasis for effective self-care ability for those withchronic conditions. Principles of self- efficacy havebeen used to develop self- management skills;extensive testing revealed relief of debility and

108 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalschronic pain in arthritis (Holman and Lorig,1992). Perceived self-efficacy has been identifiedas a predictor of functional disability regardlessof the level of pain or disease duration(Schiaffino and Revenson, 1992).Social learning can be an important route tohealth promotion since people learn throughvicarious experience (Bandura, 2004). Healthprofessionals need to take account of thiswhen working with patients to plan their care.Nurses can use self-efficacy–orientated educationto support patient (and family) empowermentand achieve health improvement. Thefocus for support using the self-efficacy conceptmay be on the patient, carer or the parent (deMontigny and Lacharite, 2005). Parental selfefficacyis very relevant to the care of the childwith conditions such as eczema, since effectivemanagement is highly dependent on the parent’seffective engagement in the treatment plan.Work has been undertaken to examine parentalself-efficacy in other related contexts, such aschildhood asthma self-management (Hanson,1998; Grus et al., 2001).There is a distinction between the concepts ofself-efficacy and locus of control, which requiresconsideration when planning patient education.Self-efficacy reflects beliefs in control overaction (such as the belief in your ability to manageyour child’s eczema symptoms), whereasthe locus of control conveys beliefs in controlover outcomes (such as the parent’s ability toimprove their child’s eczema symptoms). Theseare distinct but interrelated ideas.Application of self-efficacy theoryto the dermatology clinicAs a basis for informing the development ofinterventions to enhance self-efficacy, the followingstrategies to enhance or provide sourcesof self-efficacy, as identified by (Bandura, 1997),are summarised:1. Personal accomplishment2. Vicarious experience (learning through theexperience of others; this may be powerfullymodelled by patients or carers in a similarsituation or health professionals)3. Verbal persuasion4. Regulate emotional behaviour (primarily,the management of stress and anxiety whichmay impair learning)Their practical application will now beillustrated within the context of a dermatologyconsultation.■■■Personal accomplishment and verbal persuasion:Personal accomplishment can leadto stronger efficacy beliefs than other strategiesof influence. This involves reinforcing(acknowledging and encouraging) instanceswhen patients effectively engage in successfulhealth behaviour, such as managing toapply topical medications in the correctorder. It is important to assess the patient’sself- management ability and to give themperformance feedback, including verbal persuasionto encourage them to build on whatthey are already doing well.Vicarious experience: This refers to socialmodelling, where opportunities are providedto help the patient learn from others.This may include health professionalsdemonstrating effective practices, such asa wet-wrapping technique by a parent,or creating group-learning opportunitieswhere there is sharing of good practice bya patient or parental carer with others ina similar social learning situation. Grouplearning also provides a resource-efficientopportunity for patient or parental carereducation; this may include exposure towell-organised patient support groups suchas the Psoriasis Association or the NationalEczema Society.Regulation of emotional behaviour: Bandura(1997) highlights how emotional and physicalarousal may interfere with the performanceof a desired behaviour. Supporting thepatient to regulate such emotions involvesexamining the patient’s mood state andemotional responses to their condition andexploring coping strategies that suit them.This may involve, for example, triggeringan opportunity to raise awareness fordiscussion, such as using a quality-of-life

Helping patients make the most of their treatment 109questionnaire as a basis for discussing thepsychosocial impact of their condition orof their usual coping methods, adaptiveand maladaptive, such as exercise or excessivealcohol intake, respectively. The patientcan be directed to strategies to help themmanage stress and anxiety more effectivelythrough pursuing relaxation opportunities,such as returning to social hobbieswhich have been curtailed due to a lack ofself-esteem or engaging them in the use ofrelaxation methods such as progressiverelaxation, yoga or mindfulness-based stressreduction techniques (a training techniqueto focus attention in the present moment)(Kabat-Zinn et al., 1998).There is a need to promote active engagementwith health promotion materials reflection,clarification and interpretation of the person’sknowledge, attitudes and beliefs as well astheir involvement in health-related decisionmaking(Kettunen et al., 2001). In practice,this will require exploration at follow-upclinics any questions regarding the informationsupplied or discussion of priority issueshighlighted, such as the sequencing of topicaltreatments.Increasingly, interventions are being developedto help improve chronic illness managementand treatment adherence, whichincorporates a range of educational measuresbased on theory. This is well illustratedin the asthma field, with studies such as thatby Schaffer and Tian (2004) utilising anaudio tape and booklet alone and combined,with the tape based on Protection MotivationTheory (Rogers and Prentice-Dunn, 1997).Others include the use of individual actionplanning based on Bandura’s self-cognitivetheory (van der Palen et al., 2001). Wangberg(2008) study utilised an internet-based diabetesself-care intervention tailored to enhanceself-efficacy. This highlights the scope todevise systematic interventions, based ontheory related to motivation or self-efficacyor coping, that may enhance the likelihoodof effective learning and behavioural changerelated to self-management.The challenge of promoting treatmentadherenceEvidence-based health care may identifytreatments that are potentially effective for groupsof patients; however, these are fundamentallydependent on the patient’s behaviour to ensurethe method of application. A major problem formany people living with chronic illness, includingthose with skin conditions, is that they are on anumber of medications and they fail to utilise theirtreatment effectively; this may be due to a lack ofknowledge, skill, confidence or motivation.One example of the problem is illustrated bypsoriasis, with research evidence of the problemsof treatment adherence. A study by Richards et al.(1999) reported high levels of ‘non-compliance’with treatment. Several factors are likely to contributeto this situation. Survey evidence of expectationsof treatment highlights the high levels ofdissatisfaction (Krueger et al., 2001; Richardset al., 2001; Psoriasis Association and Beresford,2002), with many giving up their treatment. Suchevidence conveys the need for more consistenteducation, but other studies highlight the timeburden of treatment (Finlay and Coles, 1995).These findings are significant since patients’treatment expectations may affect their adherenceto therapy.The reasons for poor treatment adherence arecomplex. The situation involves a considerationof patient beliefs and behaviour. This is nowexplored in more detail by examining the processby which the health professional engageswith the patient during consultation when outliningthe treatment plan.The importance of the concordanceprocessEffective adherence to treatment requires morethan a traditional expectation of compliance,namely doing what the health professionalexpects ‘should’ be done. If adherence is to beimproved, the process must involve activelyengaging with the person ‘based on a negotiationabout medication between health care

110 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsprofessional and patient that respects patients’beliefs and wishes’ (Royal Pharmaceutical Societyof Great Britain, 1997).The concordance process requires that boththe patient and health care professional participateto reach an agreement on the nature ofthe problem (illness) and the treatment plan;their agreement needs to draw on the experiences,beliefs and wishes of the patient todecide when, how and why to use medicines(Medicines Partnership, 2003). Both partiesneed to treat each other as partners and recogniseeach other’s knowledge skills to improvedecision-making (Atkins and Ersser, 2008).Patients’ views are no less important whenmaking decisions about what is suitable for thepatient to ensure a match to their preferencesand lifestyle. Through such a process of negotiation,it is more likely that there will be cooperationwith and so adherence to the agreedplan. Therefore, some of the strategies fordeveloping a negotiated approach may includethe following elements:■■■■■■■Listening to patient’s beliefs and expectations;Dealing sensitively with patient’s emotionsand concerns;Helping patients to make informed choices;Giving explanations and rationales for treatmentoptions;Negotiating outcomes of consultations thatboth the prescriber and patient are satisfiedwith;Giving clear instructions to patients abouttheir medication;Checking the patient’s understanding andcommitment to treatment.As an example, treatment adherence problemsare a common cause for apparent failurethat feature in atopic eczema and thisincludes factors such as the patient or parentalcarer having a poor understanding of disease(Fischer, 1996). In this context, there maybe a discussion about enhancing the parent’scapacity to avoid trigger factors, managingthe child’s sleep disturbance or finding betterways of communicating with professionalsregarding treatment. Related concordanceconcerns may include the parent’s ability tomanage successfully topical applications suchas emollients, antibiotic and steroid creams.Some studies have attempted to enhance concordancewithin a dermatology context, forexample, with improved adherence to compressiontherapy for patients with venous legulcers (Brooks et al., 2004).To ensure effective use of treatment, it is necessaryto explore what the patient understandsby their treatment regimen within the consultation,since it may reveal areas of confusion.Evidence suggests that problems of adherencestem more from a disbelief in their efficacyto use prescribed medication effectivelythan from disease activity or pain (Taal et al.,1993). Furthermore, common problems arisefrom the need to manage a number of medicationsand from trying to sequence topical applicationseffectively. Also, there can be a lack ofunderstanding of the conditions under which‘as required’ drugs can be used appropriately.Practitioners also need to explore expectationsof treatments. Qualitative research evidencesuggests that dermatology patients may notshare precisely the same views with dermatologyprofessionals about what criteria are importantin judging effectiveness; as in the case ofthose living with psoriasis (Ersser et al., 2002).In addition, if a person expects their treatmentto work quickly but in practice, the medicationis effective only after sustained treatment over anumber of weeks, such as coal tar or calcipotrioluse in psoriasis, there is a high risk that suchtreatment may be abandoned prematurely. Thismay also apply to the situation in which thepatient believes their medication is designed tohelp with one symptom when it is for another,such as in the case when topical steroids may beused with the intention of controlling eczema,but when infected, an antimicrobial agent wouldbe required.There is a need to give consideration thereforeto the range of factors affecting both thepatients or carers’ treatment choice (preference)and use in practice and to recognise the relatededucational opportunities. The following discussionswill take place within the context of thehealth care consultation, to which we now turn.

Helping patients make the most of their treatment 111The therapeutic consultationOver-emphasis on technology tends toovershadow therapeutic modalities thatcan have real significance. Nurses mustrecognise that they do not create change inpeople, rather they participate in the processof change to the extent that they bringknowledge to the situation and recognisethat the healing process has the potentialfor healing beyond that which we recognisetoday. (Rogers, 1992, p. 61)To help the patient make the most of their treatment,there is a fundamental need for healthprofessionals to create effective opportunitiesfor open communication within the context ofthe dermatology consultation. The consultationprovides the key opportunity for effective educationand support. It is paradoxical that withinthe discussion of evidence-based treatment indermatology care, very little attention is paid tothe quality of the consultation opportunity asa human interaction that can profoundly influencethe patient’s behaviour, treatment planand the final outcome of the care. Some attentionhas been paid to these issues in nursing ingeneral (Ersser, 1997; Kinmouth et al., 1998;Watson, 1999), with limited attention in thedermatology nursing context (with some exceptions,e.g. Courtenay et al., 2009). General practiceresearch has paid attention to consultationissues amongst GPs and nurses (Kinmouth et al.,1998); however, this remains a neglected areawithin the dermatological literature.The quality of the consultation and its outcomeis directly dependent on the quality of thepractitioner–patient relationship and the abilityto ensure that they optimise opportunitiesfor education and support. Typically, nurses arewell placed to do this should they allow timeto assess and plan for patients’ support need,although it is also essential for the dermatologist–patientconsultation when making crucialdecisions about treatment plans. This may alsoapply to nurse–prescriber–patient consultationsin some countries such as the UK.The literature from the social psychology literatureon therapeutic professional relationshipsTable 7.3 Features of therapeutic-helping relationships.FeatureSelf-awarenessBeing genuine andauthenticCommitted to patientparticipation in careEmotional involvementand closenessEmpathyIllustrative supportingreferencesFreshwater (2002), Egan(1994), Peplau (1988),Krikoriam and Paulanka (1982)Jourard (1971), Truax et al.(1974), Mitchell et al. (1977)Brearley (1990), Hays andDimatteo (1984), Roberts et al.(1995)Jourard (1971), Strang (1982)Morse et al. (1992), Truax et al.(1974), Mitchell et al. (1977)Trust Watson (1985), Bernado (1984)Unconditionalpositive regard/warmth/caringGeanellos (2005), Sellick(1991), Stickley and Freshwater(2002), Combs et al. (1971),Mitchell et al. (1977), Morseet al. (1992)reveals common features which apply to alltherapeutic and helping relationships. There isalso evidence of the exploration of the distinctivetherapeutic opportunities that nurses may havethrough helping patients with everyday livingactivities as well as treatments (Ersser, 1997); theseare summarised and exemplified in Table 7.3.Central to all the features of therapeuticrelationships is the capacity for self-awarenesswithin the health professional, as a prerequisitefor enhancing the therapeutic quality of theconsultation (Ersser, 1997; Freshwater, 2002).These features help to create the opportunityfor effective patient education and supportdescribed previously. Taking the example of theconcordance process, this is much more likelyto be effective when there is a commitment topatient involvement, empathy to their concernsand preferences, unconditional positive regardand self-awareness regarding the health professional’sown preferences and predispositionsrelated to patient care. However, these featuresof therapeutic relationships cannot be takenfor granted as being ever present; for example,

112 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsSellick (1991) found that nurses had a strongerdesire to control relationships than other professionals,such as occupational therapists.Through the nurse–patient relationship, thenurse has scope to meet the patient’s expectationsfor seeking help, including their need toreceive support to develop their abilities andindependence and play their part in managingtheir condition.To achieve this, nurses may contribute as aresource and catalyst for the patient by raisingmutual awareness of their needs on their journeyfrom dependence to independence; this isachieved through the formation of an attachment,providing the patient with a basis for support(Ersser and Watkins, 2007). Attachmentrelationships are common in helping relationshipsand times of need (Ersser, 1997).Attachment theory is relevant to adults as wellas children – and remains an important theoryin the social psychology literature (Rholes andSimpson, 2006). It is concerned with adultattachment styles and the psychological underpinningsand how these make an impact onthe outcomes of different attachment styles.Dependence and anxiety may be reduced andthe patient can explore new coping mechanismsadapted to new awareness and divertedinto positive control over the experience ofsymptoms/illness. McCluskey (2005, pp. 86–87)describes the consequences of an effectiveattachment as follows: ‘The care-seeker has thesubjective experience of accessing competence.When this happens, the instinctive system forcare-seeking will shut down and the exploratorysystem within the individual will havemore energy to engage with the problems of living.’The appropriate caregiver response to thepatient’s (or parental carer) need is to put themin touch with their competence to act and reactivatetheir emotional, physical and intellectualcapacity and resources applied to the individual(Ersser and Watkins, 2007).There is evidence of distinctive therapeuticopportunities for education and support providedwithin nursing therapeutic or helping relationships.This may include meeting a range ofpatient needs through the provision of skilledbodily or intimate physical care such as washingand moisturising the skin Lawler, 1991; Ersser,1997). Furthermore, there is evidence of a recognitionof the integrated nature of care of mindand body, with an emphasis on maximising thetherapeutic opportunities that exist within ordinarydaily care, such as skin hygiene or helpingto apply treatments events, which providetherapeutic opportunities to integrate the meetingof both physical and psychological needs(Chapman, 1986; Taylor, 1994).Therefore, in conclusion, there is a need forthe health professional to cultivate an accessible,effective consultation style, building on establishedpsychological principles on therapeutic/helping relationships, as a basis for helping orempowering the person to be able to engageactively in contributing to the management oftheir own health.Prescribing skin-related products andopportunities for medicines educationThe prescription and administration of medicinesprovides a substantial opportunity tohelp people make the most of their treatmentthrough teaching the patient about how to usetheir treatment most effectively. Nurses have anestablished role in drug administration, ensuringthat suitable medication is delivered at theright dose, time and by the appropriate route.Therefore, whether through drug administrationor prescription, health professionals have substantialopportunities to ensure suitable treatmentselection taking into account patient needsand preferences and taking of medicines toimprove treatment adherence and effectiveness.Treatment adherence and successful medicinemanagement are dependent on effective educationand support, which if planned and deliveredeffectively nurse prescribers are well placedto provide. Consideration is needed of the valueof investing sufficient time to explain effectivelyintricate treatment regimens to the patient, andin doing so, take account of their lifestyle sothat the guidance is adapted to the individualand their level of knowledge. This is likely toimprove the effective use of medicines and their

Helping patients make the most of their treatment 113Box 7.1 Mechanisms availablefor the prescribing supply andadministration of medicines■■■■■■Patient-specific directionsPatient group directionsSpecific exemptions covering supply oradministration – as contained in medicineslegislationNurse-independent prescribingPharmacist-independent prescribingSupplementary prescribing bynurses, pharmacists, optometrists,Physiotherapists, radiographers andchiropodists/podiatristsSource: Department of Health (2006).Reproduced under the terms of the Click-Use licence.efficacy and reduce the time required to dealwith the consequences of poor adherence. Nurseprescribing consultations should prioritise theseopportunities for education and support, sinceinvariably their focus is not on diagnosis.The prescribing of treatments within dermatologyis no longer confined to medical practitionersin some countries, such as the UK, butnow by others such as suitably trained nurses,pharmacists and podiatrists. Membership ofthe Nurse Prescribing sub-group of the BritishDermatological Nursing Group continues toincrease rapidly.The mechanisms available for the prescribingsupply and administration of medicines issummarised in Box 7.1 (Department of Health,2006).These different mechanisms will now bebriefly outlined. Note these are only relevant forcountries within the UK.Patient-specific directionsA patient-specific direction (PSD) is the traditionalwritten instruction, from a doctor, dentist,nurse or pharmacist-independent prescriber,for medicines to be supplied or administered toa named patient (Department of Health, 2006).The majority of medicines are still supplied oradministered using this process. In primary care,this might be a simple instruction in the patient’snotes. Examples in secondary care includeinstructions on a patient’s ward drug chart. Asa PSD is individually tailored to the needs of asingle patient, it should be used in preferenceto a patient group direction (PGD), whereverappropriate.Patient group directionsA PGD is a written instruction for the supply oradministration of a licensed medicine (or medicines)in an identified clinical situation, wherethe patient may not be individually identifiedbefore presenting for treatment. Patients mayor may not be identified, depending on the circumstances(DH, 2006). A PGD is drawn uplocally by doctors, pharmacists and other healthprofessionals and must meet certain legal criteria.Each PGD must be signed by a doctor ordentist, as appropriate, and a pharmacist andapproved by the organisation in which it is tobe used, typically a PCT or NHS Trust. PGDscan only be used by specified registered healthcare professionals, acting as named individuals,including nurses, health visitors, paramedics andpodiatrists. Each PGD has a list of individualsnamed as competent to supply/administer underthe direction.Independent prescribingThe development of independent prescribingis part of a drive to make better use of nurses’and pharmacists’ skills and to make it easier forpatients to get access to the medicines that theyneed. From 1 May 2006, ‘Nurse IndependentPrescribing’ (formerly ‘Extended FormularyNurse Prescribing’) was expanded. This allowsnurses to prescribe any licensed medicine for anymedical condition that a nurse prescriber is competentto treat, including some controlled drugs.It allows virtually any licensed medicine in theBritish National Formulary (see part XVIIB(ii) of

114 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsthe Drug Tariff) to be prescribed (Department ofHealth, 2006). Pharmacist-independent prescribingnow permits suitably prepared pharmaciststo prescribe any licensed medicine for any medicalcondition that they are competent to treat.In the UK, all first-level registered nurses, registeredmidwives, registered specialist communitypublic health nurses and registered pharmacistsmay train to be independent prescribers. Furtherinformation on nurse-independent prescribingcan be found on the Department of Health(Department of Health, 2008) website, whichshould be checked regularly for updates.Supplementary prescribingSupplementary prescribing was introduced inApril 2003 for nurses and pharmacists. It wasextended to physiotherapists, chiropodists/podiatrists, radiographers and optometristsin May 2005. Supplementary prescribing isa voluntary prescribing partnership betweenthe independent prescriber (doctor or dentist)and supplementary prescriber, to implementan agreed patient-specific clinical managementplan (CMP), with the patient’s agreement(Department of Health, 2006). Followingagreement of the CMP, the supplementaryprescriber may prescribe any medicine for thepatient that is referred to in the plan, untilthe next review by the independent prescriber.There is no formulary for supplementary prescribingand no restrictions on the medicalconditions that can be managed under thesearrangements. It will also be appropriate inspecific situations, for instance, when workingwithin a team where a doctor is accessibleor for specific long-term conditions, betweenmedical reviews (Department of Health, 2006).Supplementary prescribers can prescribe controlleddrugs and unlicensed medicines in partnershipwith a doctor, where the doctor agreeswithin a patient’s CMP. From July 2006, chiropodists/podiatristsphysiotherapists, radiographersand optometrists are also able to prescribecontrolled drugs as supplementary prescribers,but only where there is a patient need and thedoctor has agreed in a patient’s CMP.The training for supplementary prescribingis incorporated into nurse and pharmacistindependentprescribing. All professional groupsmust register their supplementary prescribingqualification with their regulatory bodybefore beginning to prescribe. Further informationcan be found on the Department of Health(2003, 2008, 2009) website. See Table 7.4 formore sources of information on non-medicalprescribing.Table 7.4 Sources of information on non-medicalprescribing.1. Department of Health (DH) website: The DH websiteis regularly updated and has comprehensiveinformation on all aspects of prescribing.A section on ‘Non-Medical Prescribing guidance’can be found in the ‘Policy and guidance A–Z’.This includes ‘Improving Access to Medicines – theDH guide to implementation of nurse- andpharmacists-independent prescribing’ April 2006.www.dh.gov.uk/nonmedicalprescribing2. Clinical Knowledge Summaries (CKS): CKS guidanceon common conditions and symptomsmanaged in primary care is available in a varietyof formats. Full guidance provides concise informationto support decision-making in the consultationand more detailed background information for useas a learning resource. CKS Patient InformationLeaflets (PILs) provide guidance for people whoare not health care professionals and give anoverview of the condition, side-effects, advice onself-management, information on treatment optionsand sources of further help. CKS Drugs – lists thedrugs recommended and links them to the conditionand situation in which they are recommendedwww.cks.nhs.uk3. Medicines and Health care products RegulatoryAgency (MHRA): The MHRA website containsinformation about the legal framework governingthe prescribing, supply and administration ofmedicines (www.mhra.gov.uk).4. Other useful websites• British National Formulary (BNF):http://bnf.org/bnf/• Examples of patient group directions (PGDs):www.portal.nelm.nhs.uk• Medicines Partnership Programme: www.medicines-partnership.org(continued)

Helping patients make the most of their treatment 115Table 7.4 (continued)• National Electronic Library for Health: www.nelh.nhs.uk• NHS Drug Tariff for England and Wales: http://www.ppa.org.uk/ppa/edt_intro.htm• NHS National Practitioner Programme: www.wise.nhs.uk• National Prescribing Centre: www.npc.co.uk• Nursing and Midwifery Council: www.nmc-uk.org• Prescribing news: www.nurse-prescriber.co.uk• Royal Pharmaceutical Society of Great Britain:www.rpsgb.orgConclusionThose living with long-term conditions arerequired to a degree to self-manage their conditionwith the support of health professionals toensure that treatment is utilised effectively. Thisissue is often highly problematic since many peopledo not know how to use their treatment tooptimum levels, leading to difficulties of treatmentsbeing ineffective, due to poor adherence.Optimal treatment adherence is that which hasarisen from a planned consultation between thepractitioner and patient, embracing educationand support, to ensure that treatment and conditionbeliefs and expectations are understood andacted upon. The systematic assessment of educationalneeds is a vital component of helping aperson to live with their chronic skin condition.A concordance process provides an optimal modelfor engaging the patient in decisions regardingtheir treatment. However, there is also a needto recognise the limitations of self-managementwhen the person cannot manage their conditioneffectively. This needs to be built into the educationalprocess to ensure that the person utilisesthe health service effectively. Non-medical prescribingis an important strategy for improvingaccess to medicines and promoting educationsurrounding medicines management – providedby suitably qualified staff who can both prescribeand teach patients about their medication andhow to use it for optimum benefit.ReferencesAtkins, S. and S.J. Ersser (2008). Clinicaldecision-making and patient-centredcare. In: Higgs, J., Jones, M., Loftus, S.,Christensen, N. (Eds), Clinical Reasoningin the Health Professions. Oxford:Butterworth-Heinemann.Bandura, A. (1977). Social Learning Theory.Englewood Cliffs, NJ: Prentice Hall.Bandura, A. (1989). Human agency in socialcognitive theory. American Psychologist,44(9): 1174–1184.Bandura, A. (1997). Self-efficacy: The Exerciseof Control. New York: Freeman.Bandura, A. (2004). Health promotion bysocial cognitive means. Health Education andBehaviour, 31(2): 143–164.Beresford, A. (2002). Psoriasis AssociationMembers Questionnaire Survey.Northampton: Psoriasis Association.Bernado, M.L. (1984). Developing theprofessional nursing relationship. NursingForum, 21(1): 12–14.Bodenheimer, T., T. MacGregor et al. (2005).Nurses as leaders in chronic care. BritishMedical Journal, 330: 612–613.Brearley, S. (1990). Patient Participation.London: Royal College of Nursing.Brooks, J., S.J. Ersser et al. (2004). Nurselededucation sets out to improve patientconcordance and prevent recurrence of legulcers. Journal of Wound Care, 13(3): 111–116.Chapman, G. (1986). Social action theoryand psychosocial nursing. In: Kennedy, R.,Heymans, A., Tischler, Y. (Eds), The Familyas In-Patient: Families and Adolescentsat the Cassel Hospital. London: FreeAssociation Books.Chinn, D.J., T. Poyner et al. (2002).Randomized controlled trial of a singledermatology nurse consultation in primarycare on the quality of life of childrenwith atopic eczema. British Journal ofDermatology, 146(3): 432–439.Combs, A.W., D.L. Avila et al. (1971). HelpingRelationships: Basic Concepts for the HelpingProfession. Boston: Allyn and Baron.

116 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsCourtenay, M., N. Carey et al. (2009). Nurseprescriber–patient consultations: A casestudy in dermatology. Journal of AdvancedNursing, 65(6): 1207–1217.de Montigny, F. and C. Lacharite (2005).Perceived parental efficacy: Concept analysis.Journal of Advanced Nursing, 49(4): 387–396.Department of Health (2002). Expert PatientProgramme: A New Approach to ChronicDisease Management for the 21st Century.London: The Stationery Office.Department of Health (2003). SupplementaryPrescribing by Nurses and Pharmacists with theNHS in England: A Guide for Implementation.London: The Stationery Office.Department of Health (2004). Improving ChronicDisease Management. Department of Health.Department of Health (2005a). SupportingPeople with Long Term Conditions.Department of Health.Department of Health (2005b). Self-care – AReal Choice: Self Care Support A PracticalOption. Department of Health.Department of Health (2006). MedicineMatters: A Guide to Mechanisms for thePrescribing, Supply and Administration ofMedicines. D. o. H. C. P. G. Department ofHealth National Practitioner Programme,Department of Health.Department of Health (2008). SupplementaryPrescribing. Retrieved 24 April 2009,from www.dh.gov.uk/en/Healthcare/Medicinespharmacyandindustry/Prescriptions/TheNon-MedicalPrescribingProgramme/Supplementaryprescribing/index.htm.Department of Health (2009). The Non-Medical Prescribing Programme.Retrieved 254 April 2009, fromhttp://www.dh.gov.uk/en/Healthcare/Medicinespharmacyandindustry/Prescriptions/TheNon-MedicalPrescribingProgramme/index.htm.Egan, G. (1994). The Skilled Helper: A ProblemCentred Management Approach to Helping.New York: Brooks/Cole Publishing Company.Ersser, S.J. (1997). Nursing as a TherapeuticActivity: An Ethnography. Aldershot:Avebury Press.Ersser, S.J. and F. Cowdell (2009). AnExploratory and Developmental Study ofSelf-management Needs in Adults withMild to Moderate Psoriasis. Bournemouth:Centre for Wellbeing & Quality of Life,Bournemouth University.Ersser, S.J., S. Latter et al. (2007). Psychologicaland educational interventions for atopiceczema in children. Description: CochraneDatabase of Systematic Reviews, 3:CD004054. (DOI: 10.1002/14651858.CD004054.pub2.)Ersser, S.J., H. Surridge et al. (2002). Whatcriteria do patients use when judging theeffectiveness of psoriasis management?Journal of Evaluation in Clinical Practice,8(4): 367–376.Ersser, S.J. and P. Watkins (2007). Psychosocialinterventions in dermatology: An analysisof the nursing contribution. AnnualPsychodermatology Meeting. Medical Societyof London.Eysenbach, G. and J. Till (2001). Ethicalissues in qualitative research on internetcommunities. British Medical Journal,323(7321): 1103–1105.Finlay, A.Y. and E.C. Coles (1995). The effectof severe psoriasis on the quality of life of369 patients. British Journal of Dermatology,132(2): 236–244.Fischer, G. (1996). Compliance problems inpaediatric atopic eczema. Australasian Journalof Dermatology, 37(Suppl 1): S10–13.Freshwater, D. (2002). Therapeutic Nursing:Improving Patient Care through Self-Awareness and Reflection. London: Sage.Geanellos, R. (2005). Sustaining wellbeing andenabling recovery: The therapeutic effectof nurse friendliness on clients and nursingenvironments. Contemporary Nurse, 19(1–2):242–252.Gillis, A.J. (1993). Determinants of a healthpromoting lifestyle: An integrative review.Journal of Advanced Nursing, 18: 345–353.Grus, C.L., C. Lopez-Hernandez et al. (2001).Parental self-efficacy and morbidity inpediatric asthma. Journal of Asthma, 38(1):99–106.

Helping patients make the most of their treatment 117Hanson, J. (1998). Parental self-efficacy andasthma self-management skills. Journal of theSociety of Paediatric Nurses, 3(4): 146–154.Hays, R. and M.R. Dimatteo (1984). Towarda More Therapeutic Physicians–PatientRelationship. In: Duck, S.W. (Ed.), PersonalRelationships 5: Repairing PersonalRelationships. London: Academic Press.Holman, H. and K. Lorig (1992). Perceivedself-efficacy in self-management of chronicdisease. In: Schwarzer, R. (Ed.), Self-Efficacy:Thought Control of Action, pp. 305–323.Washington, DC: Hemisphere.Jourard, S.M. (1971). The Transparent Self.New York: Van Nostrand.Kabat-Zinn, J., E. Wheeler et al. (1998).Influence of a mindfulness meditation-basedstress reduction intervention on rates of skinclearing in patients with moderate to severepsoriasis undergoing phototherapy (UVB) andphotochemotherapy (PUVA). PsychosomaticMedicine, 60(5): 625–632.Kettunen, T., M. Poskiparta et al. (2001).Empowering counselling – a case study:Nurse–patient encounter in hospital. HealthEducation Research, 16(2): 227–238.Kinmouth, A.L., A. Woodcock et al. (1998).Randomised controlled trial of patientcentred care of diabetes in general practice:Impact on current wellbeing and futuredisease risk. The Diabetes Care fromDiagnosis Research Team. British MedicalJournal, 317(7167): 1202–1208.Krikoriam, D.A. and B.J. Paulanka (1982).Self-awareness: The key to a successful nurse–patient relationship. Journal of PsychosocialNursing and Mental Health Services, 20(6):19–21.Krueger, G., J. Koo et al. (2001). The impactof psoriasis on quality of life – Results of a1998 National Psoriasis Foundation patientmembershipsurvey. Archives of Dermatology,137(3): 280–284.Lawler, J. (1991). Behind the Screens: Nursing,Somology and the Problem of the Body.Melbourne: Churchill Livingstone.Marks, R. (2000). Who will advise patientsabout matters dermatological in the newmillennium? Archives of Dermatology, 136:79–80.McCluskey, U. (2005). To Be Met as a Person:The Dynamics of Attachment in ProfessionalEncounters. London: Karnac.Medicines Partnership (2003). MedicinesPartnership Project Evaluation Toolkit.London: Medicines Partnership.Mitchell, K., J. Bozanth et al. (1977).A reappraisal of the therapeutic effectivenessof accurate empathy, possessive warmthand genuineness. In: Gurucan, A., Raizin,A. (Eds), Effective Psychotherapy. Oxford:Pergamon Press.Morse, J., J. Bortoff et al. (1992). Beyondempathy: Expanding expressions of caring.Journal of Advanced Nursing, 17: 809–821.Niebel, G., C. Kallweit et al. (2000). Directversus video-based parental educationin the treatment of atopic eczema inchildren. A controlled pilot study [Direkteversus videovermittelte Elternschulungbei atopischem Ekzem im Kindesalter alsErganzung facharztlicher Behandlung. EineKontrollierte Pilotstudie]. Hautarzt, 51:401–411.Peplau, H.E. (1988). Interpersonal Relations inNursing. Houndmills: Palgrave Macmillan.Psoriasis Association (UK) and Beresford, A.(2002) Report of the Psoriasis AssociationMembers Questionnaire Survey, PsoriasisAssociation and Leo Pharmaceuticals.Rholes, W.S. and J.A. Simpson (2006). AdultAttachment. New York: The GuildfordPress.Richards, H.L., D.G. Fortune et al. (2001). Thecontribution of perceptions of stigmatisationto disability in patients with psoriasis. Journalof Psychosomatic Research, 50(1): 11–15.Richards, H.L., D.G. Fortune et al. (1999).Patients with psoriasis and their compliancewith medication. Journal of the AmericanAcademy of Dermatology, 41(4): 581–583.Roberts, S.J., H.J. Krouse et al. (1995).Negotiated and non-negotiated patientinteractions: Enhancing perceptions ofempowerment. Clinical Nursing Research,4(1): 67–77.

118 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsRogers, M.E. (1992). Prelude to the 21stCentury. Commemorative Edition: Noteson Nursing. F. Nightingale. Philadelphia:Lippincott, J.B.Rogers, R.W. and S. Prentice-Dunn(1997). Protection motivation theory. In:Gochman, D.S. (Ed.), Handbook of HealthBehavior Research 1: Personal and SocialDeterminants, pp. 113–132. New York:Plenum Press..Royal Pharmaceutical Society of Great Britain(1997). From compliance to concordance:Achieving shared goals in medicine taking.Report of the working group at the RoyalPharmaceutical Society which enquired intothe causes of medicine taking problems.London: RPSGB.Schaffer, S.D. and L. Tian (2004). Promotingadherence: Effects of theory-based asthmaeducation. Clinical Nursing Research, 13(1):69–89.Schiaffino, K.M. and T.A. Revenson (1992).The role of perceived self-efficacy, personalcontrol and causal attributions in adaptationof rheumatoid arthritis: Distinguishingmediator from moderator effects. Personalityand Social Psychology Bulletin, 18:709–718.Sellick, K.J. (1991). Nurses interpersonalbehaviours and the development of helpingskills. International Journal of NursingStudies, 28(1): 3–11.Shortridge-Baggett, L.M. and J.J. van der Bijl(1996). International collaborative researchon management self-efficacy in diabetesmellitus. Journal of the New York StateNurses Association, 27(3): 9–14.Shui, A. (2006). A case study of the educationprocess for diabetes self-managementin a nurse-led centre in Hong Kong.A Unpublished PhD thesis. University of(Southampton). Southampton: School ofNursing and Midwifery.Staab, D., T.L. Diepgen et al. (2006). Agerelated, structured educational programmesfor the management of atopic dermatitisin children and adolescents: Multicentre,randomised controlled trial. British MedicalJournal, 332: 933–938.Staab, D., U. von Rueden et al. (2002).Evaluation of a parental training programfor the management of atopic dermatitis.Pediatric Allergy and Immunology, 13: 84–90.Stickley, T. and D. Freshwater (2002). The artof loving and the therapeutic relationship.Nursing Inquiry, 9(4): 250–256.Strang, J. (1982). Psychotherapy by nurses – somespecial characteristics. Journal of AdvancedNursing, 7: 167–171.Surridge, H.R. (2005). Exploring parental needsand knowledge when caring for a child witheczema. Patient Magazine of the NationalEczema Society.Taal, E., E. Rasker et al. (1993). Health status,adherence with health recommendations,self-efficacy and social support in patientswith rheumatoid arthritis. Patient EducationCounseling, 20: 63–76.Taylor, B.J. (1994). Being Human: Ordinarinessin Nursing. Edinburgh: Churchill Livingstone.Truax, C.B., H. Altmann et al. (1974).Therapeutic relations provided by variousprofessionals. Journal of CommunityPsychology, 2(1): 33–36.Tsay, S.L. (2003). Self-efficacy training forpatients with end-stage renal disease. Journalof Advanced Nursing, 43(4): 370–375.van der Palen, J., J.J. Klein et al. (2001).Behavioural effect of self-treatment guidelinesin a self-management program for adults withasthma. Patient Education and Counseling,43(2): 161–169.Wangberg, S.C. (2008). An internet-baseddiabetes self-care intervention tailored to selfefficacy.Health Education Research, 23(1):170–179.Watson, J. (1985). Nursing: The Philosophyand Science of Caring. Colorado: AssociatedUniversity Press.Watson, J. (1999). Postmodern Nursing andBeyond: Redefining Nursing for the 21stCentury. Edinburgh: Churchill Livingstone.

Part2Principles of illness management


Psoriasis8Rebecca PenzerIntroductionPsoriasis is a chronic inflammatory conditionthat is thought to affect around 2% of thepopulation in the UK and the USA. It was firstdistinguished as a unique diagnosis in the 19thcentury, prior to that it was often mistaken forother conditions such as leprosy (Franklin andGlickman, 1986). Since that time numerous differentpresentations have been identified with awide range of morphological features. This haslead to questions about whether all these presentationsare indeed the one disease that is calledpsoriasis, or a range of conditions with somesimilarities. From a histopathological pointof view, it is not always possible to distinguishpsoriasis from other chronic inflammatory conditions;this will depend to an extent on thetime at which a biopsy is taken. Whilst the verytypical clinical appearance allows experiencedpractitioners to reach the right diagnosis, effectivetreatment becomes the next challenge. Thischapter will consider the biology of psoriasisand explore the various treatment options availableand how their efficacy might be enhanced.Specific issues about coping with psoriasis andits impact on quality of life are discussed, withreference made to Chapter 6 where generic issuesof skin disease and mental health are consideredin detail.History of psoriasisEarly references to skin diseases can be found inthe Old Testament of the Bible. Translations fromHebrew into English meant that skin diseasesbecame known as leprosy, even though they clearlydid not describe the disease we now know as leprosy.In Ancient Greek, the word ‘lepra’ was usedto describe skin that was scaly and rough whichrelates much more closely to the symptoms ofpsoriasis than those of leprosy. The word ‘psora’was used by the Greeks to describe itchy skinconditions. This is somewhat strange in view ofthe fact that today some medical textbooks makeclaim to the fact that psoriasis is not an itchy skincondition.In the late 18th century two dermatologistsRobert Willan and Thomas Bateman describedpsoriasis as Willan’s lepra, a term used to describethe typically dry and scaly lesions. By the mid-19th century an Austrian doctor Ferdinand vonHebra finally labelled the disease by what is now

122 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsits modern name of psoriasis. The 20th centurysaw the distinctions made between all the variousdifferent types of psoriasis.Who gets psoriasis?Exact figures about the proportions of populationsthat have psoriasis do vary. However inCaucasian populations it is thought that around2% have psoriasis. The incidence is less inAfricans (0.7%), Asians and Native Americans(Camisa, 2004a). It affects men and womenequally. The average age of onset is 30; however,psoriasis may be experienced for the firsttime much earlier than this or indeed much later.There do appear to be two peaks of onset, onein early adulthood and the other in later life(Williams, 1997).There is little doubt that there is a geneticcomponent to psoriasis; the earlier the psoriasisoccurs and the more severe the disease, thestronger the familial association. However, monozygotictwins (i.e. those that come from onefertilised egg that divides) will not always bothhave psoriasis. This suggests that it is likely thatenvironmental factors play a role in the developmentof active symptoms.The understanding of the genetic componentsof psoriasis is constantly increasing as researchallows ever more detailed examination of thehuman genome. There are a number of chromosomes(e.g. chromosome 6 and 17) which carrygenes that seem to increase the likelihood ofdeveloping psoriasis, i.e. they are not causativegenes but instead they increase the susceptibilityof an individual to develop the condition. Asthere are a number of different genes which codefor psoriasis, the way the psoriasis appears, whenit appears and how it responds to treatment varyenormously.Psoriasis, like all chronic skin conditions, isnot contagious. This is important to stress toindividuals when they are initially diagnosedwith the condition as they may worry aboutpassing the disease onto others.Biology of psoriasisAt a simple level, psoriasis is characterised byan over proliferation of keratinocytes, i.e. skincells replicating too quickly. The number ofproliferative cells in the basal layer doubles andthe normal cell cycle (which is around 28 days)is speeded up by seven times, the transit timebecoming around 4 days (although this willvary depending on disease severity). Not onlydoes over proliferation occur but incomplete celldevelopment, that is abnormal keratinocyte differentiation,is also seen. The granular layer iseither absent or reduced and hyperkeratosis andparakeratosis develop. This hyperproliferationis accompanied by inflammation and vascularchanges. Skin cells heap up into plaques and arethen shed in noticeable clumps.Clinically, a typical psoriatic plaque is salmonpink in Caucasian skin and a slightly darkershade of normal skin tone for skin types4–6. The actual colour of the plaque may bemasked by a covering of silvery, white skinscales. Because of the high level of vascularactivity within the psoriatic plaques, there is aproliferation of blood vessels near the surfaceof the plaque. This accounts for the change incolour of the skin and also explains a uniquesymptom of psoriasis known as Auspitz sign.This describes the symptom of pin-prick bleedingwhen the skin is scratched or knockedby the slightest trauma. The hyperkeratosisleads to induration or skin thickening so thata plaque is raised from the rest of the skinsurface.The simple description of psoriasis beinga hyperproliferative disorder with significantinflammatory components belies a complex cascadeof immune stimulated reactions that occurin the skin. Understanding of these processesis increasing, but the picture is still somewhatincomplete. However, it is reasonable to describepsoriasis as an immune-mediated conditionin which T-cells play a significant role; indeed,psoriasis is recognised as the most prevalentT-cell-mediated inflammatory condition seen inhumans (Kreuger, 2002).

Psoriasis 123T-cells are a type of lymphocyte (other lymphocytesbeing B-cells and natural killer cells) andthey play an important role in cell-mediatedimmunity. It is well recognised that T-lymphocytesinfiltrate the skin where psoriatic plaques occurand more recently it has been possible to identifythe sub-types of these T-cells as CD4 and CD8 T-lymphocytes. It is not entirely clear what causesthis initial activation of the T-cells; however,once activated they move into the bloodstreamand from there into the dermis by ‘squeezing’through the blood vessel walls. Here they arereactivated; CD4 cells into Type 1 helper cells(TH1) and CD8 cells into Type 1 cytotoxic cells.Reactivation occurs through contact with antigenpresenting cells. Together these two types of cellsinitiate an inflammatory cascade as inflammatorycytokines, whereby interferon gamma (IFN-γ)and tumour necrotising factor alpha (TNF-α)are produced. These cytokines incorporate withproinflammatory chemicals which in turn causethe keratino cytes to hyperproliferate. In patientswithout psoriasis, this inflammatory process isa response to a physical, biological or chemicaltrigger which threatens (or causes) injury. Oncethe injury is resolved, the inflammatory processis switched off. In patients with psoriasis, itis thought that the immune system mistakenlyrecognises the body’s cells as foreign, triggeringthe repair response causing inflammation. Thisresponse is not ‘switched off’ in the way that it isfollowing an actual injury and skin cells continueto proliferate.Comorbidities associated with psoriasisThere are a number of diseases which are associatedwith psoriasis; some of which have beenrecognised for a long time and others whichhave emerged from more recent research.The well-recognised comorbidities include psoriaticarthritis (PSA) (which is discussed in the nextsection), psychological/psychiatric disorders andinflammatory bowel disease, particularly Crohn’sdisease. Research has confirmed that the associationsbetween psoriasis and these conditions arewell established. Thus up to 30% of those withpsoriasis have joint pain (Osborn and Wilke,2004). The impact on quality of life for those withpsoriasis is comparable to those who have cancer,arthritis and depression (Rapp et al., 1999) andpatients with inflammatory bowel disease are upto seven times more likely than the normal populationto develop psoriasis (Christophers, 2007).There also appears to be an increased risk ofmalignancy in those with psoriasis; however,whilst this may be associated with underlyingimmunological changes in the skin, it is alsolikely that some treatments (notably PUVA andhigh-dose methotrexate) lead to an increasedrisk of malignancy (Gulliver, 2008).Whilst not strictly speaking comorbidities,there does seem to be a link between psoriasisand certain lifestyle choices, namely smokingand drinking. For example, a study carried outin Italy found that there was a negative effect onthe severity of psoriasis (particularly in women)in those who smoked (Fortes et al., 2005).A particularly strong association has beenshown between smoking and palmoplantarpsoriasis with smokers five times more likely tosuffer from the disease than non-smokers (Naldiet al., 2005). The likelihood of alcohol abuseis increased in patients with psoriasis with aGerman study showing that increased alcoholconsumption was seen twice as frequently inpatients with moderate to severe psoriasis thanin hospital-based controls. It is not clear if psoriasisis a risk factor for tendency to smokingor excessive drinking, but both the behaviourswill increase the risk of mortality (Sommeret al., 2006). The direction of the associationbetween psoriasis and drinking and smoking isnot clear. It is still not certain whether smokingand drinking are risk factors for developingpsoriasis or whether they are behaviours thatpeople develop in order to help them cope withhaving psoriasis.More recently research has turned its attentionto making connections between diseaseswhich are known to have a chronic inflammatoryassociation and particularly those that aremediated by proinflammatory T-helper type 1cytokines (as psoriasis is). In a review article,

124 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsGulliver (2008) summarises what he calls theemerging comorbidities: obesity, dyslipidaemia,hypertension and glucose intolerance (otherwiseknown as metabolic syndrome) all showincreased prevalence in people with psoriasis.For obesity and diabetes, at least, it seems thereis a greater prevalence in people with severe diseasethan those with mild disease.Because of the greater prevalence of cardiovascularrisk factors in those with psoriasis, ithas been suggested that psoriasis might be anindependent risk factor in itself for cardiovascularevents including myocardial infarction. Inother words just the very fact of having psoriasismakes an individual at higher risk of havingcardiovascular events. The evidence hereis mixed. However, what does seem clearer isthat patients with psoriasis appear to havean increased risk of coronary artery calcification(which predisposes to atherosclerosis)and psoriasis is an independent risk factor forcoronary artery calcification. It might thereforebe expected that those with psoriasiswould have a lower life expectancy than thosewithout, here again the evidence is not whollyclear; however, a study in 2007 indicated thatfor those with severe disease there was a significantlyincreased risk of mortality(Gelfandet al., 2007). When comparing those withsevere psoriasis to those without psoriasis, thefigures from the study indicated that men died3.5 years earlier and women 4.4 years earlierthan the normal population.Further research is needed in this field toclarify the relationships between psoriasisand the aforementioned comorbidities. Theprocesses which lead to low-grade persistentinflammation as is seen in psoriasis are commonto these conditions. Thus obesity is associatedwith low grade chronic inflammationmediated by levels of circulating TNF-α, IL-2,IL-6 and C-reactive protein. Metabolic syndromeand atherosclerosis show similarities topsoriasis in that Th 1 cytokines drive all threeprocesses.As there is increased understanding of theimportance of the inflammatory process, treatmentswill increasingly look to tackle the causesof the inflammatory cascades within the skin.The biological therapies which are discussedlater in this chapter will be key in this process.When discussing these associations withpatients it is important not to create unwarrantedanxiety. Patients need to know thatthere is a theoretical link between psoriasis andcardiovascular diseases but the evidence is stillbeing collected and analysed. It seems that thelinks are most important for those with severedisease. Thus ‘switching off’ the severe inflammatoryresponse quickly may be important notonly to reduce the level of psoriasis, but also todecrease the risk of experiencing other inflammatorydisease processes.Clinical variants of psoriasisChronic plaque psoriasisThis is the most common form accounting forabout 80% of those with psoriasis. Also knownas psoriasis vulgaris, where vulgaris means common,it is characterised by well circumscribed,scaly plaques. These plaques can range in shape(although they are usually round or oval) andsize from millimetres in diameter to many centimetres(Figure 8.1). The most common sitesare extensor surfaces, i.e. elbows and knees, thelower back or sacrum, natal cleft, genitalia andthe scalp. More-often-than-not the lesions aresymmetrical, i.e. they appear on both knees orboth elbows; however, the lesions on each sideare not necessarily identical. Psoriasis oftenoccurs on the hairline and can creep downFigure 8.1 Plaque psoriasis. (Source: Reprinted fromGraham-Brown and Burns, 2006.)

Psoriasis 125over the forehead, down the neck and into andaround the ears. In reality plaques can occuranywhere, although appearance on the face isconsidered rare.If chronic plaque psoriasis (CPP) occurs inflexural areas, the appearance will be quite differentfrom other areas of the body. Because ofthe heat and occlusive nature of flexures, thescale rubs off leaving a bright red shiny area ofskin. There may be a fungal or bacterial infectionpresent along with the psoriasis. This typeof psoriasis is sometimes known as inverse psoriasis(Figure 8.2).CPP on hands and feet (palmar/plantar psoriasis)also has a somewhat different appearance.Individual plaques may not be seen, butthickened fissured skin, often more apparent onthe dominant hand, will be in evidence. In orderto distinguish this from a contact dermatitis forexample, a careful history and an assessment forpsoriasis on other parts of the body, for examplein the nails, is needed.When psoriasis occurs in the scalp, the scalingcan become particularly thickened as the hairprevents the scale from shedding (Figure 8.3).As the scale develops it can cover the wholescalp which feels tight and uncomfortable; ithas been described as feeling like wearing aswimming cap. Although hair loss may seemmore extensive than normal, this is not permanentand patients can be reassured that hair willgrow back.Figure 8.2 Inverse psoriasis. (Source: Reprinted fromWeller et al., 2008.)Figure 8.3 Scalp psoriasis. (Source: Reprinted fromGraham-Brown and Burns, 2006.)Guttate psoriasisThe lesions in guttate psoriasis (GP) are generallysmaller than those in CPP and appear as ifsplattered across the body in a rain-drop pattern.The plaques are also generally less induratedand less scaly. GP occurs most commonlyon the trunk and proximal areas of extremities,it is also more likely to present on the face(Figure 8.4). This type of psoriasis seems toaffect children and young adults predominantlyand often occurs after a streptococcal throatinfection. It affects around 18% of the psoriasispopulation. For some, the acute appearanceof GP is their only experience with psoriasis. Itclears relatively quickly within a 4-week periodand they do not experience the condition again.For others, especially those with a strong familyhistory of psoriasis, the guttate form is an initialflare and it then changes into the more chronicform of plaque psoriasis.

126 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsgeneralised pustular psoriasis (GPP). Someclinicians consider PPP to be a totally differententity from other types of psoriasis. About70–80% of patients who have PPP will not haveany other psoriatic lesions elsewhere on thebody (Figure 8.6). It is also worth noting thatsignificantly more women than men suffer withFigure 8.5 Nail psoriasis. (Source: Reprinted from Graham-Brown and Burns, 2006.)Figure 8.4 Guttate psoriasis. (Source: Reprinted fromGraham-Brown and Burns, 2006.)Nail psoriasisPsoriasis of the nails is relatively commonaffecting up to 50% of people who have psoriasis.Both finger and toe nails can be affected,although it would seem that fingernails aremore commonly involved (Figure 8.5). Thevarious different apparatus of the nail can beinvolved. If the nail matrix is affected, the waythat the nail grows will be altered; this may berelatively mild with small pits appearing in thenail plate surface. However, more serious effectscan be seen when psoriasis affects the nail bedleading to thickened nails; if the hyponichiumis also affected, the result is lifting of the nailfrom the nail bed leading to onycholysis.Pustular psoriasisThere are two main variants of this type ofpsoriasis, palmar plantar pustulosis (PPP) andFigure 8.6 Palmar plantar pustulosis. (Source: Reprintedfrom Graham-Brown and Burns, 2006.)

Psoriasis 127PPP and that its onset is generally later in life.It is very strongly associated with smoking. Itsappearance is of pustules against a backgroundof erythema and scaling. Pustules at differentstages will be present at any one time. Initiallythey are yellowish in colour (although the contentsare sterile) and when the pustule breaks,the skin forms brownish macules.GPP should be considered a dermatologicalemergency where the patient is generallyfebrile and unwell. Whilst GPP affects bothsexes equally, like PPP it tends to occur laterin life (around 50) and can evolve from a preexistingpsoriasis or occur without any psoriasishistory. It is relatively rare with onlyaround 2% of the psoriasis population everexperiencing GPP. A strong trigger factor forthe development of GPP appears to be commencementon, or withdrawal from, systemicsteroids; however, infection or other drugreactions may also cause GPP. GPP can affectany part of the body but seems to have a predilectionfor flexural areas. There are hundredsof superficial pustules on widespread,irregular patches of bright red skin. Thesepatches tend to have serpiginous or wavy borderswhich move as the pustules coalesce andthen desquamate.Erythrodermic psoriasisErythrodermic psoriasis (EP) is another dermatologicalemergency; those who experience EPusually have pre-existing CPP. The usual characteristicsof CPP disappear as EP progresses;the skin becomes generally inflamed with nonoticeable plaques and there is generalisedexfoliation (Figure 8.7). Trigger factors includeemotional stress, response to systemic illnessand alcoholism; however, the most noticeablecause of EP is the inappropriate use of potentsteroids (topical, oral and injectable). LikeGPP, EP is potentially life threatening and thepatient will need to be hospitalised for intensivenursing care.The various variants of psoriasis may be confusedwith other skin diagnoses. Table 8.1 liststhe common confusions.Psoriatic arthritisIt is thought that between 6% and 10% of thosewith psoriasis suffer from inflammatory arthritisknown as PSA or psoriatic arthropathy (Figure8.8). However, it is also thought that the numberwho suffer from general joint stiffness is moreFigure 8.7 Erythrodermic psoriasis. (Source: Reprinted fromWeller et al., 2008.)Figure 8.8 Psoriatic arthritis. (Source: Reprinted fromWeller et al., 2008.)

128 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 8.1 Differential diagnoses for psoriasis.Type of psoriasis Key clinical features May be confused withChronic plaque psoriasisGuttate psoriasisInverted psoriasisNail psoriasisErythrodermic psoriasisClear demarcation between psoriaticskin and normal skinExtensive scalingPin-prick bleedingAppears on extensor surfacesRain drop type lesions on trunk and armsOften follows a throat infectionIn flexural areasBright redShineyClear edgePitting of the nail plateHyperkeratosis of the nail bed leadingto thickened nails and lifting of the nailplateGeneralised erythemaExfoliationHistory of chronic plaque psoriasisNummular eczemaLichen simplex chronicusPityriasis roseaFungal infectionFungal infection of the nailAgeing nails which will thicken especiallyif subject to traumaOther causes of erythroderma, e.g. drugreaction, eczemalike 33% (Osborn and Wilke, 2004). The pathogenicmechanisms which cause PSA include, likethose in the skin, chemical mediators for inflammationand the interaction of T-cells and macrophages.Clinically it may appear as rheumatoidarthritis, although crucially the patient remainsseronegative. Those people who have PSA arealso very likely to have nail involvement (80%)and that nail involvement is often very destructive.The majority (66%) find that the jointinvolvement occurs after the lesions appear onthe skin; however, for 15% it is around the sametime as the cutaneous signs appear and for 15%it is before there are any cutaneous lesions. Thedifferent clinical presentations of PSA are outlinedin Box 8.1.Mild to moderate arthritis may be successfullymanaged using non-steroidal anti-inflammatorydrugs. More severe disease is likely toneed to be managed by a rheumatologist andwill involve systemic treatments similar to thoseused to treat cutaneous disease.Physical symptoms that accompanypsoriasisFrom the description of the clinical symptomsof psoriasis above, it becomes clear whatthe physical symptoms may be. Like so manychronic skin diseases, psoriasis makes it verydifficult for the sufferer to feel comfortable intheir own skin. There are a number of constantreminders reflecting the fact that their skin is‘switched on’ with a myriad of inflammatoryand proliferatory activities taking place.ScalingIn a multi-centre European study, it was foundthat nearly 78% of the 330 people in the studyfound that scaling was a problem related totheir condition (de Korte et al., 2005). As hasalready been described, psoriatic plaques are

Psoriasis 129Box 8.1 Clinical presentations of PSASymmetric polyarthritis■ Looks and behaves almost exactly like rheumatoid arthritis;■ Generally affects the proximal joints of the fingers, but can affect any joint;■ Is the most common form of PSA.Asymmetric oligoarticular arthritis■ Oligo means few, thus this type of arthritis by definition must affect five or fewer joints;■ Dactylis may be seen, this describes the ‘sausage’ shape of fingers or toes when the distalinterphalangeal joint is affected;■ Later onset of oligoarticular arthritis in large joints has the best prognosis.Distal interphalangeal joint arthritis■ This could be described as the ‘classic’ appearance of PSA, where only the distal interphalangealjoints are affected.■ It affects around 5% of those with PSA.Arthritis mutilans■ A highly destructive form of PSA, there is osteolysis (dissolution of the bone) in the smalljoints of the hands;■ Occurs in 1–2% of those with PSA;■ Seems to be linked to early onset disease and has a poor prognosis.Spondylitis and sacroiliitis■ On X-ray, changes seem to be consistent with ankylosing spondylitis and sacroiliitis; howeversymptoms may be absent.characterised by over production of keratinocyteswhich are shed from the skin in noticeableclumps. This will often limit a person’slife in that they restrict activities due to theembarrassment of the ‘snowstorm’ they create.This may be about restricting the colourof clothing chosen so that white skin scales donot show up against dark coloured clothing,or it may be about limiting holiday choicesby not staying in a hotel because of all theskin cells left in sheets or on the floor. In asmall unpublished study (Ersser et al., 2000)in which patients were asked to describe howthey felt about their psoriasis, one persondescribed it thus:It is extraordinary how much skin is beingproduced. When it is like that I mean I thinkone can get into a mindset of being sort ofrevolted with one’s own body. At home if I’mthe last to bed, I get up and there’s flakes allover the settee … I brush it on the floor andthen get a hoover so that when people comedown in the morning they are not confrontedwith it. (p. 8)Related to scaling is the thickness or indurationof the plaque. Whilst this symptomseems to be of less importance to the patientthan scaling, it is important as a measure oftreatment success. A plaque that is resolving

130 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsbecomes flat so that when a finger is run overit there is no change in texture between thenormal skin and the plaque. Psoriasis tends toclear from the centre of the plaque outwards,so the patient will not see the plaque decreasein size, instead it will become flat in the middlewith an ever decreasing ring around the edge.It is important to feel the skin when lookingto see if the plaques are resolving as a plaquecoloured mark will remain on the skin foraround 2 weeks after the plaque flattens. Thisis because it takes that time for the superficialblood supply to return to normal (see later forfurther details).InflammationThe over proliferation of skin cells is accompaniedby an increased superficial blood supplyto the plaques. Because the capillaries runclose to the surface of the skin they are easilybroken. For the patient this means that the skincan be broken through scratching or knockingit leading to pin-prick bleeding (described earlier).This can be very distressing as it makesa mess of bedding and clothing and also makethe plaques more obvious. The redness of theplaques may also be made more obvious byuse of treatments and emollients. This is becausethe superficial white scale on the surface isremoved exposing the inflammation of theplaque. Patients with psoriasis will also oftencomplain that their skin feels extremely hotand sensitive; this is probably explained by theinflammation of the plaques.Pain and pruritusPsoriasis is not often described as painful, butit can be sore especially if the skin is very dryand cracked and/or scratching has led to damageof the skin surface. It is, however, very oftenitchy. About 74% in the de Kort study reporteditch being a major symptom with only 38% and12% reporting soreness and pain respectively(de Korte et al., 2005). This is contrary to somedermatological textbooks which report psoriasisas a non-itchy condition. This may be becauseunlike in eczema, itch is not one of the key diagnosticclues in psoriasis, but many patients findthe itching associated with psoriasis unbearableat some point or other.You know terrible itching sort of makes youfeel quite nervous. ... and sometimes you can’tsleep for itching. I was going to a wedding onSaturday and I was terribly itchy. I couldn’t goto the wedding and it was just horrible really.(Ersser et al., 2000, p. 10).Trigger factors in psoriasisIt is generally agreed that for psoriasis symptomsto manifest themselves there must be agenetic susceptibility (either inherited or spontaneous)along with an external trigger factor.These trigger factors are numerous and variedand science is gradually revealing the pathophysiologicalmechanisms that make themoccur. Some patients will be very clear on whatthey feel triggers their psoriasis or what makesit feel worse. Others feel that their psoriasishas ‘a life of its own’ and that it improves andworsens randomly with no easily identifiabletrigger factors. Thus, as with so many thingsabout psoriasis, the story is never totallystraightforward. Trigger factors will impactupon people in different ways and to differentextents.Koebner phenomenonOne of the classic features of psoriasis is its tendencyto Koebnerise, that is to form along theline of injury or trauma. The trauma may be anacute episode such as a surgical incision or alow-grade long-term influence like the constantrubbing of a garment. Where a linear incisionis made, the psoriasis is likely to follow the lineof the scar rather than forming in its usual ovalshape. Patients who are undergoing non-essentialsurgical interventions should be warned ofthe possibility of Koebnerisation.

Psoriasis 131Streptococcal throat infectionIt is commonly observed that throat infections,tonsillitis and pharyngitis can trigger GP; this isparticularly seen in children and young adults. Itis known, therefore, that streptococcal infectionscan lead to the onset of this specific type of thedisease. The mechanism for this is thought to bethe effect of superantigens released by the streptococcalbacteria activating T-cells and drivingthe skin to produce psoriatic lesions.DrugsThere are certain classes of drugs, which will insome cases trigger an onset or aggravate psoriasis:■■■LithiumChloroquine-based anti-malarialsBeta-blockersWhere possible it is advisable for patients andtheir health care professionals to seek alternativesto the above systemic medications. For thosewith severe bipolar disease, lithium is sometimesthe only effective treatment, which makes discontinuingit because of worsening psoriasis difficult.A small study in Scotland demonstrated that byintroducing the supplement inositol the diseaseseverity of those on lithium could be reducedwhen compared to those who were given a placebo(Allan et al., 2004). The recommendationfrom the study was that for patients who couldnot be withdrawn from lithium, inositol as a supplementis worth considering.Ultraviolet light exposureFor a small, but not insignificant number ofpeople (around 10%) exposure to ultraviolet (UV)light is an aggravating (rather than therapeutic)factor.StressPsychological stress has for many years beenlinked with exacerbations of psoriasis. In the last10 years, there has been a major increase in theamount of scientific evidence which helps toexplain the relationship between the brain andthe skin – it has been labelled the ‘brain-skinaxis’. The relationship between the brain and theskin is explored in more detail in Chapter 6.Researchers have looked at the physiologicalchanges that happen when psoriasis sufferers(compared to controls) are subjected to a numberof stress tests. It was shown that the patientswith psoriasis who were stress-responsive hadan abnormal response of the hypothalamus–pituitary–adrenal axis when exposed to stress.It was suggested that this could lead to an upregulationof the inflammatory mediators that lead tothe physical manifestations of psoriasis (Richardset al., 2005).Treatments for psoriasisTreatments for psoriasis can be divided intotopical and systemic. Topical products are generallyused to manage mild to moderate psoriasisand systemic therapies the more severe endof the disease spectrum. Topical therapies maybe used to treat more severe disease in combinationwith systemic regimes especially wherein-patient or day-care treatment is available, forexample coal tar or short-contact dithranol incombination with UV light therapy. There havebeen relatively few recent breakthroughs forpsoriasis therapy, particularly for the treatmentof mild to moderate disease. The 21st centuryhas, however, seen major developments in thefield of immunologic treatments for severe disease.Camisa (2004a) details a timeline of breakthroughsin psoriasis therapy (p. 3).Patients seem to have variable results withtopical treatments in particular. It does seemto be the case that what will work for one persondoes not work for another, even thoughtheir disease severity and motivation seem to beequivalent. It is true, however, that some peopledo not have good results from topical therapiesbecause they do not concord. It is vital, therefore,that patients with psoriasis receive supportand encouragement when using topical therapies

132 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsand that their expectations of level of clearanceand timescales are realistic. Further informationon helping patients to concord with treatmentcan be found in Chapter 7. There is also a subsetof people that, despite their best efforts witha topical product, do not see any positive result.This group should be referred to a DermatologyDepartment. Further information about referralguidelines is given at the end of this chapter.Topical therapiesEmollientsAs psoriasis is a dry skin condition, a key lineof treatment for all types of psoriasis, exceptperhaps inverse psoriasis, is emollient therapy.Emollients will not resolve plaques, nor will theystop hyperproliferation; however, they do reducethe signs of scaling and they certainly make theskin much more comfortable. Emollients maybe applied topically and/or used whilst washing.They are often underutilised in psoriasis care,but should be the first treatment option in allcases. Chapter 5 has further details about selectingand using emollients.Vitamin D analoguesVitamin D3 is naturally synthesised in theepidermis. The mechanism involves naturalUVB falling on the skin and converting 7-dehydrocholesterol into vitamin D which thenbinds with vitamin D binding protein. In thisform, the vitamin D is transported around thebody to the liver and kidneys where it undergoesa number of hydroxylations (additionof oxygen and hydrogen molecules) beforebecoming the active substance 1,25-dihydroxyvitaminD3, otherwise known as calcitriol.Receptors for the action of calcitriolcan be found in human epidermis and also inmelanocytes, Langerhans cells, fibroblasts,endothelial cells, T-lymphocytes, macrophagesand granulocytes (Camisa, 2004c). Calcitriolhas been shown to inhibit cell proliferationand induce terminal differentiation within theepidermis. It also affects calcium homeostasisby stimulating the absorption of both calciumand phosphate through the small intestine andby promoting mineralisation and osteolysis inthe bones. The synthetic vitamin D analogues(calcipotriol, tacalcitol and calcitriol) work inthe same way as naturally occurring calcitriol,inhibiting cell proliferation and encouragingthe skin cells to mature normally.Calcipotriol is more effective than tacalcitoland calcitriol (Ashcroft et al., 2000) andless calciotrophic (i.e. less likely to impact oncalcium levels) than calcitriol. The systematicreview undertaken in 2000 showed that calcipotriolwas more effective than coal tar, combinedcoal tar 5%, allatonin 2% and hydrocortisone0.5% and short-contact dithranol. When measuredat 6 weeks it was more effective thanpotent topical steroids, although this effect wasreversed by 8 weeks (Ashcroft et al., 2000).Interestingly in a further study carried outin The Netherlands where calcipotriol treatmentwas compared with short-contact dithranoltreatment in a day-care setting, dithranoltreatment was seen as more effective (van deKerkhof et al., 2006). Thus, where skilled staffare available within a day-care setting, the useof dithranol could be considered as a first linetreatment. Its efficacy is significant; however,as is described later in this section, its applicationand potential side effects are considerablewhich can make its use outside a clinicalsetting, undesirable.Method of applicationVitamin D analogues are designed for use instable CPP. In practical terms, the vitamin Danalogues are relatively easy to apply. Theyare odourless and come in cream or ointmentformulations, so the most appropriate type ofproduct can be selected. Amounts and contraindicationsare outlined in Table 8.2. Each brandof vitamin D analogue recommends a differentquantity per application. Where the manufacturermakes a specific recommendation itis quoted in Table 8.2. The cream or ointmentshould be applied to the plaque and rubbed in

Psoriasis 133Table 8.2 Key differences between the vitamin D analogues.Vitamin D3 analogue Amount used Special instructionsCalcitriol(Silkis)Calcipotriol(Dovonexcream and scalpapplication)Calcipotriol andbetamethasonediproprionate(Dovobet ointment)Tacalcitol(Curatodermointment)• No more than 210 g/week (i.e. 30 g or60 FTUs per day)• No more than 35% body surface area• Twice-daily application• ‘Apply an even layer’• No more than 100 g/week (adult) (i.e.14 gper day or 28 FTUs)• 75 g/week (children over 12)• 50 g/week (children 6–12)• Twice-daily application• ‘Apply cream thickly’• No more than 100 g/week (i.e.15 g per dayor 30 FTUs)• No more than 30% of body surface area• Once-daily application• 70 g/week (i.e. 10 g per day or 20 FTUs)• Once-daily application• ‘Apply sparingly’• Use with caution on those who are ontreatment that affects calcium levels,e.g. thiazide diuretics• Contraindicated for people with liver orkidney problems and those being treated forcalcium homeostasis• Not for use in children• Use of face with caution due to possibleirritation• Avoid use on face• Avoid exposure to natural or artificialsunlight• Contraindicated for patients with knowncalcium disorders• Can be used in children over 6• As with Calcipotriol• Not to be used in the flexures• Not to be used on infected skin• Not to be used under occlusion• Not for use in children under 18• Not to be used in conjunction with othersteroids• Not to be used for more than 4 weeksat a time• Contraindicated for patients with knowncalcium disorders• Not recommended for use in childrenSource: Datapharm (2009).Note: NB It may be helpful to explain to patients that 1 finger tip unit (FTU) is approximately half a gram, it is then possible towork out how many FTUs it is safe to use per day.gently; however, if any is left on the skin, clothingshould not be worn straight away as thismay rub off the product. Side effects includeslight stinging or irritation on application whichshould resolve shortly after application. If calcitriolor calcipotriol get onto sensitive skin, forexample the face, they may cause more severeirritation and erythema. However, tacalcitolcan be used on the face and in flexures. It isimportant that patients are instructed to washtheir hands after application of the product sothat they do not inadvertently get it onto moresensitive skin.Calcipotriol is also available as a scalp application.It is in a liquid form which is usefulfor treating psoriasis once the scale has beenremoved. Table 8.3 outlines how scalp treatmentsshould be applied.

134 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 8.3 Scalp treatments.Type of scalp psoriasis Type of treatment Application techniqueLength of time to leavetreatment onThickened and scalyThin scale but activepsoriasisScalp is dry but noactive psoriasisMaintenance and/oradjunct to othertreatmentCoal tar, salicylic acidand coconut oilCalcipotriol lotionCalcipotriol/betamethasonegelClobetasol proprionateshampooPart hair into sections workingaround the scalpFor each section rub treatmentinto the scalp. Once whole scalp iscovered, gently massage into scalpUse comb gently to loosen anyscale. Apply just once dailyAs above but apply morning andevening.As above but once a day.Apply no more than 7.5 ml to dryscalp and wash off.Preferably overnight (but if notfor at least half an hour).Protect pillow with oldpillowcase or wear shower cap;Wash out following morning.Leave on throughout day andnight and then shampoo offOnce applied to dry scalp,leave for 15 minutes beforeadding water lathering andwashing off.Coconut oil As per coal tar product Overnight if possibleCoal tar shampoo Apply as a regular shampoo 2–3times per week. Rinse out. Mayneed to use less frequently if beingused for maintenance purposesLeave on scalp for a fewminutes before rinsing.The patient should be warned that it maytake up to 4 weeks to see any positive impact ofthe treatment, that this is normal and that theyshould persevere.Calcipotriol and betamethasone diproprionateA combination treatment containing both a vitaminD analogue and a potent steroid is the mostrecent addition to the topical treatments for stableplaque psoriasis. It has been shown to beboth quicker acting and more effective at reducingdisease severity than calcipotriol on its own(Guenther et al., 2002). This same study showedthat there was no statistical or clinical differencein the outcomes of using the combined productonce or twice a day. It has consequently becomerecommended as a once-daily treatment.Method of applicationThis is a once-daily treatment and should beapplied in sufficient quantities to cover theplaque and then be gently rubbed in. As withcalcipotriol it may not matter if some ointmentgets onto unaffected skin, but this should beavoided where possible. Due to the inclusion ofpotent topical steroids, it is not recommendedthat the combination treatment should be usedfor more than 4 weeks. The British NationalFormulary suggests that further courses maybe given after a period of not less than 4weeks (British Medical Association and RoyalPharmaceutical Society of Great Britain, 2008).The combination calcipotriol/steroid ointmentmay be helpful for an initial treatment of plaquepsoriasis as it seems to be quicker acting; onceresolution of the plaques begins this may be

Psoriasis 135maintained by shifting the treatment regime tocalcipotriol alone.Calcipotriol combined with other therapiesWhen used in conjunction with narrowbandUVB, calcipotriol appears to have a UVB sparingeffect. A placebo-controlled trial showed thatthose in the active group (i.e. where calcipotriolwas used) needed a significantly lower UVB dosagethan those in the control group (Woo andMcKenna, 2003). Although there was no significantdifference in Psoriasis Area Severity Index(PASI) and quality of life measures betweenthe active and control group at the end of thestudy, at 8 weeks the PASI had improved to asignificantly greater extent in the active group.The UVB sparing effect of calcipotriol could beimportant in offering an option which decreasesthe carcinogenicity of the UVB therapy.A small study involving 40 patients lookedat whether combining calcipotriol with acitretinwas more effective than acitretin on its own.Their results suggested that calcipotriol mayenhance the clinical outcomes when acitretin isused. The duration of treatment and total doseof acitretin required to achieve clearance wasslightly lower in the combination group, butthis difference did not achieve significance (Rimet al., 2003).Coal tarBeing one of the oldest treatments for psoriasis,it remains a moderately effective option; howeverit is rarely popular with patients. Productstend to have a tar smell associated with them,although the weaker strengths have a less potentaroma. The main potential side effects associatedwith coal tar include skin irritation andfolliculitis. It is thought that coal tar works byreducing epidermal thickness and by suppressingepidermal DNA synthesis. It is a complex substancecontaining some 10,000 different compoundsof which only 50% have been identified(Camisa, 2004b). Some researchers are workingon identifying which compounds within coaltar are actively anti-psoriatic in the hope thatby distilling these out a more acceptable andyet effective treatment may become available(Arbiser et al., 2006).A number of studies have been carried outcomparing the efficacy of calcipotriol and coaltar. The systematic review carried out in 2000confirmed that calcipotriol was more effective(Ashcroft et al., 2000). Like calcipotriol, coaltar can be used in combination with UVB; this isknown as the Goeckerman regime named afterthe doctor who first published the use of thismethodology in 1925. Coal tar enhances sensitivityto the UVB and may be UVB sparing. Tarand UVB therapy offered within a health carefacility (day care) continues to provide treatmentthat over a period of time improves treatmentresistantpsoriasis. In a small study, 100% ofpatients had 75% improvement in their PASI atthe end of a 12-week treatment programme usingthe Goeckerman regime with narrowband UVB(Lee and Koo, 2005).There have been some concerns about thecarcinogenicity of coal tar. There is no doubtthat coal tar does contain some carcinogenicsubstances as has been demonstrated by animaland occupational studies. There is, however,no research within the dermatological field ofthe use of coal tar preparations and whetherthese increase the risk of internal skin tumours(Roelofzen et al., 2007).Method of applicationOn a day-to-day basis in primary care, weakcoal tar solutions are useful for widespreadsmall plaques of psoriasis as treatment doesnot need to be accurately applied to theplaques only. They can be applied 2–3 timesper day. These weaker solutions will sink intothe skin and a patient can get dressed after this.However, there is always a risk of some stainingand it may be easier for patients to applythe treatment at a point in time when they canwear ‘messy’ clothes afterwards. There is noevidence to support the amount that shouldbe used; however enough to cover the areascomfortably is a sensible suggestion. Coal tarpreparations should be applied following the

136 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalslie of the hair in order to reduce the likelihoodof folliculitis.In a health care facility, where strongerstrengths of tar may be used, tubular nettingbandages can be applied afterwards to keepthe tar close to the skin. It is impractical to getdressed during this kind of treatment; someunits are therefore advocating ‘short contact’coal tar. Where it is left on for 4–6 hours andthen washed off and an emollient applied. Thisis particularly useful in a day-care setting wherea patient can come in for a set period of timeand then leave.Tar is particularly helpful for the managementof scalp psoriasis. In combination with coconutoil and salicylic acid, it can be successfully usedto descale thickened plaques. Tar-based shampoosmay be used in conjunction with othertreatments or in less severe scalp psoriasis maybe sufficient to keep the condition under controlwithout the need for other treatments. Table8.3 outlines how scalp treatments should beapplied.DithranolAlso known as anthralin, the active ingredientswere originally extracted from the bark of theBrazilian araroba tree. During World War I asynthetic version was synthesised.Dithranol affects the synthesis of cell DNAand has a pronounced anti-proliferative effect.It also appears to have a rapid effect on thenormalisation of epidermal differentiation. Inboth these ways, it is an effective treatment forpsoriasis. However, it does have a number ofside effects including irritation and staining,although it has the advantage of being odourless.Its effects may be enhanced by the use ofthe Ingram regime, which includes UVB as wellas topical treatment.Method of applicationIn order for dithranol to be most effective, itmust be carefully applied. Dithranol in a zincoxide paste is most commonly used in hospital/day-carefacilities. The initial concentrationis 0.1% and this in increased every 2–3 days (oraccording to how well the patient will tolerateit). Here the preparation is carefully appliedto the plaques using a spatula and then ‘fixed’using talc which is applied using a makeshiftpowder puff. This helps to keep the paste inplace and minimises smudging onto good skin.This can then be covered with stocking netbandages and left in place for up to 24 hours.Removal of the paste can be difficult if justwater is used; cotton wool soaked in a mineraloil is effective at removing the dithranol prior togetting in the bath.Dithranol can be used on an outpatientbasis, but is probably only useful if limited largeplaques are present and the patient is well motivated.In this instance, short-contact dithranolcan be used. A cream-based product (againstarting at 0.1%) is carefully applied to theplaques using a gloved finger or cotton budand left in place for any period up to an hour.The amount to be applied is sufficient to coverthe plaque and be rubbed in, but not excessivelyor the chance of the product rubbing offonto clothes and furnishing is increased. At thelower strengths, patients might be able to tolerateleaving the product on overnight. Patientsshould gradually increase the strength of productused and the amount of time it is left on(starting at 10 minutes and working up toan hour). When the strength is increased, theamount of time it is left on should be temporarilydecreased. It is possible to use this on thescalp; however as with the skin, the productcan stain hair, particularly if blonde.For both methods of application this is aonce-daily treatment. The products should notbe applied to sensitive areas, e.g. face or flexuresor to sore or pustular psoriasis. Dithranolitself can cause soreness; if this is prolonged,the strength should be reduced or the amountof time left on decreased. If this does notresolve the problem, the treatment has to bestopped.CorticosteroidsPotent topical steroids on their own are rarelyused to treat plaque psoriasis in the UK. In othercountries, topical steroids may be more commonplace. The rationale for not making use of them

Psoriasis 137extensively is the increased chance of reboundand the potential for triggering an episode ofGPP. This being said, mild to moderate steroidsare commonly used to treat psoriasis in flexuralareas, the face and genitalia, as few other productsare licensed for treatment in these areas.As shown in Table 8.3, steroids are also used totreat scalp psoriasis.Vitamin AAlso known as a topical retinoid, its mode ofaction is not entirely understood. However, itdoes appear to modulate cell proliferation andincrease differentiation. It is marketed as beingsuitable for mild to moderate plaque psoriasisand should not be used on more than 10% ofbody surface area. Its main side effect appearsto be skin irritation; to help counter this twostrengths have been developed, 0.05% and 0.1%.Method of applicationA thin layer should be applied to the plaqueonly and gently rubbed in. It may be advisableto start at the lower strength first before movingonto the higher strength. One small study suggestedthat using the product as short contact(product was left on for 20 minutes and thenwashed off with water) leads to less side effectsand equal efficacy (Veraldi et al., 2006).Systemic therapiesPhototherapyFor the majority of people with psoriasis, exposureto ultraviolet radiation improves their condition.There are a small minority of around 10%who have light sensitive psoriasis; for them exposureto UV radiation can cause psoriasis to worsenor develop. The term phototherapy includestherapeutic use of both UVA and UVB light.The principle underpinning both wavelengths ofUV radiation is that they suppress the immuneresponse within the skin and thus dampen downthe cascade of immunological changes whichoccur to trigger psoriasis. The most concerningside effect on a long-term basis is the developmentof skin cancer. For this reason, careful monitoringof the cumulative doses administered is importantand it is usual to limit the course of treatmentgiven to individuals. Other more immediate sideeffects can include skin dryness and erythema.There is mixed evidence about whether emollientsshould be used prior to UVB and PUVAtreatments. Because they reduce scaling it isargued that there is improved penetration of theUV radiation; however, it has been shown thata number of emollients have a UV protectivecapacity (at different parts of the UV spectrum)and thus reduce the efficacy of the light therapy(Otman et al., 2006). It is also likely that factorssuch as plaque thickness, how much emollient isapplied and when it is applied will have a roleto play. The recommendations by Otman et al.(2006) were no more specific than to say thatif emollients were to be used prior to UV therapiesthat they should have minimal UV blockingeffects. Box 8.2 shows emollients from theBritish National Formulary that they found hada sun protection factor of less than 1.2 for UVB,UVA and PUVA. Previous researchers had statedthat protection factor of 1.2 or higher representeda reduction in UV transmittance of 17%or more which was thought to be clinically significant(Hudson-Peacock et al., 1994).UVBMost individuals who have ultraviolet treatmentfor their psoriasis will be treated with UVB (narrowband)initially. This usually involves threeBox 8.2 Emollients that have aSPF of less than 1.2 suitable foruse with UV therapy■■■■■■■Aveeno creamCalmurid creamDermol 500 lotionDoublebase creamEmulsiderm emollientEmulsifying ointmentOilatum gel

138 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsexposures a week which are generally carriedout in a Dermatology Department. To ensure themost appropriate starting dose of UVB, a patient’sback is exposed to a number of different UVBdoses and the dose that produces a small amountof erythema after 24 hours is the dose that thefirst treatment is calculated upon. This is knownas the minimal erythemal dose (MED). The speedat which these doses increase will depend to anextent on the individual’s skin type and theirresponse to the therapy. During the administrationof the UVB, individuals must wear glassesto protect their eyes and men should protect theirgenitalia with a jock strap. It is important that thesame garment is used for each treatment, otherwiseburning may result. If there are no lesions onthe face, a full facial shield should be worn as wellas goggles.PUVAFor UVA to be effective, it has to be given in combinationwith an oral medication called 8 meth oxypsoralen(8MOP). Natural psoralens have beenused for hundreds of years in India where theyhave been used to treat vitiligo; their main actionis to increase photosensitivity. This then makesthe UVA a very effective treatment for psoriasis.Because it must be given in conjunction with anoral medication which can cause a number of sideeffects listed in Table 8.4, PUVA therapy is usuallygiven if UVB has not been successful. Box8.3 lists the possible contraindications for givingPUVA. In a similar way to the MED testing forUVB therapy, minimal phototoxic dose (MPD) iscalculated for PUVA.The medication is taken 1–2 hours prior to thetreatment being administered. Once the 8 MOPhas been taken, the individual must wear eyeprotection and avoid sun exposure for at least12 hours. Sunglasses or coated normal glassesmust be tested to ensure that they are preventingpenetration of UV radiation. Gastrointestinalupsets can be lessened if the medication is takenwith a small meal. It is advisable that eachtime the tablets are taken, the amount of foodingested is more-or-less the same to ensure a consistentserum level of 8 MOP. As with UVB, menTable 8.4 Possible side effects of PUVA.Acute sideeffectsNauseaPruritusDizzinessFlu-likesymptomsHeadacheErythema(burning)Box 8.3 Contraindications forgiving PUVA■■■■■■Chronic side effectsSkin cancerMalignant melanoma: evidencesuggests that there is an increase inthe long-term, although the risk is notthat pronounced.Squamous cell carcinoma(SCC): there isa substantial increase in those who havehad PUVA.Basal cell carcinoma: small increased riskbut not as significant as SCC.Eye diseaseCurrently there is no clear evidenceto link PUVA with increasedexperience of cataracts where eyeprotection is used.Refusal to wear eye protectionMelanoma and non-melanoma skincancersPhotosensitising medicationPregnancyCataractsPhotosensitivity disorders (e.g. lupus,albinism)should wear genital protection. A facial shieldshould be used if there are no facial lesions.For those who find that 8MOP induces toomany of the below acute side effects, topicalPUVA may be helpful. The individual immersesthemselves in a bath in which 8MOP solutionis dissolved and is then exposed to the UVA inthe same way. Exact protocols will vary; however,the UVA can be given immediately after

Psoriasis 139the bath and there is no need to wear eye protectionfollowing treatment. Whilst serum levelsof 8MOP are lower, the therapeutic benefitsappear to be as good if not better during bathPUVA than oral PUVA. There also appear to befewer side effects (Cooper et al., 2000). BathPUVA requires more 8 MOP and is thereforemore expensive; however, it remains a viableoption for those who do not respond to, or whomay be excluded from oral PUVA. Cost can bereduced by the use of a polyethylene sheet in thebath which reduces the amount of water thatcomes into contact with the skin and thereforethe amount of psoralen needed to create the correctdilution (Streit et al., 1996).Topical psoralens can also be applied tolocalised areas such as hands and feet when thepsoriasis just affects these areas. As with bathPUVA, there are none of the acute systemic sideeffects with this method of treatment (exceptpotential burning). The UVA light is then justdirected at those areas using hand and footPUVA machines.MethotrexateMethotrexate is a relatively old treatment whichhas been used in psoriasis since the late 1960s.There are relatively few randomised controlledtrials looking at its efficacy; however, it is consideredto be a very useful drug for the managementof severe psoriasis. Its downsides are thedegree to which it has adverse systemic effects.It is an anti-proliferative drug, that is it affectscell DNA and stops psoriatic skin cells fromdeveloping. It does this by inhibiting folic acid,thus natural levels of folic acid in patients onmethotrexate are likely to be lower. For patientswith psoriasis, the dosage is kept low and givenonce a week at the same time. It is usually takenorally (starting at a low dose of 2.5 or 5 mgworking up to a maximum dose of 20–25 mgdepending on blood results and effect), but canalso be given as an intramuscular injection. Thislatter technique is useful if the patient is particularlyaffected by nausea. Before commencing apatient on methotrexate, they must be counselledas to the potential side effects (listed in Table 8.5)Table 8.5 Potential side effects of methotrexate.Side effectsNotesLeukopenia and thrombocytopeniaOral and plaque ulcerationLower levels of folic acidTeratogenicityHepatotoxicityPulmonary toxicityFalling white blood cell and platelet counts indicate bone marrowtoxicity and the treatment should be discontinued. Generally occurs8–11 days after commencement of treatment.Can indicate toxicity.Can lead to decreases in red blood cells and possible megaloblasticanaemia. A dose of 1–5 mg of folic acid is usually given daily (excepton the day when the methotrexate is taken). This does not seem tocompromise the therapeutic efficacy of the methotrexate.Some evidence to suggest this, sexually active fertile individuals shouldtake birth control precautions.This is a major clinical concern as it is known that prolonged use ofmethotrexate increases the risk of fibrosis and eventual cirrhosis of theliver. This is made more likely there is a high alcohol intake. Blood testsare helpful to indicate liver function, but they do not indicate fibrosis.For this a liver biopsy is needed which itself carries risks.Is unusual and can present as a non-productive cough with orwithout fever.

140 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsand the likely impact it will have on their lifestyle(e.g. need to reduce alcohol intake). Subsequentlyregular blood monitoring is needed, particularlyto ascertain kidney and liver function. Kidneyfunction is important as the drug is secretedthrough the kidneys and any decrease in functioncould increase the likelihood of toxicity.CiclosporinThe effectiveness of ciclosporin in psoriasis wasfirst seen as a serendipitous result of treating apatient following a kidney transplant with thedrug and seeing the positive effect on the skin. Asa relatively modern treatment for psoriasis, therehave been randomised controlled trials showingits efficacy at doses between 2.5–5.0 mg/kg/day(Griffiths et al., 2000). Like methotrexate it doeshave some potent systemic side effects so it isreserved for treating severe psoriasis.Its therapeutic action is through its effects onthe T-cells thus helping to inhibit the stimulationof cytokines which cause cell proliferation seenin psoriasis. Dosing of ciclosporin can be challengingas absorption (through the small intestine)is incomplete (around 30%) and hugelyvariable (4–89%) (Camisa, 2004d). Thus, theway that the drug is formulated will significantlyaffect the bioavailability of the drug and patientsshould not be switched between formulationswithout careful consideration of this fact.As with other systemic medications,ciclosporin has a range of side effects, fromthe relatively mild to the more severe. Theside effects of most concern are those relatedto nephrotoxicity and the resultant kidneyfunction damage and hypertension. The likelihoodof a patient experiencing these negativeside effects is increased by prolonged time onthe drug and higher dosages. Kidney functionand blood pressure must be closely monitored.Ciclosporin is also known to interact with anumber of drugs; some of which will decreaseciclosporin levels in the blood and others whichwill increase them (see Table 8.6). More minorside effects are listed in Box 8.4; these usuallydisappear once the patient has been taken offthe ciclosporin.Table 8.6 Drugs which alter serum levels ofciclosporin.Drugs which increaseciclosporin levelsBromocriptineDanazolKetoconazoleFluconazoleItraconazoleErythromycinVerapamilNicardipineDiltiazemMethyltestosteroneOral contraceptivesDrugs which decreaseciclosporin levelsPhenytoinPhenobarbitolCarbamazepineRifampinIntravenous trimethaprimSulfamethoxazoleBox 8.4 Minor symptomsassociated with ciclosporin■■■■■■RetinoidsGum hyperplasiaTremorHypertrichosisHeadacheNauseaParesthesiaThis is the generic name given to a range of medicationsall related to vitamin A. For psoriasis treatmentthe specific retinoid which is used is knownas acitretin. It works by altering keratinisation andepidermal differentiation having anti-proliferative,anti-inflammatory and anti-keratinising effects on

Psoriasis 141the skin (Naldi and Griffiths, 2005). Retinoids arecomplex drugs with many possible side effects;however, they are effective at treating psoriasis(Griffiths et al., 2000), and as mentioned previouslyused in conjunction with PUVA their effectmay be enhanced thus allowing for a reducedexposure to UV radiation.Retinoids can affect hepatic function andlead to hyperlipidaemia. It is also highly teratogenicand therefore not suitable for pregnantwomen or women who are considering becomingpregnant. Women should take contraceptiveprecautions for 2 years after discontinuing retinoidtherapy (Griffiths et al., 2000). Commonless severe side effects include dry mucousmembranes including eyes, lips and throat (ifa patient’s lips do not become dry it is reasonableto assume they are not complying withtreatment or the dosage is sub-therapeutic) (seeBox 8.5 for further common skin related sideeffects).BiologicsBiologics represent a new generation of drugswhich have been developed to treat chronicBox 8.5 Common skinand mucous membrane changesseen with use of acitretin■■■■■■■■■■■Dry mucous membranes including drylips (cheilitis), dry mouth, dry eyes anddry nasal mucosaAltered skin sensation–skin feels stickyDry skinDermatitisFlare of psoriasisPeeling of finger-tips, palms or solesSkin fragilityItchHair lossHair texture changeNail changes including paronychiaimmune-mediated inflammatory conditionssuch as psoriasis (but also rheumatoid arthritisand chronic inflammatory bowel conditionssuch as Crohn’s disease). In common with othersystemic drugs, they are reserved for those whohave severe disease, and in addition, it is usualfor patients to have unsuccessfully tried theother systemic options before being offered biologicdrugs. This section briefly considers thethree biologic drugs that are currently availablefor the treatment of plaque psoriasis in the UK.However, new biologic drugs are being developedand this list in unlikely to be exhaustivefor very long. For example the National Institutefor Health and Clinical Excellence is due to publishits technology appraisal on Ustekinumab(which is a human monoclonal antibody) inSeptember 2009.The basic principle of biologic drugs isthat they interfere with a very specific part ofthe inflammatory process thus preventing thedevelopment of psoriatic lesions. Because thedrugs are so targeted it is hoped that the longtermside effects will be less than other systemicmedications, but there is no long-termdata that categorically confirms this judgement.Some considerable attention is being given,by the British Association of Dermatologists,to collecting data about the effects of biologicdrugs thus creating what is called a biologicsregister (British Association of Dermatologists,2007).In April 2009, there were three biologicdrugs available for the treatment of severeplaque psoriasis. Table 8.7 outlines whatthe three drugs are, the dosage and recommendationsfrom NICE as to how and whenthey should be prescribed. A fourth drug(Efalizumab, Raptiva) was available untilFebruary 2009 when three patients experiencedsevere adverse effects. As a consequence ofthis, the European Medicines Agency issuedrecommendation that the product should notbe marketed, that no further prescriptionsshould be issued and that those already on thedrug should talk to their doctor about findingan alternative (European Medicines Agency,2009).

142 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 8.7 Biologic drugs and prescribing regimes.Name Mode of action Recommended prescribing regime DeliveryEtanercept (Enbrel)Known as a geneticallyengineered recombinantprotein, it binds to TNF-αmolecules preventing themfrom activating skin cellsthus preventing inflammation(Jackson et al., 2007).Twice weekly doses of 25 mg for up to24 weeks or until remission occurs, shouldfurther treatment be needed the same doseshould be followed (i.e. it is an intermittenttreatment).Suitable for individuals with PASI 1 of 10 ormore and a DLQI 2 of 10 or moreShould be discontinued after 12 weeks ifthe response is inadequate, i.e. there is aless than 75% reduction in PASI or lessthan 50% reduction in PASI accompaniedby a 5 point reduction in DLQI (NationalInstitute for Health and Clinical Excellence,2006)An initial 5 mg/kg infusion over 2 hours,followed by further 5 mg/kg infusions at2 and 6 weeks. Subsequent infusions arethen given at 8-week intervalsSuitable for individuals with PASI of 20 ormore and a DLQI of 18 or moreShould be discontinued after 10 weeks ifthe response is inadequate, i.e. there is aless than 75% reduction in PASI or lessthan 50% reduction in PASI accompaniedby a 5 point reduction in DLQI (NationalInstitute for Health and Clinical Excellence,2008a)An initial dose of 80 mg followed by 40 mginjections every other week starting 1 weekafter the initial dose.Suitable for individuals with PASI of 20 ormore and a DLQI of 18 or moreShould be discontinued after 16 weeks ifthe response is inadequate, i.e. there is aless than 75% reduction in PASI or lessthan 50% reduction in PASI accompaniedby a 5 point reduction in DLQI (NationalInstitute for Health and Clinical Excellence,2008b)SubcutaneousinjectionsInfliximab (Remicade)Known as a monoclonalantibody it binds to all threeforms of TNF-α thus affectingthe inflammatory processInfusionAdalimumab (Humira)Known as a monoclonalantibody which binds withTNF-α blocking interactionwith cell-surface receptorsand limiting the promotion ofinflammatory pathwaysSubcutaneousinjection1 PASI is the Psoriasis Area Severity Index which is a validated method for assessing disease severity. Further details about howto carry out a PASI assessment are given in Appendix 1.2 DLQI is the Dermatology Life Quality Index which is a validated questionnaire that assesses the impact that skin disease hason quality of life. It is discussed in further detail in Chapter 6.

Psoriasis 143Each biologic drug will have its own contraindicationswhich can be found in theBritish National Formulary (British MedicalAssociation and Royal Pharmaceutical Societyof Great Britain, 2008), Electronic MedicinesCompendium (Datapharm, 2009) and summarisedin the British Association of DermatologistsGuidelines (Smith et al., 2005).However, a concern which is relevant to allbiologic drugs is that of infection includingrisk of tuberculosis. All psoriasis patients beingconsidered for biologic therapies must have achest X-ray and a Mantoux test, both of whichmust be negative prior to commencing therapy.If for any reason, there is doubt about theresult or an individual can’t have a Mantouxtest as they are on immunosuppressive therapythey should be referred to a thoracic physician(Smith et al., 2005).Nursing careTable 8.8 gives guidelines for a nursing assessmentfor patients about to undergo biologictherapies. It is modified from an article byJackson et al. (2007).It is also important that the patient receivesfull information about the implications ofusing biologics prior to commencement oftreatment. Not only should patients be awareof the potential side effects (see Table 8.9), butthey also need to know about the commitmentto therapy. All treatments except for etanerceptare considered ongoing treatments that willrequire injections or infusions on a long-termbasis.Other systemic drugs forpsoriasisThere are a number of other drugs whichmay occasionally be used for the treatmentof psoriasis particularly when the alternativesexplored above are not suitable. In a systematicreview (Griffiths et al., 2000), the evidence forthe use of these four alternatives was reviewed.In summary their findings were as follows:Hydroxyurea: One study fulfilled the inclusioncriteria and it suggested that hydroxyureadoes improve psoriasis in some patients.It was suggested that it may be a helpfuldrug for individuals who could not takeciclosporin or methotrexate.Fumaric acid esters (fumarates): These werethe drugs for which there was most evidence;they are widely used in Germanspeaking countries. Although initial sideeffects of gastric upset (up to 66%) andflushing (up to 33%) were reported, theserarely stopped people continuing with thedrugs and other more serious side effectswere rare. It was concluded that fumaratesare helpful in treating moderate to severepsoriasis.Azathioprine: There were no recent studiesrelating to this drug and it is rarely used.Sulphasalazine: One randomised controlledtrial showed it was effective, although 25%had side effects bad enough to make themstop taking the drug.Service provision for those who needtreatment for psoriasisThe general rule is that those with mild to moderatedisease should be cared for in primarycare, whilst those with moderate to severe diseaseshould be referred for specialist care withina hospital environment. The National Institutefor Health and Clinical Excellence (NICE) clarifiedwhat specialist services should provide (seeBox 8.6); at the same time they published referraladvice which classified the level of urgencywith which someone should be referred (see Box8.7) (National Institute for Clinical Excellence,2001).As well as specialist services within hospitals,there is an ever increasing number of specialistpractitioners working in community settings.

144 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 8.8 Nursing assessment guide for those about to be prescribed biologics.QuestionRationaleAre you currently or have you in the past2 weeks experienced any of the following:• Fever• Night sweats• Sore throat• Runny nose• Face pain• Ear ache• Toothache• Cough• Breathing problems• Painful urination• Blood in urine• Antibiotic use• Headache• Wound complication• Severe fatigueHave you had any recent surgery?• If so were there any complications?• Did you experience any drainage from yourincision?Have you had a recent flu vaccination or othervaccination?Are you taking any other medication?Do you have any of the following medicalconditions: heart failure, haematological orneurological disease or any malignancies?Could you be pregnant?Have you gained or lost weight since yourprevious treatment?Did you have any hypersensitivity last time youreceived your biologic medication?What was your response to your previoustreatment?Any of these could indicate infectionSurgery poses an infection risk which usually requires biologic therapyto be postponedLive vaccines are contraindicated in people receiving biologic therapybecause of the infection riskPossible drug interactions should be consideredThese conditions may affect the ability to safely use biologic drugsand must be carefully assessedBiologics should be avoided in women who are pregnant, trying toconceive or are breast feedingWeight may affect dosing, so changes may need to be madeThese may be nurse specialists who providea range of services across primary care andbetween hospitals and primary care trusts orGeneral Practitioners with a specialist interest indermatology. The most commonly seen nursingroles include:■Clinical nurse specialists in dermatology willsee patients in their own homes or in clinicsand generally help with chronic disease managementfor adults and children. Often theywill work in such a way as to improve liaisonbetween dermatological care provided in a

Psoriasis 145Table 8.9 Potential side effects of biologic drugs.Name of drug Very common symptom (1/10) Common symptom (1/100 1/10)EtanerceptInfliximabAdalimumab• Bacterial infections (including upper respiratorytract, bronchitis, cystitis and skin infections)• Injection site reaction• Injection site reaction (including pain, swelling,redness and pruritus)• Allergic reactions• Pruritus• Fever• Viral infection• Serum sickness-like reaction• Headache, vertigo, dizziness• Flushing• Lower respiratory tract infection, upper respiratorytract infection, sinusitis, dyspnoea• Abdominal pain, diarrhoea, nausea, dyspepsia• Increased liver enzymes• Urticaria, rash, pruritus, hyperhidrosis, dry skin• Infusion related (including injection site reaction,chills, oedema, pain)• Lower and upper respiratory tract infections,viral infections, candidiasis, bacterial infections• Dizziness, vertigo, headache, neurologic sensationdisorders• Cough, nasopharangeal pain• Diarrhoea, abdominal pain, stomatitis, mouthulceration, nausea• Increased hepatic enzymes• Rash, dermatitis, hair loss• Musculoskeletal pain• Pyrexia• Fatigue■hospital and that received in the community.This feature of the role may be emphasised assome are called dermatology liaison nurses.They may or may not be nurse prescribers.Nurse practitioner will do some of theabove, but is also likely to have a significantdiagnostic role. They are likely to be a nurseprescriber.Measuring quality of lifeQuality of life measures allow health carepractitioners to ascertain, using an objectivemeasure, how psoriasis is impacting on anindividual. As with many chronic skin conditions,psoriasis can severely impact on thequality of life of an individual. This may notbe directly related to the severity of the disease,for example someone with minor disease maybe severely affected by it and another personwith severe disease may be able to cope with it,thus not allowing it to impact on their qualityof life. It is therefore important for healthcare professionals not to make assumptionsabout how an individual is affected by theirskin condition. These are discussed further inChapter 6.ConclusionPsoriasis is a complex multifactorial immunemediatedinflammatory condition of hyperproliferation.There appears to be a genetic

146 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 8.6 What specialist servicesshould be able to provide forpatients with psoriasisSpecialist services are in a position to:■ Confirm or establish the diagnosis;■■Provide in-patient and day-care services;Provide, in conjunction with otherhealth care professionals, advice on thecondition and its treatment, togetherwith social and psychological support;■ Assess and supervise the use of phototherapyand PUVA, as well as oralretinoids, cytotoxic therapy and immunosuppressivetherapy;■ Treat psoriasis that is unresponsive totherapies tried in primary care, or toresolve problems where the patientcannot tolerate such treatment;■ Offer acute treatment in patients withsevere conditions such as EP or GPP;■ Provide and support specialist nursingservices working in primary and secondarycare;■ Provide assessment and advicefor patients with painful psoriaticarthropathy.susceptibility to the condition which is then triggeredby one or more of a number of factors,which are often difficult to determine. Thereare a number of different clinical variants.The treatments for psoriasis are either topicalor systemic. Topical treatments have very variableeffects partly due to concordance withtreatment issues, but also due to the fact thatindividuals do seem to respond in an individualmanner to topical therapies. For those whodo not respond to topical therapies providedin primary care, referral to specialist servicesis likely to be the next option. Systemic therapiesare generally more effective; however, theBox 8.7 Referral criteria tospecialist servicesReferral to specialist services, which maybe prompted by features such as sleepdisturbance, social exclusion, reducedquality of life or reduced self-esteem isadvised if:■ **** The patient has generalised pustularor erythrodermis psoriasis.■ *** The patient’s psoriasis is acutelyunstable.■ *** The patient has widespread GP(so that he/she can benefit from earlyphototherapy).■ ** The condition is causing severesocial or psychological problems.■ ** The rash is sufficiently extensive tomake self-management unpractical.■ ** The rash is in a sensitive area (suchas face, hands, feet, genitalia) and thesymptoms particularly troublesome.■ ** The rash is leading to time off workor school which is interfering withemployment or education.■ ** The patient requires assessmentfor the management of associatedarthropathy.■ * The rash fails to respond to managementin general practice. Failure isprobably best based on the subjectiveassessment of the patient. Sometimesfailure occurs when patients are unableto apply the treatment themselves.■ **** should be seen immediately(within 1 day)■ *** should be seen urgently (it is recommendedthat this is within 2 weeks)■ ** should be seen soon (no specificrecommendation as to timelines)■ * should be seen as a routine patient(no specific recommendation as totimelines)

Psoriasis 147older ones have significant side effects whichcan limit their usability. A new generation ofbiological therapies are now available to thosewith severe disease who have not responded toother systemic therapies. Health care professionalswho work with patients with psoriasismust be aware of the potentially enormousimpact that it has on mental health and qualityof life issues. Readers are directed to Chapter 6for further detail on this topic.ReferencesAllan, S., G. Kavanagh et al. (2004). The effectof inositol supplements on the psoriasisof patients taking lithium: A randomized,placebo-controlled trial. British Journal ofDermatology, 150: 966–969.Arbiser, J., B. Govindarajaran et al. (2006).Carbazole is a naturally occurring inhibitor ofangiogenesis and inflammation isolated fromantipsoriatic coal tar. Journal of InvestigativeDermatology, 126(6): 1396–1402.Ashcroft, D., A. Po et al. (2000). Systematicreview of comparative efficacy andtolerability of calcipotriol in treating chronicplaque psoriasis. British Medical Journal,320(7240): 963–967.British Association of Dermatologists (2007).Biologics Intervention Register. Retrieved 15April 2009, from www.badbir.org.British Medical Association and RoyalPharmaceutical Society of Great Britain (2008).British National Formulary 55. Retrieved 17March 2008, from www.bnf.org.Camisa, C., Ed. (2004a). The clinical variants ofpsoriasis. In: Handbook of Psoriasis. Malden:Blackwell Publishing.Camisa, C., Ed. (2004b). UVB phototherapyand coal tar. In: Handbook of Psoriasis.Malden: Blackwell Publishing.Christophers, E. (2007). Comorbidities inpsoriasis. Clinics in Dermatology, 25(6).Cooper, E., R. Herd et al. (2000). Acomparison of bathwater and oral deliveryof 8-methoxypsoralen in PUVA therapy forplaque psoriasis. Clinical and ExperimentalDermatology, 25(2): 111–114.Datapharm (2009). Electronic MedicinesCompendium. Retrieved 15 April 2009, fromwww.emc.medicines.org.de Korte, J., J. Van Onselen et al. (2005).Quality of care in patients with psoriasis:An initial clinical study of an internationaldisease management programme. Journal ofthe European Academy of Dermatology andVenereology, 19(1): 35–41.Ersser, S., R. Penzer et al. (2000). Researchreport: Pruritus in psoriasis, School ofNursing and Midwifery, University ofSouthampton.European Medicines Agency (2009). PressRelease – European Medicines Agencyrecommends suspension of marketingauthorisation of Raptiva (efalizumab).Retrieved 15 April 2009, from http://www.emea.europa.eu/humandocs/PDFs/EPAR/raptiva/2085709en.pdf.Fortes, C., S. Mastroeni et al. (2005).Relationship between smoking andclinical severity of psoriasis. Archives ofDermatology, 141(12): 1580–1584.Franklin, S. and M. Glickman (1986).Lepra, psora, psoriasis. Journal of theAmerican Academy of Dermatology, 14(5):863–866.Gelfand, J., A. Troxel et al. (2007). The risk ofmortality in patients with psoriasis: Resultsfrom a population-based study. Archives ofDermatology, 143: 1493–1499.Graham-Brown, R. and T. Burns (2006).Lecture Notes: Dermatology (9th edition).Oxford: Blackwell Science.Griffiths, C., C. Clark et al. (2000). Asystematic review of treatments for psoriasis.Health Technology Assessment, 4(1): 1–125.Guenther, L., F. Cambazard et al. (2002).Efficacy and safety of a new combination ofcalcipotriol and betamethasone diproprionate(once or twice daily) compared to calcipotriol(twice daily) in the treatment of psoriasisvulgaris: A randomized, double blind,

148 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsvehicle-controlled clinical trial. BritishJournal of Dermatology, 147(2): 316–323.Gulliver, W. (2008). Long-term prognosis inpatients with psoriasis. British Journal ofDermatology, 159(Suppl 2): 2–9.Hudson-Peacock, M., B. Diffey et al. (1994).Photoprotective action of emollients inultraviolet therapy of psoriasis. BritishJournal of Dermatology, 130(3): 361–365.Jackson, K., S. Maguire et al. (2007). Biologictherapies in psoriasis: The key role of thedermatology nurse specialist. DermatologicalNursing, 6(1): s1–s11.Kreuger, J. (2002). The immunologic basis forthe treatment of psoriasis with new biologicagents. Journal of the American Academy ofDermatology, 46(1): 1–23.Lee, E. and J. Koo (2005). Modern modified‘ultra’ Goeckerman therapy: A PASIassessment of a very effective therapy forpsoriasis resistant to both prebiologic andbiologic therapies. Journal of DermatologicTreatment, 16(2): 102–107.Naldi, L. and C. Griffiths (2005). Traditionaltherapies in the management of moderateto severe chronic plaque psoriasis: Anassessment of the benefits and risks. BritishJournal of Dermatology, 152: 597–615.Naldi, L., L. Chatenoud et al. (2005). Cigarettesmoking, body mass index and stressful lifeevents as risk factors for psoriasis: Resultsfrom an Italian case control study. Journal ofInvestigative Dermatology, 125(1): 61–67.National Institute for Clinical Excellence(2001). Referral Advice: A Guide toAppropriate Referral from General toSpecialist Services. London: NICE.National Institute for Health and ClinicalExcellence (2006). Etanercept andEfalizumab for the Treatment of Adultswith Psoriasis: NICE Technology Appraisal.London: NICE.National Institute for Health and ClinicalExcellence (2008a). Infliximab for theTreatment of Adults with Psoriasis:Single Technology Appraisal. London:NICE.National Institute for Health and ClinicalExcellence (2008b). Adalimumabfor the Treatment of Adults withPsoriasis: Single Technology Appraisal.London: NICE.Osborn, T. and W. Wilke (2004). Psoriaticarthritis. In: Camisa, C. (Ed.), Handbookof Psoriasis. Massachusetts: BlackwellPublishing.Otman, S., C. Edwards et al. (2006).Modulation of ultraviolet (UV)transmission by emollients: Relevanceto narrowband UVB phototherapy andpsoralen plus UVA photochemotherapy.British Journal of Dermatology, 154(5):963–968.Rapp, S., S. Feldman et al. (1999). Psoriasiscauses as much disability as other majormedical diseases. Journal of the AmericanAcademy of Dermatology, 41(3(pt1)):401–407.Richards, H., D. Ray et al. (2005). Response ofthe hypothalamic–pituitary–adrenal axis topsychological stress in patients with psoriasis.British Journal of Dermatology, 153:1114–1120.Rim, J., J. Park et al. (2003). The efficacy ofcalcipotriol acitretin combination therapyfor psoriasis: Comparison with acitretinmonotherapy. American Journal of ClinicalDermatology, 4(7): 507–510.Roelofzen, J., K. Aben et al. (2007). Coal tarin dermatology. Journal of DermatologicTreatment, 18(6): 329–334.Smith, C., A. Anstey et al. (2005). BritishAssociation of Dermatologists Guidelines onthe use of biological interventions in psoriasisin 2005. British Journal of Dermatology,153: 486–497.Sommer, D., S. Jenisch et al. (2006). Increasedprevalence of the metabolic syndrome inpatients with moderate to severe psoriasis.Archives of Dermatological Research, 298(7):321–328.Streit, V., O. Wiedow et al. (1996). Treatmentof psoriasis with polyethylene sheet bathPUVA. Journal of American Academy ofDermatology, 35(2): 208–210.van de Kerkhof, P., P. van der Valk et al. (2006).A comparison of twice-daily calcipotriolointment with once-daily short-contact

Psoriasis 149dithranol cream therapy: A randomizedcontrolled trial of supervised treatment ofpsoriasis vulgaris in a day-care setting.British Journal of Dermatology, 155(4):800–807.Veraldi, S., R. Caputo et al. (2006). Shortcontact therapy with tazarotene in psoriasisvulgaris. Dermatology, 212(3): 235–237.Weller, R., J.A.A. Hunter, J. Savin and M. Dahl(2008). Clinical Dermatology (4th edition).Oxford: Wiley-Blackwell.Williams, H.C. (1997). Dermatology HealthCare Needs Assessment. Oxford: RadcliffeMedical Press.Woo, W. and K. McKenna (2003). CombinationTL01 ultraviolet B phototherapy and topicalcalcipotriol for psoriasis: A prospectiverandomized placebo-controlled clinical trial.British Journal of Dermatology, 149(1):146–150.


9EczemaSteven J. Ersser & Julie Van OnselenIntroductionThis chapter will highlight the different types ofeczema and the relevant principles of care thatunderpin the treatment of people living witheczema. It commences with a review of whateczema is and a brief outline of the variants ofthe condition. This is followed by an overviewof what eczema is commonly mistaken for in areview of the differential diagnosis. The focusis then on the widespread form of eczema,atopic eczema, its features and key principlesregarding the care of a child with eczemaand related family care. Different treatmentoptions are examined, with due regard to differenttypes of treatment and patterns of theiruse; this includes topical treatments, occlusive,behavioural and systemic approaches. Othertypes of eczema are discussed and the relatedpatient care, including seborrhoeic eczema,contact eczema, both irritant and allergic. Thisis followed by eczemas of adulthood, includingthose common in older age, such as discoid andvaricose eczema, and their related principles ofcare and treatment.What is eczema?Eczema or dermatitis is a type of inflammatoryreaction pattern in the skin which may be provokedby a number of external or internal factors(Graham-Brown and Burns, 2006). Theterm eczema comes from the Greek for ‘boiling’,which refers to the small vesicles or blisters thatare often observed at the early acute stages ofthe disorder. Eczema and dermatitis are synonymousterms, often used interchangeably.Eczemas may be categorised as exogenous,due to an external agent, or endogenous, relatedto a constitutional factor; however, in somecases both causal factors may be present (seeBox 9.1).Some clinical images of eczema can beseen below. Endogenous eczema is exemplifiedby atopic eczema, which often presentsin early childhood – with facial involvement(Figure 9.1). Other images include seborrhoeiceczema (Figure 9.2) and exogenous eczema, suchas contact (allergic) dermatitis.Another useful distinction is that of acute andchronic eczema. Acute eczema is characterised

152 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 9.1 Eczema classificationEndogenous■ Atopic eczema (see Figure 9.1)■ Seborrhoeic eczema (see Figure 9.2)■ Discoid eczema■ Varicose eczema■ Endogenous eczema of the palms andsoles■ Asteatotic eczema (eczema craquele)Exogenous■ Primary irritant contact dermatitis■ Allergic contact dermatitis (Figure 9.3)Source: Reprinted from Graham-Brownand Burns (2006)Figure 9.2 Seborrhoeic eczema. (Source: Reprinted fromGraham-Brown and Burns, 2006.)Figure 9.1 Atopic (endogenous) eczema. (Source:Reprinted from Buxton and Morris-Jones, 2009.)this chapter. For people living with a long-termor chronic condition, specific attention is neededto support them and their families with utilisingtheir treatment effectively and appropriatelyadhering to treatment. Such issues have beenexamined in Chapter 7.by weeping crusting, blistering redness, papules,swelling and scaling. Chronic eczema may revealthese changes but it is typically less vascular andexudative, more scaly, pigmented and thickenedand more like to fissure and show lichenification(see Figure 9.4). Lichenification describes astate where the skin is dry, leathery and thickenedwith skin markings secondary to repeatedscratching or rubbing (Weller et al., 2008).Chronic eczemas may have acute flare-ups, asin the case of a child with atopic eczema havingan eczema flare due to infection. Those livingwith eczema or their carers need to understandthe triggers that may lead to acute flare-ups andtheir management; these are discussed later inFigure 9.3 Contact dermatitis (allergic) to nickel in ajean stud. (Source: Reprinted from Graham-Brown andBurns, 2006.)

Eczema 153Figure 9.4 Lichenification. (Source: Reprinted from Welleret al., 2008.)Biology and pathophysiology of eczemaAtopic eczema occurs as a result of the interactionof environmental factors with an abnormalimmune system in a genetically predisposed individual(Cork, 1997). These genetic changes causean altered immunological response to antigensand as a result immunoglobulin (Ig) E or IgE isproduced. Abnormal T-helper (T H ) lymphocytesplay a key role in the disease interacting withLangerhans cells which raises IgE and interleukinlevels and reduces interferon levels (INF-γ); thisleads to an upregulation of pro-inflammatorycells (Buxton and Morris-Jones, 2009).In atopic individuals, IgE binds to mast cellsand an antigen response causes mast cell degranulationresulting in the release of pro-inflammatorymediators and hence the development of inflamedeczematous lesions (McFadden et al., 1993). Inaddition, this response can only occur due to theadditional genetic alteration of the epidermal barrier,which allows the penetration of antigens(Cork, 1997). The primary defect is the reducedbarrier function (e.g. from filaggrin mutations)which allows protein antigens to get into the skin;leucocytes then prime T-helper cells to becomeT2 helper cells, which then release interleukin 4, 5and 13, leading to high IgE levels and othereffects (Healy, E., University of Southampton,Southampton, pers. comm.). The complex relationshipbetween the epidermal barrier dysfunctionin atopic eczema and the interaction betweengenes and the environment is usefully summarisedin (Cork et al., 2006).The normal skin barrier has lipid lamellaewhich keep high levels of water within the corneocytesand together with high levels of naturalmoisturising factors (NMFs), e.g. urea, lacticacid and urocanic acid that maintain the skin’sprotective features and keep the skin elasticand smooth (Cork, 1999). Skin barrier changesin eczematous skin include the breakdown oflipid lamellae from around the corneocytes anda decrease of up to 80% of the levels of NMF.In addition, genetic changes in atopic eczemaof the genes (including filaggrin and protease)responsible for the structure of the skin barrier(stratum corneum) result in decreased levels ofNMF within the stratum corneum (Palmer et al.,2006). This results in water loss from the corneocytes,with shrinking and cracking permittingpenetration of irritants and allergens and triggeringthe inflammatory response. The differencesbetween normal skin and eczematous skinbarriers are illustrated in Figure 9.5.The damage to the epidermal skin barrieralso results in bacterial colonisation, commonlyStaphylococcus aureus. People with atopiceczema have a total bacterial skin flora of 90%of Staphylococcus aureus compared to 30% in(a)Permeability barrier(b)Permeability barrierThe skin barrier – Normal skinH 2 ONMFH 2 ONMFH 2 OBarrier lipid lamellaeNMFH 2 OThe skin barrier – Eczematous skinH 2 ONMFH 2 ONMFDefective barrier lipid lamellaeH 2 OStratumcomeumStratumcomeumFigure 9.5 (a) Normal and (b) eczematous skin barrier.(Source: Cork, 1999.)

154 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsindividuals without atopic eczema (Hoare et al.,2000). Even when the skin has not undergoneclinical change with overt infection, Staphylococcusaureus contributes to disease activityand increases with the severity of atopic eczema(Szakos et al., 2004).Staphylococcus aureus is an environmentaltrigger in atopic eczema as it flourishes in eczematousskin. Bacterial colonisation of the skinwith Staphylococcus aureus will result in activeeczema with visible signs of infection, such asweeping, crusting and pustules, present in theskin. Therefore Staphylococcus aureus willexacerbate and sustain eczema. There are severalmechanisms that support this physiologicalresponse in eczema:(1) Protein A is a constituent of the cell wall ofstaphylococic (if protein A is injected intradermally,the substance causes initial flare,followed by delayed induration of the skin).(2) Circulating anti-staphylococcal (IgE) antibodiesare found in up to 30% of patientswith atopic eczema and can contribute tomast cell degranulation.(3) Staphylococcus aureus produces exotoxinswhich act as superantigens. These can stimulateT-lymphocytes to release massive amountsof cytokines, thereby contributing hugely tothe inflammatory response. This is illustratedin Figure 9.6 (McFadden et al., 1993).SuperantigenicexotoxinsT-cellsIL-4B-cellsStaph. aureusFigure 9.6 Superantigens diagram, illustrating the cycle ofevents that result from release of superantigenic exotoxins.(Source: Reprinted from McFadden et al., 1993.)IgEEczematouslesionsInflammatorymediatorsMast-cellsAtopic eczemaClinical features and epidemiologyAtopic eczema, or atopic dermatitis, is an itchyinflammatory skin disease, which usually involvesthe skin creases (Williams et al., 1995). Thediagnostic criteria for atopic eczema are classifiedby the following clinical picture (Williams et al.,1995) an itchy skin condition, plus three ormore of:■■■■■Past involvement of the skin creases, such asbends of the elbows or behind the knees,A personal or immediate family history ofasthma or hay fever,A tendency towards generally dry skin,Onset under the age of 2 year andVisible flexural dermatitis, as defined byphotographic protocol.The risk factors for children developing atopiceczemas include familial factors including genetics(atopy), family size and sibling order; socialclass (eczema has a higher incidence in moreaffluent social classes) and concurrent illness/disruption to family life including teething, psychologicalstress and lack of sleep (NationalInstitute for Health and Clinical Excellence[NICE], 2007).Clinical signsAtopic eczema is characterised by inflammation(redness), swelling, crusting, scaling of the skin;intensified by scratching in response to intenseitch. It may be acute with oozing and vesicles orit may be chronic with lichenification, alteredpigmentation and exaggerated surface markings.Itching is a predominant symptom that can leadto a cycle of scratching, leading to skin damageand in turn more itching (the itch–scratch cycle).A stubborn reverse pattern may occur when theextensor areas (a straight part of the body) aswell as the flexural areas (a body part that flexesor bends) are affected, for example, around theelbow (see Figure 9.7).Atopic eczema is now the commonest inflammatoryskin disease of childhood, affecting

Eczema 155Figure 9.7 Atopic eczema. (Source: Reprinted fromGraham-Brown and Burns, 2006.)around 15–20% of school children in the UK(Herd, 2000). Although only 1–2% of adults areaffected by atopic eczema, their disease is oftenmore chronic and severe (Herd et al., 1996).Atopic eczema is more frequent in childhood,especially in the first 5 years of life (Thomaset al., 2008). Young children represent the largestgroup of individuals with atopic eczema seen bydermatologists, GPs, primary care nurses andnurse specialists. Atopic eczema is the commonestof childhood dermatoses, accounting for20% of all dermatology referrals (Lewis-Joneset al., 2001). There is reasonable evidence to suggestthat the prevalence of atopic eczema hasincreased two to three-fold over the last 30years, for reasons which are unclear but possiblydue to environmental and lifestyle changes,(Williams, 1992) and in many countries thiscontinues to rise (Asher et al., 2006).Studies with twins demonstrate that geneticfactors are important in atopic eczema butother evidence strongly suggests that environmentalfactors are critical in disease expression(Williams, 1995). Allergic factors such as exposureto house dust mites may be accountable, butnon-allergic factors such as exposure to irritantsand infectious agents may also be important.Atopic eczema may be further categorised intoextrinsic and intrinsic forms, as highlighted earlierin the chapter. The former denotes individualswith evidence of raised circulating antibodiesto common allergens, whereas the latter does not.It is also established that psychological factors,such as stress, play a vital role in the course ofatopic eczema as a trigger or precipitating factor(Buske-Kirschbaum et al., 2001, 2002). Frequentexposure to infections may protect children fromexpressing atopy; this observation is based onan inverse relationship between prevalence ofeczema and family size, leading to the ‘hygienehypothesis’ (Strachan, 1989). As referred to inthe section on the biology of eczema, atopiceczema is a multifactorial condition that is influencedby the interplay between genetics and theenvironment; this interplay and its relationship tothe skin barrier is discussed in Cork et al. (2006).Some of the environmental trigger factors arenow discussed.Trigger factorsTrigger factors need to be identified and managedfollowing clinical assessment; potential factorsinclude (NICE, 2007):■■■irritants (e.g. soaps and detergents)skin infectionsallergens contact food inhalantAtopic eczema assessment should consider all theidentified trigger factors listed in Table 9.1.NICE (2007) provides guidance based on asynthesis of evidence, proposing the followingconsiderations. Inhalation allergy may be seenin children with seasonal flares, and those whoseeczema is associated with asthma and allergicrhinitis. Allergic contact dermatitis may be seenin children with exacerbations of previouslycontrolled atopic eczema or reactions to topicalpreparations. Allergy testing on the high streetor via the internet should be avoided since thereis no evidence of their value. The role of factorssuch as stress, humidity or temperature extremeshave in leading to flares is not known and assuch these factors should be avoided wherepractical.Health care professionals should consider adiagnosis of food allergy in children with atopiceczema who have previously reacted to foodwith immediate symptoms. This also applies to

156 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 9.1 Trigger factors for atopic eczema.Potential triggerfactorIrritantsContact allergensFood/dietary factorsInhalant allergensMicrobial colonisation/infectionClimateEnvironmentalfactorsSource: Adapted from NICE (2007).Source of trigger factorWool and synthetic clothing,soaps, detergents, disinfectantsand chemicalsPreservations in topical products,perfumes, metals and latexCow’s milk, eggs, peanuts, wheatHouse dust mite, animal dander,tree/grass pollens and mouldStaphylococcus aureus,Streptococcus species, Candidaalbicans, Pityrosporum yeastsand herpes simplexExtremes of temperature andhumidity and seasonal variationHard water, proximity to traffic,cooking with gas and tobaccosmokeinfants and young children with moderate tosevere eczema that has not been controlled byoptimum management, particularly if associatedwith gut dysmobility (including colic, vomitingand altered bowel habit) or failure to thrive(NICE, 2007).In general there is little evidence to support adiet free of eggs, and milk in unselected patientswith atopic eczema nor the use of a few-foodsdiet. There is, however, some evidence to supportthe use of an egg-free diet in infants withsuspect egg allergy who have positive specificantibodies (IgE) to eggs (Williams et al., 2008).With exclusion, diet consideration also needsto be given to the risks of impaired growthand development in the child. It is not knownwhether altering a breast feeding mother’s dietis effective in reducing the severity of eczema(NICE, 2007). Evidence is currently not availableto suggest the optimal feeding regimen inthe first year of life for children with establishedatopic eczema.Evidence to support the implication of environmentalfactors increasing the prevalence ofatopic eczema in developed countries is outlinedby a study showing associations between atopiceczema symptoms and the home environment(McNally et al., 2001). This highlights factorssuch as dampness in the home environment,the use of radiators in bedrooms (causing nocturnaloverheating) and upholstered furniture,bedding and carpets; all these factors encouragehouse dust mites to thrive. The study concludedthat there was an improvement in atopiceczema symptoms by controlling mite allergensthrough mattress covers and frequent vacuuming.Control of house dust mite by vacuumingis therefore advocated, based on this evidence; asimilar principle will apply to damp dusting.Significance and impact of atopic eczemaAtopic eczema is a significant disease. Childrenwith atopic eczema are a high-priority group foreffective intervention. Few individuals experiencehandicap in adult life with the very chronicform of atopic eczema. However, the onset ofdisease occurs before the age of 2 years in 90%of newly diagnosed cases. The intractable itch ofatopic eczema can cause sleep loss, misery tochildren and disruption to family life (Williams,1997). Atopic eczema can be a disfiguring andvery burdensome due to the unrelenting itch anddesire to scratch. Scratching damages the skin,disturbs sleep, disrupts relationships, triggersmood changes and alters affect (Lewis-Joneset al., 2001). Sleep loss is an important measureof disease intensity in children with atopic eczema(Reid and Lewis-Jones, 1995).Atopic eczema is the cause of significant emotionaldifficulties for many sufferers as well asother family members (Elliott and Luker, 1997).The latter study of mothers caring for childrenwith severe atopic eczema highlights the extraburden of normal childcare and the additionalhousework generated by the disease. Elliott andLuker found that mothers described the majortask in keeping their child entertained in order toprevent scratching. This is further compoundedby the fact that such children were often found tobe irritable and had short concentration spans.There is a substantial economic cost of eczemato the patient (Kemp, 2003) and the health service(Verboom et al., 2002). Herd et al. (1996)

Eczema 157estimated that in 1996 the annual UK personalcost to patients would be £2,297 million, the costto the service £125 million with a substantialloss of school and working days. The substantialeconomic impact of the disease is supported bystudies such as that from Australia (Kemp, 2003).Measurement of the impact of skin disease onquality of life is important for our understandingand management of skin diseases. Several studiessuggest that atopic eczema has a more profoundeffect on quality of life than other skin diseases,such as acne and psoriasis (Lewis-Jones andFinlay, 1995).Therefore, it is desirable to measurethe impact on quality of life as a potential outcomeof intervention. The relationship betweenthe severity of atopic eczema in children and qualityof life has been established (Ben-Gashir et al.,2004). Problematic symptoms such as itchingcan adversely affect quality of life. Itch leads toscratching and these may have a significant impacton a child’s sleep, quality of life (Lewis-Jones et al.,2001) and family (Elliott and Luker, 1997).Due to these various impacts of atopiceczema, it is necessary to measure changes inquality of life impact as well as disease severityas a key outcome measure (further details canbe obtained in Chapters 3 and 6). Also, sincecaregivers, especially parents, are often requiredto assist with treatments, their ability and confidenceare also relevant outcomes to measure.Given that people with atopic eczema requirespecial clothing, bedding, frequent applicationsof greasy ointments (Reid and Lewis-Jones,1995), treatment adherence also becomes a relevantclinical outcome to assess. Nurses have akey role in supporting the parents of childrenwith atopic eczema. The challenge for parents ishighlighted in the research by Elliott and Luker(1997) and ongoing work by Surridge (2005) onthe challenges of appraising knowledge sourcesto find tolerable solutions to their child’seczema. Parental education is discussed later,but is also highlighted in Chapter 7, on theimportance of parental education to make themost of treatment.What is eczema commonlymistaken for?Diagnosis of eczema requires identification of itskey clinical signs (described earlier) and also differentiationfrom other skin conditions; the latteris summarised in Table 9.2.Table 9.2 Common differential diagnoses.Eczema variantDifferential diagnosisScalp and hairFace and neckSeborrhoeic dermatitis: Fine scaling (yellow/greasy) on scalp with mild erythema. Tendingto confluence.Atopic eczema: Eczematous areas especiallyof face show erythema, scaling and oozing,but much of non-eczematous skin may bevery dry.Airborne contact dermatitis: Erythema,blisters and weeping.Acute eczema: Erythema, vesicles, oozingand crusting. Always itches, hence isscratched.Psoriasis: Thick scaling and erythema extending tohairline and ears. Hair thinning may occur. Tendingto discrete paths with clear skin in between.Infantile seborrhoeic eczema: Greasy yellow-brownscales or crusting on scalp, face and napkin areawith mild erythema. May not itch.Chronic actinic dermatitis (Photosensitivity): Acuteerythema on sun-exposed area.Erysipelas/cellulitis: Intense erythema and oedema.(continued)

158 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTable 9.2 (continued)Eczema variantDifferential diagnosisPalms and solesDorsum handsGeneralisedFlexural/perineal/genitalLimbsChronic dermatitis: Dryness, mild erythema,cracks and fissures.Pompholyx eczema: Vesicles, bullae andweeping.Allergic hand eczema: Intense erythema,vesicles and blisters.Discoid eczema: Circular lesions, dry skin,moderate erythema. Very itchy.Atopic eczema: Dryness, erythema, scalingwith patchy oozing and marked scratching.Lichenification is increased line markings ofthe skin and pigmentation due to persistentscratching and rubbing.Acute eczema: Erythema, vesicles, oozingand crusting.Chronic eczema: Dry skin, background oferythema, excoriation and lichenification.Flexural eczema: Dryness, erythema, minimalscaling or oozing. Satellite lesions.Atopic eczema: Dryness, erythema, scalingand vesicles.Asteatotic eczema (craquele): Large dry flakyscales (‘crazy-paving appearance’), milderythemaChronic psoriasis: Thick scaling with silvery scalesand erythema, often in discrete patches.Palmoplantar pustulosis: Dryness, yellow sterilepustules which resolve to brown macules.Chronic irritant eczema: Dryness, mild erythema,cracks and fissures.Psoriasis: Thick scaling with silvery scales anderythema.Dermatitis herpetiformis: Small to medium vesicleson an erythematous and eczematized background –favours shoulder, knees and elbows.Bullous pemphigoid: Large tense bullae on anerythematous and eczematized background.Tinea (excluding palms and soles): Erythema, mildscaling with a raised advancing edge and clearingcentre.Flexural psoriasis: Erythema, minimal scaling, plaqueforms and bilaterally symmetrical, less likely to bescratched.Tinea cruris: Erythema, minimal scaling and unilateral.Keratosis pilaris: Follicular papules, skin coloured orbrown, no erythema.Venous eczema: Erythema, decolourisation (due tohaemosiderin) and scaling with associated oedema,ulceration and fibrosis.Source: Based on Cox and Lawrence (1998).Eczema severity assessmentNICE (2007) recommends that clinicians shouldconsider using the assessment tools to measureeczema severity, psychological and psychosocialwell-being and quality of life. However, thetools used should be easy-to-use validated toolswhich will aid clinical management. Eczemaseverity assessment and measurement toolsshould aid the clinician to ascertain the level ofseverity of eczema and the effects of treatment.Time-consuming and cumbersome tools maynot necessarily be effective in day-to-day clinicalpractice. A selection of the commonly usedtools to assess the impact of atopic eczema inchildren, recommended by NICE (2007), is outlinedin Table 9.3.The patient-orientated eczema measure (POEM)is a useful tool for adults in self-assessing

Eczema 159symptoms and disease severity in atopic eczema.Tools assessing the effects of quality of life foradults with eczema may include the DermatologyLife Quality Index and SCORAD. These assessmenttools are discussed in more detail in Chapters6 and 3 respectively. There is a need for healthprofessionals to adopt a holistic approach toTable 9.3 Eczema severity assessment scales.Assessment toolVisual analoguescalesPatient-OrientatedEczema Measure(POEM)Children’sDermatology LifeQuality index(CDLQI)Infants DermatologyLife Quality Index(CDLQI)Dermatitis FamilyImpact (DFI)questionnaireDescriptionUse a 0–10 scale to capture thechild/patient/carer’s assessmentof severity, itch and sleep lossover the previous 3 daysPatient self-assessment formonitoring symptoms anddisease severityImpact of eczema on the childImpact of eczema on the infantImpact of eczema on the child’sparents/carereczema assess ment, taking into account of boththe severity of atopic eczema, quality of life/everydayactivities and psychosocial well-being. NICE(2007) recommends a simple holistic assessmenttool outlined in Table 9.4.Caring for children with eczemaConsultations tend to focus on the physicalaspects of the child’s problems, neglectingthose of a psychosocial nature (Fennessy etal., 2000). The health care professional shouldinclude in a holistic assessment the followingfactors:■■A detailed individualised history of the: time, onset, pattern and severity of eczema response to previous and currenttreatmentspossible trigger factorsthe impact of the condition on the child,their parents/carersdietary historygrowth and developmentpersonal and family history of atopiceczema (NICE, 2007)Specific problems such as scratching/poorsleep/family impact.Table 9.4 Holistic assessment for atopic eczema recommended by NICE (2007).Skin/physical assessmentImpact on quality of life and psychosocial well-beingCLEARNormal skin, no evidence of atopiceczemaNONENo impact on quality of lifeMILDAreas of dry skin, infrequent itching (withor without small areas of redness)MILDLittle impact on everyday activities, sleepand psychosocial well-beingMODERATEAreas of dry skin, frequent itching, redness(with or without excoriation and skinthickening)MODERATEModerate impact on everyday activities andpsychosocial well-being, frequently disturbedsleepSEVEREWidespread area of dry skin, incessantitching, redness (with or without excoriation,extensive skin thickening, bleeding,oozing, cracking and alteration ofpigmentation)SEVERESevere limitation of everyday activities andpsychosocial functioning, nightly loss ofsleep

160 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals■■■■Developmental considerations: It is importantto highlight that 10% children with severeatopic eczema display retarded growth. NICE(2007) recommends monitoring growth in childrenwith atopic eczema by regular weight andheight measurement, to assess for growth retardation.The reasons for growth retardation insevere atopic eczema are not fully understood,but chronic sleep disturbance and stress maycontribute (NICE, 2007). Growth retardationalso needs to be assessed with consideration tothe child’s diet, as children on strict eliminationdiets (which may not be clinically supervised)often exhibit nutritional deficiencies that maylead to poor growth (Lifschitz, 2008).Parental support/self-efficacy (belief in theirability to manage their child’s eczema): managingmedication and eczema symptoms andcommunicating with health care professionals.Challenge of parent and child managementof scratching and poor understanding of aneffective clinical regimen by parent.Quality of life impact: this is significant inatopic eczema and affects the entire familyincluding: Sleep disturbance, Major burden of care causing disruptionof family life, Economic cost and Treatment adherence: children witheczema are often on multiple medicationsand parents are given health guidelinesthat they often struggle to put into practice.Problems of adherence stem morefrom a disbelief in their ability to useeffectively what they are prescribed thanfrom disease activity (Taal et al., 1993).Other forms of childhood eczemaSeborrhoeic dermatitisIn infancy, seborrhoeic dermatitis is also commonlyknown as ‘cradle cap’ (infantile seborrhoeic dermatitis)and occurs on the scalp, face, flexures,nappy area and occasionally can be generalised. Itpresents with erythema and yellow greasy scales;it is self-limiting, not itchy and generally resolvesover several weeks (see Figure 9.2). The aetiologyof seborrhoeic dermatitis is unclear but it isbelieved to be an inflammatory reaction related tothe proliferation of a non-pathogenic skin flora,yeast called Malassezia furfur (formerly known asPityrosporum ovale). Increased keratinocyte andsebocyte turnover may also play a part.Juvenile plantar dermatosesThis is a condition mainly affecting school-agedchildren. It occurs exclusively on the plantarregions of the feet (soles) with glazed erythemaand painful fissuring. This is a form of dermatitiswhich is related to the continual wearing ofsynthetic footwear (Burns et al., 2004).Other forms of eczema in adulthoodThe following other forms of eczema are morelikely to be seen in the middle-aged patient,although these can present in any age group.Discoid eczemaDiscoid eczema describes a type of eczemawhich presents as disc-shaped, rounded areasof raised eczematous lesions. The lesions havewell-defined edges and scale; they are very itchyand occur in asymmetrical patterns all over thebody. The cause is unknown.Lichen simplexLichen simplex occurs due to the repeated rubbingor scratching of an irritated or itchy areaof skin which becomes a lichenified patch ofeczema; scaling and fissuring may also bepresent. It may appear as a single lesion or occurin multiple sites on any part of the body.PompholyxThis is a term given to eczema that typically occurson the palms, fingers, soles and toes. It presentsfollowing severe itching as clear vesicles that aredeep seated and may progress to confluent largebullae (blisters). When the bullae resolve, the skincracks and peels and is painful and susceptible toinfection (Figure 9.8) (Burns et al., 2004).

Eczema 161Figure 9.8 Infected eczema. (Source: Reprinted fromBuxton and Morris-Jones, 2009.)The following other forms of eczema are morelikely to be seen in the older patient, althoughthese can present in any age group.Asteatotic eczemaAsteatotic eczema is known as ‘eczema craquele’and describes the crackled crazy paving typeappearance of dry, scaled and fissured eczematousskin. It occurs exclusively in the olderperson, usually in winter and on the lower limbsand trunk. Asteatotic eczema is often associatedwith the overuse of soaps, overheating and lowhumidity (see Table 9.2).Varicose (venous) eczemaVaricose eczema is also known as gravitational,stasis or venous eczema. It occurs in the lowerlimbs of patients suffering from venous hypertension.An eczematous pattern is present onone or both limbs; the skin is dry, flaky, irritatedand inflamed (see Figure 9.9). The skin is fragileand can break down easily, leading to the formationof venous leg ulcers.It is not uncommon in the community to see arange of erythematous eczema-like lesions affectingthe lower leg. Although all are red, eczema isalways itchy or sore with broken skin. Superficialthrombo-phlebitis is localised to a vein and tendsto be linear and tender, whereas cellulitis is a deepdermal and subcutaneous condition, with painfulinflammation and is usually accompanied by apyrexia and diffuse oedema (Ryan, T., Universityof Oxford, Oxford, pers. comm.).Figure 9.9 Varicose eczema. (Source: Reprinted from Buxtonand Morris-Jones, 2009.)Contact dermatitisPrevalence and incidenceThe majority of occupational dermatoses consistof contact dermatitis. Irritant contact derma titisis extremely common; it is reported to be as highas 55% in people with certain occupations (e.g.health care workers and those working in catering,cleaning and hairdressing). Contact aller gicdermatitis affects 1–2% of the general UK population(English, 1999).Risk and trigger factorsThese include:■■■atopic eczema (current or a history of childhoodatopic eczema)occupations with a high exposure toallergensoccupations where repeated hand washing isessential

162 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsIrritant dermatitisIrritant dermatitis is inflammation of the skinresulting from a non-immunological reaction toexternal stimuli due to excessive contact withan irritant (e.g. detergents, soap, acids, alkaline,cement, solvents, chemicals and food). Acuteirritant contact dermatitis is often the result ofa single overwhelming exposure or a few briefexposures to the irritant or causative agent.Chronic or cumulative contact dermatitis occursfollowing repeated exposure to irritants (Bourkeet al., 2001).Allergic contact dermatitisAllergic contact dermatitis is an allergic reactionwhich only occurs in people whose skin hasbeen exposed to and previously sensitised by anallergen. Subsequent contact with the antigenelicits a specific cell-mediated sensitisation (e.g.nickel, cosmetics, perfumes, hair dye, dyes andplants) of the immune system to a specific allergen/swith resulting dermatitis or exacerbationof pre- existing dermatitis. Phototoxic, photoallergicand photo-aggravated contact dermatitisoccur when allergens are photo-allergens butit is not always easy to distinguish betweenphoto-allergic and phototoxic reactions (Bourkeet al., 2001). Phototoxic reactions result fromdirect damage to tissue caused by light activationof the photosensitising agent. Photoallergicreactions are a cell-mediated immuneresponse in which the antigen is the lightactivatedphotosensitising agent. Some patientswith atopic dermatitis and other chronic inflammatoryskin conditions become photosensitive(DermNetNZ, 2009).Acute dermatitis will follow a single exposureto an irritant or an allergen, and the allergic andeczematous manifestations observed in the skinare defined by Burns et al. (2004). The manifestationsare as follows:■■Vasodilatation of the dermis causes inflammation;Peri-vascular infiltrate of lymphocytes andpolymorphs;■■Intra-epidermal vesicles form by accumulationof fluid in cells, and may coalesce toform bullae;Vesicles and bullae will rupture to oozing,crusting, scaling and healing.Patients with allergic contact dermatitis usuallypresent with acute dermatitis at the bodysite where the allergen has been in direct contactwith the skin. Severe allergic contact reactionsmay extend outside the contact area or it maybecome generalised.Diagnosis of irritant and contact dermatitisThe key to diagnosing irritant and/or allergiccontact dermatitis is the detection of the irritantsensitising agent respectively. Sensitisation maysuddenly occur following years of trouble-freecontact with the allergen.An examination and skin/occupational historywill reveal clues and common sites of involvement,e.g.:■■■nickel – ear lobes/nape of neck (jewellery)leather – wrists (watch straps)tanning agents/adhesives – soles of feet(shoes)Patch testingPatch testing identifies whether a substance thatcomes in contact with the skin is causing inflammationof the skin (contact dermatitis) and confirmsor excludes an allergen.The guidelines for managing contact dermatitis(Bourke et al., 2001) recommend thatpatients with persistent eczematous eruptionsshould be patch tested. Patch testing shouldinclude at least to an extended series of allergens.In addition, patch testing should be undertakenby an individual who has had trainingin the investigation of contact dermatitis, prescribesthe appropriate patch tests and performspatch test readings at day 2 and day 4 forpatients undergoing diagnostic patch tests. Thedual time sequenced readings allow time for theimmunological response to evolve sufficiently.

Eczema 163(a)(b)Figure 9.10 Patch testing: (a) metal cups containing allergens; (b) positive patch test reactions. (Source: Reprinted fromGraham-Brown and Burns, 2006.)Patch testing involves testing patients with thesuspected substance (prepared allergens) and theEuropean standard battery (the European standardof allergens most widely used in patch testing)plus other likely allergens (English, 1999).The procedure for patch testing is as follows.(1) Suspected allergens are placed within smallmetal chambers called Finn chambers andare the placed on the patient’s back.(2) The patch tests are left in place for 48 hoursand then removed (the patient is instructednot to wash their back for 5 days).(3) Results are read at 48 and 96 hours using afour-point scale to score the skin reaction tothe patch tests. The scale is as follows: O no reaction a palpable oedematous reactiondevelops the reaction becomes vesicular the reaction is very strong andspreads beyond the boundary of the patch.(4) The skin reactions from patch testing areinterpreted with consideration to the patient’shistory, lifestyle and occupation. Furtherdetails on conducting patch test are illustratedin Radcliffe (1998). Clinical images depictingthe process are also given in Figure 9.10.When photo-allergic dermatitis is suspected,photo-patch testing involves application of thephoto allergen series and any other suspectedallergens in duplicate on the back. One set ofpatch tests is irradiated with ultraviolet light(5 J cm −2 ), and after 48 and 96 hours the patchtests are read in parallel (Bourke et al., 2001).Treatment options for eczemaManagement of eczema aims to relieve symptomsand prevent complications, such as infections,until remission occurs. General principles

164 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsof eczema management for mild to moderateatopic eczema include emollient therapy andtopical therapy, which include topical corticosteroidsor immunomodulators, antibacterial andantibiotics and antihistamines. In severe eczema,secondary care referral is required for phototherapyand/or systemic therapy. Severe complexconditions such as atopic eczema require amultidisciplinary approach; a model of internationalexcellence of hospital-based support isillustrated by the National Jewish Medical andResearch Center in the USA (Boguniewicz et al.,2008) and specifically nursing advances within(Nicol and Boguniewicz, 2008).Eczema treatment can only be successful ifpatients and their carers are fully supportedwith information, education and practical treatmentadvice on self-management. Advice onavoiding exacerbating and trigger factors (seeTable 9.1) including soaps, detergents, temperatureextremes and irritant clothing is importantto avoid increasing severity.Topical treatmentsEmollientsThere have been no systematic reviews on emollientsin atopic eczema (Williams et al., 2008).However, there is overwhelming clinical consensusbetween dermatology health professionalsthat emollients are essential in managingeczema in acute and chronic periods. Completeemollient therapy is advocated and every topicalpreparation that goes onto the skin shouldbe emollient based with soaps and detergentsreplaced with emollient-based products suchas emollient washes, bath and shower products(Cork, 1997; NICE, 2007). For information onemollients, see Chapter 5.Topical corticosteroidsTopical corticosteroids are highly effective astreatments for inflammatory skin conditionsand a mainstay of treatment for eczema. Theyinhibit the production and action of inflammatorymediators in the skin. It is important forpatients to understand that topical corticosteroidsrelieve symptoms but do not cure eczema.The appropriate potency for the severity andextent of eczema together with the correct applicationof topical corticosteroids is essential toreducing the risk of adverse effect. Topical corticosteroidsshould be used intermittently to controlacute eczema exacerbations and reduceinflammation and itching. They are applied inconjunction with emollients but applied at a differenttime of day to avoid diluting the steroid.The British National Formulary (BNF) (BritishMedical Association and Royal PharmaceuticalSociety of Great Britain, 2009) classifiestopical corticosteroids as mild, moderatelypotent, potent or very potent. Examples of topicalcorticosteroids available for prescriptionare listed in Table 9.5; details of constituentelements, such as antimicrobials, are given inthe current BNF (British Medical Associationand Royal Pharmaceutical Society of GreatBritain, 2009).In general, potent and very potent topical corticosteroidsshould be reserved for recalcitrantdermatoses and avoided on the face and skinflexures and in children (unless prescribed by adermatology specialist). The least-potent topicalcorticosteroid that relieves symptoms shouldbe applied (British Medical Association andRoyal Pharmaceutical Society of Great Britain,2009). Mild and moderately potent topical corticosteroidsare associated with few side effects.However, particular care is required in the useof potent and very potent topical corticosteroids.As a guide, clinicians should consider thefactors outlined in Table 9.6 when prescribingtopical corticosteroids and assessing the risk ofside effects.The current recommendation is to apply topicalcorticosteroids thinly to the affected area;no more frequently than twice daily and use theleast-potent formulation which is fully effective(NICE, 2004a; BNF, 2009). We would advocatethe use of the Finger-Tip Unit (FTU) here to enablemore precise measurement of the topical steroidbeing used. Further deatils are given later.Systemic side effects are not common andoccur through skin absorption and can rarelycause adrenal suppression and Cushing’s syndrome.Absorption is likely to be greatest whereskin is thin, broken and in flexural areas. Localside effects are outlined in Box 9.2.

Eczema 165Table 9.5 Topical corticosteroids and their potencies.Potency Formulation Proprietary nameMild Hydrocortisone 0.1–2.5% Dioderm, Efcortelan, MildisonWith antimicrobials Canesten HC (e.g. miconazole), Daktacort, Econacort, Fucidin H,Nystaform-HC, Timodine, Vioform-HydrocortisoneWith crotamitonEurax-HydrocortisoneModeratelypotentFluocinolone acetonide 0.0025%eg: Clobetasone butyrate*With antimicrobialsWith ureaSynalar 1 in 10 dilutionBetnovate-RD, Eumovate*, Haelan, Modrasone, Synalar1 in 4 dilution, Ultralanum PlainTrimovateAlphaderm, Calmurid HCPotent eg: Betamethasone valerate 0.1%eg: Mometasone furoate*betamethasone valerate 0.1%, Betacap, Bettamousse,Betnovate, Cutivate, Diprosone, Elocon*, hydrocortisonebutyrate, Locoid, Locoid Crelo, Metosyn, Nerisone, SynalarWith antimicrobials Aureocort, Betnovate-C, Betnovate-N, FuciBET, Locoid C,Lotriderm, Synalar C, Synalar N, Tri-AdcortylWith salicylic acidDiprosalicVery potent eg: Clobetasol propionate* Dermovate*, Nerisone Forte, Clarelux, EtrivexSource: Adapted from the British National Formulary (March 2009). Reproduced from National Collaborating Centre for Women's and Children'sHealth, Atopic Eczema in Children: Management of atopic eczema in children from birth up to the age of 12 years. Clinical Guideline. RCOGPress; 2007. © Royal College of Obstetricians and Gynaecologists; reproduced with permission.Table 9.6 Factors to consider when prescribing topicalcorticosteroids for eczema.Factors to considerPotencyDegree of penetrationExtent of area treatedDaily volumeAge of patientPractical applicationMild – moderate, children,face and flexures. Potent –for the body. Very potent –for the soles.Occlusion will increasepotency. Ointments arebetter for penetrating dry,scaly lesions. Creams arebetter for moist, weepinglesions.Single lesion/generalisedarea.Grams per day. How longdoes a tube last?Children and the olderperson with fragile skinrequire lower potencies.Box 9.2 Potential local sideeffects from topical corticosteroids■■■■■■■■Spread and worsening of untreatedinfectionThinning of the skin, which may berestored over a period after stoppingtreatment but the original structuremay never returnIrreversible striae atrophicae andtelangiectasiaContact dermatitisPerioral dermatitisAcne, or worsening of acne or rosaceaMild depigmentation which may bereversibleHypertrichosis also reported

166 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTopical corticosteroid applicationA practical measure devised for a practicalmeasurement technique for the application oftopical corticosteroids is the Finger Tip Unit(FTU) (Long and Finlay, 1991). One FTU is theamount of cream/ointment squeezed from thetip of an adult index finger to the first crease ofthe finger tip. One FTU (approximately 500 mg)is sufficient to cover an area that is twice thatof the flat adult palm. For treating children, anadult FTU is used but the amount of FTUs arereduced depending on the age of the child (seeFigure 9.11). The use of the FTU helps patientsto understand how much topical corticosteroidto apply to ensure full therapeutic effectiveness.Current treatment guidelines recommend thattopical corticosteroids should be stepped up ordown according to severity and clinical response(NICE, 2007). Topical corticosteroids should beused to treat inflamed eczema (flare-ups), and inbetween flares, periods of using emollients onlyare advised.Treatment of atopic eczemaAlthough there is currently no cure for atopiceczema, various interventions do exist to controlsymptoms, but the effectiveness of many treatmentshas not been established (Hoare et al.,2000). Conventional treatment consists of theapplication of emollients and topical corticosteroids,both of which have been in use for over30 years (Hanifin and Rajka, 1980; Leung, 2000).NICE (2007) advocates a ‘stepped approach’ totreatment for atopic eczema in children, whichtailors the treatment steps to the severity of atopiceczema. Emollients should always form the basisof eczema treatment and used when there is novisible eczema (see Chapter 5). The use of occlusivetechniques, such as wet and dry wrapping,One adult fingertipunit (FTU)∗Number of fingertip units (FTUs)AgeFace& neckArm& handLeg& footTrunk(front)Trunk (back)inc. buttocksAdultChildren:3–6 months1–2 years2½ 4 8 7 71 1 1½11½ 1½ 2 2 31½3–5 years1½ 2 3 33½6–10 years2 2½ 4½ 3½ 5∗ One adult fingertip unit (FTU) is the amount of ointment or cream expressed from a tube witha standand 5mm diameter nozzle, applied from the distal crease to the tip of the index finger.Figure 9.11 Diagram of FTU and chart with FTUs for treating adults and children.

Eczema 167Table 9.7 Recommendations for the ‘stepped approach’to atopic eczema management.Mild atopiceczemaModerate atopiceczemaSevere atopiceczemaEmollients Emollients EmollientsMildlypotent topicalcorticosteroidsSource: NICE (2007).Moderatelypotent topicalcorticosteroidsTopicalcalcineurininhibitorsBandagesPotent topicalcorticosteroidsTopicalcalcineurininhibitorsBandagesPhototherapySystemic therapyhas been discussed in Chapter 4. The steppedapproach is summarised in Table 9.7.Other treatments include wet wraps, bandaging(damp, occlusive body bandages eitherimpregnated with a therapeutic substance orapplied over topical preparations), behaviouralmanagement and habit reversal; these have beendiscussed extensively in Chapter 4. Complementarytherapies for atopic eczema, such asmedical herbs, are embraced by guidance fromNICE (2007) which concludes that there is insufficientevidence to make recommendations forclinical practice. For more severe atopic eczema,secondary care referral for phototherapy andsystemic therapies may be employed. The followingsection discusses other treatment options foracute and severe exacerbations of atopic eczema,including complementary therapies and treatmentprovided in secondary care settings.Managing bacterial infectionAtopic eczema is frequently complicated bybacterial infection, commonly, Staphylococcusaureus, but infection with Streptococcus pyogenes(group A Streptococcus) may also occur. NICE(2007) recommends oral antibiotics. Flu cloxacillinis active against the common bac terial skin infectionsand should be the first-line treatment forStaphylococcus aureus and streptococcal infections.Erythromycin should be used if there islocal resistance to Flucloxacillin or in childrenwith a penicillin allergy. NICE (2007) recommendsthat topical antibiotics and combinationsof topical corticosteroids and antibiotics shouldonly be used short term, for no longer than 2weeks on localised areas of skin infection only.Antiseptics are useful adjunct therapies for reducingbacterial load and are added to some emollients,bath oils, soap substitutes and washes andmoisturisers. Bacterial resistance is an ongoingissue; NICE (2007) advises that health professionalsshould be aware and follow local guidelinesfor advice on patterns of bacterial resistance toantimicrobials.Managing viral infectionViral infections also occur in atopic eczema. Themost common viral infections are herpes simplexvirus (with the complication eczema herpeticum),molluscum contagiosum, viral warts (and verrucae)and varicella (chicken pox). NICE (2007)recommends the following steps for managementof eczema herpeticum: start treatment with oralAciclovir at first suspicion of eczema herpeticum.For more severe and confirmed infection intravenousAciclovir may be required.Managing fungal infections inseborrhoeic eczemaTopical antifungals such as Ketoconazole (cream/shampoo) and Terbinafine are a well-establishedtreatment, based on trial evidence (Picardo andCameli, 2008). There is limited evidence thatoral antifungals are beneficial.For cradle cap (infant seborrhoeic dermatitis),in addition to scalp being affected, thecondition may also affect other areas of thebody such as behind the ears, in the creases ofthe neck, armpits and nappy area. It is treatedby regular use of mild baby shampoos and theuse of oil to soften the scales, avoiding olive oilwhich exacerbates the growth of the Malasseziayeast. If this is unsuccessful or the rash spreadsmore extensively, inflamed areas may require amedicated shampoo containing ketoconazoleand hydrocortisone cream.

168 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTopical calcineurin inhibitorsTopical calcineurin inhibitors are immunomodulatorytreatments, which help modulate theimmune system to reduce inflammation. Cal cineurinis a protein phosphatase 2B responsible foractivating the transcription of interleukin 2 (IL-2),which stimulates the growth and differentiationof T-cell response inhibitors (Hultsch et al.,2005); these are non-steroid drugs. Tacrolimus(Protopic ® ) and pimecrolimus (Elidel ® ) are theavailable topical immunosuppressant agentswhich may be used as alternative to (topical) steroidstopical for eczema. Tacrolimus (Protopic ® )for moderate to severe atopic eczema in patients 2years of age and above, which is not adequatelyresponding to conventional therapies such as topicalcorticosteroids (Electronic MedicinesCompendium [EMC], 2009a). Pimecrolimus(Elidel ® ) is indicated for treatment of patientsaged 2 years and over, with mild or moderateatopic dermatitis where treatment with topicalcorticosteroids is either inadvisable or not possible(EMC, 2009). NICE recommends that topicalcalcineurin inhibitors should not be used to treatmild atopic eczema or as ‘first-line’ treatments(NICE, 2004b). Tacrolimus has also now beenlicensed in the UK for intermittent use.Sedating antihistaminesSedating antihistamines in conjunction with othertherapies may help to reduce itching at night, it isthe sedating effect that is useful as eczema is nota histamine releasing condition. Paste bandagingand wet wrapping are helpful at night to preventdamage from scratching, reduce itch and help healthe skin (see Chapter 4). Behavioural approachessuch as habit reversal techniques can also be usefulin chronic atopic eczema.Behavioural management: habit reversalBehavioural management, incorporating habitreversal, for the control of damaging itchingbehaviour has been addressed in Chapter 4.Secondary care options: phototherapy and oralimmunosuppressantsPatients with moderate to severe eczema who areunresponsive to topical therapies in primary careshould be referred to secondary care. Phototherapyand other systemic treatments in children shouldonly be initiated after assessment and documentationof disease severity and assessment ofquality of life (NICE, 2007). The Primary CareDermatology Society and the British Associationof Dermatologists (PCDS and BAD) have developedreferral guidelines for all patients with atopiceczema which are outlined in Box 9.3 (PrimaryCare Dermatology Society and British Associationof Dermatologists, 2006).Patients with severe eczema should be referredto secondary care for phototherapy and systemictherapies.PhototherapyPhototherapy has an immunosuppressive actionon the skin and has a particular effect on blockingantigen-presenting Langerhans cells, alteringBox 9.3 PCDS–BAD (2006) –Referral guidelines for atopiceczemaDiagnostic doubtSevere eczema■ Failure to respond to appropriatetherapy in primary care■ Eczema not satisfactorily controlled inprimary careSevere infected eczema■ Bacterial infection■ Eczema herpeticum■ Specialist opinion for counselling patientsand families with severe socialor psychological problems related toeczema.■ Additional advice on treatment application.■ Patch testing for suspected contact dermatitis.■ Consideration for dietary manipulation.

Eczema 169eosinophil functions and altering production ofcytokines by keratinocytes (Hoare et al., 2000).Narrowband UVB (TL01) is the most commonform of phototherapy used to treat skindiseases. Narrowband refers to a specific wavelengthof ultraviolet (UV) radiation, 311–312 nm. PUVA or photochemotherapy is usedfor more severe eczema and involves a combinationtreatment that consists of psoralens (P) andthen exposing the skin to UVA (long-wave ultravioletradiation). Psoralens are compoundsfound in many plants which make the skin temporarilysensitive to UVA. Medicinal psoralensinclude methoxsalen (8-methoxypsoralen), 5-methoxypsoralen and trisoralen. Eye protectionis required; 24 hours post-oral administration ofpsoralens. Psoralens can also be applied topicallyin a bath soak or as lotion for small areas(hands and feet). The amount of UV is carefullymonitored for side effects and especially degreesof erythema and burning. A number of protocolsexist depending on the individual’s skintype, age, skin condition and other factors.Patients will generally attend hospital 2–3 timesa week for stepped administration of phototherapy(Hoare et al., 2000).Oral immunosuppressant therapiesOral immunosuppressant treatments have beenshown to be effective for severe recalcitrant casesof eczema. They act by reducing inflammationand affecting lymphocytes. The only licensedoral therapy for atopic eczema is ciclosporin, animmune suppressant drug which is also used toprevent transplant rejection. In atopic eczema,ciclosporin is indicated for the short-term treatment(8 weeks) of patients with severe atopiceczema in whom conventional therapy is ineffectiveor inappropriate. The normal dosage is 2.5–5 mg/kg/day given orally in two divided dosesfor a maximum of 8 weeks. Ciclosporin requirescareful monitoring due to side effects; monitoringshould be shared between primary and secondarycare and involves the following:■Blood pressure should be measured oncetotwice-weekly for the first month, thenmonthly thereafter.■■Kidney function should be tested by bloodand urine tests, especially creatinine levels.Other regular tests should include: completeblood count, liver function, fasting lipidlevels, uric acid.Ciclosporin can impair renal and liverfunction. Close monitoring of serum creatinineand urea is required and dosage adjustment maybe necessary. Increases in serum creatinineand urea occurring during the first few weeks ofciclosporin therapy are generally dose-dependentand reversible and usually respond to dosagereduction. Apart from a reduction in renal function,other side effects include hypertension, hirsutism,loss of appetite and nausea, paraesthesia,tremor, sensitive and bleeding gums and anincreased risk of infection. Ciclosporin can alsoincrease the risk of developing skin cancer, inparticular basal cell and squamous cell carcinoma.The increased risk of developing malignanciesand lymphoproliferative disorders(including lymphomas), some with reportedfatalities, appears to be related to the degree andduration of immunosuppression (ElectronicMedicines Compendium, 2009b).Other immunosuppressant agents used insevere atopic eczema are prescribed ‘off licence’and include: Azathioprine (a thiopurine analoguedrug that suppresses the immune systemby altering white blood cell function), oral systemiccorticosteroids, interferon gamma andintravenous immunoglobulin.Complementary therapiesNICE (2007) outlines that 60% of children withatopic eczema have tried complementary therapies.However, to date, there is limited evidenceof the effectiveness of complementary therapies inatopic eczema, as in the case of medicinal herbs(Sheenan and Atherton, 1994). The NationalEczema Society advises patients with eczema,who wish to try a complementary therapy, to goto a properly trained and registered practitioner,always let your health care professional knowabout the complementary therapy and not tosuddenly stop using prescribed eczema treatments(National Eczema Society, 2009).

170 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsSafety can also be an important issue.Complementary products sold as ‘natural’may have added synthetic ingredients; anexample being the addition of steroids withinmedicinal herbs (Graham-Brown et al., 1994).Furthermore, it cannot always be assumed thatnatural is safe. An investigation into fraudulentpractice with unregistered complementarytherapies revealed the addition of potent corticosteroids(All Party Parliamentary Group onSkin [APPGS], 1999). The sound recommendationsfrom NICE (2007) include informingpatients on the problems of fraudulent practiceand for patients to inform their health careprofessional.Treatment options for other formsof eczemaTreatment options for other forms of eczema aresummarised in Table 9.8.Behavioural treatments for eczema:psychological support and educationalinterventionEducational and psychological interventions areinvariably provided in conjunction with conventionaltherapy. Such interventions may bedirected towards adults or the parent or childTable 9.8 Treatment options for other forms of eczema.TypeTreatment optionsIrritant dermatitisContact allergicdermatitisSeborrhoeic dermatitisJuvenile plantardermatosesDiscoid eczemaLichensimplex/neurodermatitisPompholyxAsteatotic eczemaVaricose eczemaAvoidance of the irritating factor(s), liberal use of emollients and topical corticosteroids toreduce inflammation. Napkin rash can be a type of irritant contact dermatitis. Barrierproducts for treating napkin rash often contain zinc oxide, which has soothing and protectiveproperties.Topical corticosteroids are used to treat both irritant and allergic contact dermatitis. Oralantibiotics should be prescribed if there are visible signs of infection. Contact dermatitis isconsidered widespread when greater than 25% of the body is affected and the cause isknown and avoidable in future. In adults, oral prednisolone can be prescribed for 2–3 weeks,in reducing doses, when the cause is known and is avoidable in the future.Seborrhoeic dermatitis will require treatment with an antifungal cream for secondary candidalinfection. A mild steroid can also be used for up to 1 week to treat inflammation. Antifungalpreparations combined with topical corticosteroids are the first-line treatment for adults withseborrhoeic dermatitis.Emollients should be applied liberally, occlusive dressings for deep fissures and potent topicalcorticosteroids for inflammation. Wearing of trainers should be discouraged.Treatment is with emollients and potent or very potent topical corticosteroids.Patches of lichen simplex or neurodermatitis are treated with topical steroids under occlusion,to prevent habitual scratching and rubbing.Treatment is with emollients and potent topical corticosteroids. Sedating antihistamines maybe required at night as this condition produces intense itch and irritation (Figure 9.12).Treatment with emollients; humectants emollients with anti-itch properties may be helpful.Topical corticosteroids will be indicated for reducing mild erythema.Treatment is with emollients and topical corticosteroids (use ointment preparations). Patchtesting may be indicated, should contact dermatitis be suspected. Paste bandages may beapplied during the acute period. Compression (support) stockings are indicted for chronicperiods and long-term prevention. Concordance with compression therapy, leg elevation andankle movement are also important (Brooks et al., 2004).Source: Reproduced from National Collaborating Centre for Women's and Children's Health, Atopic Eczema in Children: Management ofatopic eczema in children from birth up to the age of 12 years. Clinical Guideline. RCOG Press; 2007. © Royal College of Obstetricians andGynaecologists; reproduced with permission.

Eczema 171Figure 9.12 Pompholyx. (Source: Reprinted from Buxtonand Morris-Jones, 2009.)with eczema, with parents tending to be the primaryfocus of the educational approaches andchildren the main target of psychological interventions.This section builds on principles fromChapter 7 but applies and extends them to thefield of eczema, addressing and largely focusingon key issues such as education and support forparents of children with atopic eczema. Suchinterventions provide considerable scope tonursing staff to approach the assessment andmanagement of educational and support needsin a systematic way.The importance of education, as a basis forimproving adherence to treatment, is highlightedin the NICE (2007) guidance on atopic eczema inchildren. It highlights the importance of educatingboth child and parent or carer and reinforcedat every consultation, both in written and verbalforms, with practical demonstrations covering:■■■■how much treatment to use,how often to apply treatments,when and how to step treatments up anddown andhow to treat infected atopic eczemaSuch interventions may be illustrated with theapplication to children, as in the case of atopiceczema. The suitability of the intervention willdepend on the age and developmental stage ofthe child and, therefore, the child’s ability toparticipate effectively in an educational and psychologicalintervention will vary.Since atopic eczema affects children and can bedisabling for whole families, it is generally agreedthat psychological support and education of theparent/carer are a crucial component of diseasemanagement. Little is known, however, of themeasurable effects of such interventions and themost recent systematic review of the treatmentsfor atopic eczema to date (Hoare et al., 2000),which found only limited evidence to supportpsychological treatments or educational interventions,although more recent evidence has beenfound of the value of some planned educationalapproaches (Ersser et al., 2007). Psychologicalinterventions are being incorporated into managementstrategies to reduce scratching behavioursthat exacerbate eczema (Horne et al., 1989;Giannini, 1997). Despite the fact that parentsare the primary carers for children with atopiceczema, very limited attention has been given tothe psychological support of parents (by educationalor psychological intervention). As such,the caregiver’s ability to manage their child’seczema is an important outcome and thereforethe educational or psychological supportgiven to parents is required. It could be arguedthat the general case for psychosocial interventionto improve clinical outcomes in chronicorganic disease such as eczema is establishedand in related areas such as asthma (Guevaraet al., 2003).The literature refers to a range of psychologicalinterventions that have been used inatopic eczema, such as behavioural management(Noren 1995; Bridgett et al., 1996) andcognitive behavioural therapy (Ehlers et al.,1995). Clinical observations suggest that behaviouraltechniques can be a useful adjunct totopical therapy and breaking the itch–scratchcycle is argued to be a primary clinical aim(Hagermark and Wahlgren, 1995). However,evaluative research has been limited (Simpson-Dent et al., 1999; Bridgett, 2000), especiallywith children.Educational interventions to supporteczema managementEducational interventions have also been usedto bring about behavioural change through

172 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalshealth/patient education or patient teaching forthose with eczema (Niebel et al., 2000). Theseare important since chronic disease managementrequires a degree of self-management (or caregiver/parentalsupport) and therefore educationand behavioural change (Holman and Lorig,2000). A limited number of evaluative studieshave examined the impact of parental educationon the management of children with atopiceczema (e.g. Niebel et al., 2000), although somestudies have examined the impact of educationon adults with eczema; these studies areinformative (e.g. Ehlers et al., 1995). The basisfor education is highlighted throughout thisbook, highlighting, for example, key aspects ofChapter 5 on emollient therapy, understandingtreatments for eczema – as outlined in this chapterand developing strategies to help patientsmake the most of their treatment (Chapter 7).These emphasise the need to involve the patientin education, assess educational need systematicallyand provide education in a plannedmanner.A recent systematic review has been undertakento examine the effectiveness of educationaland psychological interventions in changing outcomesfor children with atopic eczema (Ersseret al., 2007). This review was published at thetime of the production of the NICE (2007) guidanceon atopic eczema in children, but providesa more extensive account of the evidence available,information on the typical service deliverymodels in use and an extensive critique of theevidence available.Up to this stage the most recent systematicreview of the treatments for atopic eczema wasa generic review of treatments for atopic eczema(Hoare et al., 2000). Ersser et al.’s Cochranereview identified that such interventions havebeen used as an adjunct to conventional therapyfor children with atopic eczema to enhancethe effectiveness of topical therapy. The selectioncriteria for the review included randomisedcontrolled trials (RCTs) of such interventionsused to manage children with atopic eczema.Eligibility to enter the trail, assess trial qualityand extract data was independently assessed bytwo reviewers and revealed a limited number ofstudies that met the quality criteria for inclusion(n 5) and a lack of comparable data preventeddata synthesis. Some included that studiesrequired clearer reporting of trial procedures.Rigorous established outcome measures werenot always used.The main results are that five studies (RCTs)met the inclusion criteria; all interventions wereadjuncts to conventional therapy, four relatedto educational intervention (Niebel et al., 2000;Chinn et al., 2002; Staab et al., 2002, 2006).Four focused on intervention directed towardsthe parents; data synthesis was not possible.Psychological interventions remain virtuallyunevaluated by studies of robust design; the onlyincluded study (Sokel et al., 1993) examined theeffect of relaxation techniques (hypnotherapyand biofeedback) on severity. Some educationalstudies identified significant improvements indisease severity between intervention groups.The largest trial to date, conducted in Germany(Staab et al., 2006) evaluated long-term outcomesand found significant improvements inboth disease severity at 1 year (3 months to 7years, p 0.0002; 8–12 years, p 0.003; 13–18years, p 0.0001) and parental quality of life(3 months to 7 years, p 0.0001; 8–12 years,p 0.002), for children with atopic eczema.One study by Niebel et al. (2002) found thatvideo-based education was more effective inimproving severity than direct education andthe control (discussion) (p < 0.001). The singlepsychological study found that relaxation techniquesimproved clinical severity as compared tothe control at 20 weeks (t 2.13) but of borderlinesignificance (p 0.042) (Sokel et al., 1993).In conclusion, the lack of rigorously designedtrials (excluding the study by Staab et al., 2006)provides only limited evidence of the effectivenessof educational and psychological interventions inhelping to manage the condition of children withatopic eczema. Evidence from included and adultstudies (e.g. Ehlers et al., 1995; Gradwell et al.,2002) indicated that different service deliverymodels were in operation, including multiprofessionaleczema schools, which were more commonin countries such as Germany and the nurse-ledclinic model, which was utilised in the UK.These different models of service delivery requirefurther and comparative evaluation to examine

Eczema 173their cost-effectiveness and suitability for differenthealth systems.Drawing on these two reviews there areindications that there may be considerable scopefor developing nurse-led dermatology services,especially targeted at groups such as those withatopic eczema requiring educational support.Indeed the National Eczema Society has issuedguidance on developing such clinics (Penzer,2003). The systematic review by Hoare et al.(2000) of treatments for atopic eczema identifiedthe role of specialist nurses as an urgent researchpriority. An important feature in the developmentof dermatology services over recent years hasbeen the expansion of nurse-led services. Evidencefrom a survey conducted of BAD consultants forthe BAD Therapy Guidelines and Audit Committeehas indicated that there has been a majorexpansion of nurse-led services in Britain; 69%(n 183) of consultants had nurse-led clinics,which they anticipated to rise by 91% (Cox,1999); although more recent data is limited inproving new information, the anecdotal evidenceon the UK suggests that these have expandedconsiderably. These developments are consistentwith government nursing strategy to identifywhere the nursing service can expand its role andenhance its contribution to service delivery wherehealth needs are inadequately or poorly addressed(Department of Health, 2000, 2008). Indeed, theNHS plan policy document highlights nurse-ledclinics in dermatology as one of ‘10 key roles fornurses’ in the new NHS (Department of Health2000, p. 83). Despite the rapid expansion of dermatologyservices over recent years, the evaluationprogramme for the expansion of theseservices has fallen behind, especially in settingssuch as dermatology. There is also limited knowledgeof the precise nature of many of these servicesand their therapeutic impact.ConclusionThis chapter has outlined the nature of eczemaand its management. This includes a summaryof its clinical signs, differential diagnosis and itsdifferent variants, with reference to its impacton people and their families. This is accompaniedby an evidence-based summary of the keytreatments and management strategies to controleczema, highlighting the nursing contribution,especially in otherwise neglected areas suchas education and behavioural management. Theholistic measurement of eczema is also included,as a basis for more rigorous assessment andevaluation.ReferencesAll Party Parliamentary Group on Skin (1999).Report on the enquiry into fraudulentpractice in the treatment of skin disease.London: All Party Parliamentary Group onSkin, Portcullis.Asher, M.I., S. Montefort et al. (2006).Worldwide time trends in the prevalenceof symptoms of asthma, allergicrhinoconjunctivitis, and eczema in childhood:ISAAC Phase One and Three repeatmulticountry cross-sectional surveys. TheLancet, 368: 733–743.Ben-Gashir, M.A., P.T. Seed et al. (2004).Quality of life and disease severity arecorrelated in children with atopic dermatitis.British Journal of Dermatology, 150(2):284–290.Boguniewicz, M., N. Nicol et al. (2008).A multidisciplinary approach to evaluationand treatment of atopic dermatitis. Seminarsin Cutaneous Medicine and Surgery, 27:115–127.Bourke, J., I. Coulson et al. (2001). Guidelinesfor the care of contact dermatitis. BritishJournal of Dermatology, 145(6): 877–885.Bridgett, C. (2000). Psychodermatology andatopic skin disease in London 1989–1999 –helping patients to help themselves.Dermatology and Psychosomatics/Dermatologie und Psychosomatik, 1(4):183–186.Bridgett, C., P. Noren et al. (1996). AtopicSkin Disease: A Manual for Practitioners.Petersfiled: Wrightson Biomedical PublishingLimited.

174 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBritish Medical Association and RoyalPharmaceutical Society of Great Britain(2009). British National Formulary. London,British Medical Journal Publishing GroupLtd and The Royal Pharmaceutical Society ofGreat Britain.Brooks, J., S.J. Ersser et al. (2004). Nurselededucation sets out to improve patientconcordance and prevent recurrence ofleg ulcers. Journal of Wound Care, 13(3):111–116.Burns, T., S. Breathnagh et al. (2004). Rook’sTextbook of Dermatology. Oxford: BlackwellPublishing Ltd.Buske-Kirschbaum, A., A. Geiben et al.(2001). Psychobiological aspects of atopicdermatitis: An overview. Psychotherapy andPsychosomatics, 70: 6–16.Buske-Kirschbaum, A., A. Gierens et al.(2002). Stress-induced immunomodulationis altered in patients with atopic dermatitis.Journal of Neuroimmunology, 129:161–167.Buxton, P.K. and R. Morris-Jones, Eds.(2009). ABC of Dermatology (5th edition).Chichester: Wiley-Blackwell and BMJBooks.Chinn, D.J., T. Poyner et al. (2002).Randomized controlled trial of a singledermatology nurse consultation in primarycare on the quality of life of childrenwith atopic eczema. British Journal ofDermatology, 146(3): 432–439.Cork, M.J. (1997). The importance of skinbarrier function. Journal of DermatologicalTreatments, 8: S7–S13.Cork, M.J. (1999). Taking the itch out ofeczema: How the careful use of emollients canbreak the itch–scratch cycle of atopic eczema.The Asthma Journal, 4: 116–120.Cork, M.J., D.A. Robinson et al. (2006). Newperspectives on epidermal barrier dysfunctionin atopic dermatitis: Gene–environmentinteractions. Journal of Allergy and ClinicalImmunology, 118: 3–21.Cox, N.H. (1999). The expanding role ofnurses in surgery and prescribing in Britishdepartments of dermatology. British Journalof Dermatology, 140(4): 681–684.Cox, N.H. and C.M. Lawrence (1998).Diagnostic Problems in Dermatology.London: Mosby.Department of Health (2000). The NHS Plan:A plan for investment, a plan for reform.London: Department of Health, Crown.Department of Health (2008). Framing theNursing and Midwifery Contribution:Driving up the quality of care, pp. 1–21.London: Department of Health, Crown.DermNetNZ. (2009). Photocontact dermatitis.Retrieved 6 May 2009, from http://www.dermnetnz.org/reactions/photocontactdermatitis.html.Ehlers, A., U. Gieler et al. (1995). Treatmentof atopic dermatitis: A comparison ofpsychological and dermatological approachesto relapse prevention. Journal of Consulting& Clinical Psychology 63(4): 624–635.Electronic Medicines Compendium. (2009a).Summary of product characteristics (SPC)for Protopic 0.03% and Protopic 0.1%.,from http://emc.medicines.org.uk/document.aspx?documentId8884.Electronic Medicines Compendium. (2009b).Summary of product characteristics (SPC)for Neoral soft gelatine capsules andneural oral solution. Retrieved 14 April2009, from http://emc.medicines.org.uk/document.aspx?documentId4106 andhttp://emc.medicines.org.uk/document.aspx?documentid1307.Elliott, B.E. and K. Luker (1997). Theexperiences of mothers caring for a childwith severe atopic eczema. Journal of ClinicalNursing, 6: 214–217.English, J. (1999). A Colour Handbook ofOccupational Dermatology. London: MansonPublishing.Ersser, S.J., S. Latter et al. (2007). Psychologicaland educational interventions for atopiceczema in children – Description. CochraneDatabase of Systematic Reviews, 3:CD004054 (DOI: 10.1002/14651858.CD004054.pub2).Fennessy, M., S. Coupland et al. (2000). Theepidemiology and experience of atopiceczema during childhood: A discussion paperon the implications of current knowledge for

Eczema 175health care, public health policy and research.Journal of Epidemiology and CommunityHealth, 54(8): 581–589.Giannini, A.V. (1997). Habit reversal techniqueand eczema. Journal of Allergy and ClinicalImmunology, 100(4): 580.Gradwell, C., K.S. Thomas et al. (2002). Arandomized controlled trial of nurse followupclinics: Do they help patients and do theyfree up consultants’ time? British Journal ofDermatology, 147: 513–517.Graham-Brown, R. and T. Burns (2006).Lecture Notes: Dermatology (9th edition).Oxford: Blackwell Publishing.Graham-Brown, R.A.C., J.F. Bourke et al. (1994).Letters: Chinese herbal remedies may containsteroids. British Medical Journal, 308: 473.Guevara, J.P., J.P. Wolf et al. (2003). Effects ofinterventions for self management of asthmain children and adolescents: Systematic reviewand meta analysis. British Medical Journal,326: 1308–1309.Hagermark, O. and C.F. Wahlgren (1995).Treatment of itch. Seminars in Dermatology,14(4): 320–325.Hanifin, J.M. and G. Rajka (1980). Diagnosticfeatures of atopic dermatitis. Acta DermatoVenereologica (Stockholm), 92: 44–47.Herd, R.M. (2000). The morbidity and cost ofatopic dermatitis. In: Williams, H.C. (Ed.),Atopic Dermatitis, pp. 85–95. Cambridge:Cambridge University Press.Herd, R., M.J. Tidman et al. (1996). Prevalenceof atopic eczema in the community: TheLothian atopic dermatitis study. BritishJournal of Dermatology, 135: 18–19.Hoare, C., A. Li Wan Po and H. Williams(2000). Systematic review of treatmentsfor atopic eczema. Health TechnologyAssessment, 4: 1–19.Holman, H. and K. Lorig (2000). Patientsas partners in managing chronic disease –Partnership is a prerequisite for effective andefficient health care. British Medical Journal,320(7234): 526–527.Horne, D.J.D., A.E. White et al. (1989). Apreliminary study of psychological therapyin the management of atopic eczema. BritishJournal of Medical Psychology, 62: 241–248.Hultsch, T., A. Kapp et al. (2005).Immunomodulation and safety of topicalcalcineurin inhibitors for the treatmentof atopic dermatitis. Dermatology, 211:174–187.Kemp, A.S. (2003). Cost of illness of atopicdermatitis in children: a societal perspective.Pharmacoeconomics, 21: 105–113.Leung, D.Y.M. (2000). Atopic dermatitis: Newinsights and opportunities for therapeuticintervention. Journal of Allergy and ClinicalImmunology, 5(105): 860–876.Lewis-Jones, M.S. and A.Y. Finlay (1995). Thechildren’s dermatology life quality index(CDLQI): Initial validation and practicaluse. British Journal of Dermatology, 132:942–949.Lewis-Jones, M.S., A.Y. Finlay et al. (2001).The infants’ dermatitis quality of life index.British Journal of Dermatology, 144:104–110.Lifschitz, C. (2008). Is there a consensus in foodallergy management. Journal of PaediatricGastroenterology Nutrition, 47(Suppl 2):S58–S59.Long, C.C. and A.Y. Finlay (1991). The fingertipunit – a new practical measure. Clinicaland Experimental Dermatology, 16(6):444–447.McFadden, J.P., W.C. Noble et al. (1993).Superantigenic exotoxin-secretingpotential of staphylococci isolated fromatopic eczematous skin. British Journal ofDermatology, 128: 631–632.McNally, N.J., H.C. Williams et al. (2001). Atopiceczema and the home environment. BritishJournal of Dermatology, 145(5): 730–736.National Eczema Society (2009). Frequentlyasked questions on eczema: What aboutcomplementary therapies? from http://www.eczema.org/faq.php?actcli.faq_view&id_faq15&id_domain0&question&sql_indx1&faq_indx6.National Institute for Health and ClinicalExcellence (NICE) (2004a). Frequency ofapplication of topical corticosteroids foratopic eczema, 34p. London: NationalInstitute for Health and Clinical Excellence(NICE).

176 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsNational Institute for Health and ClinicalExcellence (NICE) (2004b). Tacrolimus andprimecrolimus for atopic eczema. London:NICE.National Institute for Health and ClinicalExcellence (NICE) (2007). Atopic eczema inchildren: Management of atopic eczemain children from birth up to the age of 12years, from http://www.ncc-wch.org.uk/index.asp?PageID359.Nicol, N.H. and M. Boguniewicz (2008).Successful strategies in atopic dermatitismanagement. Dermatology NursingSupplement: 1–19.Niebel, G., C. Kallweit et al. (2000). Directversus video-based parental educationin the treatment of atopic eczema inchildren. A controlled pilot study [Direkteversus videovermittelte Elternschulungbei atopischem Ekzem im Kindesalter alsErganzung facharztlicher Behandlung. EineKontrollierte Pilotstudie]. Hautarzt, 51:401–411.Noren, P. (1995). Habit reversal – a turningpoint in the treatment of atopic dermatitis.Clinical and Experimental Dermatology,20(1): 2–5.Palmer, C.N., A.D. Irvine et al. (2006).Common loss-of-function variants of theepidermal barrier protein filaggrin area major predisposing factor for atopicdermatitis. Nature Genetics, 38:441–446.Penzer, R. (2003). How to set up an eczemaclinic in primary care. London: NationalEczema Society.Picardo, M. and N. Cameli (2008). Seborrheicdermatitis. In: Williams, H.C., Bigby, M.,Diepgen, T. et al. (Eds), Evidence-basedDermatology, pp. 164–170. Oxford:Blackwell Publishing/BMJ Books.Primary Care Dermatology Society and BritishAssociation of Dermatologists (2006).Guidance for the management of atopiceczema: ECDS & BAD, from http://www.eGuidelines.co.uk/skin, 28: 372–375.Radcliffe, J. (1998). How to … conduct apatch test. British Journal of DermatologicalNursing, 2(4): 8–9.Reid, P. and M.S. Lewis-Jones (1995). Sleepdisturbances and their management inpre-schoolers with atopic eczema. ClinicalExperimental Dermatology, 20: 38–41.Sheenan, M.P. and D.J. Atherton (1994). Oneyear follow-up of children treated withChinese medicinal herbs for atopic eczema.British Journal of Dermatology, 130:488–493.Simpson-Dent, S.L., R.C.D. Staughton et al.(1999). The combined approach to chronicatopic eczema. A prospective comparisonof behavioural modification with standarddermatological treatment against standardtreatment alone. Paris: Proceedings of theInternational Congress of DermatologicalPsychiatry.Sokel, B., D. Christie et al. (1993). Acomparison of hypnotherapy and biofeedbackin the treatment of childhood atopic eczema.Contemporary Hypnosis, 10(3): 145–154.Staab, D., U. von Rueden et al. (2002).Evaluation of a parental training programfor the management of atopic dermatitis.Pediatric Allergy and Immunology, 13: 84–90.Staab, D., T.L. Diepgen et al. (2006). Agerelated, structured educational programmesfor the management of atopic dermatitisin children and adolescents: Multicentre,randomised controlled trial. British MedicalJournal, 332: 933–938.Strachan, D.P. (1989). Hayfever, hygiene andhousehold size. British Medical Journal, 299:1259–1290.Surridge, H.R. (2005). Exploring parental needsand knowledge when caring for a child witheczema. Patient Magazine of the NationalEczema Society.Szakos, E., G. Lakos et al. (2004). Relationshipbetween skin bacterial colonization and theoccurrence of allergen-specific and nonallergen-specificantibodies in sera of childrenwith atopic eczema/dermatitis syndrome. ActaDermato-Venereologica, 84(1): 32–36.Taal, E., E. Rasker et al. (1993). Health status,adherence with health recommendations,self-efficacy and social support in patientswith rheumatoid arthritis. Patient EducationCounseling, 20: 63–76.

Eczema 177Thomas, K., F. Bath-Hextall et al. (2008).Atopic eczema. In: Williams, H.C., Bigby,M., Diepgen, T. et al. (Eds), Evidence-basedDermatology. Oxford: Blackwell PublishingLtd.Verboom, P., L. Hakkaart-Van et al. (2002). Thecost of atopic dermatitis in the Netherlands:An international comparison. British Journalof Dermatology, 147(4): 716–724.Weller, R., J.A.A. Hunter, J. Savin and M. Dahl(2008). Clinical Dermatology (4th edition).Oxford: Blackwell Publishing Ltd.Williams, H.C. (1992). Is the prevalenceof atopic dermatitis increasing? Clinicaland Experimental Dermatology, 17(6):385–391.Williams, H.C. (1995). Atopic eczema – whywe should look at the environment. BritishMedical Journal, 311: 1241–1242.Williams, H.C. (1997). Dermatology: HealthCare Needs Assessment. Oxford: RadcliffeMedical Press.Williams, H., H. Forsdyke et al. (1995). Aprotocol for recording the sign of visibleflexural dermatitis. British Journal ofDermatology, 133: 941–949.Williams, H., M. Bigby et al. (2008). EvidencebasedDermatology. Oxford: BMJ Books,Blackwell Publishing.


10AcneRebecca PenzerIntroductionAcne is a condition of the pilosebaceous gland.Mild acne affects the majority of teenagers atsome point, but in one study only 14% of girlsand 9% of boys actually consulted their GPand of these 0.3% were referred to see a dermatologist(Rademaker et al., 1989). However,acne is not just a condition affecting teenagers,it can persist into adult years and for a numberof people it appears for the first time after teenageyears are left well behind. There are alsoinstances in which babies show signs of acnetypelesions (Cunliffe et al., 2001). Acne is acondition which can be effectively treated. Inorder to make the most of the treatments available,it is helpful for nurses to understand theunderlying pathology of the condition. Thereare a range of treatments available; however,patients need support to ensure that they areused appropriately and effectively.What is acne?Acne is a hormonally driven condition whichaffects the pilosebaceous gland. Sebaceousglands are found on most parts of the humanbody except for the palms of the hands and thesoles and dorsum of the feet. They are foundpredominantly on the face and scalp, but alsoexist in relatively large numbers on the chestand back. This explains the tendency for acneto appear in these areas. There is considerablevariability in the size of the glands bothbetween individuals and on different anatomicalsites on any single individual. Acne lesionsand severity assessment have been introducedin Chapter 3.The sebaceous glands respond to circulatingandrogens by producing sebum. In acne, sebumproduction is increased either because the sebaceousgland becomes overly sensitive to circulatingandrogens or because the levels of circulatingandrogens are particularly high (O’Connell andWesthoff, 2008). Testosterone is the primaryandrogen associated with acne. It is producedin the adrenal glands, the ovaries in women andtestes in men. Whilst generally thought of as amale hormone, testosterone is present in bothmales and females and becomes an importantfactor at puberty when the reproductive organsbecome active.There are four key processes which occur toproduce acne lesions.

180 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals(1) Increased production of sebum;(2) Hyperkeratinisation within the hair follicleleading to follicular plugging;(3) Increased bacterial activity within the follicleas there is enhanced colonisation withPropionibacterium acnes;(4) Release of inflammatory mediators (e.g.cytokines, tumour necrosis factor) into thefollicle and surrounding dermis causingincreased inflammation (Figure 10.1).Each of these four processes will now be consideredin turn.Increased sebum productionThe response of the body to increased circulatingandrogens (which generally begins tooccur at 7–8 years of age) is twofold. Firstly,the androgens drive changes in both sebocytesand follicular keratinocytes which leadto microcomedone formation. Microcomedonesare non-inflammatory lesions whichare considered the first lesions of acne, i.e.both inflammatory and non-inflammatory acnelesions are preceded by a microcomedone(Gollnick et al., 2003). Secondly, the androgenslead to an increase in sebum production(Gollnick et al., 2003).Sebum is made up of lipids (triglycerides,waxes, free fatty acids and squalene) and thedebris of dead fat-producing cells. As a substancein itself, it is odour free; however, bacterial activityon the sebum does produce a distinctiveodour known as body odour. Its purpose is towaterproof the skin and protect it from becomingdry and brittle. Sebum has the unique abilityto support the growth of the bacteria P. acnesand as such acne cannot occur without the presenceof sebum (Thiboutot, 2008). If the amountof sebum produced can be reduced, there is aconsequent decrease in P. acnes (Leyden andMcGinley, 1993). This mechanism is discussedHyperkeratosisThe ‘comedo’Sebum‘Zit’ or ‘pimple’AndrogenP. acnesLeakageRuptureAcute inflammatory responseFigure 10.1 Acne pathogenesis. (Source: Reprinted from Graham-Brown and Burns, 2006.)

Acne 181further in the section on treatments. It seemsthat the highest density of P. acnes is found inareas most rich in sebaceous glands (Leyden andMcGinley, 1993).Follicular pluggingIn a normal follicle, the keratinocytes are shedas single cells into the follicular channel andthen excreted. It is not fully understood whatstimulates the hyperkeratinisation in which thedead keratinocytes remain adherent in the follicularchannel leading to blockage, which canbe either partial or complete. However, initiallythese blockages lead to small virtually invisiblechanges which are the microcomedones.They may take up to 2–3 years before theyproceed into more significant acne lesions. Asthe microcomedone gets bigger and the swellingincreases behind the blockage, comedonesdevelop. These are always the precursor lesionsto acne.Comedones can either be open or closed.Open comedones (otherwise known as blackheads)are where the blockage of the follicleis high up and contents of the follicle arepushed through the follicle opening, thus beingexposed to the air. The black colour of blackheadsis not caused by dirt, although thereappears to be disagreement about its origins.Texts vary, with some saying it is due to thepresence of melanin (Ashton and Leppard,2005), others to the way that light is reflectedof the tightly compacted horny cells (Leydenand McGinley, 1993) and yet others statingit is caused by the oxidising effect of the airon the contents of the comedone (O’Toole,1997) (Figure 10.2). Closed comedones (otherwiseknown as whiteheads) do not have theircontents exposed to the air as the blockage isfurther down the hair follicle. Blackheads andwhiteheads are the non-inflammatory stage ofacne (Figure 10.3). Acne can resolve spontaneouslyat this stage never progressing to theinflammatory form of the disease. The blockagewithin the follicle allows for a build up ofsebum which becomes the ideal environment forP. acnes to proliferate.Figure 10.2 Open comedones. (Source: Reprinted fromWeller et al., 2008.)Figure 10.3 Acne with comedones. (Source: Reprintedfrom Buxton and Morris-Jones, 2009.)Increased bacterial activity andresulting inflammationEven where there is no evidence of active acne,P. acnes exists on the skin surface; indeed, theredoes not seem to be any correlation between the

182 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalslevels of P. acnes on the skin surface and severityof acne. However, some aspect of the hairfollicle itself and the microenvironment foundthere causes P. acnes to proliferate and colonisethe hair follicle leading to inflammation. Theintensity of the inflammation varies dependingon the individual which may, in part, be due tothe individual’s sensitivity to the inflammatorymediators associated with P. acnes. Althoughthe mechanisms are not fully understood, it isthought that the action of the proliferating bacteriacauses release of inflammatory cytokines,primarily CD4 + T-lymphocytes. Initially, papulesand pustules are seen. Pustules form the typicalyellow spot of acne. Because of the inflammatoryresponse, lots of white blood cells are attractedto the area where there are increased levels ofbacteria. Pus is formed largely from the deadwhite blood cells.As these inflammatory mediators move outinto the surrounding dermis, the lesions aremore likely to be nodular and/or cystic and thereis an increased likelihood of permanent scarring.Nodules are solid and larger than pustulesextending deeper into the layers of skin. They arecaused when large comedones rupture releasingtheir inflammatory contents into the surroundingskin. Because they extend deeper into the skinaffecting the dermis as well as epidermis, they dolead to scarring. Cysts occur less frequently thannodules but when they do they are even moredestructive, leading to greater levels of scarring.They are not as solid as a nodule and will oftenoccur where there are two or three nodules closetogether (Figure 10.4).Acne conglobata and acne fulminansAcne conglobata describes a situation where thereis severe nodular acne causing deep abscesses,sinuses in the skin and skin breakdown leading toulceration. There are also usually large numbersof blackheads affecting the face, neck, upper armsand trunk.Acne fulminans is a severe form of acne conglobatawhere the patient becomes systemicallyunwell. Patients will present with nodular cysticacne plus a number of other symptoms includingFigure 10.4 Acne with cysts. (Source: Reprinted fromBuxton and Morris-Jones, 2009.)malaise, fever, joint pain and/or swelling. It nearlyalways affects males and is characterised by anabrupt onset along with the above symptoms anda raised white blood cell count. It may be precipitatedby the illegal use of testosterone to boostmuscle growth; however, it can just occur spontaneously(New Zealand Dermatological SocietyIncorporated, 2009). It is considered a dermatologicalemergency and a patient presenting withacne fulminans must be referred urgently to seea dermatologist (National Institute for ClinicalExcellence, 2001).Acne conglobata and fulminans can presentas part of a syndrome known as SAPHO. Thissyndrome must include any combination of thefollowing:Synovitis (inflamed joints)Acne (conglobata or fulminans)Pustulosis (thick blister containing yellow pus)Hyperostosis (increase in bone substance)Osteitis (inflammation of the bones)

Acne 183Treatment will be multifactorial involvingcare from dermatologists and rheumatologistsin order to treat all of the symptoms.ScarringOne of the key aims of treatment is to preventscarring. Should it become evident that scarringis occurring, the patient should be referred formore intensive treatment (National Institutefor Clinical Excellence, 2001). Scarring ismore likely to occur in patients who have nodulesand/or cysts. However, tendency to scaris quite individual and each patient needs tobe assessed individually as some people willbegin to scar even with relatively mild acne(Figure 10.5).There are some marks that are left on the facepost-acne; these are lesions that are not strictlyspeaking scars. They are related to pigmentchanges. The final vestiges of the inflammatoryprocess may appear as small red maculeson the skin which will fade over the course of6 months. Post-inflammatory pigmented lesionsdescribe lesions where melanin has built up inthe skin as a result of the inflammation. Thesemay be in evidence for over a year and are oftenmore noticeable in darker skin types.True scarring can be one of two types.It can either be hypertrophic or atrophic.Hypertrophic scars (sometimes referred to askeloid scars) occur where there is excessivetissue giving the scars a raised up appearancethat may extend beyond the margins of theoriginal lesion (Mitchell and Dudley, 2002).The overgrowth of tissue is caused by excessivecollagen being laid down in that area. Afro-Caribbean skin seems to be more prone to keloidscarring than other racial groups. Atrophicscars refer to those where there is a loss of tissue,so the lesion appears depressed from thesurface of the skin. Different types of atrophicscars include:■■■Ice-pick scars: Have a well-defined irregularedge and steep sides usually occurring on thecheeks.Atrophic macular scars: These are flatter onthe skin surface and the skin may appearthin and somewhat wrinkled. Although theyare generally small on the face, they can belarger on the body; with time, they appearwhitish in colour.Follicular macular atrophy: These scars areso called because they tend to occur aroundhair follicles on the chest and back followingon from severe acne. The elastin fibres in theskin are damaged so that rather than lyingsmooth and flat they bunch up and causesmall lumps to appear in the skin lookingrather like white heads. With time, as theelastin repairs, these lesions tend to flattenout (Mitchell and Dudley, 2002).Treatment for scarringPatients need to have realistic advice about thelikely success of treatment for acne scarring.They should be reassured that hyperpigmentationwill gradually fade over time. Skin bleachingcreams should be avoided as they are likelyto cause hypopigmentation, leaving the patientwith a more permanent problem than before.At the current time, there are no treatments foracne scarring that have a good research evidencebase. Some options that patients may ask aboutare listed below.Figure 10.5 Acne scarring. (Source: Reprinted from Welleret al., 2008.)Camouflage techniques: Special covercreamscan be closely matched to skin tone

184 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsand applied to the skin to even out colourdifferences. The creams are fixed with aspray or powder so that they can be left inplace for up to a week (Davies, 2007). Forpatients with acne, this is most effective atcovering hyper or hypopigmentation; it is notterrible successful at covering scars. It cannotbe used on active inflammatory acne lesions.Steroid injections for keloid scars: These canbe helpful, but small injections should begiven over a period of time to get the bestresults and avoid side effects.Chemical peels or dermabrasion: Theseprocedures are used for atrophic scarringand aim to remove layers of skin so thatthe whole skin surface is lowered to thelevel of the scar tissue. When the new skingrows back, it is smoother and less pitted.Patients should be warned that this can beextremely painful and lead to a prolongedperiod of sore and damaged facial skin asit heals. The extent of this depends on howsevere the treatment is. Those facial peelswhich do not leave the face feeling sore areunlikely to have much long-term beneficialeffect. ‘Fillers’ may be helpful in lifting shallowdepressed scars. Treating scar tissue inthese ways requires careful assessment anddelivery of the various techniques to obtainthe optimal response. In general these treatmentsare not available on the NHS.Silicon sheets: These are worn in direct contactwith the scar. A systematic review of theevidence for the efficacy of silicon sheetsfound that there were no good studies whichmade it difficult to make a judgement abouttheir benefits (O’Brien and Pandit, 2006). Theyare, however, unlikely to cause any damage.Lasers: A systematic review of the evidencefor the use of lasers in treating acne scarringrevealed that the evidence was not sufficientlyrobust as to determine the efficacy of differentlaser treatments or in comparison with othertreatments. Whilst some case studies suggestthere might be a positive effect, the authorsof the review felt that the evidence was notstrong enough to make recommendations forpractice (Jordan et al., 2000).Who gets acne and distributionAs mentioned earlier, the majority of teenagers willexperience acne to some degree. There are, however,other age groups who can also develop acne.Impact of geneticsAs with the majority of inherited skin disorders,the pattern for heritability of acne is notstraightforward. However, research carried outon twins does suggest that the severity of acne atall ages and on all sites was influenced by geneticfactors (Evans et al., 2005). Monozygotic twinswere significantly more likely to have similarseverity of acne than dizygotic twins.Infantile acneWhilst infantile acne is unusual, it can occur usuallybetween 6 and 18 months. During the firstyear of life, both boys and girls produce androgensfrom their adrenal gland; in addition to this,boys also produce testosterone from their testes(this may explain why infantile acne seems moreprevalent in boys). In a retrospective study of 29patients with infantile acne, 24 were boys and 5were girls (Cunliffe et al., 2001). The same studysaw a range of disease severity with 17 havingsuperficial inflammatory lesions and 5 comedonallesions; it was mild in 7, moderate in 18 andsevere in 4. This study highlights the similaritiesbetween infantile and teenage acne and indeedthe management was the same (although tetracyclineswere not used as they should be avoidedin children under 12). All responded to therapy,although 11 of the children required 24 monthsof treatment. In these instances, it is importantthat the parents and family receive support andreassurance that the lesions will resolve.Acne in middle ageAlthough teenagers usually grow out of acne,for some it does persist into middle age, for othersacne appears for the first time in middle age.

Acne 185TreatmentsGeneral guidance on using treatmentWhen deciding on the type of topical treatmentto use, assessment of the type of acne the patientis presenting with is important, e.g. is it inflammatoryor non-inflammatory or a mixture ofthe two. It is also important to bear in mind thepatient’s lifestyle and what sort of treatmentsthey are willing and able to tolerate.Before discussing with the patient the possibletreatment options, it is important that thehealth care professional ensures that the patientis clear about a number of general issues aroundacne and its treatment. To start with, patientsneed to be advised that acne is not caused byany of the mythical causes such as poor hygiene,too much sex, eating chocolate or dietary habitsin general. As has been described earlier inthe chapter, acne is a complex condition causedby the interplay of a number of different physiologicalfactors. It may be helpful to explainthis to patients. Some patients may believe thattheir acne is contagious and this falsehood mustbe dispelled. Regardless of which treatments areeventually used, there are some general guidelinesabout acne management that are worthdiscussing. These are listed in Box 10.1.Box 10.1 General advice on skincare for acne prone skin(1) Avoid harsh washing and specificallydo not scrub acne affected skin.(2) It is best for the skin not to squeezespots. Certainly, if the lesion is red andnot pustular it should be left alone.However, for many patients this is difficultto adhere to, so the followingguidance is aimed at causing as littlepermanent damage as possible to theskin:(a) When trying to express the contentsof a pustule, stretch the skinon either side of the lesion using atissue rather than digging in withthe nails and squeezing.(b) Gentle pressure and squeezing oneither side of blackhead is probablythe only way to express thoselesions. Whiteheads should not besqueezed.(c) Stop squeezing if blood is seen(Mitchell and Dudley, 2002).(3) Avoid using oily products on the skin.Moisturisers may be needed as theskin between lesions can become dryand tight (especially if drying topicalagents are being used). All productsshould be labelled oil free andnon-comodogenic.(4) Foundation and cover-up makeupcan make acne worse, althoughlighter non-comodogenic products arelikely to be less troublesome.It is important that patients are aware thatthere is really no quick treatment option foracne and that results from treatment will onlybe seen over a prolonged period of time (weeksto months). In addition, due to the number ofdifferent processes that are occurring in thedevelopment of acne (i.e. increased sebum production,follicular plugging, colonisation byP. acnes and the resulting inflammation), it isoften necessary to have a combination of treatmentswhich tackle different elements of thedisease process. In order to optimise the careof patients with acne (and therefore the resultsthey experience), intervention at an early stageis vital. Often it will be a nurse who has the timeand skills to undertake this early care. This willensure that people with acne understand aboutthe process of the disease, how and why to usetreatments and importantly how to recogniseif the condition is worsening and more intensiveinterventions are needed, particularly with theaim of preventing scarring.

186 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTopical treatmentsMild to moderate acneTopical treatments are the first-line treatmentfor acne. As has been outlined earlier, noninflammatorylesions include microcomedones,open and closed comedones. If these types oflesions predominate, with few or no pustules,acne is usually termed mild. In this instance, thefirst-line treatments are ones that reduce follicularplugging anti-inflammatory properties areless important. There seems to be consensus thatin this situation the best treatment options aretopical retinoids (Gollnick et al., 2003).Topical retinoidsTopical retinoids work by reducing the abnormaldesquamation of skin cells into the follicularcanal thus reducing the plugging. Theywork on the very earliest of acne lesions, themicrocomedone, thus preventing more maturecomedones from developing. They also appearto have some anti-inflammatory properties,although these are not their main mode ofaction. Finally, because of their impact on thefollicular microclimate, they appear to enhancethe efficacy of antibacterial products such asbenzoyl peroxide (BPO) and topical antibiotics(Gollnick et al., 2003). Because of their actionon the microcomedone, retinoids can be consideredas maintenance therapy once active lesionshave been cleared.Topical retinoids describe a broad group ofpharmaceutical products which are derived fromvitamin A. Over the years, a number of different‘generations’ of retinoids have been developed.Tretinoin and isotretinoin were the first generation;the drawbacks highlighted with these productsbeing skin irritation, delayed and variableresponses, photosensitivity and exacerbation ofthe acne after 2– 4 weeks (Naito et al., 2008). Inorder to get around the problems of skin irritation,a number of different strengths and formulationswere developed including the microspherewhich was designed to release the tretinoin slowlyin a controlled manner (Gollnick et al., 2003). Itshould be noted that topical isotretinoin has asimilar effect to tretinoin, but a very differenteffect from oral isotretinoin as it has no impacton sebum production.Adapalene is a newer retinoid (known asthird generation) in which the therapeutic actionis similar to that of tretinoin, but in which theunwanted side effects of skin irritation and photosensitisationhave been reduced. Adapalenealso seems to be absorbed into the pilosebaceousduct more effectively than into the restof the skin surface, thus increasing its efficacy(Naito et al., 2008). As yet there is no Cochranereview giving evidence-based guidance as towhich retinoid is best to use; however, there hasbeen a research study indicating that whilst efficacywas similar, adapalene had fewer unwantedside effects than tretinoin microsphere gel 0.1%(Thiboutot et al., 2003).Topical retinoids can be used in women ofchild-bearing age; however, they should beadvised to avoid pregnancy whilst using them.Should an individual become pregnant whilstusing topical retinoids, they should stop thetreatment immediately. Whilst it is unlikely forthe topical product to have a systemic effect,this is a sensible precaution.How to apply a retinoid product?Usually it is best to apply these at night beforegoing to bed. The patient should be encouragedto wash the skin and dry it gently butcompletely before applying a thin layer of theproduct to the whole area to be treated, notjust the lesions. Retinoids can be applied to anyarea of the body where acne is present includingchest and back. The choice of the formulationof the product, whether a cream or a gel, willusually depend on personal preference. A gel islikely to dry the skin more and may be helpful ifthe skin surface is very greasy whereas a creamwill be more moisturising and may be helpful ifthe skin surface has a tendency to get dry. Afterapplying the treatment, the patient should washtheir hands. The possible side effects of treatmenthave already been mentioned includingredness, soreness and skin peeling and hypersensitivityto sunlight. If the former is a problem,the severity of the symptoms may be reducedby using a weaker formulation, if one is available,or by starting with less than a once-daily

Acne 187application (perhaps alternate days) and thenbuilding up to the required once a day. Patientsshould be advised to avoid overexposure to thesun and to not make use of sunbeds.Benzoyl peroxideBPO is a commonly used product for the managementof mild to moderate acne. Manyteenagers who have acne will purchase overthe-counterproducts containing BPO, and arelikely to have had varying degrees of successwith them. BPO works by releasing free radicaloxygen within the follicle itself; this has a bactericidaleffect thus reducing the bacterial load ofP. acnes (Tucker, 2008). BPO is therefore aneffective antibacterial product and particularlyuseful when there are inflammatory lesions aswell as non-inflammatory lesions. The impact ofBPO is enhanced by the use of topical retinoids;they are often used as a combination therapy.How to use BPO?Before starting to use the treatment, patientsshould be made aware that the product canbleach bedding, clothing and even hair, so careshould be taken when using it. The main sideeffect of BPO products is that they cause reddeningand soreness of the skin. This is usuallymild and can generally be overcome by startingtreatments at a low strength and/or usingthem on alternate days initially. Graduallyover time, the frequency can be increased toonce or twice daily. If the lower strengths aretolerated and they are not completely clearingthe acne, it is worth moving up to the strongerstrengths.The patient should be instructed to wash theirskin with a mild cleanser and pat the skin surfacecompletely dry. The product should thenbe applied all over the affected area, not just tothe lesions. The patient should then wash theirhands carefully. Another tip if the skin is particularlysensitive is to leave the product on forjust a short period of time initially (washing itoff after 15 minutes) and then gradually buildingup increasing amounts of time as the skintolerates the product.BPO may be used as part of a combinationregime, usually with retinoids. In theseinstances, BPO should be used in the morningand the topical retinoid in the evening. It is particularlyimportant for the patient to rememberto wash their face prior to using each differenttopical therapy.Azelaic acidThis has a similar clinical effect to BPO, butcauses less irritation and does not have the sametendency to bleach. It has reported antibacterialand comodolytic properties (Strauss et al.,2007). It is available as a 15% gel and 20%creamHow to use azelaic acid?It should be applied to clean skin twice daily,preferably in the morning and evening. Aswith BPO, if the skin is particularly sensitive,a gradual introduction of the product might behelpful.NicotinamideThis is a physiologically active form of nicotinicacid which is thought to have anti-inflammatory,bacteriostatic effects on P. acnes and reducesebum production. It is therefore most useful ifthere are inflammatory lesions in evidence.How to use nicotinamide?It should be applied to clean skin twice daily,preferably in the morning and evening. Itmay take up to 12 weeks to have a beneficialeffect.Topical antibioticsIf BPO is not tolerated, topical antibiotics particularlytopical clindamycin, erythromycin ortetracycline may be used. There are concernsabout antibiotic resistance and it is generallyrecommended that they should not be used as amonotherapy, but instead be used with a retinoidproduct. Long term use as a maintenancetherapy should also be avoided. They have aslower onset than oral antibiotics and are lesseffective (Gollnick et al., 2003). Some topicalantibiotic products already contain BPO and ithas been shown that this combination leads to areduced potential for developing P. acnes resistance(Eady et al., 1996).

188 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsHow long to use treatment for?All three of the topical treatments in this sectionneed to have been used for 2 months before assessmentas to their success or failure is made. Duringthis prolonged period of time, patients will needto have support and encouragement to continueto use treatments. Concordance will be improvedwith regular contact to discuss how the treatmentsare feeling on the skin and whether there are anyongoing problems (see Chapter 7). Ideally, patientsshould have access to telephone support.Moderate acneModerate acne differs from mild in the numberof papular and pustular lesions that are present.These are much greater in number and althoughthere will still be comedones present, the focusof treatment shifts towards managing the highburden of P. acnes which leads to significantinflammatory lesions.Oral antibioticsOral antibiotics are a commonly used treatmentfor acne, and should be considered as appropriatefor moderate to severe cases. Typically, the antibioticsof choice are tetracycline or oxytetracycline.Doxycycline may be considered for people whocannot comply with oxytetracycline or tetracycline.Lymecycline is tetracycline which is taken oncedaily and has the advantage of not needing to betaken on an empty stomach. Erythromycin might beconsidered if there is no response to the other antibiotictherapies; however, it has been increasinglyassociated with resistant strains of propionibacteriawhich may explain its lack of efficacy. It has beensuggested that erythromycin is reserved for patientsfor whom the cyclines are contraindicated, e.g. whenbreast feeding or when pregnant (Dreno et al., 2004).Trimethoprim is a final option but it is an off-licenceuse and therefore probably only to be initiatedby a specialist. Minocycline has historically beenthe preferred antibiotic; however, safety concernsincluding a greater risk of a lupus erythematosustypereaction and possible permanent skin pigmentchanges have meant that it is rarely used. ACochrane review considered the evidence in relationto the efficacy of minocycline in comparisonwith other oral antibiotics and showed no significantdifference (Garner et al., 2003).An important issue in relation to antibioticprescribing in acne is that of resistance. It wasreported that around 50% of acne sufferers inEurope were colonised with erythromycin- andclindamycin-resistant strains of P. acnes andup to 20% were colonised with cycline-resistantstrains (Dreno et al., 2004). The samepaper states that the longer someone is onoral antibiotics, the more likely it is for resistanceto develop; they estimate that at the endof a 6 months course of antibiotics, most peoplewould have developed resistant strains ofP. acnes (Dreno et al., 2004). Antibiotic resistanceshould be considered as a possible causeof failure to respond to treatment, especially ifthey have been given over a prolonged period oftime. Box 10.2 summarises the risk factors associatedwith developing resistant bacteria.The same article provides a list of recommendationsfor reducing the likelihood of developingresistant strains of P. acnes (see Box 10.3).Oxytetracycline and tetracycline are given in500 mg doses twice a day whereas doxycyclineis longer acting, thus given as a once-daily treatmentat a dose of 100 mg. Lymecyline taken oncea day in a dose of 408mg. Treatment should begiven for 3 months before an assessment as towhether it is making any improvement or not.If no improvement is seen, the antibiotic shouldbe changed; however, it should be noted thatmaximum improvement is usually seen at 4–6months. More severe cases of acne may need oralantibiotics for 2 years or more (but see commentsearlier with regards to resistance). Fatty food inparticular decreases the absorption of tetracyclineBox 10.2 Risk factors forbacterial resistance■■■■Long courses of antibioticsMultiple course of antibioticsPoor compliance with treatmentBeing close to someone who hasresistant acne.Source: Dreno et al. (2004).

Acne 189Box 10.3 Recommendations forreducing likelihood of developingresistant bacteria(1) Do not use antibiotics where otheracne treatments can be expected tobring about the same degree of clinicalbenefit;(2) Use antibiotics according to clinicalneed (e.g. should not in general beused for mild acne);(3) Do not use them as monotherapy;(4) Stop the treatment when the healthcare professional and the patient agreethat there is no further improvement orthe improvement is only slight;(5) Try to avoid using antibiotics beyond 6months;(6) Use BPO either concomitantly orpulsed as an anti-resistance measure;(7) Do not swap antibiotics without adequatejustification (i.e. if a furthercourse of antibiotics is needed, use thesame one) (p. 394).and oxytetracycline and to a lesser extent, doxycycline.Patients should be recommended wherepossible to take the antibiotics on an empty stomachto maximise their therapeutic value.The most common side effects of these antibioticsare gastrointestinal disturbances whichpatients should be warned of.It is generally agreed that clearing inflammatoryand comedonal lesions is quicker when oralantibiotics are used in conjunction with topicalretinoids and antibacterials (Gollnick et al.,2003). Thus oral treatment is not used insteadof topical treatment, but as an additional therapy.The mechanisms for improved efficacy ofcombined therapy is in part due to the differentmodes of action of the various therapeuticagents (i.e. they target different aspects of thedisease process). However, it is also thoughtthat topical retinoids affect skin permeabilitythus enhancing topical agent penetration andincreasing the cell turnover of the follicular epitheliumwhich allows more systemic antibioticto be transported to where the P. acnes resides(Gollnick et al., 2003).Hormonal therapiesThe combined oral contraceptive pill (containingboth oestrogen and progesterone) has beenshown to be effective in reducing both inflammatoryand non-inflammatory acne lesions inwomen (Strauss et al., 2007). It does not appearthat one particular combined oral contraceptivepill is particularly better than any other.However, this therapeutic option is recommendedfor women who have acne but who alsowant birth control, and as such this may be areasonable choice.Severe acneIn cases of acne that do not respond to theabove oral therapies, the final option is oralisotretinoin. Whilst usually reserved for thesevere end of the disease scale, if the acne isproving to be particularly scarring either physicallyor psychologically it may be consideredas an option earlier, when the disease is moremoderate.IsotretinoinIsotretinoin is a unique therapy because it targetsall aspects of the acne disease process. Itseffects are summarised in Box 10.4.Box 10.4 Effects of isotretinoin■■■■Decreases the size of, and secretionsfrom, the sebaceous glands;Normalises the follicular keratinisationthus preventing follicular plugging andcomedone formation;Alters the microenvironment of thefollicle so that it is not conducive to P.acnes growth;Has an anti-inflammatory effect.

190 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTaking isotretinoin can reduce the sebum productionby up to 90%; the effect of this is thatP. acnes levels decrease significantly (Gollnicket al., 2003). This in turn leads to a significantdecrease in inflammatory lesions. Most casesrespond to a single 4–6 month course. Pustulesclear more rapidly than papules and nodulesand those lesions on the face, upper arms andlegs clear more quickly than those on the trunk.Beneficial effect may take 1–2 months to noticeand occasionally the acne may worsen in thisperiod of time prior to improving. Patients needto be warned of this fact.Dosing ranges from 0.1–2.0 mg/kg but in realitydoses higher than 1.0 mg/kg are rarely used.In order to minimise potential side effects (especiallya flare-up of the acne), a starting dose of0.5 mg/kg/day for the first month may be advisable.If tolerability is not a problem, this dosemay be followed by 1 mg/kg per day for the restof the course. More severe deeper nodular acnemay need a longer treatment period.Side effectsThe side effects of oral isotretinoin are significantand require detailed discussion with thepatient to ensure full understanding of the implicationsof taking the drugs. Because one of thetherapeutic benefits of isotretinoin is as a dryingagent, patients will experience dry skin, chappedlips, dry eyes and a dry mouth. Secondary skininfections with S. aureus can also occur andshould be treated with oral antibiotics or antiseptics(depending on the level of infection).Less frequently patients may experience muscleand back aches and mild headaches, althoughthese usually resolve as the treatment progresses.Nosebleeds and skin fragility may occur. Theremay be a rise in serum lipid levels. Certainsymptoms should be taken very seriously andwarrant discontinuation of the treatment immediately.These include:■■■severe headachedecreased night visionsigns of adverse psychiatric eventsGenerally, the unwanted side effects willresolve once treatment is discontinued.Both brands of isotretinoin available inBritain contain soya oil. Some patients with peanutallergy may have cross-reactivity with soyaand this needs to be discussed. The capsules thatencase the active ingredients contain gelatinewhich may make taking the tablets unacceptableto someone on a vegetarian diet.MonitoringSerum lipid and liver function tests (LFTs)should be monitored. LFTs should be measuredas a baseline prior to the commencementof treatment and then checked at 4 and 8 weeks(although exact timings will vary depending onlocal clinical practice). If blood levels are normalat 8 weeks, further monitoring is probably notnecessary as long as the dose remains the same.Because isotretinoin is teratogenic (it can seriouslyadversely affect the unborn child), womenof child-bearing age must have a negative bloodpregnancy test before commencement of therapy.Once a negative pregnancy test has beenreceived, therapy should be started after the 2ndor 3rd day of the first menstrual period afterthe test. Current practice requires women toundergo monthly urine pregnancy tests prior toa further prescription of isotretinoin being given.It should be noted in the patient record that contraceptionand pregnancy avoidance advice havebeen discussed and understood by the patient.Different countries have different policies on theissue of pregnancy avoidance. Grewal-Fry outlinesthe policy in the USA (Grewal-Fry, 2007).Patients may well already be aware of thepotential psychological impacts of taking isotretinoinas these have been extensively coveredin the popular press. Whilst severe psychiatricchanges are unlikely, patients should be counselledabout the possibility of mood swings. Acneitself can lead to high levels of anxiety (Aktan etal., 2000) and it is not always possible to categoricallyidentify mental health changes being asa result of isotretinoin. Very occasionally severepsychiatric changes may occur with some reportsof depression and suicidal ideation (Gollnicket al., 2003). A more recent study suggestedthat there is a link between isotretinoin use anddepression in those with acne vulgaris (Azoulayet al., 2008). In a commentary on this article,

Acne 191however, the categoric results were debated withthe author questioning whether the researchmethods allowed the conclusions to be drawn(Bigby, 2008). This author states that ‘Firm conclusionsregarding the risk of depression associatedwith isotretinoin cannot be drawn’ (p.1199), although he confirms that discussionsabout the possibility of depression should be hadwith the patient. It is important, therefore thatpatients are asked about their mood and warnedof depression as a potential side effect.RelapseRelapse can occur post-isotretinoin therapy.A large study (17,351 first time isotretinoin usersover a 20-year period) looked at the prescriptionsgiven to this cohort. It identified that 41%of the patients required further acne treatments(isotretinoin or other systemic or topical therapy).Twenty six percent required a second doseof isotretinoin (Azoulay et al., 2007). The authorslooked for predictive factors for relapsing andnoted that male subjects and those under the ageof 16 were more likely to require further treatmentwith anti-acne medications. Those who hadlower doses and shorter courses also seemed moreat risk of needing subsequent anti-acne treatments.Generally, it seems to be the case that if relapse isgoing to occur it occurs most frequently in the firstyear post-treatment (Gollnick et al., 2003).Supporting patients who are taking isotretinoinPatients being prescribed isotretinoin need to besupported throughout their course of treatment.They need advice with regards to managing arange of issues (Box 10.5).It is not possible to totally ameliorate the dryingeffects of the drug, but certain protectivebehaviours may help (Box 10.6).The drug’s effect can be significantly enhancedby taking it with food. It is thought that 40%is absorbed if taken with a meal whereas only20% is absorbed if it is taken on an emptystomach (Gollnick et al., 2003). The drug can betaken as a single dose once a day or divided andtaken as two doses at different times of the day.If the drug dose is to be split, it may be helpfulfor the patient to use a dosing box to ensurethat they keep track of their tablets.Box 10.5 Checklist of topics thatneed to be discussed with patientson isotretinoin■■■■■■■■■■Change in moodContraception (in women)Dryness: eyes, mouth, lips, nose (nosebleeds),genitaliaJoint and/or muscle discomfortSun protection/avoidanceAvoiding AlcoholWaxing/exfoliatingAvoiding planned surgery/cosmeticprocedureShould not give bloodAvoid vitamin supplementsBox 10.6 Advice that mayhelp with the drying effects ofisotretinoin■■■■■■■■■Avoiding activities which dry the skin,e.g. taking hot showers/baths andusing soap;Using emollients extensively if skinbecomes dry;Not using exfolliants or topical treatmentsthat will dry the skin further.All topical acne treatments should bestopped;Not waxing;Having a chapstick handy for dry lipsand using this frequently (may need tobe hourly);Avoiding exposure to UV radiation andnot making use of sunbeds. Always usingan oil-free sunscreen of at least SPF 15;Wearing soft contact lenses or glassesare likely to be more comfortable thanhard contact lenses;Using hypromellose eye drops;Keeping a bottle of water handy at alltimes, to sip.

192 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsPreventing pregnancy is key for femalepatients who are on isotretinoin. Contraceptiveadvice should be given to all sexually activepatients. Teenagers who attend with parentsmay be unwilling to admit they are sexuallyactive; however, information should still begiven. It is advised that one or preferably twotypes of contraception are used. Depending onthe level of advice needed, the woman may needto be referred to a family planning service toensure that the most effective and suitable contraceptionis provided. Contraception must beused for a month prior to the planned start oftreatment, during treatment and for 5 weeksafter the end of treatment. This is because ittakes this length of time for the isotretinoin tobe excreted from the body completely.Although very low levels of isotretinoin maybe found in the semen of men on the drug, theseare not thought to be sufficient to harm anunborn child or their sexual partner.Newer treatments with less evidencePhotodynamic therapyA review carried out in 2008 considered thevarious uses for photodynamic therapy (PDT)including its potential role in the treatment ofacne (Morton et al., 2008). PDT is a type oflight therapy in which a photosensitising drugis applied to the skin and then a light source isshone onto the skin in order to alter, in someway, targeted cells. The light source varies andcan be a laser, filtered xenon arc and metalhalide lamps, fluorescent lamps and light emittingdiodes. When used for treating cancerouslesions, for example basal cell carcinomas,the process of applying the light to the sensitisedskin is to kill the cancer cells. In acnetreatments, the exact mechanism is not whollyunderstood but it is thought that the treatmenthas a number of effects:(1) It has an antimicrobial effect on P. acnes.(2) It causes selective damage to sebaceousglands.(3) It reduces the keratinocyte shedding andtherefore follicular blocking.A number of studies are reported by Mortonet al. (2008) showing beneficial results fromPDT both immediately after treatment and atvarious time points after the treatment. Somestudies looked at results after one treatment,others after a series of treatments. Some of thestudies reported some unpleasant side effectsincluding pain during treatment, severe erythemaafter treatment, pustular eruptions andepithelial exfoliation. Most of the studies weresmall. Few trials compare laser light therapy toconventional treatments but in one case wherePDT was compared to 1% adapalene gel theresults showed that PDT was no better thanthe gel (Hamilton et al., 2009). The conclusiondrawn by Morton et al. (2008) was that whilstthis looks like a promising treatment for inflammatoryacne on both the face and back, furtherwork needs to be done on determining the mosteffective treatment protocols.A Cochrane review looked at the evidence inrelation to laser therapy and found that trials ofblue light, blue–red light and infrared light weremore successful than light alone particularlywhen multiple treatments were used (Hamiltonet al., 2009).Psychological impactA brief discussion with teenagers with acne willquickly illuminate the degree to which ‘spots’can affect their lives. Appearing as it does, duringthe emotionally turbulent teenage years,responses to acne range from mild annoyanceto depression and even suicidal ideation. Notonly can acne cause severe psychological hardship,but it can also prevent young people fromachieving their full potential as they avoidapplying for the job they really want becauseit means being in the public eye, for example.Whilst some people with acne may requireextensive psychological support and intervention,for the majority having someone who takestheir problem seriously and works with them tofind a treatment regime which works will beall that is required. For this reason, nurses whocare for people with acne need to take the time

Acne 193to find out how the disease is impacting on lifeand work with the person to find a satisfactorytherapy. (See Chapter 6 for further informationon the psychological impact of skin disease.)ConclusionAcne results from a number of pathologicalprocesses which have been outlined in this chapter.Treatments need to be matched to the levelof disease severity and in particular the type ofacne the patient is experiencing. Patients needto have treatments clearly explained to themincluding descriptions of possible side effectsand the length of time they take to have a therapeuticimpact.ReferencesAktan, S., E. Ozmen et al. (2000). Anxiety,depression, and nature of acne vulgarisin adolescents. International Journal ofDermatology, 39(5): 354–357.Ashton, R. and B. Leppard (2005). DifferentialDiagnosis in Dermatology. Oxford: RadcliffePublishing Ltd.Azoulay, L., D. Oraichi et al. (2007).Isotretinoin therapy and the incidence ofacne relapse: A nested case-controlled study.British Journal of Dermatology, 157(6):1240–1248.Azoulay, L., L. Blais et al. (2008). Isotretinoinand the risk of depression in patientswith acne vulgaris: A case-crossover study.Journal of Clinical Psychiatry, 69(4):526–532.Bigby, M. (2008). Does isotretinoin increase therisk of depression. Archives of Dermatology,144(9): 1197–1199.Buxton, B.K. and R. Morris-Jones (2009). ABCof Dermatology (5th edition). Oxford: WileyBlackwell.Cunliffe, W., S. Baron et al. (2001). A clinicaland therapeutic study of 29 patientswith infantile acne. British Journal ofDermatology, 145: 463–466.Davies, V. (2007). The use of camouflage in skinconditions. Dermatological Nursing, 6(4):16–20.Dreno, B., V. Bettoli et al. (2004). Europeanrecommendations for the use of oralantibiotics for acne. European Journal ofDermatology, 14: 391–399.Eady, E., J. Cove et al. (1996). The effects ofacne treatment with a combination of benzoylperoxide and erythromycin on skin carriage oferythromycin resistant propionibacteria. BritishJournal of Dermatology, 34(1): 107–113.Evans, D., K. Kirk et al. (2005). Teenage acne isinfluenced by genetic factors. British Journalof Dermatology, 152: 505–594.Garner, S., E. Eady et al. (2003). Minocylcinefor acne vulgaris: Efficacy and safety.Cochrane Database of Systematic Reviews,(1): Art No. CD002086.Gollnick, H., W. Cunliffe et al. (2003).Management of acne – A report from a globalalliance to improve outcomes in acne. Journalof the American Academy of Dermatology,49(1): S1–S37.Graham-Brown, R. and T. Burns (2006).Lecture Notes: Dermatology (9th edition).Oxford: Blackwells.Grewal-Fry, R. (2007). The managementof patients on isotretinoin in the USA.Dermatological Nursing, 6(2): 26–29.Hamilton, F., J. Car et al. (2009). Laser andother light therapies for the treatment ofacne vulgaris: Systematic review. BritishJournal of Dermatology, 160(6): 1273—85.Jordan, R., C. Cummins et al. (2000). Laserresurfacing for facial acne scars. CochraneDatabase of Systematic Reviews (3): Art No.CD001866.Leyden, J. and K. McGinley (1993).Coryneform bacteria. In: Noble, W. (Ed.),The Skin Microflora and Microbial SkinDisease. Cambridge: University Press.Mitchell, T. and A. Dudley (2002). Acne – The‘At Your Fingertips’ Guide. London: ClassPublishing.Morton, C., K. McKenna et al. (2008).Guidelines for topical photodynamic therapy:An update. British Journal of Dermatology,159: 1245–1266.

194 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsNaito, A., S. Ovaisi et al. (2008). Topicalretinoids for acne vulgaris. CochraneDatabase of Systematic Reviews (3): Art No.CD007299.National Institute for Clinical Excellence(2001). Referral Advice: A Guide toAppropriate Referral from General toSpecialist Services. London: NICE.New Zealand Dermatological SocietyIncorporated (2009) DermnetNZ. Retrieved25 March 2009, from www.dermnetnz.org.O’Brien, L. and A. Pandit (2006). Silicongel sheeting for preventing and treatinghypertrophic and keloid scars. CochraneDatabase of Systematic Reviews (1).O’Connell, K. and C. Westhoff (2008).Pharmacology of hormonal contraceptivesand acne. Cutis, 81(1 Suppl): 8–12.O’Toole, M., Ed. (1997). Miller-KeaneEncyclopedia and Dictionary of Medicine,Nursing and Allied Health. Philadelphia: WBSaunders.Rademaker, M., J. Garioch et al. (1989). Acnein schoolchildren: No longer a concern fordermatologists. British Medical Journal,298(6682): 1217–1220.Strauss, J., D. Krowchuk et al. (2007).Guidelines of care for acne vulgarismanagement. Journal of the AmericanAcademy of Dermatology, 56(4): 651–663.Thiboutot, D. (2008). Overview of acne and itstreatment. Cutis, 81(1 Suppl): 3–7.Thiboutot, D., R. Thieroff-Ekerdt et al. (2003).Efficacy and safety of azelaic acid (15%) gel asa new treatment for papulopustular rosacea:Results from two vehicle-controlled, randomisedphase III studies. Journal of the AmericanAcademy of Dermatology, 48(6): 836–845.Tucker, R. (2008). The use of over-the-counterproducts in acne vulgaris. DermatologicalNursing, 7(1): 11–18.Weller, R., J.A.A. Hunter, J. Savin and M. Dahl(2008). Clinical Dermatology (4th edition).Oxford: Blackwell Publishing.

11Skin cancer and itspreventionRachel Duncan, Julie Van Onselen, Steven J. ErsserIntroductionCancer is the commonest cause of death inpeople aged 50–64; one in four people die ofcancer (Office of National Statistics, 2009). Skincancer is the most frequently diagnosed cancer inthe UK, and rates of melanoma have risen fasterthan any other major cancer (Cancer ResearchUK, 2009a). The All Party Parliamentary Groupon Skin (APPGS, 2003) enquiry into the treatment,management and prevention of skincancer reports that the incidence of skin cancerhas doubled within the last 20 years. The incidenceand referral rate for skin cancer is alsorising, due to greater public awareness. Lack ofeducation and training in skin cancer by GPs ishighlighted in the APPGS (2003) enquiry. TheAPPGS (2008) highlights the need for emphasisbeing placed on improving education amongstall those who have contact with people withskin conditions and especially in primary care.Nurses have a key role in skin cancer prevention,detection and in the support and treatmentof those who develop skin cancer. Specifically,the APPGS argue for each dermatology unithaving a clinical nurse specialist (CNS) in skincancer at a ratio of one full-time employee per160,000 of the population (APPGS, 2008).This chapter introduces the epidemiologyof skin cancer and locates this within the UKpolicy context. Three main sections then follow,embracing key diagnostic groupings ofpre- and cancerous skin lesions; these includepre- malignant skin lesions, non-melanoma skinlesions and melanoma. The final section outlinesthe causation, risk prevention and early detectionof skin cancer and the key role nurses andother health professionals can play, especially, inprimary care.Skin cancer epidemiology: the scaleof the problemIn UK, around 9000 cases of melanoma arediagnosed annually and, although mortalityrates are relatively low, they account for 80%of skin cancer deaths with incidence rising rapidly(Cancer Research UK, 2004, 2009c; RoyalCollege of Physicians [RCP], 2007). Nonmelanomaskin cancer (NMSC) is relativelycommon (approximately 100,000 cases/year(Cancer Research UK, 2009b).Placed within a policy context, the Departmentof Health (DH) aims to reduce by 20% thenumber of deaths from cancer in people below

196 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals75 years by 2010 (Department of Health, 2000,2007). Half of all cancers may be prevented bypromoting awareness and changes in lifestyle(DH, 2007); for skin cancer, this is a priority(Health Development Agency, 2002). The newgovernment’s National Awareness and EarlyDiagnosis Initiative supports local interventionsto raise public awareness of cancer and seek helpsooner (Cancer Research UK, 2009d).Melanoma is a cancer which affects alladult age groups. Incidence rates are highestin people over 75 years, and whilst rare inyoung people; it is the second most commoncancer diagnosed in 20–39 year olds (CancerResearch UK, 2009c). Men and women areoften equally affected, but in some countries aslight female preponderance is seen (Karim-Koset al., 2008).The incidence of melanoma is small comparedto other cancers, with 9,583 new casesrecorded in the UK in 2005 (Cancer ResearchUK, 2009a) but large increases have occurredover the last few decades. The number of peopleliving with melanoma in the UK, known as theprevalence, is estimated to be between 24,500and 31,000 (Forman et al., 2003). Knowing theprevalence of a disease is important when planningfuture resources. A substantial number ofdeaths occur in younger people. It is predictedthat the incidence of melanoma will continue torise steeply, yet mortality rates will remain thesame (Mackie, 2003).Pre-malignant skin lesionsCommon types of pre-malignantskin lesionsActinic keratosisActinic keratosis (AK) or solar keratoses arepre-malignant skin lesion showing early changesof increase in keratosis (see Figure 11.1).AKs present as scaly, erythematous, hyperpigmentedcrusty lesions, predominantly insun-exposed skin, often the back of the hands,face and scalp. They are very common in olderFigure 11.1 Actinic (solar) keratoses. (Source: Reprintedfrom Graham-Brown and Burns, 2006.)people, and there is a high prevalence inpatients receiving chronic immunosuppressionsuch as organ transplant recipients. Evidencesuggests that most AKs are the result of chronicexposure to ultraviolet (UV) light. A small percentagemay have the potential to progress tosquamous cell carcinoma (SCC) (de Berkeret al., 2007).Bowen’s diseaseBowen’s disease usually presents as a single erythematousscaly patch or plaque on sun-exposedskin (see Figure 11.2). Bowen’s disease is a formof intra-epidermal carcinoma in situ, which mayprogress to an invasive SCC and is also referredto as intra-epidermal SCC (Buchanan andCourtenay, 2006).

Skin cancer and its prevention 197recommendations from the British PhotobiologyGroup (de Berker et al 2007) are outlined inTable 11.1.Destructive treatments for AK may includecryotherapy, photodynamic therapy (PDT), surgery,laser chemical peels and dermabrasion.Table 11.1 British Photobiology Groups recommendationsfor the topical treatment of AK.Recommended AKtopical therapyRationale for AK treatmentFigure 11.2 Bowen’s disease. (Source: Reprinted fromGraham-Brown and Burns, 2006.)Diagnosis of pre-malignant skinlesionsDiagnosis is generally made on clinical examination.Differential diagnosis for AK may includesuperficial basal cell carcinoma (BCC), Bowen’sdisease, SCC and amelanotic melanoma. If thereis any clinical doubt, a punch biopsy will be performedto confirm diagnosis (de Berker et al.,2007).Treatment of AKActinic keratosis and Bowen’s disease aretreated with topical or destructive treatment.Topical treatment may include emollients,sun blocks, salicylic acid ointment,topical non-steroidal anti-inflammatory agents(Diclofenac), topical cytostatic preparation(fluorouracil) and topical immune responsemodulators (Imiquimod). Topical treatmentNo therapyEmollient therapySun blockSalicylic acidDiclofenac gel(Solaraze ® )Fluorouracilcream (Efudix ® )Imiquimod(Aldara ® )21% AK respond spontaneouslyover 12 months.Management of clinical manifestationsonly. Emollients do notreverse biological process.Long-term application is preventativeagainst further AKdevelopment.Removes overlying keratin anddoes not reverse biologicalprocess.Moderate efficacy for AK treatmentand clearance of lesions, thistreatment is well tolerated withminimal side effectsApplication: Apply by smoothingcream into lesion twice daily untilclearance (for up to 60–90 days).Good efficacy for AK treatmentand clearance of lesions; this treatmentis less well tolerated due toside effects of soreness.Application: Apply thinly once ortwice a day until clearance.Moderate efficacy for AK treatmentand clearance of lesions; thistreatment is less well tolerateddue to side effects of pruritus andapplication site pain, burning andirritation.Application: Apply thrice a week,for 4 weeks, leave on skin for 8hours and then wash off.Source: Adapted from de Berker et al. (2007).

198 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsThese therapies will be discussed in more detailin the non-melanoma section of this chapter.Prevention of pre-malignant lesionsand reoccurrence of AKEvidence suggests the regular use of sunscreensreduces the number of AKs. Patients should beadvised on sun protection measures and advisedto regularly use and apply sunscreens (de Berkeret al., 2007).Non-melanoma skin lesionsBasal cell carcinomaBasal cell carcinoma (BCC) is also commonlyreferred to as a rodent ulcer or basalioma. BCCis the most common type of cancer in Europe,Australia and the US Caucasian populationbut it is rare in Africans, Afro-Caribbean andAsians; and extremely rare in oriental races.BCCs arise due to solar damage and ionisingradiation; they also occur in burn scars andvaccination sites (Burns et al., 2004). There isa worldwide increase in the incidence of BCCs,and the significant aetiological factors includea genetic predisposition and exposure to UVradiation (sun exposure in childhood is indicated).Other risk factors include: increasingage, males, fair skin types I and II, immunosuppressionand arsenic exposure (Telfer et al.,2008). The tendency to develop multiple BCCsis a feature of Gorlin syndrome (basal cell naevussyndrome).BCC is defined as a malignant tumour, whichrarely metastases and is composed of cells similarto those in the basal area of the epidermisand its appendages (Burns et al., 2004) (seeFigure 11.3). BCC is a slow growing but locallyinvasive tumour which infiltrates tissues througha three- dimensional growth pattern. BCCs willcontinue to develop and grow and may causeextended local tissue invasion and destruction,Figure 11.3 Basal cell carcinoma. (Source: Reprinted fromGraham-Brown and Burns, 2006.)particularly, on the face, head and neck (Telfer etal., 2008).Types of BCCThere are several types of BCC and classicallythey arise in skin of a normal appearance. Theycan also vary in size from a few millimetres toseveral centimetres in diameter. There are severaldifferent clinical presentations of BCC,which are outlined in Table 11.2 (DermNet NZ,2009a).Diagnosis and definitionof high- and low-risk BCCsBCCs are diagnosed by examining the suspectlesion in good light and with the optional aidof a dermatoscope. If clinical doubt exists, apunch biopsy may be performed. Imaging techniquesmay also be used where bony involvementis suspected (Telfer et al., 2008). BCCsare treated with either surgery or other noninvasivetechniques. The chosen treatmentalmost always results in a cure; although BCCscan reoccur at the same sites. Metastatic BCCis extremely rare and can be fatal; this involvesa BCC that has spread to the lymph glands andother organs.The British Association of Dermatologists(BAD) guidelines for the management of BCC

Skin cancer and its prevention 199(Telfer et al., 2008) recommend that high-riskBCCs, defined as those most likely to reoccur, areexcised with predetermined margins or Mohsmicrographic surgery is performed. High-riskBCCs also includes previous treatment failureand patients who are immunosuppressed. Thefeatures of high-risk BCCs are defined bythe factors in Table 11.3.Table 11.2 Different clinical presentations of BCC.Nodular BCCSuperficial BCCMorphoeic BCCPigmented BCCBasisquamous BCC• Most common type on the face• Small, shiny, skin-coloured or pinkish lump• Blood vessels cross its surface• May have a central ulcer so its edges appear rolled• Often bleeds spontaneously then seem to heal over• Cystic BCC is soft, with jelly-like contents• Rodent ulcer is an open sore• Micronodular and microcystic types may infiltrate deeply• Often multiple• Upper trunk and shoulders, or anywhere• Pink or red scaly irregular plaques• Slowly grow over months or years• Bleed or ulcerate easily• Also known as sclerosing BCC• Usually found in mid-facial sites• Skin-coloured, waxy, scar-like• Prone to recur after treatment• May infiltrate cutaneous nerves (perineural spread)• Brown, blue or greyish lesion• Nodular or superficial histology• May resemble melanoma• Mixed BCC and SCC• Potentially more aggressive than other forms of BCCSource: Reproduced from DermNetNZ (2009a).Table 11.3 Factors affecting the prognosis of BCC.Tumour sizeTumour siteTumour type and definition of tumour marginsGrowth pattern/histological subtypeFailure of previous treatment (recurrent tumours)Immunocompromised patientsSource: Reprinted from Telfer et al. (2008).

200 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTreatment of BCCLow-risk BCCs, tumours that do not conferwith the features in Table 11.3, are generallytreated with a variety of destructive surgery andnon-surgical techniques.Curettage and cautery and cryotherapy proceduresmay be used. Cryotherapy, althoughconvenient and less expensive than surgery orradiotherapy, has poor cure rates in comparisonwith surgery and radiotherapy, especiallyfor lesions greater than 2 cm; surgery also providesa better cosmetic effect (Bath-Hextalland Perkins, 2008). Carbon dioxide laser is anuncommon treatment with poor evidence tosupport its use. Non-surgical techniques includetopical immunotherapy, PDT and radiotherapy.Topical immunotherapyThere is a good evidence for using topicalimmunotherapy to treat primary and superficialBCC (Telfer et al., 2008). Imiquimod is theonly topical immunotherapy licensed for theBCCs but is not indicated for BCCs on the face(Electronic Medicines Compendium [EMC],2009). Imiquimod cream is applied over thetreatment area, including 1 cm of skin surroundingthe BCC. Before applying Imiquimodcream, patients should wash the treatment areawith mild soap and water and dry thoroughly.Sufficient cream should be applied once a day (atbedtime is ideal) and rubbed into the treatmentarea until the cream vanishes. Imiquimod creamremains on the skin for approximately 8 hours;showering and bathing should be avoided. Afterthis period it is essential that Imiquimod creamis removed with mild soap and water, and thehands are washed thoroughly (EMC, 2009).Imiquimod cream can be applied for 12 weeksand treatment response can then be assessed.If the treated tumour shows an incompleteresponse, a different therapy should be used.A rest period of several days may be taken if thelocal skin reaction to Imiquimod cream causesexcessive discomfort to the patient, or if infectionis observed at the treatment site. In the lattercase, other appropriate measures should betaken (EMC, 2009).During therapy and until healed, affected skinis likely to appear noticeably different from normalskin. Local skin reactions, such as pruritus,burning, irritation and pain on applicationsite, are common but these reactions generallydecrease in intensity during therapy or resolveafter cessation of Imiquimod cream therapy(EMC, 2009).Photodynamic therapyPhotodynamic therapy (PDT) is a procedurewhich causes a photochemical reaction withintumour cells due to the reaction with a photosensitisingagent (methyl aminolevulinate cream),red light and cellular oxygen. This proceduredestroys the targeted tumour cells by apoptosisand necrosis (Buchanan and Courtenay, 2006).PDT is indicated for superficial BCCs, Bowen’sdisease and AK. A PDT light source is used by atrained clinician within a dermatology clinic. Thelesion is prepared by gentle decaling; a photosensitisingagent is applied and several hours later(usually between 3 and 6 hours to allow the drugto concentrate in the cancer cells), the lesion isthen illuminated with red light. Following treatment,the lesion site will form a scab, which willfall off after 3 weeks. More than one lesion canbe treated in a session, and PDT can be repeatedafter a 4-week interval (National Institute forHealth and Clinical Excellence [NICE], 2006b).RadiotherapyRadiotherapy is a less commonly used therapyto treat BCCs. It is effective for primary andrecurrent BCC and is generally suitable forhigh-risk older patients who are unable to toleratesurgery. Good cosmetic results are achievedusing superficial radiotherapy (generated atup to 170 kV) as once-weekly treatments forseveral weeks (Telfer et al., 2008).Prevention of BCCAdvice on sun protection and sunscreens iscrucial, as people with BCCs have a high riskof developing further BCCs; also they have anincreased risk of developing other skin cancers.

Skin cancer and its prevention 201Patients should be advised to complete skin selfexamination(SSE) and seek the opinion of aclinician if they have any suspected moles orother skin lesions.Squamous cell carcinomaSquamous cell carcinoma is defined as a malignanttumour arising from the keratinocytes of theepidermis (see Figure 11.4). SCC has the potentialto metastasise; spread is almost always bythe lymphatic route (Burns et al., 2004). UnlikeBCCs, SCCs do not often arise in healthy skinand usually present as an indurated nodularkeratinising or crusted tumour, or as an ulcerwithout the evidence of keratinisation. SCC is thesecond most common skin cancer, and the incidencehas been rising since the 1960s (Preston,1992). Aetiology is usually related to chronic UVlight exposure, especially in fair-skinned individuals,those with albinism or xeroderma pigmentosum.SCC may also develop as a result ofprevious exposure to ionising radiation, arsenic;or within chronic wounds, scars, burns or frompre-existing lesions, such as Bowen’s disease(Motley et al., 2002).Diagnosis of SCCThe diagnosis of SCC is generally established byhistology. Punch biopsies will be performed toprovide a tissue sample, which will be assessedby histology and a report produced outliningthe pathological pattern (e.g. adenoid type),Figure 11.4 Squamous cell carcinoma. (Source: Reprintedfrom Buxton and Morris-Jones, 2009.)cell morphology (e.g. spindle cell SCC), degreeof differentiation (e.g. poorly or well differentiated)and the histological grade. SCC gradingis by Borders’ classification system; grades 1, 2and 3 denote ratios of differentiated to undifferentiatedcells (Motley et al., 2002).Treatment of SCCThe treatment of choice for all resectable SCCsis surgical excision; Mohs surgery is recommendedfor high risk and recurrent SCCs. Smalland well-defined, low-risk SCCs are generallytreated by curettage and cautery or cryotherapy.Radiotherapy may be indicated for non-resectabletumours (Motley et al., 2002).Prevention of SCCPatients with SCCs require follow-up for recurrentskin cancer. Patients should be instructedin self-examination. Early detection and treatmentimproves patient survival from recurrentdisease. Ninety-five percent of local recurrencesand 95% of metastases are detected within5 years (Motley et al., 2002).Cutaneous T-cell lymphomaLymphomas are generally carcinomas of thelymphatic system; however, lymphomas canoccur in the skin with no evidence of diseaseelsewhere. They are referred to as primary T-celllymphomas and account for 65% of lymphoma’saffecting the skin. Cutaneous T-cell lymphomas(CTCL) refer to a serious but uncommonskin condition in which there is an abnormalneoplastic proliferation of lymphocytes with a‘T’ subtype (thymus derived).Mycosis fungoidesMycosis fungoides is the most common type ofCTCL presenting as patches or lumps composedof white cells called lymphocytes. It generallyfollows a low-grade clinical course, oftenpersisting slowly over years in a patch stage,then slowly progressing to the tumour stage(DermNet NZ, 2009b) (see Chapter 13 forfurther detail).

202 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsPrimary cutaneous CD30+ lymphoproliferativedisordersThis is the second most common group ofCTCL and accounts for about 30% of allCTCL cases. This group includes primary cutaneousanaplastic large cell lymphoma, whichpresents as solitary or localised nodules ortumours. Prognosis is usually good but theremay be regional lymph node involvement for10% of patients. The other common type inthis group is lymphomatoid papulosis, withlesions occurring predominantly on the trunkand limbs; they clear spontaneously but mayscar (DermNet NZ, 2009b).Sézary syndromeSézary syndrome (sometimes referred to as ‘redman syndrome’) is the name given when T-celllymphoma affects the skin of the entire body.The skin is also thickened, dry or scaly andusually very itchy. Examination usually revealsthe presence of neoplastic T cells (Sézary cells)in skin, lymph nodes and peripheral blood.The prognosis of Sézary syndrome is generallypoor with a median survival between 2 and 4years; infection caused by immunosuppressionis the main cause of death (DermNet NZ,2009b).Treatment of CTCLTreatments of CTCL depend on the tumour, site,stage, distribution, age and general health of thepatient. Various treatments may include topicalsteroids, phototherapy, photophoresis, topicalnitrogen mustard, chemotherapy, radiotherapy,interferons and oral retinoids.What is melanoma?Melanoma occurs after the malignant transformationof melanocytes (Barnhill et al., 1993).The melanocyte is a skin cell, which is found inthe epidermis. Its most important physiologicalfunction is to produce melanin, one of thepigments responsible for skin colour. This helpsto protect the skin from damage caused byUV radiation from the sun. Most melanocytesare found in the skin and it is for this reasonthat most melanomas are known as cutaneousmelanomas (see Figure 11.5).At first melanomas grow horizontally. The basementmembrane, a barrier separating the epidermisfrom the dermis, acts as a mechanical barrier,preventing the melanoma from invading deeperinto the skin. Early stages of melanoma that arelimited to the epidermis are called melanoma insitu and are curable. If the melanoma cells growvertically through the basement membrane to thedermis, it is known as an ‘invasive’ melanoma.The depth that the melanoma grows into theskin provides important prognostic information.The measurement, known as the Breslowthickness, is taken from the granular layer ofthe epidermis to the base of the tumour (Robertset al., 2002) and is measured in millimetres with asmall ruler called a micrometer (see Figure 11.6).The greater the Breslow thickness, the greater thechance the cancer may spread to other areas ofthe body via the lymphatic or blood stream.Introduction to melanomaMelanoma is a rare type of skin cancer whichaffects all age groups. Although melanoma isthe major cause of skin cancer mortality, it isusually curable if detected and treated at anearly stage (Scottish Intercollegiate GuidelinesNetwork [SIGN], 2009).Figure 11.5 Cutaneous melanoma. (Source: Reprinted fromGraham-Brown and Burns, 2006.)

Skin cancer and its prevention 203Risk factorsGranular cell layerExtension of tumourinto dermisDepth in mmFigure 11.6 Breslow thickness. (Source: Reprinted fromGraham-Brown and Burns, 2006.)Type of melanomaMelanomas are categorised according to clinicaland pathological parameters into four maintypes: superficial spreading melanoma, nodularmelanoma, acral lentiginous melanoma andlentigo maligna melanoma.Superficial spreading melanoma is the mostcommon type, accounting for approximately 70%(Cancer Research UK, 2009c). This type oftengrows slowly over a period of months or yearsand approximately 50% of patients will give ahistory of a pre-existing apparently benign lesion.The classic clinical presenting features include anirregular lateral margin, irregular multicolouredcentral pigmentation and a history of growth(Mackie, 2000). They are commonly found on thetrunk in men and the leg in women, and patientsare often in their fourth or fifth decade of life.The second most common type is nodularmelanoma. These often present as raised lesionswhich bleed easily and are ulcerated. Althoughoften dark in colour, they may be colourless oramelanotic. Lentigo maligna melanoma tendsto occur on the face of elderly patients withextensive chronic sun damage. Lentigo malignamelanoma should not be confused with lentigomaligna, a type of melanoma in situ. Acrallentiginous melanoma, whilst rare, is the mostcommon type of melanoma seen in Asians andpeople with dark skin. It is often found on thepalms, soles, under fingernails and toenails andcan affect mucous membranes.Melanoma occurs most commonly in fairskinnedpersons, especially those with a historyof significant sun exposure. Whilst sun exposureis thought to be a risk factor for melanoma, therelationship is not straightforward. The exactcause of melanoma is not known. Patients oftenhave freckles, red hair and tan poorly. Havingmultiple naevi is a powerful predictor of risk ofmelanoma.Cutaneous melanoma can occur anywhere onthe skin. Most frequently it is found on the leg inwomen (particularly between the knee and ankle)and on the trunk (especially the back) in men. Inelderly people, melanomas develop most commonlyon the face (Austoker, 1994). Figure 11.7depicts the distribution of melanoma on parts ofthe body by sex.Diagnosis of primary melanomaAs primary melanomas are clearly visible onthe surface of the skin, most melanomas arefirst detected by the patient or a spouse examiningthe skin and then bought to the attentionof the GP. The three major features ofmelanoma (in terms of diagnostic importance)in a skin lesion are as follows: (1) a changein size of the lesion, (2) the presence of anirregular outline or edge around the lesionand (3) the presence of three or more colourswithin the lesion. Other minor signs includea lesion with a diameter greater than 7 mm,inflammation, oozing or a change in sensation.Head andneck 22%Trunk 38%Arm 17%Leg 15%Not specified 8%Head andneck 14%Trunk 17%Arm 21%Leg 42%Not specified 7%Figure 11.7 Distribution of melanoma on parts of the bodyby sex. (Source: Cancer Research UK, 2009a.)

204 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsThe ABCDE guidance formula is anothercommonly used clinical guide for the diagnosisof early melanoma; see Box 11.1.It is recommended that patients with a lesionsuspicious of melanoma are referred to a doctortrained in the specialist diagnosis of skin cancer,normally a dermatologist (National Institutefor Health and Clinical Excellence, 2006a). InEngland, it is a requirement for patients to beseen within 2 weeks of referral, as early diagnosisand treatment represents the best chance ofcure (Department of Health, 2006). In order tomeet this target set out in the National CancerPlan (2000), most hospitals have designated skincancer clinics.At the skin cancer clinic an assessment will beundertaken; a clinical history will be ascertained,and the lesion examined, often with the aid ofa dermatoscope (see Chapter 3). Suspiciouslesions should be biopsied with a 2 mm marginof skin often using a local rather than generalanaesthetic promptly. The National Cancer Plan(Department of Health, 2000) provides detailson the referral arrangements.A record of the patients treatment plan agreedby the multidisciplinary team (MDT) whosecore members should include a dermatologist,a plastic surgeon, a histopathologist, a specialistnurse, a radiotherapist and an MDT coordinator(Department of Health, 2000) should berecorded in the patient’s notes.Treatment of primary melanomaFollowing a histological examination of the suspiciouslesion, the treatment for primary cutaneousBox 11.1 ABCDE guidance to therecognition of melanoma■■■■■A = AsymmetryB= BorderC= ColourD= Diverse structureE= Elevationmelanoma is wide local excision under local orgeneral anaesthetic (Roberts et al., 2002). Thepurpose of this treatment is to minimise the riskof local recurrence. The excision margins specifiedin the UK Guidelines (Roberts et al., 2002)are determined by the Breslow thickness of thelesion, as described and depicted earlier (Figure11.6).At the same time, a sentinel lymph nodebiopsy (SLNB) may be performed in patientswith thick tumours in order to discover if themelanoma has spread from the skin to the lymphnodes. The sentinel lymph node(s), the firstlymph node to which cancer may have metastasised,is identified by injecting a blue dye ora radioactive material, or both, into the skin atthe site of the primary melanoma. The surgeonthen uses a scanner to find the lymph node(s)containing the radioactive substance or looks forthe lymph node(s) stained with dye. The lymphnodes are surgically removed and examined histologically.If the sentinel lymph node containsmetastatic melanoma, then the surroundinglymph nodes are often removed during a subsequentprocedure known as a lymphadenectomy.Whilst there is no proof to date that SLNB leadsto an overall survival benefit for all patients, it isan accepted staging procedure. Its availability topatients is not standardised across the UK.Adjuvant treatmentsAdjuvant treatment can be defined as any treatmentin addition to surgery which may reducethe risk of recurrence. There is currently noneof proven benefit (Roberts et al., 2002) butpatients should be referred for entry into clinicaltrials, examples of which include bevacizumab(AVAST-M).Follow-upIt is recommended that patients are followed up‘to reduce morbidity and mortality through thedetection of metastatic disease and other primarymelanomas’ (Sober et al., 2001, p. 6). Itis estimated that 4–8% of patients diagnosed

Skin cancer and its prevention 205with a primary melanoma may develop a furtherprimary melanoma within the first 3–5 yearsfollowing diagnosis (Levi et al., 2005). It is suggestedthat ‘all patients with invasive melanomashould be followed up at three monthly intervals,for three years. Thereafter patients with melanomasless than 1.0 mm thick may be dischargedbut others should be reviewed 6 monthly for afurther two years’ (Roberts et al., 2002).Physical examination, by a health professional,is the mainstay of follow-up interventions.The site of the primary tumour and theadjacent skin should be examined for localrecurrences and local metastatic disease; thedraining lymph node basins should be examinedfor lymphadenopathy; and the remaining skinshould be examined for other suspicious lesionssuch as other primary melanoma (Roberts et al.,2002). Routine investigations, such as bloodtests and X-rays, contribute little to recurrencedetection (Kersey et al., 1995), as mostmelanoma recurrences produce symptoms orcan be found by physical examination.Metastatic melanomaMelanoma can spread to virtually any organor tissue such as the skin, subcutaneous tissue,lymph nodes, lung, gastrointestinal tract, liver,bone and brain (Essner, 2001). The majorityoccurs in the first 3 years after diagnosis(Shumate et al., 1995; Poo-Hwu et al., 1999).Many of the first metastases, after treatmentof the primary tumour, develop in the regionallymph nodes or in the skin close to or at the siteof the primary tumour (McCarthy et al., 1988;Dickers et al., 1999).Skin metastases often present as nodules butthey may be inflammatory, cicatrical or bullouslesions (Lookingbill et al., 1993). They arenormally flesh coloured, although they may bered, purple, brown or black and about a thirdare pigmented or ulcerated (Evans et al., 2003).Often round or oval in appearance, they can benon-tender, non-painful, solid, firm or rubberyin texture (Strohl, 1998). They can be moveableor fixed and vary in size and may presentas single or multiple nodules in the skin (Strohl,1998). Skin metastases can be found by palpationand visual examination, and diagnosisis most commonly confirmed by histologicalanalysis following a biopsy: needle, incisional orexcisional (Balch et al., 1994).Lymph nodes are oval- or bean-shaped structures,found scattered throughout the body ingroups, located along the length of the lymphaticsystem (Tortora and Derrickson, 2005). Lymphnodes containing metastatic melanoma are generallymore firm and rubbery, and are non-tendercompared with inflammatory nodes, which areusually softer, more resilient and tender (Balchet al., 1994). Lymph nodes can therefore befound by palpation but diagnosis is confirmedby histological analysis following a biopsy: needle,incisional or excisional (Balch et al., 1994).The signs and symptoms of distant metastasesto the lungs, liver, bone or brain depend on thesite of relapse and on whether they are at singleor multiple sites. Metastatic disease remainsrelatively resistant to current treatments withdacarbazine (an alkylating agent) being thecurrent single chemotherapy agent of choice(Roberts and Crosby 2008).SurvivalTo allow the health professional to identify thosepatients most at risk of developing metastases,offer prognostic information to patients and theirfamilies and to compare treatment results, theAmerican Joint Committee on Cancer (AJCC)melanoma staging system classifies patients’ diseaseinto tumour (T), regional lymph nodes (N)and distant metastases (M) (Kim et al., 2002).From this classification, melanomas are groupedinto four stages, stages I–IV.In Stage I and II, patients have a primarytumour but there is no evidence that the cancerhas spread to the lymph nodes or distantly.Patients have favourable overall survival outcomesof up to 95% (Kim et al., 2002) (AJCC).Although patient age, site of the primarymelanoma, level of invasion of the tumour andgender have been identified as prognostic factors,tumour thickness and the presence of ulcerationof the lesion are the most powerful predictors of

206 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalssurvival in patients in Stage I and II (Balsh et al.,2001). The 7th edition of the AJCC melanomastaging system will be published in the spring of2009 and it is likely that the number of mitosesper square millimetre will also be included as anindependent prognostic predictor.The strongest indicator of survival is tumourthickness: the thinner the Breslow thickness, thebetter the prognosis (Table 11.4). Most patientsdiagnosed with melanoma have thin tumours. Atotal of 57.8% of patients in the South AustralianCancer registry from 1994 to 2000 had tumours0.75 mm in thickness (Luke et al., 2003).Ulceration of the primary tumour carries a worseprognosis compared to non-ulcerated lesions.In Stage III, patients have developed a lymphnode metastasis or intransit/satellite lesion buthave no distant metastases. The number of metastaticnodes, tumour burden and the presenceand absence of melanoma ulceration are the mostpowerful predictors of survival in Stage III diseasepatients. In Stage IV disease, patients havedeveloped distant metastases with the anatomicsite of these metastases being the most significantpredictor of survival (Kim et al., 2002). Patientswith metastases in visceral sites have a poorerprognosis compared with those with metastasesat non-visceral sites (i.e. skin, subcutaneous anddistant lymph nodes) (Kim et al., 2002).Psychological impact of a diagnosisof skin cancer and the roleof the CNSA diagnosis of cancer can be one of the mostdevastating events of a person’s life (Buckman,1996). An individual’s emotional response tohearing that they have cancer may be complexand include an array of emotions such as anxiety,shock, anger, denial, fear and uncertainty(Van der Molen, 1999). Until recently, little hasbeen known about the specific impact of thediagnosis of skin cancer and the specific needsof this client group, but an audit undertakenthrough the use of focus groups of patients withmelanoma found that many patients reportedfeelings of shock and blankness when learningof the diagnosis (Wright et al., 2004). Theway in which the diagnosis is communicatedcan affect the individual’s adjustment to thedisease and his or her attitude to treatment(Buckman, 1996). It is therefore recommendedthat health professionals, including the CNSwho should be present during this consultation,who inform patients that they have skin cancerhave attended a communication skills course(National Institute for Health and ClinicalExcellence, 2006a).Table 11.4 Illustration of a 5-year survival rates for patients diagnosed with cutaneous melanoma at each stage.IA IB IIA IIB IIC IIIA IIIB IIICTa: Non-ulceratedmelanomaT1a95%T2a92%T3a79%T4a67%N1aN2a67%N1bN2b54%N1aN2a52%N328%Tb: Ulcerated melanomaT1b91%T2b77%T3b63%T4b45%N1bN2bN324%Source: Kim et al. (2002) and American Joint Committee on Cancer (2002).

Skin cancer and its prevention 207The CNS plays a vital role in supportingpatients with skin cancer; a role recognised byNICE (National Institute for Health and ClinicalExcellence, 2006a) in the Manual for ImprovingOutcomes for People with Skin Tumours includingMelanoma. Often the CNS will be designatedthe patient’s ‘key worker’ who co-ordinates theircare across many disciplines and thus acts as apermanent fixture in their journey. To help theCNS identify the most ‘at risk’ patients and providethe appropriate intervention, Perkins (1993)describes four psychosocial phases. The first twoare important at the time of diagnosis. Duringpsychosocial Phase 1, known as the existentialcrisis, acute anxiety is often experienced due toa poor knowledge of melanoma and ‘anticipatorygrief due to the fear of dying’. During thisphase, the CNS may reduce the patient’s anxietyby providing information. The need for informationappears greatest at the time of diagnosis.Whilst the type of information required variesaccording to the stage of the patient (Bonevskiet al., 1999), information pertaining to diagnosis,test results and treatment, risk of recurrence,life expectancy, effect of the disease on work andfamily life is most desired (Bonevski et al., 1999;Schofield et al., 2001).Nationally produced written materials by‘Cancerbacup’ (Macmillan Cancer Support,2009), Cancer Research UK (Cancer Help;Cancer Research UK, 2009e), ‘Marc’s Line’(Melanoma and Related Cancers of the Skin)(Wessex Cancer Trust, 2004) and the BritishAssociation of Dermatologists (2009) providegeneric information. However, informationoutlining local services, including names of keypersonnel and contact details, and relevant andlocal and national support groups should be provided(National Institute for Health and ClinicalExcellence, 2006a). The offer and acceptance ofwritten information should always be recordedin the patient’s notes. In addition, a permanentrecord of the consultation at which treatmentoptions were discussed should be offered (NICE,2006a). Whilst it is recommended that patientsshould receive targeted information throughouttheir cancer journey (SIGN, 2003), this can bedifficult to achieve since patients with skin cancermake few visits for diagnosis and treatment,many of which are brief outpatient visits. Analternative means of providing informationmay be via structured information programmeswhereby patients diagnosed with melanoma areinvited to participate in a group meeting such asthat described by Brandberg et al. (1996).To help patients to deal with ‘anticipatorygrief due to the fear of dying’ suggestedby Perkins (1993), the CNS may help by offeringsimple interventions such as signpostingpatients to relevant self-help groups, facilitateemotional disclosure, listening and respondingto their worries and concerns and helping themto normalise their experiences (Thompson,2009). The CNS should ascertain individualpatient’s coping styles and teach appropriatecoping strategies if appropriately trainedto do so. A randomized control trial ofpatients with melanoma found that a 6-weekstructured, psychiatric group interventionimproved outcomes in terms of affective statesand coping style at 6 weeks follow-up andat 6 months follow-up (Fawzy et al., 1990).A later study by Fawzy et al. (2003) found thata 6-week structured, psychiatric group interventionwhich included health education was associatedwith a survival advantage, after adjustingfor gender and Breslow thickness.In the second psychosocial phase (Phase 2),referred to as accommodation and mitigation,‘patients feel physically healthy, yet areconstantly living with the fear that the diseasemay return’ (Perkins, 1993, p. 162). Nationallyorganised support, specific to patients with adiagnosis of melanoma, is limited to a telephonesupport, ‘Marc’s Line’ and therefore manypatients rely on the CNS whom they are likely tohave established a good report with. Those whoare identified as struggling to come to terms withtheir diagnosis should be referred to an appropriateindividual within the extended skin cancerteam such as the clinical psychologist.SurgerySurgical excision is the recommended treatmentfor all primary melanoma and most NMSC,

208 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsalthough various non-surgical treatments areappropriate for some NMSC subtypes. Preoperativeassessment should include whether thepatient has allergies to latex and whether theyare on medications, such as anticoagulants, steroidsor aspirin.Written consent prior to the procedure isessential. Most common post-operative complicationsinclude bleeding, infection and scarring.Surgery is most often carried out using a localrather than a general anaesthetic most often asday case by trained dermatologists or plasticsurgeons, although occasionally, very complexsurgery as an in-patient may be required.Primary surgery for melanoma involves anumber of stages. Initially, a biopsy includinga narrow margin of normal skin is taken andthe resulting defect can almost always be closeddirectly. After analysis of the biopsy, a widerexcision may need to be performed accordingto the thickness of the tumour in the biopsyand the resulting defect can often be closeddirectly but the size or anatomical site of somedefects may dictate the use of skin flaps orskin grafts. Increasingly, sentinel node biopsy,a procedure whereby the first draining lymphgland is removed, is performed at the sametime as wider excision of a melanoma in orderto provide extra prognostic information aboutthe patient. This is performed by specificallytrained surgeons only and usually as part of aclinical trial.The same reconstructive ladder applies toNMSC and these tumours are most commonlytreated at a single operation. Following the procedure,patients need to be provided with writteninstructions to assist them in caring for theirwound, provide them with information aboutsuture removal and care of grafts and flaps inpost-operative period. A number of patients willhave surgery that will result in disfigurementparticularly if it involves the head and neck area.Sustained psychological support is essential bothbefore and after the treatment to enable patientsto adjust psychologically and socially to theirdisfigurement and to develop coping strategies(NICE, 2006a). After the surgery, patients mayneed access to prosthetic, camouflage and lymphoedemaservices.Causation, risk preventionand early detectionThe Department of Health (DH) aims to reducecancer deaths in patients below 75 years by20% by 2010 (Department of Health, 1999,2000b, 2007). At least half of all cancers arepreventable by promoting awareness and changinglifestyle (DH, 2007), especially skin cancer(Health Development Agency, 2002).The International Cancer (International CancerResearch Funding Organisations, 2008) highlightsUS educational prevention research withyoung people. Although childhood sun exposureis an important preventable factor, since riskdevelops in childhood (Armstrong and Kricker,2001) through genetic mutation and learnt riskbehaviour, educating this group remains problematic.Adolescents continue to seek exposure tosecure a tan (e.g. Melia et al., 2000; Cokkinideset al., 2002). Recent qualitative evidence suggeststhat in young women sun-related behaviours arecomplex but their activities in the sun are directedtowards meeting their physical and psychologicalcomfort needs and not health protection(Norton, 2008). A review argues that preventionis also valuable later in life, especially for thosewith high childhood sun exposure (Armstrongand Kricker, 2001). Achieving attitude and UVprotectivebehaviour in adults, who may be parents,may result in good practice being passed tochildren (parental risk-behaviour predicts that byyoung people; Cokkinides et al., 2002). However,adults received limited attention in preventivestudies.Attitudes and behavioural changeLimited knowledge and unsafe sun practicescontinue in the UK (Miles et al., 2005; Officeof National Statistics, 2009). Research isrequired to promote and evaluate behaviouralchange to prevent cancer and promoteearly detection (National Cancer ResearchInstitute, 2005). The SunSmart campaign aimsto achieve this by ‘action … to inform andempower patients so that they can play anactive role in decisions’, but delivery models

Skin cancer and its prevention 209other than UV-awareness campaigns are notdetailed (Department of Health, 2007; CancerResearch UK, 2009f). A review of evidence ofprimary care prevention proposes due cautionwhen drawing from US/Australian strategies(Melia et al., 2000). Melanoma preventionguidelines advise sun-avoidance and effectivesunscreen/clothing use (Royal College ofPhysicians, 2007).Using theory on effective behaviour change islikely to maximise the effectiveness of lifestyleinterventions (Berwick et al., 2000; NationalInstitute for Health and Clinical Excellence,2007). Research applying the Self-efficacy Theory(Bandura, 1996, 1997) highlights it as an importantpredictor of healthy behaviours (Havaset al., 1998; Rosal et al., 1998; Clark and Dodge,1999). Ajzen’s Theory of Planned Behaviour(Ajzen, 1991, 2001) is the most widely appliedmodel of beliefs, attitudes and intentions thatprecede action (Connor and Sparks, 2005).Nursing intervention and promotingself-examinationEvidence suggests primary care nurses canreduce cancer risk by promoting early detection/referral (Austoker, 1994; Taylor and Roberts,1997; Oliveria et al., 2002). Nurses are a substantialhealth education resource (Bradfordand Winn, 1997; Latter et al., 2000; Runcimanet al., 2006). Studies of nurse-led interventionsto increase cancer awareness or change behaviourhave been successful (e.g. Koinberg et al.,2004; Sharp and Tischelman, 2005). However,most initiatives have not been applied to skincancer prevention, involve self-examination only(e.g. Oliveria et al., 2002), have a limited theorybase and do not evaluate education to reducerisk behaviour (Oliveria et al., 2004).A systematic review by Saraiya et al. (2004)argues for research focused on health outcome,patient behaviour and the ‘role of the non-physicianprovider to help identify if counselling skills tochange behaviour might be better suited to providerswith the time and skills, such as a nurse’(p. 444); however, there is little evidence of suchstudies. Also, resource-efficient models of servicedelivery are required for primary care. Nursescan effectively increase self-efficacy in targetedpatient telephone interventions (Wong et al.,2005) with review evidence finding these safeand acceptable (Bunn et al., 2004).This section focuses on self-examination forprimary disease; however, it also embraces selfexaminationfor metastatic disease. The literatureprimarily focuses on the former, not the latter.Since primary and secondary prevention are keynursing roles, these are covered in some detail.Do patients perform self-examinationcorrectly?Patients’ ability to perform self-examination correctlyhas not been assessed previously. The UKnational guidelines (Roberts et al., 2002) do notclearly specify what would constitute a competentSSE. Specific body sites should be examinedand there is a need to search for both metastaticdisease and other primary melanomas should be.For competence to be achieved, an individualmust possess the appropriate knowledgeand skills, be confident to perform the skillsafely and trust their own ability to performthe skill without direct supervision. Elementswere taken from the definition of competenceused by Roach (1992). Whilst it is purportedthat females in the general population aremore knowledgeable about melanoma thenmen (Bourke et al., 1995; Miller et al., 1996;Melia et al., 2000), the only insight pertainingto the level of knowledge possessed by patientsactually diagnosed with melanoma comes froma small retrospective study by Regan et al.(1995). Here, patients ‘did not clearly knowwhy the examination was being performed orwhat was being searched for’ (p. 13) duringself- examination even after regularly submittingto the clinical examination at follow-up.However, if metastases were detected, patientsdid recognise the importance of their find andreported it: 50% contacted their GP; 28% contactedthe hospital; but 22% waited for thenext outpatient appointment. Knowledge ofskin changes and abnormalities has been foundto reduce individuals delay in seeking medical

210 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsattention for melanoma (Oliveria et al., 1999a).Confidence to carry out SSE for primary skinlesions has been found to be poor (Carli et al.,2002). It is not known how confident individualsdiagnosed with melanoma feel to performself-examination or to detect metastatic disease.The level of trust placed in the hospital healthprofessional and in themselves to perform selfexaminationis also not known. From the limitedliterature available on patient’s knowledge,confidence and trust, it is impossible to concludeif patients are able to perform self-examinationcorrectly.Factors which may encourage or inhibitthe performance of self-examinationThere is little evidence to suggest which factorsmay encourage individuals to perform selfexamination,for metastatic melanoma. Areview of the literature on SSE, which is advocatedfor the detection of primary skin cancer,including melanoma, and the detection of primarymelanoma, suggests that many factorsmay be involved. It is acknowledged that thefactors which may encourage or deter an individualfrom performing self-examination, todetect primary disease, may be different fromthose involved in the detection of metastaticdisease.Socio-demographic factorsIn SSE, several socio-demographic factors suchas gender, age, educational attainment, maritalstatus and cohabitation have been investigated.Females are more likely to self-detecttheir melanoma (Weinstock et al., 1999; Bradyet al., 2000) and have been found to performSSE for primary disease more often than males(Girgis et al., 1991; Hill et al., 1991; Berwicket al., 1996; Miller et al., 1996; Robinson etal., 1998). Similarities in both genders havehowever also been found (Robinson et al.,2002). Men are more likely to present withmelanomas located on the back (Hanrahanet al., 1998). Individuals with melanomas onnon-visible areas may incur difficulties in bothdetecting the primary tumour and performingself-examination. In addition, men are alsoless knowledgeable about melanoma and haveless favourable attitudes (Brandberg et al.,1996; Miller et al., 1996). The psychologicalapproaches to danger posed by melanoma maybe different for men and women (Robinson etal., 2002).Age and educational attainment have beenfound to both encourage and discourage the performanceof self-examination (Girgis et al., 1991;Friedman et al., 1993; Balanda et al., 1994;Robinson et al., 1998; Oliveria et al., 1999b).Elderly patients have a lower rate of detectioncompared to younger people and are more likelyto be diagnosed with thicker tumours which havea poorer prognosis (Roder et al., 1995). Thismay result from a failure to identify changes tomelanoma more often than younger patients(Hanrahan et al., 1998) or as a result of a lessfrequent inspection of their skin compared toyounger people.Surprisingly, Miller et al. (1996) found thatelderly patients are more likely to do selfexaminations.In primary disease, patientswith a low median educational attainment aremore likely to present later, whilst those frommore affluent areas generally have thinnermelanomas at the time of detection (Bonettet al., 1989; Roder et al., 1995). Patientswith melanoma with a lower socioeconomicstatus are more likely to die of their disease(Vagero and Persson, 1984). Lower socioeconomicstatus has also been associated withless knowledge and awareness of melanoma.Research by Koh et al. (1996) confirms theimportance of having a spouse in detectingmany primary melanomas. In their study, aspouse was the third most common person(after the index patient and a physician) todetect a melanoma. Having a spouse or partnermay provide encouragement or help tocarry out the procedure (Brady et al., 2000).This may be especially important when examininginaccessible areas since it has beenreported that melanoma arising on more visiblebody areas are more likely to be diagnosedat an early stage (Hemo et al., 1999). Higherrates of self-examination have been found inthose married or cohabitating (Balanda et al.,1994).

Skin cancer and its prevention 211Physical factorsA direct plea from a health professional toa patient instructing them to perform selfexaminationmay be a prime motivator(Weinstock et al., 1999). It is suggested that ‘bydirectly informing patients of their risk of thedevelopment of melanoma and skin cancer duringhealth care visits, physicians or nurses canpromote SSE’ (Robinson et al., 1998, p. 755).The literature does not describe which person isbest to make this plea or teach self- examination,although both hospital medical and nursing staffmay be involved (Poo-Hwu et al., 1999). Perssonet al. (1995) suggest that this individual shouldhowever be trusted by the individual receivingthe request. Previously highlighted as importantbeneficial factors are the following: havingheard or read about self-examination (Petro-Nustus and Mikhail, 2002); possessing knowledge(Champion, 1991); (Hajii-Mahmoodi etal., 2002; Jirojwong and MacLennan, 2003)and being motivated (Petro-Nustus and Mikhail,2002).The number of visits made to the health professionalhas been shown to be associated withincreased performance of self-examination(Robinson et al., 2002) and attendance at theoutpatient clinic has been found to be stronglyassociated with the practice of SSE for bothfemales and males (Oliveria et al., 1999a). Itmay provide an opportunity for health professionalsto reinforce the importance of selfexaminationand to promote skin awareness forit is known that behaviours that are reinforcedare more likely to be repeated (Redman, 1997).Weinstock et al. (1999) reported that one ofthe reasons given by the general public for notperforming self-examination was simply notthinking about it. Having the skin of the bodypurposely looked at by a health professional,during the physical examination, may be animportant factor (Weinstock et al., 1999). Itmay also act as a reminder.Knowledge of self-examination and feelingconfident are important in encouragingan individual to perform self-examination(Celentano and Holtzman, 1983). Having ahigh level of confidence in performance wasone of the three strongest predictors of SSE,although the measurement used to measurethis independent variable was not described(Robinson et al., 2002).Psychological factorsEarlier in this chapter, the phases of reactions todiagnosis of cancer were highlighted (Perkins,1993); these psychological effects have relevanceto behaviour related to self-examination. Duringpsychosocial Phase 1 (existential crisis), acuteanxiety is often experienced due to a poorknowledge of melanoma and ‘anticipatorygrief’. However, it is argued that some anxietymay cause the individual to act (Redman,1997) and therefore promote the performanceof self- examination. However, extreme anxietyor distress may inhibit patients from ‘seeking’professional advice and following through withrecommendations (Trask et al., 2001). Perkins(1993) suggests that by recognising key psychosocialphases, health professionals may identify themost ‘at risk’ patients and provide the appropriateintervention.Patients who are well informed aboutmelanoma and their risk of metastases, andtherefore, ‘have a concern for their disease orperceive themselves susceptible to developingcancer may be better able to look afterthemselves and engage in appropriate selfcare’ (Brown et al., 2000, p. 1148). It hasbeen reported that one of the reasons givenby the general public for not performing selfexaminationwas that they did not believeit to be necessary (Weinstock et al., 1999).Patient’s perceived risk to developing metastasesand understanding of melanoma andthe purpose of self-examination, particularlyBreslow thickness, is not known. In addition,a belief that self-examination is importantmay also be required (Rosella, 1994). InPhase 2, referred to as accommodation andmitigation, ‘patients feel physically healthy,yet are constantly living with the fear thatthe disease may return’ (Perkins, 1993, p.162). Self-examination may assist individualsto keep their fears in check. The emotionsexperienced by individuals before, during and

212 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsafter self-examination are not known. In bothbreast cancer (Persson et al., 1995) and testicularcancer (Cook, 2000), it is suggestedthat patients may experience feelings of fearand anxiety when performing self-examinationsince it involves trying to find somethingsuspicious (Frank and Mai, 1985; Rutledgeand Davis, 1988; Persson et al., 1995). Womendescribed that they would be terrified if theyfound a lump during breast self-examination(Persson et al., 1995). This may discourageits performance. In contrast, it is speculatedthat the regular practice of self-examinationcould reassure individuals and therefore reduceanxiety, if no evidence of metastases werefound (Best et al., 1996). Thus the performanceof self-examination would be encouraged.Whilst as mentioned, Phases 1 and 2 are relevantto those diagnosed with primary disease,in Phase 3 recurrence of the disease occurs.This can be a time of great anxiety for thepatient and their family since there are fewertreatment options available. In Phase 4, thereis general deterioration and decline as the diseaseadvances. The goal here is the palliationof symptoms.Teaching of self-examinationfor metastatic diseaseMetastases may become apparent in betweenhospital visit (Basseres et al., 1995) and mayoccur many years after the initial diagnosiswhen follow-up visits at the hospital have ceased(Kelly et al., 1985). Patients can find recurrences(Dickers et al., 1999) and therefore it is advisedthat they should be taught how to examinetheir own skin. Whilst many patients who havebeen taught how to perform self-examinationdo carry out the health professional’s request,often they do not have the necessary knowledgeor skills to do so competently as a consequenceof current teaching methods (Duncan, 2005).An MDT approach to teaching using innovativeaids is suggested (Duncan, 2005). Self-examinationshould be reinforced at each outpatientappointment and appropriate written materialsprovided, i.e. ‘How to check your lymph nodes’(Wessex Cancer Trust, 2004).Sun prevention activitiesThe UK national skin cancer prevention programmeSunSmart was launched in 2003 and iscommissioned by the UK Health Departmentsand run by Cancer Research UK. SunSmartprovides evidence-based information aboutskin cancer and sun protection and can beaccessed at http://info.cancerresearchuk.org/he althyliving/sunsmart (Cancer Research UK,2009f) (see Box 11.2).Sunscreens and SPFSunscreens can be both chemical absorbers andphysical blockers. Chemical absorbers work byabsorbing UV radiation and can be further differentiatedby the type of radiation they absorb,UVA or UVB, or both. Physical blockers workby reflecting or scattering the UV radiation(DermNet NZ 2009c).Sun protection factor is a worldwide system,stating how much protection a sunscreenprovides, applied to the skin at a thickness of2 mg/cm 2 . The test works out how much UVradiation (mostly UVB) it takes to cause barelydetectable sunburn on a given person with andwithout sunscreen applied. For example, if ittakes 10 minutes to burn without a sunscreenand 100 minutes to burn with a sunscreen,then the SPF of that sunscreen is 10 (100/10).There is no recognised international measurementof UVA sun protection factors (DermNetNZ, 2009c). In the UK, a star system is used.Sunscreens can have anywhere from 0 to 5stars. The number of stars is not an absolutemeasure and depends on how much UVB protectionthe sunscreen offers (Cancer ResearchUK, 2009f). In due course, a new EU symbolis being introduced to convey the UVA andUVB protection offered by some UV protectionproducts.A sunscreen with an SPF of 15 providesgreater than 93% protection against UVB.Protection against UVB is increased to 97%with SPF of 30+. The difference between anSPF 15 and an SPF 30 sunscreen may not havea noticeable difference in actual use as the effectivenessof a sunscreen has more to do with how

Skin cancer and its prevention 213Box 11.2 SunSmart – advice onsun protection and prevention ofskin cancerSunburn can greatly increase the risk of skincancer. Do not let yourself be caught out –use shade, clothing and sun protection factor15+(SPF15+) sunscreen to protect you.Sunburn – Don’t let sunburn catch youout. Whether at home or abroad, useshade, clothing and SPF15+ sunscreen toprotect your skin.Clothes and sunglasses – Cover up witha T-shirt, hat and sunglasses.Sunscreens – Buy sunscreen with SPFof at least 15 ‘broad-spectrum’ sunscreenswith a star rating of four stars or more. AnSPF 15 is advised as it represents the bestbalance between protection and price andprovides over 90% protection.Sun beds – Are not a safe alternative totanning. The more you use a sun bed thegreater your risk of skin cancer. Using a sunbed once a month or more can increaseyour risk of skin cancer by more than half.So when the tan fades, the damage remains.UV index – Know your skin type andwork out your risk of burning. Check the UVIndex for the day on the Met Office website(www.metoffice.gov.uk/weather/europe/europe_uv.html). Keep out of the middaysun (12.00–15.00 hrs) and seek the shade.Vitamin D – Amount of sun needed tomake enough vitamin D is always lessthan the higher amounts that cause tanningor sunburn.Fake tan – If you really want to changethe colour of your skin, it is safer to use afake tan product on your skin than tan outin the sun or under a sun bed. Fake tandoes not protect your skin from the sun.Protecting children – Young skin is delicateand very easily damaged by the sun.All children, no matter whether they taneasily or not, should be protected from thesun and are at risk.Working outdoors – Protecting yourselfif you work outside during the day. Try toavoid unnecessary midday sun exposure,cover up and use sunscreen.Source: Adapted from SunSmart website(Cancer Research UK, 2009f).much of it is applied, how often it is applied,whether the person is sweating heavily or beingexposed to water. Hence, a sunscreen withSPF15+ should provide adequate protection aslong as it is being used correctly. However, mostpeople apply their sunscreen at about one-thirdthe thickness used for testing; they fail to applyit to all exposed areas of skin; and they forgetto reapply it every couple of hours. Therefore,the actual protection may be a lot less than thetests indicate. The BBC Weather internet pagesprovide guidance on the UV Index providedwith weather reports and also give updatedinformation on UV Index, offering a basis forguiding to protective behaviour (BBC WeatherCentre, 2009).ConclusionThis chapter has outlined the nature of skincancer, its epidemiology, clinical presentation,causes and treatment. The different types ofpre-malignant, non-melanoma and melanomacancer have been presented, categorised andexamined. Attention has been given to thecrucial importance of prevention, patientbehaviour, preventative strategies such as selfexaminationfor both primary disease andmalignant melanoma. Reference has also beenmade to reactions to diagnosis and the importanceof patient support. The nurse’s role inprevention, education and support are of crucialimportance and the protective activitiesthat the public can undertake to reduce theirrisk of UV-related damage have been highlighted.

214 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsReferencesAjzen, I. (1991). The theory of plannedbehaviour. Organisational Behaviour andHuman Decision Processes, 50: 179–211.Ajzen, I. (2001). Nature and operation ofattitudes. Annual Review of Psychology,52: 27–58.All Party Parliamentary Group on Skin(APPGS) (2003). Enquiry into the Treatment,Management and Prevention of Skin Cancer.London: All Party Parliamentary Group onSkin, Portcullis.All Party Parliamentary Group on Skin (APPGS)(2008). Skin Cancer-Improving Prevention,Treatment and Care. London: APPGS.American Joint Committee on Cancer. (2002).Melanoma of the Skin. In: Greene, F.L.,Page, D.L., Balsh, C.M., Fleming, I.D.and Morrow, M. (eds.) American JointCommittee on Cancer: Cancer StagingManual. (6th edn) New York, SpringerVeralog.Armstrong, B.K. and A. Kricker (2001). Theepidemiology of UV induced skin cancer.Journal of Photochemistry and PhotobiologyB-Biology, 63(1–3): 8–18.Austoker, J. (1994). Melanoma: Preventionand early diagnosis. British Medical Journal,308(3944): 1682–1686.Balanda, K.P., J.B. Lowe et al. (1994).Enhancing the early detection of melanomawithin current guidelines. Australian Journalof Public Health, 18(4): 420–423.Balch, C.M., N.R. Pellis et al. (1994). Oncology.In: Schwartz, S., Shires, G.T., Spencer, F.C.(Eds), Principles of Surgery. New York:McGraw-Hill Incorporated.Balsh, C.M., S.J. Soong et al. (2001).Prognostic factors analysis of 17,600melanoma patients: Validation of theAmerican Joint Committee on CancerMelanoma Staging System. Journal ofClinical Oncology, 19(16): 3622–3634.Bandura, A. (1996). Social Foundations ofThought and Action: A Social CognitiveTheory. Englewood Cliffs, NJ: Prentice Hall.Bandura, A. (1997). Self-efficacy: The Exerciseof Control. New York: Freeman.Barnhill, R.L., C. Marhn et al. (1993).Neoplasms: Malignant melanoma. In:Fitzpatrick, T.B., Sisen, A.Z., Wolff,K., Freedburg, I.M., Austin, K.F. (Eds),Dermatology in General Medicine. NewYork: McGraw-Hill.Basseres, N., J. Grob et al. (1995). Costeffectivenessof surveillance of stage 1melanoma – A retrospective appraisal basedon a 10 year experience in a dermatologydepartment in France. Dermatology, 191(3):199–203.Bath-Hextall, F. and W. Perkins (2008). Basalcell carcinoma. In: Williams, H.C., Bigby,M., Diepgen, T. et al. (Eds), Evidence-basedDermatology. Oxford: Blackwell Publishing/BMJ Books.BBC Weather Centre (2009). The Sun – how theindex works. BBC Weather. Retrieved 8 May2009, from http://www.bbc.co.uk/weather/world/features/sun_index.shtml.Berwick, M., C. Begg et al. (1996). Screeningfor cutaneous melanoma by skin selfexamination.Journal National CanadianInstitute, 88(1): 17–23.Berwick, M., S. Oilveria et al. (2000). A pilotstudy using nurse education as an interventionto increase skin self-examination for melanoma.Journal of Cancer Education, 15(1): 38–40.Best, D., S. Davis et al. (1996). Testicularcancer education: A comparison of teachingmethods. American Journal of HealthBehaviour, 20(4): 229–241.Bonett, A., D. Roder et al. (1989).Epidemiological features of melanoma inSouth Australia: Implications for cancercontrol. Medical Journal Australia, 15(9):502–504, 506–509.Bonevski, B., R.P.H. Sanson-Fisher et al. (1999).Assessing the perceived needs of patientsattending an outpatient melanoma clinic.Journal of Psychosocial Oncology, 17(3/4):101-118.Bourke, J., M. Healsmith et al. (1995).Melanoma awareness and sun exposure inLeicester. British Journal of Dermatology,132(2): 251–256.Bradford, S. and M. Winn (1997). Practicenursing and health promotion: A case

Skin cancer and its prevention 215study. In: Siddell, M., Jones, L., Katz,J., Perberdy, A.I. (Eds), Debates andDilemmas in Promoting Health. A.Reader. Basingstoke: Macmillan and OpenUniversity Press.Brady, M.S., S.A. Oliveria et al. (2000). Patternsof detection in patients with cutaneousmelanoma. Cancer, 89(2): 342–347.Brandberg, Y., M. Bergenmar et al. (1996). Sixmonthfollow-up effects of an informationprogramme for patients with malignantmelanoma. Patient Education andCounselling, 28(2): 201–208.British Association of Dermatologists (BAD)(2009). Skin cancer. Patient Information andLeaflets, 3 May 2009, from http://www.bad.org.uk//site/574/default.aspx.Brown, J., P. Butow et al. (2000). Psychologicalpredictors of outcome: Time to relapse andsurvival in patients with early stage melanoma.British Journal of Cancer, 83(11): 1448–1453.Buchanan, P. and M. Courtenay (2006).Prescribing in Dermatology. Cambridge:Cambridge University Press.Buckman, R. (1996). Talking to patients aboutcancer. British Medical Journal, 313(7059):699–700.Bunn, F., G. Byrne et al. (2004). Telephoneconsultation and triage: Effects on healthcare use and patient satisfaction. CochraneDatabase of Systematic Reviews, 18(4):CD004180.Burns, T., S. Breathnagh et al. (2004). Rook’sTextbook of Dermatology. Oxford: BlackwellPublishing Ltd.Cancer Research UK (2004). Brief sheets: SkinCancer. CRUK.Cancer Research UK (2009a).Malignant Melanoma – Cancerstats,from http://info.cancerresearchuk.org/cancerstats/types/skin/incidence/.Cancer Research UK (2009b). UK SkinCancer Incidence Statistics, from http://www.cancerhelp.org.uk/help/default.asp?page=3010.Cancer Research UK (2009c). MalignantMelanoma Mortality by Age and Sex,from http://www.cancerresearchuk.org/cancerstats/types/skin/mortality/?a=5441and http://www.cancerresearchuk.org/cancerstats/type/skin/in/#age.Cancer Research UK (2009d). TheNational Awareness and Early DiagnosisInitiative (NAEDI). Retrieved 3 May2009, from http://info.cancerresearchuk.org/publicpolicy/naedi/?a=5441.Cancer Research UK (2009e). Cancer Help.Retrieved 3 May 2009, from http://www.cancerhelp.org.uk/.Cancer Research UK (2009f). SunSmart.Retrieved 3 May 2009, from http://info.cancerresearchuk.org/healthyliving/sunsmart/.Carli, P., V.D. Giorgi et al. (2002). Melanomadetection rate and concordance between selfskinexamination and clinical evaluation inpatients attending a pigmented lesion clinic inItaly. British Journal of Dermatology, 146(2):261–266.Celentano, D. and D. Holtzman (1983). Breastself examination: An analysis of self reportedpractice and associated characteristics.American Journal Public Health, 73(11):1321–1323.Champion, V.L. (1991). The relationship ofselected variables to breast cancer detectionbehaviours in women 35 and older. OncologyNursing Forum, 18(4): 733–739.Clark, J. and N. Dodge (1999). Exploringself-efficacy as a predictor of diseasemanagement. Health Education andBehaviour, 26: 72–89.Cokkinides, V.E., M.A. Weinstock, M.C.O’Connell and M.J. Thun (2002). Use ofindoor tanning sunlamps by US youth, ages11–18 years, and by their parent or guardiancaregivers: Prevalence and correlates.Pediatrics, 109(6): 1124–1130.Connor, M. and P. Sparks (2005). Theory ofplanned behaviour and health behaviour.In: Connor, M., Sparks, P. (Eds), PredictingHealth Behaviour: Health and Practice withSocial Cognition Models. Maidenhead: OpenUniversity.Cook, N. (2000). Teaching and promotingtesticular self examination. Nursing Standard,14(24): 48–51.de Berker, D., J. McGregor et al. (2007).Guidelines for the management of actinic

216 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalskeratosis. British Journal of Dermatology,156(2): 222–230.Department of Health (1999). Saving Lives:Our Healthier Nation. London: TheStationery Office.Department of Health (2000). The NHSCancer Plan: A Plan for Investment, aPlan for Reform. London: The StationeryOffice.Department of Health (2006). Cancer WaitingTargets – A guide Version 5. Retrieved 6 May2009, from http://www.performance.doh.gov.uk/cancerwaits.Department of Health (2007). What the CancerReform Strategy means to Patients. London:Crown.DermNet NZ (2009a). Basal cell carcinoma.Retrieved 20 April 2009, from http://www.dermnetnz.org/lesions/basal-cell-carcinoma.html.DermNet NZ (2009b). Cutaneous T-celllymphoma. Retrieved 27 April 2009, fromhttp://www.dermnetnz.org/dermal-infiltrative/cutaneous-t-cell-lymphoma.html.DermNet NZ (2009c). Sunscreens. Retrieved 27April 2009, from http://www.dermnetnz.org/treatments/sunscreens.html.Dickers, T.J., G.M. Kavanagh et al. (1999).A rational approach to melanoma followupin patients with primary cutaneousmelanoma. British Journal of Dermatology,140(2): 249–254.Duncan, R. (2005). A Survey of the Factorswhich Influence Patients Diagnosed withCutaneous Melanoma to Perform Self-Examination for Metastatic Disease.Birmingham, Birmingham, UK.Electronic Medicines Compendium (2009).Summary of product characteristics (SPC) forImiquimod cream.Essner, R. (2001). Is it worthwhile to detect andresect metastases early? Melanoma Research,11(Suppl 1): S2.Evans, A.V., F.J. Child and R. Russell-Jones(2003). Zosteriform metastasis frommelanoma. British Medical Journal, 326:1025–1026.Fawzy, F.I., N. Cousins et al. (1990).A structured psychiatric intervention forcancer patients. 1. Changes over time inmethods of coping and affective disturbance.Archives General Psychiatry, 47(8): 720–725.Fawzy, F.I., A.L. Canada et al. (2003).Malignant melanoma: Effects of a briefstructured psychiatric intervention on survivaland recurrence at 10 year follow-up. Archivesof General Psychiatry, 60(1): 100–103.Forman, D., D. Stockton et al. (2003). Cancerprevalence in the UK: Results from theEUROPREVAL study. Annals of Oncology,14(4): 648–654.Frank, J. and Mai, V. (1985). Breast SelfExamination in Young Women: More HarmThan Good? The Lancet 2(8456): 645–7.Friedman, L.C., S. Bruce et al. (1993). Skinself-examination in a population at increasedrisk for skin cancer. American Journal ofPreventative Medicine, 9(6): 359–364.Girgis, A., E.M. Campbell et al. (1991).Screening for melanoma: A community surveyof prevalence and predictors. Medical Journalof Australia, 154(5): 338–343.Hajii-Mahmoodi, M., A. Montazeri et al. (2002).Breast self examination, knowledge, attitudesand practices among female health care workersin Tehran.” Breast Journal, 8(4): 222–225.Hanrahan, P.F., P. Hersey et al. (1998). Factorsinvolved in presentation of older people withthick melanoma. Medical Journal Australia,169(8): 410–414.Havas, S., K. Treimen et al. (1998). Factorsassociated with fruit and vegetableconsumption among women participatingin WIC. Journal of American DieteticAssociation, 98: 1141–1148.Health Development Agency (2002). CancerPrevention: A Resource to Support LocalAction in Delivering The NHS Cancer Plan.London: Health Development Agency.Hemo, Y., M. Gutman et al. (1999). Anatomicalsite of primary melanoma is associated withdepth of invasion. Archives of Surgery,134(2): 148–150.Hill, D., V. White et al. (1991). Cancerrelated beliefs and behaviours in Australia.Australian Journal Public Health,15: 14–23.International Cancer Research FundingOrganisations. (2008). International Cancer

Skin cancer and its prevention 217Research Portfolio, from http://www.cancerportfolio.org/index.jsp.Jirojwong, S. and R. MacLennan (2003). Healthbeliefs, perceived self efficacy and breast selfexaminationamong Thai migrants in Brisbane.Journal of Advanced Nursing, 41(3): 241–249.Karim-Kos, H.E., E. de Vries et al. (2008).Recent trends of cancer in Europe:A combined approach of incidence, survivaland mortality for 17 cancer sites sincethe 1990’s. European Journal Cancer, 44:1345–1389.Kelly, J., M. Blois and R.W. Sagebiel (1985).Frequency and duration of patient followup after treatment of a primary malignantmelanoma. Journal of the American Academyof Dermatology, 13(5): 756–760.Kersey, P., N. Iscoe et al. (1995). The value ofstaging and serial follow-up investigationsin patients with completely resected primarycutaneous melanoma. British Journal ofSurgery, 72(8): 614–617.Kim, C.J., D.S. Reintgen et al. (2002). The newmelanoma staging system. Cancer Control,9(1): 9–15.Koh, H., A. Geller et al. (1996). Detection andearly prevention strategies for melanomaand skin cancer: Current status. Archives ofDermatology, 132(4): 436–442.Koinberg, I.L., B. Fridlund et al. (2004). Nurseledfollow-up on demand or by a physicianafter breast cancer surgery: A randomisedstudy. European Journal of OncologyNursing, 8: 109–117.Latter, S., P. Yerrell et al. (2000). Nursing,medication education and the new policyagenda: The evidence base. InternationalJournal of Nursing Studies, 37(6): 469–479.Levi, F., L. Randimbison et al. (2005). Highconstant incidence rates of second cutaneousmelanomas. International Journal of Cancer,117(5): 877–879.Lookingbill, D., N. Spangler et al. (1993).Cutaneous metastases in patients withmetastatic carcinoma: A retrospective studyof 4020 patients. Journal of the AmericanAcademy of Dermatology, 29(2 Pt 1): 228–236.Luke, C., B. Coventry et al. (2003). Arecutaneous melanomas of a specified thicknessshowing deeper levels of invasion? AsianPacific Journal of Cancer, 4(4): 307–311.Mackie, R.M. (2000). Primary CutaneousMalignant Melanoma: A Guide to Clinical,Differential Diagnosis and CurrentManagement. Edinburgh: Lothian Print.Mackie, R.M. (2003). Cancer Scenarios: AnAid to Planning Cancer Services in Scotlandin the Next Decade. 06 Malignant Melanomaof the Skin. Edinburgh: Scottish ExecutivePublications.Macmillan Cancer Support (2009).Cancerbacup. Retrieved 3 May 2009, fromwww.cancerbackup.org.uk/.McCarthy, W., H. Shaw et al. (1988). Time andfrequency of recurrence of cutaneous stage1 malignant melanoma with guidelines forfollow-up study. Surgery Gynecology andObstetrics, 166(6): 497–502.Melia, J., L. Pendrey et al. (2000). Evaluationof primary prevention initiatives for skincancer: a review from a UK perspective.British Journal of Dermatology, 143:701–708.Miles, A., J. Waller et al. (2005). SunSmart?Skin cancer knowledge and preventativebehaviour in a British populationrepresentative sample. Health EducationResearch, 20(5): 579–585.Miller, D., A. Geller et al. (1996). Melanomaawareness and self examination practices:Results of a United States survey. Journal ofthe American Academy of Dermatology, 34:962–970.Motley, R., P. Kersey et al. (2002).Multiprofessional guidelines for themanagement of the patient with primarycutaneous cell carcinoma. British Journal ofDermatology, 146: 18–25.National Cancer Research Institute (2005).Strategic Plan 2005–2008. London: NCRI.National Institute for Health and ClinicalExcellence (2006a). Guidance on CancerServices: Improving Outcomes for Peoplewith Skin Tumours including Melanoma: TheManual. London, NICE.National Institute for Health and ClinicalExcellence (NICE) (2006b). Photodynamictherapy for non-melanoma skin tumours

218 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals(including premalignant and primarynon-metastatic skin lesions). Retrieved 23April 2009, from http://www.nice.org.uk/nicemedia/pdf/ip/IPG155guidance.pdf.National Institute for Health and ClinicalExcellence (2007). The Most Appropriate Meansof Generic and Specific Interventions to SupportAttitude and Behaviour Change at Populationand Community Levels. London: NICE.Norton, E.A. (2008). A Grounded Theoryof Female Adolescent Behaviour in theSun: Comfort Matters. Bournemouth:Bournemouth University.Office of National Statistics (2009). Cancer.National Statistics. Retrieved 19 April 2009,from http://www.statistics.gov.uk/CCI/nugget.asp?ID=915&Pos=2&ColRank=1&Rank=310.Oliveria, S.A., P.J. Christos, A.C. Halpern, J.A.Fine, R.L. Barnhill and M. Berwick (1999a).Patient knowledge, awareness, and delayin seeking medical attention for malignantmelanoma. Journal Clinical Epidemiology,52(11): 1111–1116.Oliveria, S.A., P.J. Christos et al. (1999b).Evaluation of factors associated with skinself-examination. Cancer EpidemiologyBiomarkers and Prevention, 8(11):971–978.Oliveria, S.A., J.F. Altman et al. (2002). Useof nonphysician health care providersfor skin cancer screening in the primarycare setting. Preventive Medicine, 34(3):374–379.Oliveria, S.A., S.W. Dusza et al. (2004). Patientadherence to skin self-examination – Effectof nurse intervention with photographs.American Journal of Preventive Medicine,26(2): 152–155.Perkins, P.J. (1993). Psychosocial support andmalignant melanoma. European Journal ofCancer Care, 2(4): 161–164.Persson, K., I. Johansson et al. (1995). Breastself examination. A survey of frequency,knowledge and attitudes. Journal of CanadianEducation, 10(3): 163–167.Petro-Nustus, W. and B. Mikhail (2002).Factors associated with breast selfexamination among Jordanian women. PublicHealth Nursing, 19(4): 263–271.Poo-Hwu, W., S. Ariyan et al. (1999). Followuprecommendations for patients withAmerican Joint Committee on Cancer StagesI–III. Malignant melanoma. Cancer Control,86(11): 2252–2258.Preston, D.S. (1992). Non-melanoma cancers ofthe skin. New England Journal of Medicine,327: 1649–1662.Redman, B. (1997). The Practice of PatientEducation. St Louis: Mosby.Regan, M., C. Reid et al. (1995). Malignantmelanoma, evaluation of clinical follow-upby questionnaire survey. British Journal ofPlastic Surgery, 38: 11–14.Roach, S. (1992). Human Act of Caring:A Blueprint for the Healthcare Professional(Revised edition). Ottawa: Canadian HealthAssociation Press.Roberts, D. and T. Crosby (2008). Cutaneousmelanoma. In: Williams, H.C., Bigby, M.,Diepgen, T. et al. (Eds), Evidence-basedDermatology. Oxford: Blackwell Publishing/BMJ Books.Roberts, D.L.L., A.V. Anstey et al. (2002). U.K.guidelines for the management of cutaneousmelanoma. British Journal of Dermatology,146(1): 7–17.Robinson, J., D. Rigel et al. (1998). Whatpromotes skin self-examination? Journalof the American Academy of Dermatology,39(5): 752–757.Robinson, J.K., S.G. Fisher et al. (2002).Predictors of skin self-examinationperformance. Cancer, 95(10): 135–146.Roder, D.M., C.G. Luke et al. (1995). Trendsin prognostic factors of melanoma in SouthAustralia 1981–1992: Implications for healthpromotion. Medical Journal Australia,162(1): 25–29.Rosal, M.C., J.K. Ockene et al. (1998).Coronary Artery Smoking InterventionStudy (CASIS): 5 year follow up. HealthPsychology, 1(7): 476–478.Rosella, J.D. (1994). Testicular cancer healtheducation: An integrative review. JournalAdvanced Nursing, 20(4): 666–671.

Skin cancer and its prevention 219Royal College of Physicians (2007). ThePrevention, Diagnosis, Referral andManagement of Melanoma of the Skin: ConciseGuidance to Good Practice. Number 7 ClinicalStandards: Royal College of Physicians andBritish Association of Dermatologists. London:Royal College of Physicians.Runciman, P., H. Watson et al. (2006).Community nurses’ health promotion workwith older people. Journal of AdvancedNursing, 55(1): 46–57.Rutledge, D. and Davis, G. (1988). Breast SelfExamination Compliance and the HealthBelief Model. Oncology Nursing Forum15(2): 175–9.Saraiya, M., K. Glanz et al. (2004).Interventions to prevent skin cancer byreducing exposure to ultraviolet radiation:A systematic review. American Journal ofPreventive Medicine, 27(5): 422–466.Schofield, P.E., L.J. Beeney et al. (2001). Hearingthe bad news of a cancer diagnosis: TheAustralian melanoma patient’s perspective.Annals of Oncology, 12: 365–371.Scottish Intercollegiate Guidelines Network(SIGN) (2003). Cutaneous melanoma:A National Clinical Guideline. Section 10Information for Patients, from www.sign.ac.uk/guidelines/fulltext/72/section10.html.Scottish Intercollegiate Guidelines Network(SIGN) (2009). Cutaneous melanoma:A National Clinical Guideline, from http://www.sign.ac.uk/pdf/sign72.pdf.Sharp, L. and C. Tischelman (2005). Smokingcessation for patients with head and neckcancer. Cancer Nursing, 28(3): 226–235.Shumate, C.R., M.M. Urist et al. (1995).Melanoma recurrence surveillance, patient orphysician based? Annals of Surgery, 221(5):566–571.Sober, A.J., T.Y. Chuang et al. (2001).Guidelines for care for primary cutaneousmelanoma. Journal of the American Academyof Dermatology, 45(4): 579–586.Strohl, R.A. (1998). Cutaneous manifestationsof malignant disease. Dermatology Nursing,10(1): 23–25.Taylor, P. and D. Roberts (1997). Skin cancerprevention. Nursing Standard, 11(50):42–45.Telfer, N., G. Colver et al. (2008). Guidelinesfor the management of basal cell carcinoma.British Journal of Dermatology, 159:35–48.Thompson, A. (2009). Psychosocial impact ofskin conditions. Dermatological Nursing,81(1): 43–47.Tortora, G.J. and B.H. Derrickson (2005).Principles of Anatomy and Physiology.New Jersey: John Wiley & Sons.Trask, P., A. Paterson et al. (2001).Psychological characteristics of individualswith non-stage iv melanoma. Journal ofClinical Oncology, 19(1): 1844–1850.Vagero, D. and G. Persson (1984). Risks,survival and trends of malignant melanomaamong white and blue collar workers inSweden. Social Science and Medicine, 19(4):475–478.Van der Molen, B. (1999). Relating informationneeds to the cancer experience: 1. Informationas a key coping strategy. European Journal ofCancer Care, 8(4): 238–244.Weinstock, M.A., R. Martin et al. (1999).Thorough skin examination for the earlydetection of melanoma. American Journal ofPreventative Medicine, 17(3): 169–175.Wessex Cancer Trust (2004). How to CheckYour Lymph Nodes. Southampton: WessexCancer Trust.Wong, K., F.K. Wong et al. (2005). Effectsof nurse-initiated telephone follow-up onself-efficacy among patients with chronicobstructive pulmonary disease. Journal ofAdvanced Nursing, 49(2): 210–222.Wright, S., Becker, S., Smith, J. & South WestCancer Intelligence Service Skin CancerTumour Panel (2004). Use of focus groups toinform the development of skin cancer patientinformation. Bristol. South West CancerIntelligence Service.


12Infective skinconditions andinfestationsSteven J. ErsserIntroductionHealthy skin provides a tough barrier to keepout allergens and pathogens but if this barrierfunction breaks down or is penetrated,infections and infestations can cause disease(Gawkrodger, 2003). Skin infections and infestationsare common problems and nurses needto be confident in their assessment and management.This includes not only treating thephysical problem and ensuring patients andtheir families understand how to use the treatmentscorrectly, in order to be effective, but alsoaddressing practical considerations and reducingpotential for recurrence if possible. This chapterwill look at bacterial, viral and fungal skininfections and infestations. Risk factors such asage and concomitant conditions, treatment and,where possible, prevention will be consideredfor each subgroup.Infections and infestations are common andmany are treated by the primary care team. Itis therefore important to understand the fundamentalsof diagnosing these common skin conditions.Children, parents and patients who missschool or work while waiting for proper diagnosiscontribute to the financial burden of thesecommon conditions which are usually very easilytreated. Infections such as impetigo and tineaare highly visible and can lead to stigmatisationand create difficulties for children at school(Popovich and McAlhany, 2007). Impetigo isalso very contagious and therefore easily spread.Early access to appropriate diagnosis andtreatment can alleviate these aspects. Nurseprescribers in the community have much tocontribute to the improvement of health careprovision for dermatology patients (Courtenayet al., 2007), but this does mean that there is acontinuing need for nurses to receive additionaleducational support to be ‘upskilled’ and confidentin the assessment and management ofsuch problems. There have long been calls fornurses with experience in dermatology nursingto be available in every primary care settingso that patients with skin conditions can allhave access to quality dermatological care fromappropriately informed nurses. An increase inthe number of such nurse-clinicians would allowfor greater support and advice for people withskin conditions and those that are affected. Inaddition and very importantly, it would lead toan improvement in the dissemination of accurateinformation and treatments and encouragegreater adherence to therapies (APPGS, 2008).

222 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsWhile Watson and de Bruin’s (2007) work focuseson the experiences of patients with psoriasis, itclearly demonstrates how influential the doctor/patientrelationship is to the patient’s selfconcept:the participants all agreed that theywould have felt more empowered by their doctorshad they empathised with their suffering,given good explanations about the disease andtreatment and been alert to their related underlyingemotional struggles. Such findings can betransferred across the spectrum of dermatologicaldisease and for patients it cannot be overemphasisedthat a caring, empathetic nurse istherefore important for holding and addressingthe patients’ physical and psychologicalwell-being.Skin infections (bacterial, viral and fungal)and infestations (parasites or mites which canbe direct as in scabies or lice or indirect, e.g.bedbugs or fleas) cover a huge spectrum. Theymay range from minor conditions which neverthe-lesscan be embarrassing and uncomfortableto life-threatening infection where patientsare systemically unwell. Dermatology is a veryvisual and practical field where touch is alsoimportant and nurses need an ability to recognisethe changes which infection may make inthe appearance and feel of skin along with anability to accurately describe what they observeand feel. With this need to touch skin must alsocome education of the patient and public ininfection control measures, i.e. hand washing topromote best practice in preventing transmission(Docherty, 2001).In this chapter, the most commonly seenbacterial, viral and fungal infections areconsidered.Bacterial skin infectionsImpetigoImpetigo is a highly infectious superficial bacterialskin infection which is most frequentlyseen in children (Figure 12.1). It is more commonin the summer (Loffeld et al., 2005).Both Staphylococcus aureus (S. aureus) andFigure 12.1 Impetigo. (Source: Graham-Brown andBurns, 2006.)Streptococcus pyogenes (group A – haemolyticstreptococcus, GABHS) can cause this type ofsuperficial pyoderma or purulent skin disease.In British general practice, 2.8% of childrenaged 0–4 years and 1.6% of children 5–15years consult their GP about impetigo each year(McCormick et al., 1995). It is the most commonform of bacterial infection in individualswith human immunodeficiency virus (HIV).Primary impetigo is direct bacterial invasionof skin which was previously normal whereassecondary impetigo occurs in skin where thereis some underlying skin disease, for exampleatopic eczema or scabies, disrupting the skinbarrier. Impetigo is characterised by inflammationand infection localised in the epidermis.Impetigo is also classified as non-bullous or bullous.Non-bullous impetigo is sometimes alsotermed impetigo contagiosa, although this terminologymay be used at times synonymouslyas any impetigo.Non-bullous impetigo is the most commontype and accounts for more than 70% of cases(Burr, 2003). It is more common in childrenover the age of 2 years. Initial lesions are thinwalled vesicles on skin which has previouslybeen normal. Subsequently any areas where theskin barrier has been disrupted, for exampleminor abrasions, insect bites or atopic eczema,may be infected. The initial lesions rupture leavingerosions which are covered by the yellowishbrown or honey-coloured crusts which arevery characteristic of the condition. Individual

Infective skin conditions and infestations 223lesions enlarge to 1–2 cm and satellite lesionsappear. These can coalesce resulting in largerareas of crusted involvement. The infection canoccur on any part of the body but the face, especiallyaround the mouth and nostrils, extremitiesand buttocks are common. The problem usuallyremains localised. Widespread impetigo is mostcommon in secondarily infected or impetiginisedeczema. Diagnosis is not usually difficult. Themost important point to remember is that anyunderlying skin disease, for example shingles,cold sores, fungal skin infections and eczema,needs recognition and must also be treated(Resnick, 2000). Although not painful, impetigocan be itchy and sore.Bullous impetigo is less common and characterisedby vesicles and bullae which rupture lesseasily and can persist for several days (Koninget al., 2003). There are usually fewer lesionsand it can affect the trunk more commonly thanin non-bullous impetigo. It is more commonin infants and children under 2 years of age.Neonatal bullous impetigo tends to occur in theinguinal area and on the buttocks. The lesionsappear to develop on intact skin as a result oflocalised toxin production by S. aureus. It can beconfused with thermal burns, blistering disorders(e.g. bullous pemphigoid), herpes infections andStevens–Johnson syndrome (Koning et al., 2003).CausesBullous impetigo is always caused by S. aureus.Non-bullous impetigo can be caused by staphylococcior streptococci; it is possible to cultureboth organisms from lesions in many cases(Resnick, 2000). Historically in Britain S. aureuswas the main cause of impetigo in the 1940sand 1950s after which S. pyogenes was the maincausative agent for about 30 years. Currently S.aureus is the dominant cause again (Koninget al., 2003) with 10% of impetigo cases inBritain due to S. pyogenes.PrognosisThe prognosis is generally good. Impetigo canbe self-limiting but will usually persist andspread if untreated and be a source of infectionfor others. Local and systemic spread can rarelyresult in cellulitis, lymphangitis or septicaemia(Koning et al., 2003). Severe progression suchas septic arthritis, pneumonia and osteomyelitisare very rare and usually limited to thosewith acquired in inherited immune deficiencies(Resnick, 2000). Post-streptococcal glomerularnephritis is a serious but rare complication whileguttate psoriasis can also occur but probablyonly in those already genetically predisposed.ManagementKoning et al.’s (2003) review of 36 treatmentsfor impetigo highlight that there is no standardtherapy for impetigo. Trials show that Penicillinis not effective for impetigo and there is little evidencesupporting the value of disinfecting measures.Knowledge of local resistance patterns onthe basis of surveillance of specimens should beincorporated into any regional guidelines.(1) Consider taking a swab for microscopy,culture and sensitivity of in non-bullousimpetigo of purulent material or bullae fluidin bullous impetigo especially if MRSA is apossibility (Box 12.1). If the child or adult issystemically unwell, consider taking bloodfor blood cultures.(2) Hygiene measures to reduce the spread toothers: Careful hand washing, use of individualtowels and bedding, avoidance ofskin-to-skin contact with the child or adultuntil lesions have been treated.(3) Children should stay away from nurseryor school until the lesions have stoppedBox 12.1 Bacterial swabMoisten the tip of the swab;Apply to the affected skin;Rotate the swab between the fingers topick up debris;Put into transport medium.Source: RCN/BDNG (2008).

224 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsblistering or crusting or they have had48 hours of antibiotics.(4) In limited disease topical antibiotics, forexample fusidic acid, may be sufficient(other topical antibiotics seem less effective)(Koning et al., 2003).(5) Oral Flucloxacillin or Erythromycin, althoughthere is insufficient evidence that they are betterthan topical (Koning et al., 2003).(6) If culture reveals both staphylococcus andstreptococcus, both pathogens must be treatedwith appropriate antibiotics.(7) Most importantly any underlying skincondition must also be treated, e.g. impetiginisedatopic eczema should be treatedconcurrently with appropriate topical corticosteroidsand emollients (Charman andLawton, 2006).Folliculitis and related conditionsFolliculitis is an acute pustular infection ofmultiple hair follicles. A furuncle or boil isa localised acute abscess formed in hair folliclesnext to each other and a carbuncle is adeep abscess of the skin and subcutaneoustissue formed in a group of follicles which ispainful. Anything which tends to increase thenumbers of skin surface bacteria may lead tothe develop ment of folliculitis (Resnick, 2000)and this can include occlusion, overhydrationand maceration. Folliculitis is more commonin tropical climates and in those who livein overcrowded conditions or practice poorhygiene. It is also more common in patientswho are obese, have diabetes mellitus or weartight occlusive clothing.Follicular pustules occur in hair bearingareas such as the legs, face, buttocks and groin.In women it can happen after hair removal byshaving or waxing and in men it can affect thebeard area. It is usually, but not always, causedby S. aureus. Boils appear as tender, red pustuleswhich grow over a few days into a largered lump under the skin surface. It may burstthrough the skin releasing pus or may graduallysettle without bursting. They often occuron the face, neck, scalp, axillae and perineum asthe bacteria survives best in moist areas. Theycan recur. Large boils or carbuncles can result insystemic illness.Furuncles, carbuncles and other abscessesappear to be the most frequently reported clinicalmanifestations of MRSA (Nathwani et al.,2008).Management(1) Swabs should be taken for bacterial culturefrom the lesion only if: furuncles or boilsare recurrent, there is a history of spread inthe family or close contacts, the infectionis severe or MRSA is suspected (Nathwaniet al., 2008).(2) Acute staphylococcal infections should betreated with antibiotics in either topical orsystemic forms.(3) Furuncles and carbuncles can be treated surgicallyby lancing or incision and drainageif they are 5 cm in diameter (Gould et al.,2009), and if cellulitis is not present antibioticsmay not be required.(4) Recurrent and chronic cases are more difficultto treat and measures to help break thecycle of infection are needed (BAD, 2007).Antiseptic washes, for example iodine orchlorhexidine, can be used. Nasal carriageof staphylococcus should be treated withtopical antibiotic, e.g. Mupirocin.(5) Other family members should be swabbedand if carriers should also be treated.(6) Hands and finger nails should be kept cleanand short and clothing washed frequentlyusing a hot wash.(7) Obese patients should be advised about theneed to lose weight to reduce the survival ofbacteria in the skin folds.Staphylococcal scalded skin syndromeThis is an acute toxic illness usually seen ininfants but can affect adults with renal failureor immunodeficiency (BAD, 2006). It is causedby S. aureus which produces a toxin leadingto damage of a key protein called desmogleinwhich binds skin together. The resulting shedding

Infective skin conditions and infestations 225of sheets of superficial parts of the epidermisresembles a scald, giving rise to the name of thecondition (Gawkrodger, 2003).The original infection can be minor, forexample a graze or sticky eye, after whicha patchy red rash will develop and quicklyspread and increase in size. There is oftenredness around the mouth but there is nomucosal involvement of the lips or eyes whichdifferentiates this from the more serious toxicepidermal necrolysis (TEN). TEN is a similarlooking condition but rare in children andnearly always caused by a drug reaction. Thebaby or child is usually miserable and feverishand the condition is painful. A thin layerof skin will loosen, with fluid-filled blisters orjust with sheets of skin sliding off the underlyingareas (BAD, 2006). If large areas ofdenuded erythematous areas occur, there willbe exudate with possible electrolyte imbalanceand the risk of septicaemia.Management(1) Swab surface fluid or pus for bacterialculture.(2) Give systemic antibiotics: including Flucloxacillinor Erythromycin which may need tobe given intravenously.(3) Clean skin gently and apply emollient, e.g.Liquid and White Soft Paraffin, NPF ointment(WSP:LP 50:50).Cellulitis and erysipelasCellulitis is a relatively common infection ofthe dermis and subcutaneous tissues, oftendue to streptococci (Figure 12.2). Erysipelasis an infection of the dermis only with a welldefined,raised edge which usually affects theface or lower leg or areas where there is lesssubcutaneous tissue. It can be hard to distinguishbetween the two and in practice theterms may be used interchangeably (Kilburnet al., 2003). Important precipitants includetinea pedis, lymphoedema venous insufficiencyand being overweight as they all lead to skinbarrier breakdown and the consequent entrypoints for infection (DTB, 2003). CellulitisFigure 12.2 Cellulitis. (Source: Graham-Brown and Burns,2006.)presents with an acute onset of red, painful, hot,swollen, smooth, shiny and tender skin, sometimeswith bullae. There may also be systemicupset with nausea, shivering, malaise, fevers andrigors. It usually affects one limb only, nearlyalways a leg. Some cases arise through a breakin the skin, e.g. bites, burns and scalds and cuts,eczema or ulcers.It is important to distinguish between cellulitisof the leg and varicose eczema as thetwo are often confused due to the erythematousinflammation found in both conditions(Quartey-Papafio, 1999). However, there areother clinical features by which to differentiatethe two conditions. Crusting or scaling isthe most important sign in varicose eczemaand not present in cellulitis where the skin issmooth and shiny. Small vesicles are commonin varicose eczema. These break down withthe release of serous fluid which dries to formcrusts which coalesce. Such blister formation israre in cellulitis. Itching is present in varicose

226 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalseczema but not cellulitis and the patient mayhave a history of varicose veins or deep veinthrombosis.Varicose eczema should always be consideredin the differential diagnosis of cellulitis ofthe leg. In varicose eczema, intravenous antibioticsare unnecessary. Treatment will be neededwith 1:10,000 potassium permanganate solutionand topical steroid and emollients (Quartey-Papafio, 1999).Management(1) There are no published UK guidelines orconsensus for treating cellulitis.(2) Hospital admission is advisable for neonates,the immunocompromised or thoseunwell with co-existing disease, those withsevere cellulitis or with periorbital cellulitisand those who lack support at home or arenot improving on treatment (DTB, 2003).(3) Treatment with phenoxymethylpenicillin orbenzylpenicillin can be started ‘blind’ for milduncomplicated cellulitis, as unless there is alikely portal of entry or secondary blistering,it is usually difficult to identify a specificbacteriological cause (DTB, 2003).(4) Drawing around the extent of the infectionwith a permanent marker pen can help totrack for future comparison.(5) Flucloxacillin may be given in addition andthis is common practice in more severe cases.Whether these are given orally or intravenouslywill depend on the patient’s condition.(6) Co-existing disease such as leg ulcers, toewebintertrigo, lymphoedema, venous insufficiency,leg oedema and obesity should alsobe addressed.(7) Recurrence is common (up to 30%) (DTB,2003). There is a strong association withoedema and multiple episodes of cellulitis(Cox, 2006) where the vicious cycle ofoedema predisposing to cellulitis and cellulitisbeing a cause of persistent oedema mustbe appreciated. Cox suggests that interventionssuch as the reduction of oedema ormore prolonged antibiotic therapy mayreduce the risk of recurrent infection.Viral infectionsHerpes simplexHerpes simplex virus (HSV) is a very commonacute, self-limiting vesicular eruption.Humans are the only natural host of HSV andthe virus does not survive for long in the externalenvironment (Goodyear, 2000). It is highlycontagious and spreads by direct contact withinfected individuals when the virus comes intocontact with mucosal surfaces or broken skin.In primary infection, a non-immune person isexposed to contaminated saliva or secretionsfrom the pharynx, genitalia or eyes at closecontact. The virus penetrates the epidermisand replicates in the epithelial cells at the siteof the infection (Gawkrodger, 2003) in the primaryinfection. The latent non-replicating virusthen travels down to the dorsal root ganglionwhere it can lie dormant. At some later date,following exposure to a trigger it can reactivateand travel back down the sensory nerveand reinfect the epithelial cells at the nerveending. This ability to recur is a hallmarkof HSV infection. It usually happens at thesame site, e.g. cold sore. Common triggers arecolds, strong sunlight, stress and menstruation(Docherty, 2001). HSV is preceded by tinglingor burning in the affected area – the prodromalphase. The highest rate of HSV infections is inthe first 5 years of life and then after the onsetof sexual maturity (Goodyear, 2000). It is rareunder 6 months of age due to passive transferof maternal antibodies.There are two types of HSV. Type 1 is usuallyfacial or non-genital and Type 2 is genital due tosexual contact but crossover is seen.Primary infection usually occurs in childrenwhich may often go unrecognised as they aresub-clinical. In those with symptoms, acuteinflammation of the gums and mouth (gingivostomatitis)is common. The children havevesicles on their lips and mucous membraneswhich rapidly erode and are painful. Clusters ofvesicles arise on a background of erythema andover about 10–12 days erode to become crustedlesions. Children are miserable, may be pyrexial

Infective skin conditions and infestations 227and can have problems eating and drinking. Insevere cases, intravenous fluids may be needed.Some children may also have corneal involvement.There may be local lymphadenopathy.This can last for about 2 weeks.Herpetic whitlowThis is a local painful presentation where apainful vesicle or pustule is found on a finger.Type 2 HSV occurs as a primary infection dueto sexual contact in young adults as acute vulvovaginitis,penile or perianal lesions sometimeswith associated dysuria, difficulties in passingurine, fever, headache and muscle pains.Differential diagnosisHSV may be confused with impetigo. The viruscan be cultured or identified by immunofluorescencefrom a swab (Box 12. 2).Box 12.2 Viral swabUse the appropriate medium;Pierce the roof of the blister and placeswab in the fluid and rotate.Source: RCN/BDNG (2008).ComplicationsComplications are rare but serious (Gawkrodger,2003). Secondary bacterial infection is usuallydue to S. aureus. Eczema herpeticum whereeczema becomes infected with herpes simplexis a serious potentially fatal complication(Figure 12.3). Disseminated herpes simplexcan occur in neonates or immunosuppressedpatients. Chronic and atypical lesions can occurin patients with HIV. Herpes encephalitis is aserious complication. Lastly, infection with HSVis the most common cause of recurrent erythemamultiforme (Gawkrodger, 2003).Figure 12.3 Eczema herpeticum. (Source: Graham-Brownand Burns, 2006.)Management(1) Mild HSV may not require any treatment.Those with more severe disease will requiresymptomatic treatment with oral fluids andparacetamol.(2) Recurrent or mild facial or genital HSVcan be treated with aciclovir topically fivetimes daily for 5 days. This helps to reducethe length of the attack and the durationof viral shedding if given early. Viral sheddingoccurs when the virus is active andtransmittable. More severe episodes requireoral aciclovir. Those with recurrent attacksmay require prophylactic treatment withaciclovir.(3) Intravenous aciclovir may be needed forsevere attacks in the immunosuppressed andthose with eczema herpeticum.(4) Genital herpes can be treated with valacicloviror famciclovir. Barrier contraceptionmethods are advised during intercoursewhich ideally should be avoided while thepatient is symptomatic.Varicella zoster (chickenpox)Varicella is an acute, highly infectious diseasecaused by the varicella zoster virus (VZV)which also causes shingles. It is typically adisease of childhood (Macartney and McIntyre,2008) with an incubation period of 7–21 days.

228 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsIt is communicable from 5 days before a rashdevelops until 6 days after. The disease is characterisedby a widespread maculopapular rashwhich often starts on the trunk and then movesto the limbs. Lesions are often seen at all stagesat once: vesicles, papules and crusted lesions.Fever and general malaise are also present.Management(1) Treatment is supportive.(2) Paracetamol may be given for pyrexia.(3) Traditionally lotions, for example calaminelotion, are used. The effect of calamine lotionon pruritis has not been evaluated but it hasa good safety profile and Tebruegge et al.(2006) report some symptomatic relief. Theyfound limited evidence to support the use ofsystemic antihistamines in this context.(4) Lukewarm baths may provide some reliefand light cotton clothing is probably morecomfortable (Shuru, 2003).(5) Scabs should not be picked but allowed tofall off spontaneously.(6) Children with sores in their mouths may bereluctant to eat or drink, so small amountsof clear liquids should be encouragedfrequently.(7) Aciclovir can reduce the number of dayswith fever in otherwise healthy childrenbut its effect on soreness and itching is notcertain (Klassen et al., 2005).(8) Live attenuated varicella vaccines are nowlicensed for use in some countries (not theUK) and are a potential strategy for theprevention of morbidity from varicellainfection. Macartney and McIntyre’s 2008review of the efficacy and safety of vaccinesfor the post-exposure prophylaxis againstvaricella shows that varicella vaccineadministered within 3 days to children followinghousehold contact with a varicellacase reduced infection rates and severity ofcases but did not adequately address safetyaspects.(9) Neonates with chickenpox should betreated with parenteral aciclovir regardlessof immune function to reduce the risk ofsevere disease.(10) Neonates and children and adults who areimmunocompromised and have been exposedto the virus may require prophylaxis withvaricella-zoster immunoglobulin (VZIG).ComplicationsIn healthy children, the disease is mostly selflimiting.The most common complication issecondary bacterial infection (Macartney andMcIntyre, 2008). However, there are the moreserious well-recognised complications of pneumoniaand encephalitis, dehydration, hepatitisand ataxia and these usually lead to hospitalisation.Women who contract varicella in the first20 weeks of pregnancy have a 2% risk of thefoetus developing congenital varicella syndromewith women who contract varicella in the lasttrimester being at increased risk of pneumonia.The onset of varicella in pregnant women from5 days prior to delivery to 2 days after can resultin neonatal varicella in 17–30% (Macartney andMcIntyre, 2008).VZV also remains dormant in the dorsal gangliaof individuals and can reactivate to causeherpes zoster. Primary infection usually provideslifetime immunity but secondary infections dooccur.Immunocompromised patients are at particularrisk from primary VZV infection or reactivation.Herpes zoster (shingles)Herpes zoster or shingles is an acute selflimitingvesicular eruption occurring in a dermatomal(localised area of skin that has itssensation via a single nerve from a single nerveroot) distribution. It is caused by a reactivationof VZV. It is not known what causes this but ismore likely in the elderly, those who are understress or immunosuppressed.It always occurs in people who have previouslyhad varicella (chickenpox). The virus lies dormantin the sensory root ganglion of the spinalcord and when reactivated, the virus replicatesand travels down the nerve to the skin to inducethe cutaneous lesions of shingles. Viraemia (the

Infective skin conditions and infestations 229presence of virus in the bloodstream) is frequentand involvement may be disseminated(Gawkrodger, 2003). The thoracic dermatomesare involved in 50% of cases. Involvement of theophthalmic division of the trigeminal nerve isparticularly common in the elderly.PresentationPain, tenderness and paraesthesia in the dermatomemay precede the eruption by 3–5 days.These are followed by erythema and groups ofvesicles scattered in the dermatomal area. Thevesicles become pustular and then form crusts(Figure 12.4). Secondary infection can occur.These separate after 2–3 weeks and leave scarring.Herpes zoster is usually unilateral and caninvolve adjacent dermatomes. Local lymphadenopathyis common. Shingles recurs in about 5%of cases.ComplicationsSerious complications can occur depending onwhich nerve is involved (Gawkrodger, 2003).Opthalmic disease: If the first trigeminaldivision is affected, corneal ulcers and scarringcan result.Motor palsy: The viral involvement mayspread from the posterior horn of the spinalcord to the anterior horn which resultsin a motor disorder. Cranial nerve palsy orFigure 12.4 Herpes zoster. (Source: Graham-Brown andBurns, 2006.)paralysis of the diaphragm or other musclegroups can happen.Disseminated herpes zoster: Immunosuppressedpatients can develop confluenthaemorrhagic involvement which spreadsand can become necrotic or gangrenous.Postherpetic neuralgia: The pain of shinglesmay go on long after the rash has disappeared.Neuralgia is rare in patients under40 years of age but affects a third of thoseover the age of 60 years and usually subsideswithin 6 months but may go on formore than a year.Management(1) The goals of treatment are to shorten theattack, reduce pain, deal with complicationsand prevent postherpetic neuralgia if possibleand to treat pain should it occur (BAD,2004).(2) In mild disease, treatment is symptomaticwith rest and analgesia. Basic hygieneshould be maintained (Docherty, 2001)and the principles of care for chickenpoxapplied.(3) Any secondary bacterial infection may makethe neuralgia worse and should be treatedwith antibiotics.(4) Patients should stay away from youngbabies and the immunocompromised andmay need to stay off work for 2–3 weeks(BAD, 2004).(5) More severe cases may be treated if seenwithin 72 hours of onset with acicloviror famciclovir to reduce the lengthof the attack and reduce viral shedding.Immunosuppressed patients will needintravenous aciclovir.(6) Except in the immunosuppressed, oral prednisolonecan reduce the incidence of postherpeticneuralgia. There is evidence to showthat gabapentin which was originally developedto treat epilepsy, but is now widelyused to relieve neuropathic pain, may beeffective but ineffective in acute pain (Wiffenet al., 2005). In severe cases, referral to painclinics may be needed.

230 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsMolluscum contagiosumMolluscum contagiosum is a viral skin infectionseen most often in normal immunocompetentchildren. They usually present as single ormultiple (usually no more than 20), discrete,smooth, pearly papules with a classic dimple(van der Wouden et al., 2006) (Figure 12.5).The infection is caused by a pox virus and followscontact with infected people or contaminatedobjects. They occur worldwide but aremore common in areas with warm climates withan association with swimming pool use, age, livingin close proximity and skin-to-skin contactwhile gender, seasonality and hygiene show noassociation (Braue et al., 2005). Infection is rareunder the age of 1 year and most common in the2- to 5-year age group. Affected people and theparents of affected children frequently seek helpfor social reasons; for children name calling andbullying are not uncommon. A large proportionof the parents interviewed by Braue et al.(2005) reported that they were moderately orgreatly concerned and these concerns focused onphysical issues such as scarring, itching and thechance of spread to peers, pain and the effectsof treatments.The estimated incubation period varies from14 days to 6 months. The lesions grow slowlyand can reach a diameter of 5–10 mm in 6–12weeks. They usually resolve spontaneouslywithin 6–9 months without leaving scars but theduration of individual lesions and the entire episodecan be very variable with some lasting for3–4 years (van der Wouden et al., 2006) and thevirus may spread to other areas of skin. Traumasuch as scratching may result in pus, crustingand the destruction of the lesion.It should be noted that there is also a sexuallytransmitted variant which occurs in genital, perineal,pubic and surrounding skin. Molluscumcontagiosum has also been observed with otherdiseases in people with a damaged immune systemand people with HIV infection are particularlyprone (van der Wouden et al., 2006). Asimmunodeficiency progresses in HIV-infectedindividuals, they become more common andresistant to treatment. Multiple lesions on atypicalareas such as the face and neck are oftenseen. There is limited data on the disease coursein this group.Management(1) The option of no treatment is reasonableespecially in young children (van derWouden et al., 2006).(2) Cryotherapy can be very effective but is painfuland not usually tolerated by children.(3) Topical therapies include salicylic acid orpodophyllotoxin cream. Crystacide creamcan be used off license and 5% Imiquimodcream can be used in difficult cases.(4) A recent review of treatments could find noreliable evidence for any of the treatmentscurrently used (van der Wouden et al.,2006) and recommends that until better evidenceon treatment options is found, lesionsshould be left to heal naturally.Viral wartsFigure 12.5 Molluscum contagiosum. (Source: Graham-Brown and Burns, 2006.)Warts (verrucae) are common cutaneous tumoursdue to infection via direct inoculation

Infective skin conditions and infestations 231but may also be found on faces or genitalia.Their surfaces interrupt skin lines. Some facialwarts can resemble a thread or filament (filiformappearance).Figure 12.6 Viral warts. (Source: Graham-Brown andBurns, 2006.)of epidermal cells with human papillomavirus (HPV) and most people will experiencethem at some time in their life (Figure 12.6).They are spread by touch, sexual contact orindirectly via fomites or inanimate objectsor substances capable of carrying infectiousorganisms. They are common in children andthe immunosuppressed are particularly susceptible.Approximately 50% of renal transplantpatients develop warts within 5 years oftransplantation. The epidermis becomes thickenedand hyperkeratotic due to vacuolationof keratinocytes infected by the wart viruswhereby the keratinocytes become filled withfluid-filled vesicles bounded by a membranewithin the cytoplasm. Up to half of commonwarts disappear spontaneously in childrenwithin 6 months. Benign warts almost neverundergo malignant transformation in immunocompetentindividuals. Sterling et al. (2001)advise that periungual warts in combinationwith genital HPV disease warrant carefulattention. In immunosuppressed patients, dysplasticchange is quite common and there isoften a poor correlation between clinical andhistological appearance.Common wartsThese are dome-shaped papules or nodules withpapilliferous surfaces. They are rough, scaly,pink or skin-coloured and usually multiple. Theyare most common on hands or feet in childrenPlane wartsThese are smooth, flat-topped papules whichare often light brown in colour. They are mostcommon on the face and dorsum of hands andusually multiple and painless. They are hard totreat and eventually resolve spontaneously. Theycan Koebnerise, i.e. appear in areas where theskin is injured.Plantar wartsThese are common in children and adolescentsand can be solitary or multiple. They usuallyhave a rough surface and affect the soles of feet,are painful and covered by callus. They growinto the dermis due to pressure.Genital wartsIn females they are found on the vulva, perineumand vagina. In males they are found onthe penis. The perianal area can be affected inthose who have anal sex. They may be smallbut can grow into large cauliflower-like lesions(Gawkrodger, 2003).Management(1) No treatment is a valid option but pain,interference with function, cosmetic embarrassmentand risk of malignancy are indicationsfor treatment (Sterling et al., 2001).An immune response is needed for clearance,so immunocompromised patients maynever show clearance.(2) The majority can be treated in primary care.There is no treatment which is 100% effectiveand different types of treatment mayneed to be combined. Gibbs and Harvey(2006) found a considerable lack of evidenceon which to base the rationale oftopical treatments for warts, although theyfound evidence to support the use of simpletopical treatments containing salicylic acid.There was less evidence for the efficacy ofliquid nitrogen.

232 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals(3) In hand and foot warts, the hyperkeratoticareas can be pared down with a pumicestone and allows for topical treatment.There are many wart paints now available,most of which contain salicylic acid. Thisis a keratolytic which slowly destroys thevirus-infected epidermis. They should beapplied after bathing which will help tomoisten the warts. Treatment needs to becontinued for at least 3 months. Wart paintsare not suitable for the management offacial and anogenital warts or warts on ornear areas of atopic eczema.(4) Topical treatments should always be triedbefore cryotherapy. Cryotherapy with liquidnitrogen is painful and should not becarried out on small children. It should beapplied every 2–3 weeks and can be carriedout on hand, foot and genital warts. It cancause blistering, scarring and damage to nailgrowth. Hypo- and hyperpigmentation canoccur in skin types 5 and 6.(5) Surgical removal by curettage or blunt dissectionfollowed by cautery may be usefulfor filiform warts on the face and limbs butcan result in scarring.(6) Patients with anogenital warts should bemanaged by genito-urinary physicians toexclude the possibility of other sexuallytransmitted infections (Sterling et al., 2001).(7) While many children under 3 years of agehave vertical transmission of anogenitalwarts, sexual transmission (and thereforesexual abuse) should always be considered,especially in older children with no wartselsewhere. This emphasises the need forcareful physical examination and historytakingas well as thorough assessment of thesocial and family dynamics (Wyatt, 2008).Hand, foot and mouth diseaseThis occurs as epidemics in young children andis due to coxsackie A16 virus. Children presentwith oral blisters or ulcers, red-edged vesicleson the hands and feet and mild fever. It usuallyfades within a week.Management(1) Supportive measures only are needed, e.g.paracetamol, encouragement with oral fluids.Kawasaki diseaseThis is an acute systemic vasculitis involvingsmall and medium arteries with a predilectionfor coronary arteries. Peak occurrence in thewinter and spring has been reported with peakincidence in children aged 9–11 months with arange of 6 months to 5 years. It is the secondcommonest vasculitic illness of childhood andassociated with the development of systemicvasculitis complicated by coronary and peripheralarterial aneurysms and is the commonestcause of acquired heart disease in childrenin the UK (Brogan et al., 2002). The causativeagent is unknown but clinical and epidemiologicalfeatures are strongly suggestive of an infectioustrigger, although there is no correlationwith any specific viruses (Brogan et al., 2002;Harnden et al., 2009).There is no diagnostic test for this illness seenin young children, so diagnosis is based on clinicalcriteria which are:Fever of 5 days duration plus four of the following:(1) Conjunctivitis which is bilateral, bulbar andnon-suppurative;(2) Lymphadenopathy which is cervical and| 1.5 cm;(3) Polymorphic rash with no vesicles orcrusts;(4) Changed lip or oral mucosa with redcracked lips, ‘strawberry’ tongue or diffuseerythema of the oropharynx;(5) Changes of the extremities initially with erythemaand oedema of palms and soles. Atthe convalescent stage, peeling of skin fromthe fingertips is seen.It can be diagnosed with less than four ofthese features if coronary artery aneurysms aredetected (Brogan et al., 2002).

Infective skin conditions and infestations 233Management(1) This aims to reduce inflammation and preventthe occurrence of coronary arterialaneurysms (CAA) and arterial thrombosis.(2) Early treatment with aspirin and intravenousimmunoglobulin has been shown toreduce the occurrence of CAA.Fungal infectionsSuperficial fungal skin infections are very commonin people of all ages (Penzer, 2005). Theyare usually considered mild but can be unpleasantand difficult to eradicate; this underlinesthe need for accurate assessment and treatment.They can be more serious in immunosuppressedpeople. They can also lead to compromised skinbarrier function which can predispose to bacterialinfections such as cellulitis. They can be dueto two groups of fungi:(1) Dermatophytes (ringworm): multicellularfilaments or hyphae;(2) Yeasts: unicellular forms which replicate bybudding (Gawkrodger, 2003).Dermatophyte (ringworm) infectionsThese fungi reproduce by spore formation.They invade and colonise the stratum corneumof the skin and keratinised tissues, e.g.hair and nails (Clayton, 2000) and induceinflammation by delayed hypersensitivity or bymetabolic effects. They are classified by associatingthe Latin word for the body part theyaffect with the word tinea: thus tinea capitis(scalp ringworm), tinea corporis (ringworm onthe body), tinea pedis (ringworm of the foot)and tinea cruris (ringworm of the groin andupper thighs), tinea unguium (ringworm of nailplate).They are caused by three groups of fungalorganisms: Trichophyton, Microsporum andEpidermophyton. These organisms can alsobe distinguished as anthrophilic if they prefer‘living on’ human bodies or zoophilic if associatedwith animals. Zoophilic organisms will also liveon humans (Clayton, 2000).Tinea capitisThis is usually seen in pre-adolescent children.Adult cases are rare. The key symptoms arescalp hair loss and scaling. Sometimes there isa black-dot pattern (studded with broken-offhairs) (Figure 12.7). Acute inflammation witherythema and pustule formation may also occur.Infection may also be associated with painfulregional lymphadenopathy. In some cases,kerions or boggy tumours studded with pustulesmay develop which may be misdiagnosedas bacterial abscesses. A generalised eruptionof small itchy papules particularly around theouter helix of the ear, although it can occur anywhere,can occur as a reactive phenomenon or‘id’ response (Higgins et al., 2000; Gonzálezet al., 2007).Fungus can either penetrate the hair shaft(endothrix infection) or penetrate the hair shaftand grow over the outside of the hair shaftat the same time (exothrix infection). Someother conditions can be confused with tineacapitis (Health Protection Agency, 2007). Inalopecia areata, there is rarely inflammationin the area of alopecia and no scaling or itching.Seborrhoeic dermatitis occurs in childrenof all ages but the scaling is diffuse and thereis seldom associated hair loss. Scalp psoriasisproduces more scaling.Figure 12.7 Tinea capitis. Source: Graham-Brown andBurns, 2006.

234 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsThe pattern of tinea capitis has changed in theUK over the past 10 years (Health ProtectionAgency, 2007) with a significant rise in the incidenceand prevalence of causes of infection dueto the anthrophilic organism, Trichophyton tonsurans(T. tonsurans), which causes endothrixinfection. The main focus of the infection hashistorically been linked to Afro Caribbeancommunities and therefore cities where thereare long standing or recently established blackcommunities but the Health Protection Agency(2007) makes it clear that infection can occurin any child irrespective of their ethnic origin.Indeed Higgins et al. (2000) recommend that asit is now so widespread it should be consideredin the diagnosis of any child over 3 months witha scaly scalp.Laboratory diagnosisSpecimens should be taken whenever possibleto confirm the diagnosis as systemic therapywill be required. Skin scrapings (Box 12.3) orbrushings which include hair and hair fragments(Box 12.4) should be used and sent for mycology.Cut hair is not helpful because of theendothrix nature of the infection; hairs shouldbe plucked. Culturing of the scrapings allows foraccurate identification of the organism. Theseshould be repeated after treatment to determinewhether the treatment has been effective ornot. The use of Wood’s light examination is notusually helpful as T. tonsurans is an endothrixinfection so does not fluoresce.Box 12.3 Skin scraping sampleHold a blunt blade at an angle of 45degrees;Scrape along the active scaly edge of thelesion without cutting the patient;Wipe the blade edge or catch the keratinscale onto the black filter paper container.Source: RCN/BDNG (2008).Box 12.4 Hair debrisIdentify affected hair follicles and removeskin, hair and/or debris for collectionsuing a firm toothbrush.Fold inside the black filter paper container.Source: RCN/BDNG (2008).Management(1) Treatment must be systemic. Most superficialfungal infections can be treated topically.However tinea capitis (like fungalnail infections) always requires systemicmedication (González, 2007) as the infectionis found at the root of the hair folliclewhich cannot be reached by topicalagents.(2) Incision and drainage of kerions is not helpfuland must be avoided.(3) Removal of surface crusts from a kerion isoften helpful as it relieves itching and secondaryinfection. It can be painful but canbe done gently after soaking the kerion withlukewarm water or saline (Health ProtectionAgency, 2007).(4) Griseofulvin remains the only licensedtreatment for scalp ringworm in the UK.Absorption is improved if taken with fattyfoods. The dose is at least 10 mg/kg per dayfor 6–8 weeks but up to 20 mg/kg may berequired (Higgins et al., 2000).(5) Terbinafine is now well documented fortreatment at doses based on weight: 20 kg,62.5 mg/day; 20–40 kg, 125 mg/day and40 kg, 250 mg/day for 4 weeks. Terbinafinetablets only are available. The newer treatments(Terbenafine, Itraconazole) are similarto Griseofulvin and may be preferred becausethe treatment durations are shorter and allhave reasonable safety profiles (Gonzálezet al., 2007). However, they are not licensed

Infective skin conditions and infestations 235for use in the UK and are not all availablein paediatric suspensions (Health ProtectionAgency, 2007).(6) The use of a topical treatment, for exampleselenium sulphide or ketaconazole shampoo,or another topically active antifungal,for example Terbenafine cream, is recommendedfor the first 2 weeks of therapy asthis may allow the scalp to heal and preventformation of crusts where there arekerions (Health Protection Agency, 2007).Carriers should also be given a topicalpreparation.(7) Hairbrushes and combs should be cleanedwith simple bleach or Milton (Higgins et al.,2000).Parents are often horrified that their child hasa fungal infection and need reassurance thatthis is not due to a worm (Broomhead, 2007).Children do not need to be kept off school(Health Protection Agency, 2007) as althoughtheoretically there is a potential risk to noninfectedchildren; the method of spread is notclear and the infected child is likely to have beenat school for sometime before detection of theinfection. Exclusion is probably too late to preventspread and in addition only reinforces achild’s isolation.Other children in the household should alsobe examined. Adults in contact with tinea capitiscan very rarely develop tinea corporis.Tinea corporisThis term covers infections of the trunk andlimbs with characteristic annular or ring-likelesions which are usually unilateral. They appearas pink scaly plaques or papules which extendoutwards and heal form the centre (Figure 12.8).The degree of inflammation depends on whetherthe infection is anthrophilic, for example T.rubrum or tonsurans when the lesions are usuallyless erythematous, or zoophilic, for exampleΜ. canis, which produces erythematous scalylesions (Clayton, 2000). It is common in childrenof all ages and adults but rare cases havebeen seen in the newborn.Figure 12.8 Tinea corporis. (Source: Graham-Brown andBurns, 2006.)Tinea crurisThis is rare before puberty but is frequently seenin adolescent males and adults. Erythematousand scaly lesions extend symmetrically fromthe groin down the inner thigh and may containpustules at the edges. Lesions are often veryitchy. The causative fungi are either T.rubrum, T.interdigitale or E. floccosum. The last is alwaysthe cause of outbreaks in groups of sportspeopleor those living in close communities with sharedbathing facilities, for example boarding schools(Crawford and Hollis, 2007).Tinea pedis or athlete’s footThis is the most common form of tinea in temperateclimates (Clayton, 2000). It occurs moreoften in males than females but rarely beforepuberty. The responsible fungi are all anthrophilicwith T. rubrum the commonest species. It usuallystarts in the toe spaces, often between the 4thand 5th toe with peeling, white skin and fissureswhich are usually itchy. It can spread to the toesand soles of the feet. T. rubrum usually results infine dry scaling on the toes which can become

236 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsmore widespread and chronic. T. interdigitalesresults in small clear vesicles which can spreadonto the dorsum of the foot before they ruptureand dry with a scaly edge.DiagnosisScrapings can be taken for microscopy.Management(1) These lesions respond well to topical antifungals,for example imidazole creams, Clotrimazoletwice daily for 2–4 weeks or Terbinafine twicedaily for 7–10 days, which is said to be mosteffective (Crawford and Hollis, 2007).(2) Particularly in tinea pedis, patients shouldbe educated about the importance of goodfoot hygiene and careful drying, especiallybetween the toes because moisture encouragesfungal growth. Patients should alsobe advised to change socks and shoes frequentlyif they become moist with cottonsocks and natural fibre shoes providing betterventilation. The wearing of flip flops incommunal showering facilities or lockerrooms should also be advised.(3) It is particularly important to treat tineapedis in those who are prone to cellulitis.Tinea unguiumOnychomycosis or invasion of the nailplates by species of dermatophytes (mostlyTrichophyton rubrum) is one of the most commondermatological conditions (Figure 12.9).It is very rare in children but increases withage with toenails more commonly affectedthan finger nails. It is often associated withexisting fungal skin infections, e.g. tinea pedis.Although sometimes considered to be a trivialcosmetic problem, it is relentlessly progressiveand in the elderly can give rise to complicationssuch as cellulitis and in those with diabetesor peripheral vascular disease can furthercompromise the limb. It can affect choice offootwear and mobility. It is therefore not surprisingthat it gives rise to many medical consultationsand absence from work (Robertset al., 2003).Figure 12.9 Fungal toenail. (Source: Graham-Brown andBurns, 2006.)It is clinically classified as (Hay and Moore,2004):(1) Distal and lateral subungual onychomycosis(DLSO): This is the most common andnearly always due to dermatophyte infection.It often starts with a streak or patchof discoloration, white or yellow at thefree edge of the nail plate, often near thelateral nail fold. It then spreads to thebase of the nail and may become darkerbrown or black. The nail plate then thickensand lifts from the nail bed (onycholysis).Surrounding skin nearly always showssigns of tinea pedis. It commonly starts asone affected nail with other digits invadedlater. There may be a marked variation inthe degree of damage.(2) Superficial white onychomycosis (SWO): Socalled due to the ‘creamy’ white discolouration,distally this is less common than DLSOand affects the surface of the nail platerather than the nail bed. The dorsal surfaceof the nail plate is eroded in well-circumscribedpowdery white patches where the

Infective skin conditions and infestations 237white material can be easily scraped away.Toenails are usually affected. Onycholysis isunusual.(3) Endonyx onychomycosis: The organisminvades the nail plate from the top surfacepenetrating deep into the nail plate. There iswhite creamy discolouration. The nail plateis scarred with pits and lamellar splits. Itis usually caused by dermatophytes whichcause endothrix scalp infections, notablyT. soudanense.(4) Proximal subungual onychomycosis (PSO):Fungi invade the nail bed and plate via thecuticle. The lanula (half moon) of the nailappear as patches of white or yellow discolouration.This is a rare variety of dermatophyteinfection which is now more commonparticularly associated with immunosuppressedpatients or those with diabetes orperipheral vascular disease. It is thereforeimportant to think about intercurrent disease,especially HIV in these cases.Differential diagnosisThe changes of the nail plate and bed can bemimicked by psoriasis, although fine pittingof the nail plate is never seen in fungal infections.Irregular buckling of the nail can be seenin eczema and in lichen planus there may be aridged or dysplastic nail. Candida can cause paronychiaof the nail where there is a tender areaof infection where the nail and skin meet at theside or the base of a finger or toenail. However,this usually affects the nail plate proximallyand laterally while the free edge is often sparedinitially. Ringworm of the finger nails is rarelysymmetrical and it is common to find the nailsof only one hand affected.ManagementThis is not a trivial problem and affects manypatients’ quality of life, functional activity andgeneral well-being. On the grounds of complications,there is a real need to treat. Toenails cantake 12 months to grow out and 70–80% curerates can be expected with fingernails taking 6months with a cure rate of 80–90% (Robertset al., 2003). It is therefore vital that patientsunderstand the nature of the disease and how itis spread along with an acceptance of the longtermnature and slow clinical improvement ofantifungal treatments.(1) Careful clinical examination of the skin ofthe feet and of the palms is essential.(2) Treatment should not be started on clinicalgrounds alone because although 50% ofnail dystrophies are due to fungal infectionit is not always possible to identify these.A nail sample and clippings should be sentfor mycological examination (Box 12.5).The sample needs to be from nail tissuewhere active disease is present which maymean paring down the nail with a scalpeland clippers to access the nail bed anddebris in the middle of the suspected area ofinfection (Buchanan, 2006). Sampling whitesuperficial nail infection involves scrapingthe upper surfaces of the nails with a curetteor scalpel.(3) Evidence for the effective use of topicaltherapies to treat dermatophyte nail infectionsis limited (Crawford and Hollis, 2007)and systemic treatments are usually used.These include Terbinafine, Itraconazole,Griseofulvin.(4) Proper early treatment of tinea pedis andtinea manum (ringworm of the hand)would almost certainly reduce the prevalenceof tine unguium (Hay and Moore,2004). Candida species can be treatedtopically with an imidazole lotion orcream twice daily to the nail fold or oralItraconazole for 14 days.Box 12.5 Nail clipping sampleIdentify the active edge of the nail;Clip carefully and catch the keratin piecesin the black filter paper container.Source: RCN/BDNG (2008).

238 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals(5) Early diagnosis and treatment is the mosteffective way to manage onychomycosis(Buchanan, 2006), so patient and carer educationis fundamental.(6) Effective treatment of concomitant tineainfections of the skin, e.g. tinea pedis, to tryand prevent ongoing nail involvement andinfection is very important.(7) Patients also need practical advice on foot andnail care especially if they are high risk, e.g.elderly, those with psoriasis, diabetes, peripheralvascular disease or immunocompromised.(8) Advice should cover a good foot care regimeencompassing:■■■■■■■■■■Daily washing with warm (not hot)water and mild soap or soap substitute;Careful drying, especially between toewebs;Moisturising of dry, scaly skin on feetand heels with emollient, although thisshould be avoided between toes;Avoiding the use of dusting powderbetween toes;Socks, tights and shoes should fit welland socks and tights should be changedevery day;Daily checking for any redness, itchingor swelling of skin between and aroundtoes and any changes in colour, shape,thickness or smoothness of nails;Cutting toe nails straight across in linewith toe shape and avoiding cuttingclose to corners of nails;Seeking advice for treatment of cornsand calluses;Prompt advice if fungal infection issuspected;Possible referral to a podiatrist.Buchanan (2006).Tinea incognitoThis is not a specific type of lesion but describesan infection where the usual clinical signs of tineahave been modified by the application of topicalcorticosteroids. The rash may have become morewidespread and the active margins may be lost.Yeast infectionsThese infections are common (Crawford andHollis, 2007) and generally caused by commensalorganisms; organisms which normally liveon the skin (particularly of the oral cavity andgenital tracts) in symbiosis with their humanhosts. This non-parasitic relationship becomespathogenic when opportunistic situations whichfavour its multiplication arise. This is commonwhile patients are taking oral antibiotics or oralcontraceptives or in patients who are immunosuppressed.Candida albicans is a commensal of the mouthand gastrointestinal tract which can result inopportunistic infection (Gawkrodger, 2003).There are predisposing factors which good nursingadvice may help patients to address:(1) Moist and opposing skin folds: advisepatients to dry the skin well after washingespecially in skin folds with the use of individualtowels;(2) Obesity patients require advice about weightreduction strategies;(3) Immunosuppressed patients require educationabout such opportunistic infections in orderto recognise them and seek advice early;(4) Pregnancy(5) Poor hygiene: patients need advice aboutgood skin hygiene and careful drying;(6) Humid environments: patients should beadvised to avoid skin occlusion in order toaid healing and prevent recurrence;(7) Wet work occupations: offer advice aboutcareful hand drying and hand protectionduring wet work, e.g. gloves;(8) Use of broad-spectrum antibiotics should beavoided unless necessary.PresentationYeast infections may present in a number of differentways.Genital thrush commonly presents as anitchy, sore vulvovaginitis. Mucous membranesare inflamed and white plaques adhere tothese. There may be a white vaginal dischargeor penile discharge. Thrush can be spread bysexual intercourse.

Infective skin conditions and infestations 239IntertrigoThere is a moist macerated appearance to thissuper-infection with Candida albicans in the submammary, axillary or inguinal folds and in theinterdigital clefts. Red macerated skin with satellitelesions just ahead of the advancing edge isvery distinctive of candida.OralWhite plaques stick to the buccal mucosa(Figure 12.10). Unlike leukoplakia (white plaqueson the mucous membranes), these can be scrapedoff and leave small bleeding points underneath.Broad-spectrum antibiotics, false teeth, poor oralhygiene and poorly sterilised feeding equipmentin babies can predispose to this.SystemicSystemic candidiasis can occur in immunosuppressedpatients. Red nodules or pustules areseen in the skin.Management(1) There is little evidence on the optimal treatmentof candidal skin infections.(2) It is generally agreed that general measuressuch as good hygiene and careful dryingshould be improved and other predisposingfactors addressed.(3) Topical imidazoles, for example clotrimazole,ketaconazole, are recommended forfirst-line treatment.(4) Oral treatment is required for people withsevere or extensive disease or when topicaltreatment has failed.(5) Oral Fluconazole is recommended as thefirst-line treatment if systemic treatment isneeded.(6) In children under the age of 12 years specialistadvice should be sought.Pityriasis versicolorThis is a chronic yeast infection which is oftenasymptomatic. It is seen in adolescents andadults but not younger children. It is characterisedby pigmentary changes, often on thetrunk and proximal parts of the limbs. Brownor pinkish oval or round scaly patches are seen(Gawkrodger, 2003) (Figure 12.11). In tannedor pigmented skin, the lesions may be hypopigmented.It is caused by overgrowth of a yeastcalled Pityrosporum orbiculare. It is common inyoung adults.Management(1) Topical imidazole antifungal, e.g. Canestenor Daktarin, or alternatively selenium sulphideshampoo (Selsun) or ketaconazoleshampoo should be applied and showeredoff after 5–10 minutes three times a weekfor 2 weeks. The best way to do this maybe to lather the shampoo on the scalp andthen allow the lather to sit on the skin.Figure 12.10 Candida albicans. (Source: Weller etal., 2008.)Figure 12.11 Pityriasis versicolor. (Source: Graham-Brownand Burns, 2006.)

240 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsWhile redness and scaling rapidly improves,colour disturbances can take months torecover.(2) Recurrence is common, so patients need tobe made aware of the difference betweenprolonged repigmentation and recurrence ofthe active condition.(3) For resistant cases, Itraconazole 200 mgdaily for 7 days may be given.InfestationsInfestations are defined as the harbouringof insect or worm parasites in or on the body(Gawkrodger, 2003) and these are also commonpresenting problems in primary care.ScabiesScabies is a contagious parasitic infection ofthe skin endemic throughout the world witha global prevalence of 300 million but particularlyproblematic in areas of poor sanitation,overcrowding and social disruption(Strong and Johnstone, 2007). Despite itsincidence, it is often missed or misdiagnosed.It can affect people of any age but is mostlyseen in children, young adults, elderly peopleespecially those in institutions and those whoare immunocompromised. It is more commonin overcrowded situations and in urban areas.It is a huge source of embarrassment and miseryfrom severe itching and sleepless nights.Disease control is often hampered by inappropriateor delayed diagnosis and poor treatmentcompliance (Heukelbach and Feldmeier,2006).It is caused by the Sarcoptes scabeii mite andspreads from person to person by direct skincontact which includes sexual, though transfervia clothing or furnishings is possible. The pregnantfemale lays eggs in burrows in the stratumcorneum; 50–72 hours later, the larvae appearand make new burrows. They mature, mate andrepeat this 10- to 17-day cycle. Physical findingsinclude burrows (Figure 12.12), erythematousFigure 12.12 Scabies burrow. (Source: Graham-Brown andBurns, 2006.)papules, excoriations, nodules, vesico-pustularor bullous lesions and secondary bacterialinfection. The classic sites of infection arebetween the fingers, the wrists, axillary areas,female breasts (particularly the skin of the nipples),peri-umbilical area, penis, scrotum andbuttocks (Strong and Johnstone, 2007). Infantsare usually affected on the face, scalp, palmsand soles. There are more pustules in youngerchildren. The condition is very itchy which isoften worse at night. The host immune reactionto the presence of mites and their productsin the epidermis (Heukelbach and Feldmeier,2006) is the source of much of the itchingand can appear about a month after initialinfection and persist for up to 6 weeks aftertreatment.Crusted (Norwegian) scabies is much moresevere and is associated with extreme incapacityand immunosuppression such as in HIVinfection. This form of scabies presents with ahyperkeratotic dermatosis which can resemblepsoriasis and lymphadenopathy and eosinophiliamay also be present. Itching may be surprisinglymild. These patients are highly infectiousand may harbour millions of mites which mayalso be on the scalp (Strong and Johnstone,2007). Complications are few but secondarybacterial infection with S. aureus or GroupA Streptococcus can occur. Scabies is a riskfactor for developing acute post-streptococcalglomerulonephritis (Heukelbach and Feldmeier,

Infective skin conditions and infestations 2412006). In crusted scabies, a generalised lymphadenopathyis common and secondary sepsiscan lead to death.DiagnosisThis is usually made on clinical grounds and goodhistory-taking. Other family members may beinfected and although they may be asymptomatic,more classically itching which starts at the sametime amongst family members or those living in aninstitution, indicates scabies. Differential diagnosisincludes atopic eczema, allergic contact dermatitis,insect bites, papular urticaria and impetigo.Microscopic identification of the mite can bemade by picking out a mite from a burrow witha needle. Alternatively, scrapings can be lookedat in the same way.ManagementThe management of scabies falls into two equallyimportant halves:(1) Getting rid of the patient’s own scabies andensuring that all family and those who havehad prolonged contacts are treated, even ifthey are asymptomatic. This means checkingwho lives at home and who visits regularlyand ensuring the patient knows how toapply the treatment correctly.(2) Making sure that the patient and contactsdo not catch it again which means that allfamily members and sexual contacts mustbe treated too, whether they say they areitchy or not (BAD, 2004).Of the topical scabicides in use (Maliathon,Permethrin and Sulphur), on recent review,Permethrin appears to be the most effective(Strong and Johnstone, 2007). This must beapplied correctly in order to be effective.Procedure:(1) All those who need treatment should applyit at the same time.(2) Avoid bathing before application as thisincreases absorption into the blood andremoves the treatment from their site ofaction on the skin (BNF, 2008).(3) Treatment should be applied to the wholebody, including the scalp, face, neck andears.(4) Special care needs to be taken with genitalia,flexures, fingernails, webs of the fingersand toes.(5) Leave the treatment on for at least 12 hoursbefore washing off.(6) When hands are washed during this period(or a child’s nappy changed), treatmentshould be reapplied.(7) Apply two treatments 1 week apart.(8) Ordinary washing of clothes and bedding issufficient (BAD, 2004).Ivermectin, an oral antihelminthic appears tobe an effective (off license) treatment (Strongand Johnstone, 2007) and may be useful in themanagement of crusted scabies and epidemics.Plant derivatives, for example neem, turmericand tea tree oil, are promising future treatments(Heukelbach and Feldmeier, 2006).Following effective treatment, itching cantake up to 6 weeks to subside unless reinfestationoccurs. This allows time for lesions to healand for eggs and mites to reach maturity (i.e.beyond the longest incubation interval), if treatmentfails (Strong and Johnstone, 2007). Scabiesnodules can take longer to subside and topicalcorticosteroids may be indicated.LiceLice are flat, wingless blood-sucking insectsthat lay their eggs or nits on hairs and clothing.There are two species: body lice (includes headlice) and pubic lice. These are often very stigmatisingconditions.Body liceThe body louse is usually seen in people living inpoor social conditions and is spread by infestedbedding and clothing. Excoriation is commonand lichenification and pigmentary changes mayoccur. The lice are seen on the clothing, not theperson. It can be treated by washing clothing andbedding and topical application of maliathon orpermethrin.

242 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsHead lice (Pediculosis capitis)These are a worldwide phenomenon and affectpeople of all ages but are very common amongchildren with those aged 4–11 years most affected(Wyndham, 2008). The itching usually starts at theside and back of the head and the scratching oftenresults in secondary infection and matted hair.The nits or eggs are often easier to see than thelice (Gawkrodger, 2003). They are more commonin girls and in urban areas and spread by head tohead contact. For reasons which are unclear, somechildren experience persistent head lice infestationswhich last weeks, or even years (Gordon, 2007).For many of these children and their families, thisis very problematic and the strain and difficultieswhich should not be underestimated are welldocumented by Gordon. The families she studiedexperienced ostracisation and social isolation andfeelings of failure as parents. They sought helpfrom a multitude of services while trying to keepthe lice a secret from their communities and welldemonstrated the ways in which head lice madethem lose their sense of perspective.ManagementThis needs to be with the pediculicide to whichthe lice are most likely to be sensitive and willvary from district to district. Maliathon, permethrinor carbaryl lotion are all commonlyused. Shampoos are too weak to be effective solotion or liquid preparations should be used.Alcoholic preparations are most effective butcan be irritant (BNF, 2008).(1) Apply pediculicide to all areas of the scalp andto all the hairs from their roots to their tips.(2) Leave on for 12 hours before washing offand repeat after a week to kill any lice whichhave hatched out after the first application.(3) If lice are found after the second treatment,then treatment should start again with a differentpediculicide.(4) Alcohol-based lotions can sting but shampooswhich are on for a short time are lesseffective.(5) Hair should also be combed on a daily basiswith the help of a good light and a magnifyingglass. Combing (which can be verytime consuming) should go on until noliving lice have been found for 2 weeks. Usinga conditioner to lubricate the hair make maycombing easier. The comb should be washedregularly to remove lice and eggs (BAD, 2008).Pubic licePubic lice results in severe itching with secondaryinfection and eczema. Maliathon or permethrinshould be applied to all the body andany secondary infection treated. Sexual partnersalso need to be treated.AIDS and the skinAcquired immune deficiency syndrome (AIDS) iscaused by the HIV which affects immunocompetentcells including CD4 T-cells and macrophages.Dermatological involvement in AIDS hasbeen appreciated since the first recognition of thedisease (Bunker and Gotch, 2004). The proportionof patients with skin complications and thenumber of these manifestations in any one patientincrease as HIV progresses and AIDS develops.The incidence and severity of several commondermatological conditions covered in this chapter,for example herpes simplex and herpes zoster,folliculitis, viral warts, mollusca, tinea and scabies,are increased in patients with HIV, often incorrelation with their CD4 count. Skin diseasemay therefore provide the first suspicion of thediagnosis of HIV infection and may also presentwith unusual signs and symptoms, coexist withother pathologies or be altered by treatment, allof which may make them a challenge to diagnoseand manage. As highlighted by Bunker and Gotch(2004), good history-taking and examination istherefore vital.ConclusionThe success of treatments relies on bothnurses and parents, carers and patients workingtogether. As nurses, we need to explore the

Infective skin conditions and infestations 243extent to which patients follow advice abouttreatments and medications. This means discussionand exploration with patients usingopen questioning as this is more likely to leadto admission about potential difficulties withadherence. Education is vital to explain pathomechanismsand medication. The patient’s levelof knowledge about the disorder needs to beassessed so that gaps can be filled in. Treatmentrationale and ramifications of non-adherenceneed to be discussed and instructions simplified,adjusted or interpreted if necessary (Popovichand McAlhany, 2007) to ensure understanding.Adherence is likely to be better when the patientbelieves the medication is safe. The tailoring ofmanagement to meet individual needs and thesimplification of treatment regimens to makethem realistic and achievable are also essential.Niggermann (2005) also suggests the useof reminders or practical tips such as the use ofcalendars and tick boxes to reduce medicationomissions. The importance of follow-up whichis appropriate and negotiated with the patientwill also enhance the relationship of trustwhich Popovich and McAlhany (2007) suggestimproves the level of adherence.The first step towards a successful outcomein the management of all these infections andinfestations is accurate diagnosis but this mustbe coupled with adherence to management toprevent the risk of further spread and achievepositive outcomes. Education is therefore key.ReferencesAll Parliamentary Group on Skin (APPGS)(2008). Commissioning of Services for Peoplewith Skin Conditions. London: APPGS.Braue, A., G. Ross, G. Varigos and H. Kelly(2005). Epidemiology and impact ofchildhood molluscum contagiosum: A caseseries and critical review of the literature.Pediatric Dermatology, 22(4): 287–294.British Association of Dermatologists (BAD)(2004). Scabies Patient InformationLeaflet. London: British Association ofDermatologists.British Association of Dermatologists (2006).Staphylococcal Scalded Skin Syndrome:Patient Information Leaflet. London: BritishAssociation of Dermatologists.British Association of Dermatologists (2007).Boils Patient Information Leaflet. London:British Association of Dermatologists.British Association of Dermatologists(2008). Head Lice Patient InformationLeaflet. London: British Association ofDermatologists.British National Formulary (BNF) (2008). No56 London: BMJ Publishing.Brogan, P.A., A. Bose, D. Burgner et al.(2002). Kawasaki disease: An evidencebased approach to diagnosis, treatment, andproposals for future research. Archives ofDisease in Childhood, 86: 286–290.Broomhead, C. (2007). Fungal infections of theskin and nails. Practice Nurse, 33(9):25–29.Buchanan, P. (2006). Onychomycosis:Managing patients at risk. Journal ofCommunity Nursing, 20(6): 35–40.Bunker, C. and F. Gotch (2004). AIDS andthe skin. In: Burns, T., Breatnach, S., Cox,N., Grifiths, C. (Eds), Rook’s Textbook ofDermatology (7th edition), pp. 26.1–26.41.London: Blackwell Science.Burr, S. (2003). Impetigo. In: Barnes, K. (Ed.),Paediatrics: A Clinical Guide for NursePractitioners, pp. 70–72. London: ElsevierScience.Charman, C. and S. Lawton (2006). Eczema:What Really Works. London: Robinson.Clayton, Y.M. (2000). Superficial fungalinfections. In: Harper, J., Oranje, A. andProse, N. (Eds), Textbook of PaediatricDermatology, pp. 447–467. Oxford:Blackwell Science.Courtenay, M., N. Carey and J. Burke (2007).Independent extended nurse prescribing forpatients with skin conditions: A nationalquestionnaire survey. Journal of ClinicalNursing, (16): 1247–1255.Cox, N. (2006). Oedema as a risk factor formultiple episodes of cellulitis/erysipelas of thelower leg: A series with community followup.British Journal of Dermatology, (155):947–950.

244 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsCrawford, F. and S. Hollis (2007). Topicaltreatments for fungal infections of the skinand nails of the foot. Cochrane Database ofSystemic Reviews, (3): Art No: CD001434.DOI:10.1002/14651858. CD001434.pub2.Docherty, C. (2001). Infections and infestations.In: Hughes, E., Van Onselen, J. (Eds),Dermatology Nursing: A Practical Guide.London: Churchill Livingstone.Gawkrodger, D. (2003). Dermatology: AnIllustrated Colour Text. London: ChurchillLivingstone.Gibbs, S. and I. Harvey (2006). Topical treatmentsfor cutaneous warts. Cochrane Database ofSystematic Reviews, (3): Art No: CD001781.DOI:10.1002/14651858.CD01871.pub2.González, U., T. Seaton, G. Bergus, J.Jacobson and C. Martinez-Monzon (2007).Systemic antifungal therapy for tineacapitis in children. Cochrane Databaseof Systemic Reviews, (4): Art No:CD004685. DOI:10.1002/14651858.CD004685.pub2.Goodyear, H. (2000). Herpes simplex virusinfections. In: Harper, J., Oranje, A.,Prose, N. (Eds), Textbook of PaediatricDermatology, pp. 321–328. Oxford:Blackwell Science.Gordon, S.C. (2007). Shared vulnerability:A theory of caring for children with persistenthead lice. The Journal of School Nursing,23(5): 283–292.Gould, F.K., R. Brindle, P.R. Chadwick etal. on behalf of the MRSA Working Partyof the British Society for AntimicrobialChemotherapy (2009). Guidelines (2008) forthe prophylaxis and treatment of methicillinresistantStaphylococuus aureus (MRSA)infections in the United Kingdom. Journalof Antimicrobial Chemotherapy AdvanceAccess, published12 March 2009.Graham-Brown, R. and Burns, T. (2006).Lecture Notes: Dermatology (9th edition).Oxford: Blackwell Science.Harnden, A., R. Mayon-White, R. Perera, D.Yeates, M. Goldacre and D. Burgner (2009).Kawasaki disease in England: Ethnicity,deprivation and respiratory pathogens. ThePediatric Infectious Disease Journal, 28(1):21–24.Hay, R. and M.K. Moore (2004). Mycology. In:Burns, T., Breatnach, S., Cox, N., Grifiths, C.(Eds), Rook’s Textbook of Dermatology (7thedition), pp. 31.1–31.101. London: BlackwellScience.Health Protection Agency (2007). Tinea Capitisin the United Kingdom. A report on itsDiagnosis, Management and Prevention.London: Health Protection Agency.Heukelbach, J. and H. Feldmeier (2006).Scabies. The Lancet, (367) 9524, 1767–1774.Higgins, E.M., L.C. Fuller and C.H. Smith(2000). Guidelines for the management oftinea capitis. British Journal of Dermatology,143: 53–58.Kilburn, S., P. Featherstone, B. Higgins, R.Brindle and M. Severs (2003). Interventionsfor cellulites and erysipelas. (Protocol)Cochrane Database of SystematicReviews, (1): Art No: CD004299.DOI:10.1002/.14651858. CD004299.Klassen, T.P., L. Hartling, N. Wiebe andE. Belsecl (2005). Acyclovir for treatingvaricella in otherwise healthy children andadolescents. Cochrane Database of SystematicReviews, (4): Art No: CD002980. DOI:10.1002/14651858. CD002980.pub3.Koning, S., A.P. Verhagen, L.W.A. vanSuijlekom-Smit, A. Morris, C.C. Butler,J.C. van der Wouden (2003). Interventionsfor impetigo. Cochrane Database ofSystematic reviews, (2): Art No: CD003261.DOI:10.1002/14651858.CD003261.pub2.Loffeld, A., P. Davies, A. Lewis and C. Moss(2005). Seasonal occurrence of impetigo:A retrospective 8-year review (1996–2003).Clinical and Experimental Dermatology, 30:512–514.Macartney, K. and P. McIntyre (2008). Vaccinesfor post-exposure prophylaxis againstvaricella (chickenpox) in children and adults.Cochrane Database of Systematic Reviews, 3:Art No: CD001833. DOI:10.1002/14651858.CD001833.pub2.McCormick, A., D. Fleming and J. Charlton(1995). Morbidity Statistics from GeneralPractice. Fourth National Study 1991–1992.London: HMSO.Nathwani, D., M. Morgan, R.G. Masterton et al.(2008). Guidelines for UK practice for the

Infective skin conditions and infestations 245diagnosis and management of methicillinresistantStaphylococcus aureus (MRSA)infections in the community. Journal ofAntimicrobial Chemotherapy, (61): 976–994.Niggermann, B. (2005). How can we improvecompliance in pediatric pneumology andallergology? Allergy, 60(6): 735–738.Penzer, R. (2005). Common superficial fungalinfections of the skin. Nursing in Practice,Jul/Aug 31–34.Popovich, D. and A. McAlhany (2007).Accurately diagnosing commonlymisdiagnosed circular rashes. PediatricNursing, 33(4): 315–320.Quartey-Papafio, C.M. (1999). Importance ofdistinguishing between cellulitis and varicoseeczema of the leg. British Medical Journal,318: 1672–1673.Royal College of Nursing/British DermatologicalNursing Group (2008). Competencies foran Integrated Career and CompetencyFramework for Dermatological Nursing, pp.48–49. London. Royal College of Nursing.Resnick, S.D. (2000). Staphylococcal andstreptococcal skin infections: Pyodermasand toxin-mediated syndromes. In: Harper,J., Oranje, A., Prose, N. (Eds), Textbookof Paediatric Dermatology, pp. 369–372.Oxford: Blackwell Science Ltd.Roberts, D.T., W.D. Taylor and J. Boyle (2003).Guidelines for treatment of onychomycosis.British Journal of Dermatology, 148(3):402–410.Shuru, D. (2003). Varicella (chickenpox). In:Barnes, K. (Ed.), Paediatrics: A ClinicalGuide for Nurse Practitioners, pp. 227–229.London: Elsevier Science.Sterling, J.C., S. Handfield-Jones andP.M. Hudson (2001). Guidelines for themanagement of cutaneous warts. BritishJournal of Dermatology, 144(1): 4–11.Strong, M. and P.W. Johnstone (2007).Interventions for treating scabies. CochraneDatabase of Systematic Reviews, (3): Art No:CD0032 0. DOI:1002/14651858. CD000320.pub2.Tebruegge, M., M. Kuruvilla and I. Margarson(2006). Does the use of calamine orantihistamine provide symptomatic relieffrom pruritis in children with varicella zosterinfection? Archives of Disease in Childhood,91: 1035–1036.van der Wouden, J.C., J. Menke, S. Gajadinet al. (2006). Interventions for cutaneousmolluscum contagiosum. CochraneDatabase of Systemic Reviews, (2): ArtNo: CD004767. DOI:10.1002/14651858.CD004767.pub2.Watson, T. and G.P. de Bruin (2007). Impactof cutaneous disease on the self-concept: Anexistential – Phenomenological study of menand women with psoriasis. DermatologyNursing, 19(4): 351–364.Weller, R., J.A.A. Hunter, J. Savin and M.Dahl (2008). Clinical Dermatology (4thedition). Oxford: Blackwell Publishing.Wiffen, P.J., H.J. McQuay, J.E. Edwardsand R.A. Moore (2005). Gabapentinfor acute and chronic pain. CochraneDatabase of Systematic Reviews, (3): ArtNo: CD005452. DOI: 10.1002/14651858.CD005452.Wyatt, H. (2008). Non-accidental injury indermatology. Dermatological Nursing, 7(4):30–36.Wyndham, M. (2008). Picture. CommunityPractitioner, 81(2): 33.


13Less common skinconditionsRebecca PenzerIntroductionIt is something of a challenge to select the mostcommon, uncommon skin conditions to includein this chapter. The conditions that have beenincluded here are the ones that someone workingin a general setting is most likely to see.Those working in a specialist area are likelyto see all of them at some point in time. Alsoincluded in this chapter are some conditionswhich do not fit easily into any of the otherchapters and are actually quite common, e.g.rosacea and pityriasis rosea.The structure of this chapter is to provide anoutline of the disease itself; the way it presentsand its pathogenesis and then to describe thetreatments that are relevant to each condition,along with evidence for selection of the treatmentif any is available. Any specific nursingcare activities will be included in the section ontreatment. This chapter will not repeat the informationgiven in previous chapters about theimportance of considering quality of life, concordanceand psycho-social impact, although ofcourse all these issues will be pertinent.Blistering conditionsBlisters can appear in the skin as a result of anumber of causes. These include:■■■■■Congenital in which there are faults in theway the layers of skin adhere together;Physical in which the skin splits because ofsome kind of injury, e.g. sheering forces;Infections which cause disruption in the layersof the skin (usually the epidermis) whichlead to blistering, e.g. impetigo;Inflammation in its acute phase can lead tosecondary blistering, e.g. eczema;Immunobullous disease in which immunologicallymediated damage leads to splittingof the layers of skin either between the dermisand the epidermis or between the layersof the epidermis, e.g. bullous pemphigoid(Graham-Brown and Bourke, 1998).In this section, the focus will be on the morecommon congenital diseases and the immunobullousdiseases.

248 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsEpidermolysis bullosaThis describes a group of inherited blisteringdisorders which generally present early in life,although milder forms of the disease may notpresent until later in life. The autosomal dominantforms of epidermolysis bullosa (EB) requirejust one parent to have the faulty EB gene andthe autosomal recessive forms require bothparents to pass on an EB gene. This geneticallydetermined group of conditions are characterisedby the fact that the layers of skin do notadhere to each other normally, leading to splitsbetween the layers of skin. Where these splitsoccur will determine the exact type of EB thatan individual experiences (see Table 13.1).TreatmentThe treatment for all forms of EB focus on protectingthe skin, minimising trauma and reducingthe likelihood of infection. A syste maticreview found that there was no reliable trialevidence for other interventions for treating EB(Langan and Williams, 2009). The more severeforms will also involve ensuring adequate nutritionalintake and surgery to manage scarringwhich can cause ‘webbing’ to develop betweenTable 13.1 Summary of the types of epidermolysis bullosa.Type of EBType ofinheritanceLevel ofcleavage Subtype Location of blisters Course of diseaseEB simplexAutosomaldominantWithin thebasal cells ofthe epidermisGeneralisedAreas of trauma orfrictionIntense levels of blistering startingas a neonate, which heal withoutscarring but can lead to severe incapacitycontinuing into adulthood.As above, although onset maybe delayed until adolescence oradulthood.Very rare. Can be fatal to infantshowever may subside as the childgrows up.Weber–CockayneHands and feetfollowing traumaDowlingMearaGeneralised severeform. Blisters presentat birth, face, trunkand limbs. Mayinvolve mouth, GIand respiratory tractsWidespread includingmouth andpharynxJunctionalAutosomalrecessiveWithin laminalucida ofthe basementmembranezoneSubepidermalwith loss ofanchoringfibrilsEroded areas are widespread andhard to heal. Begin in neonatalperiod. Child often dies early dueto sepsis.DystrophicAutosomalrecessiveWidespread includingmouth, pharynxand eyesBlisters appear either from trauma orspontaneously and heal with scarring.If mouth/pharynx is involved, therecan be problems with eating and eyescarring can lead to blindness. Nailsand teeth are abnormal and squamouscell carcinomas may develop inatrophic areas.Less serious than recessive butscarring does occur and blisteringcontinues throughout life.AutosomaldominantSmaller blistersgenerally appearingon limbs and areas oftrauma

Less common skin conditions 249fingers and toes. Thus, consideration must begiven to soft furnishing, padded with sheepskinsand soft clothes that do not rub or scratch. Thechild must always be handled with great careto minimise the amount of blistering caused byfriction and trauma. For those who have thevarious forms of EB simplex, healing occurswithout scarring and although this may takesome time it does usually happen. Dystrophicforms of EB, particularly the recessive forms,will scar and require great care to be given todressings and preventing infections.The most important feature of any dressingsthat are used is that they are non-adherent andthat they can stay in place for a number of dayswithout requiring changing. Thus a secondaryabsorbent dressing may need to be placed over theprimary non-adherent one. Dressings should notbe stuck to the skin but secured with light bandagesor cotton tubular dressings. If dressings dobecome stuck to the skin, it may cause less traumato remove them whilst soaking in a bath duringbathing (Ly and Su, 2008). Pain relief duringdressing change is likely to be necessary; the choiceof pain relief dependant on the level of pain. Forsome, Entonox may provide sufficient relief duringthe dressing change and avoids the problemsof drowsiness associated with some pain relief.Nutritional problems occur most commonlyin the more severe forms of EB; junctional, dystrophicrecessive and Dowling Meara. From anearly age, neonates can develop blisters in theirmouths, the lips and on the tongue which makefeeding very painful. This may be helped by usingteething gel and white soft paraffin on the lips, butoral feeding may in the end prove too difficult. Inthis instance, a long-term nasogastric tube shouldbe used. Breast feeding is rarely successful as thechild’s face becomes blistered whilst suckling andrubbing against its mother’s breast.At all ages, EB sufferers are likely to have highcalorific requirements due to the calories requiredfor wound healing. This in combination with thedifficulty of eating orally can mean that maintainingadequate nutrition is extremely challenging.Gastrostomy feeding may be necessary.Physiotherapy will be helpful for those withdystrophic recessive EB in order to help minimisethe contractions caused by scarring.EB in all its forms can be a distressing condition,particularly as it occurs so early in lifeand as there is little effective treatment, onlysymptom management. It is important that anaccurate diagnosis is made early on so that theparents know what to expect by way of diseaseseverity. For those with the recessive form of thecondition there is unlikely to have been any previousexperience of the disease. It is importantthat parents have the opportunity to discuss thelikelihood of having subsequent children withthe disease, with a genetic counsellor. Prenataldiagnosis is possible.Immunobullous diseasesBullous pemphigoidThe most common of the immunobullous conditions,bullous pemphigoid predominantly affectsthe older population usually occurring in theseventh or eighth decade. It affects men andwomen equally. The split in the skin is subepidermalleading to tense fluid filled blistersin which the roof of the blister is the full thicknessof the epidermis (Figure 13.1). The split isFigure 13.1 Bullous pemphigoid. (Source: Reprinted fromGraham-Brown and Burns, 2006.)

250 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalstriggered by the presence of a specific antibody,its action is directed at the basement membranecomplex (probably the hemidesmosomes (seeChapter 2). The blisters often occur in flexuresand around 50% of patients have lesions onthe mucous membranes, the mouth being mostcommonly affected (Wojnarowska et al., 2002).Prior to the blisters developing, it is usual forpatients to experience an irritating erythematousrash which may look somewhat urticarial. Theblisters themselves may be haemorrhagic (bloodfilled).Diagnosis is usually confirmed by a biopsywhich should be taken from the edge of a newblister. This will show the subepidermal split.Direct immunofluorescence will show the antibodieslining up along the basement membranesof the cells. The disease is self-limiting and blisterswill eventually stop forming; however this maytake years, so treatment is usually necessary anddesirable.TreatmentIntensity of treatment will depend on the severityof the disease. The overall aim of treatment isto suppress the symptoms of blister formation,pruritis and urticaria, so that quality of life ismaintained. This is generally achieved by immunosuppressionof some description. Because thepatient population is generally elderly, the treatmentof symptoms with potent immunosuppressioncan cause a level of morbidity or evenmortality, thus treatments must be closely monitoredand there is a significant need for expertnursing care.For more mild to moderate disease controlmay be gained by the use of very potent topicalsteroids (particularly 0.05% clobetasol proprionate)alone. This may be sufficient to gaincontrol and oral therapies may not be needed. Areview of the evidence for BP treatment regimesshows that there is little consensus about exactlevels of oral treatment (Wojnarowska et al.,2002). However, the evidence does indicatethat oral corticosteroids (usually prednisolone)should be used to control new blister formationin severe forms of the disease. 1 mg/kg isthe commonly recommended starting dose forextensive disease, although in reality the dosagemay not be directly related to patient weight anda starting dose of 60 mg is often used. The qualityof evidence of the effectiveness of any of theother oral therapies is low; azathioprine is themost common additional treatment used, butthe studies looking at its steroid sparing effectsare conflicting (Wojnarowska et al., 2002).However, it may be added into a treatmentregime if steroids alone are not halting blisterformation. In severe disease, topical therapiesare often used alongside the oral therapy.High doses of steroids in elderly patients areassociated with significant levels of morbidity andoccasionally mortality. Careful monitoring forglucose in the urine and increased blood pressureshould be routine. Monitoring the patient’s temperaturewill help indicate if an infection is developing.Eroded areas should be swabbed and sentfor culturing if there are signs of infection.Helping patients to remain comfortable andmanaging the blisters are key nursing roles. Newblister formation should be logged each day as amethod of determining treatment efficacy, i.e. iftreatment is working, the number of new blistersdeveloping each day will reduce and eventuallystop. New blisters need to be broken using minimalskin trauma. Making a small incision with ablade is more effective than lancing with a needleas the incision is less likely to reseal than a hole.The skin should be left in place in order to forma natural dressing over the dermis. If topical steroidsare being applied to the lesions, it is easierto apply the product to a non-adherent dressingand then onto the skin – cream is preferable to anointment. The dressing should be secured usinga light bandage or cotton tubular bandage, nottape. Maintaining skin hygiene is important inview of the large areas of open skin. Daily bathingwith an antiseptic emollient may be helpful,although no evidence could be found to supportthis. Bland petrolatum emollients (e.g. white softparaffin/liquid paraffin) can be helpful to maintainskin comfort particularly in the old blistersites where the skin tends to be dry.Treatment is gradually reduced over time andthen stopped once it appears that the patient isin total remission. Wojnarowska et al. (2002)recommend that treatment is reduced every 1–2

Less common skin conditions 251months and also states that the appearance ofthe occasional lesion should not lead to increasein treatment, rather should be taken as an indicationthat the condition is not being over treated.It is possible for people to experience relapsesafter periods of remission at which point treatmentmay need to be introduced again.PemphigusThis describes a group of disorders in whichthe skin splits at different levels within the epidermis.There is dissolution of the intracellularcement which holds the epidermal keratinocytestogether caused by an antibody that actsdirectly on these intracellular proteins. The epidermalcells then no longer hold together andflaccid, easily broken blisters appear. The mostcommon type of pemphigus (pemphigus vulgaris)is still very rare (probably around 1 in amillion), although it is seen more commonly inAshkenazy Jews and Indians. It tends to affecta younger age group than bullous pemphigoid,striking 50- to 60-year olds.Because the skin splits within the epidermis,the blisters have very thin roofs to them and theskin becomes extensively eroded very quicklyleading to fluid and protein loss and the potentialfor severe skin infections. In addition to this,the mouth and other mucosal surfaces are commonlyaffected with the consequent difficultywith eating and drinking. Patients with pemphiguscan quickly become very unwell.Treatment and nursing care are similar to bullouspemphigoid, being based on immunosuppressionthrough high dose oral steroids. Thepatient is likely to be hospitalised and nursingcare should include monitoring for the effects ofhigh steroid doses along with fluid balance andcare of the skin erosions (blisters will usuallyburst themselves as they are so fragile). In additionoral care is likely to be needed.have classic skin signs are systemic lupuserythematosus (SLE), systemic sclerosis, morpheaand dermatomyositis. Here SLE and systemicsclerosis will be considered in greaterdetail.Systemic lupus erythematosusSystemic lupus erythematosus is seen mostcommonly in young women of child bearingage. Its progression is usually through aseries of exacerbations followed by periods ofremission (Figure 13.2). Systemically it affectsmany organs as well as the skin, includingjoints, heart and pericardium, lungs, kidneys,brain and haemopoietic system. The disease ischaracterised by the development of cytotoxicantibodies and immune complexes (Graham-Brown and Bourke, 1998). The symptomsof SLE are outlined in Box 13.1. (Note thatthe first four symptoms are also present incutaneous lupus erythematosus when systemicdisease is not present (or only very mildly).Connective tissue disordersIn this section, the skin signs related to connectivetissue disorders will be considered.Examples of connective tissues diseases thatFigure 13.2 Lupus. (Source: Reprinted from Weller et al.,2008.)

252 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 13.1 Clinical features of SLEErythematous plaque on face but also onneck, ears or scalp;Follicular plugging;Scarring in the plaques which can lead topermanent hair loss when on the scalp;Mouth, nasal epithelium and conjunctivamay also be affected;Photosensitivity (more marked in SLE);Raynaud’s phenomenon;Diffuse patchy hair loss;‘Butterfly patch’ across the face, moreaccurately described as a blotchy, evanescent,erythematous rash which is morewidely distributed than just across noseand cheeks (Graham-Brown and Bourke,1998);Vasculitis.Treatment for SLEEarly treatment of plaques with potent topicalsteroids is important to minimise scarring.Advice about avoiding sun exposure should alsobe given. Otherwise, the mainstay of treatmentfor SLE is immunosuppressive comprising oforal steroids and/or azathioprine.Systemic sclerosisAn autoimmune disease of unknown cause, systemicsclerosis is 3–4 times more common inwomen than in men and usually starts betweenthe ages of 30–40 (although later in men) (NewZealand Dermatological Society Incorporated,2009). It is a multisystem disease in which vasculopathyof small arteries produce symptomsaffecting the gastrointestinal (GI) tract, lungs,kidneys, heart, liver, nervous and musculoskeletalsystems (Graham-Brown and Burns, 2006).The typical skin symptoms are created by ‘thickeningof the skin’; there is also destruction of thehair follicles and sweat glands. Box 13.2 liststhese symptoms. Note that a milder form of theBox 13.2 Clinical features ofsystemic sclerosisTight shiny face;Loss of facial wrinkles;Beaked nose;Narrowing of the mouth with perioralfurrowing;Facial telangiectasia;Raynaud’s phenomenon;Tightening of the skin on digits creatingprogressive contractures;Painful ulcers at ends of fingers which canprogress to resorption of underlying terminalphalanges;Calcinosis.condition is called CREST. When there is no systemicdisease but skin sclerosis is present this isknown as morphea.Treatment for systemic sclerosisNo treatment has been shown to be effective fortreating systemic sclerosis.Drug reactionsDrug-related eruptions of the skin may becaused by a substance which has been used systemicallyor one that has been applied topically.The level of severity of a drug reaction will vary;however, in most cases, the only way to resolvethe eruption is to remove the individual fromthe medication that has caused the problem. Inthis section, a number of different types of druginducedskin eruptions will be considered. Foreach type, the drugs that are most likely to causethe reaction are listed in the relevant boxes,please note (these are not necessarily comprehensive.It is worth remembering that if anindividual is sensitive to a particular drug, theymay also react to different drugs that are chemicallysimilar. The skin can respond adversely in

Less common skin conditions 253Box 13.3 Common drugs thatcan cause fixed drug reactionsBox 13.4 Categories of drugs thatcan cause toxic erythemaPhenolphthaleinTetracyclinesSulphonamidesQuinineParacetamolChlordiazepoxideNon-steroidalanti-inflammatoriesAntibioticsAntihypertensivesNon-steroidal antiinflammatoriesBarbituatesHydantoinsa wide, varied way to drugs. Whilst morbilliformtype reactions are common, the skin mayrespond in a number of other ways, e.g. takingon vasculitic or acneiform appearance (Graham-Brown and Bourke, 1998).Fixed drug reactionsAs the name suggests, fixed drug reactionsare oval-shaped lesions that are either solitaryor multiple, and sometimes have a blisteredcentre. They occur quickly after taking thesensitising drug (within a few hours) and willreoccur, usually in the same place, each timethe drug is taken see Box 13.3. They leavebehind a hyperpigmented area of skin. Thelesions can occur anywhere on the body butfrequently appear on mucosal surfaces includinglips and genitalia.Toxic erythemaThe skin may respond adversely in a numberof different ways; toxic erythema describes themost common morbilliform presentations wherethere are symmetrical erythematous macules andpapules, larger more confluent patches or urticatedplaques. These initial presentations mayprogress into a more severe picture, e.g. drughypersensitivity syndrome (DHS) (see later) ortoxic epidermal necrolysis. Patients with a suppressedimmune system, for example those whohave the human immunodeficiency virus (HIV),are more susceptible to drug reactions of this type(Box 13.4).Drug hypersensitivity syndromeThis is a serious type of drug reaction whichhas an 8% mortality rate (New ZealandDermatological Society Incorporated, 2009). Itgenerally occurs 1–8 weeks after the medicationis commenced and has three key symptoms: fever,skin rash and organ involvement which generallyoccur in that order. The rash starts with papulesand pustules against a background of erythemaand may progress to erythroderma and/or a generalexfoliative picture. The degree to which theorgans are being affected should be monitoredthrough blood tests assessing liver function andeosinophilia. The cause of DHS is unclear; thereis some thought that it is caused by a defect in theliver which affects the way it metabolises certaindrugs or that it is related to a co-infection withherpes virus 6. What is more certain is that thereis a genetic component to DHS and thus relativesshould be counselled (Box 13.5).Drug-induced skin pigmentationThere are a wide range of skin pigmentationscaused by drugs; indeed it is thoughtthat 10–20% of all cases of acquired skin pigmentationare related to drugs (New ZealandDermatological Society Incorporated, 2009).Although the pigmentation is usually benign,it can become socially unacceptable and mayhave a significant psychological impact on thepatient. In most instances, stopping the drugwill mean that the skin colour returns to normal;however, this may take some time and insome instances becomes permanent.

254 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsBox 13.5 Drugs that can cause DHSAbacavir Diltiazem NSAIAAllopurinol Gold salts PhenobarbitoneAtenolol Isoniazid PhenytoinAzathioprine Lamotrigine SulfasalazineCaptopril Mexiletine SulphonamidesCarbamazepine Minocycline TrimethoprimClomipramineNevirapineDapsoneOxicamPigmentation in the skin may occur for anumber of reasons. These include:■■■■Accumulation of certain heavy metals inthe dermis following dermal vessel damage.Sufficient accumulation of the heavy metalwill cause pigment change without any associatedincrease in the level of melanin.Drug–pigment complexes might be formedwith melanin in the skin, exposure to sunlightcan trigger this reaction.Other drugs will trigger the accumulation ofmelanin as a non-specific post-inflammatorychange. This may be worsened by exposureto sunlight.Some drugs can cause pigmentation bydirectly accumulating and/or reacting withsubstances in the skin.Table 13.2 taken from www.dermnetnz.orgoutlines the clinical features associated with thedrugs that are most likely to cause pigmentation.Treatment involves stopping the drug involvedif the pigmentation is causing distress. However,as can be seen from Table 13.2, most pigmentarychanges are aggravated (and often triggered)by exposure to the sun. Therefore adviceabout sun protection is critical to reducing theproblems associated with pigmentary changes.Drug-induced photosensitisationPhotosensitisation reactions can be divided intotwo broad groups: those that are phototoxicand those that are photoallergic with the formerbeing more common.Drugs that may cause photosensitisation arelisted in Box 13.6.Phototoxic sensitisation describes a directdamage to skin tissue caused by the light activatingthe photosensitising substance. The reactioncan occur at virtually any time post-exposure tothe photosensitising substance and light, fromimmediately to hours afterwards. Its appearanceis usually that of sunburn (it may be accompaniedby vesicles and blisters); however, amiodaroneand sunlight turn the skin a blue-greencolour in sensitive individuals. The reactiononly occurs in the sun-exposed sites. In additionnail changes may be seen with the nails liftingfrom the nail bed (onycholysis). For those withdarker skin colours, this may be the only sign ofthe drug-induced photosensitisation.Photoallergic sensitisation is usually causedby topical applications and is a cell-mediatedimmune response in which the antigen is thelight activated, photosensitising agent. It is characterisedby an eczematous type, itchy reactionthat can spread to anywhere on the body andwill appear 24–72 hours after the exposure tothe photosensitising substance and sunlight.Treatment involves avoiding where possiblethe medications that lead to photosensitisation.However, in many instances, the therapeuticvalue of the drugs will outweigh thephotosensitisation risks and the patient shouldbe given information and support to protecttheir skin from the sun using sunscreens, clothingand avoidance.

Less common skin conditions 255Table 13.2 Drugs that can cause pigmentary changes.Drug/drug groupClinical featuresAntipsychotics (chlorpromazineand relatedphenothiazines)PhenytoinAntimalarialsCytotoxic drugsAmiodarone• Bluish-grey pigmentation, especially in sun-exposed areas.• Pigmentation is cumulative and some areas may develop a purplish tint.• Pigmentation of the conjunctiva in the eye may also occur, along with cataracts and cornealopacities.• 10% of patients develop pigmentation of the face and neck resembling chloasma (clearlydefined, roughly symmetrical dark brown patches).• Fades after a few months when drug has been stopped.• About 25% of patients receiving chloroquine or hydroxychloroquine for several yearsdevelop bluish-grey pigmentation on face, neck and sometimes lower legs and forearms.• Continuous long-term use may lead to blue-black patches, especially in sun-exposed areas.• Nail beds and corneal and retinal changes may also develop.• Busulfan, cyclophosphamide, bleomycin and adriamycin have all produced hyperpigmentationto some degree.• Banded or diffuse pigmentation of nails often occurs.• Blue-grey pigmentation in sun-exposed areas (face and hands).• Photosensitivity occurs in 30–57% of patients whilst 1–10% show skin pigmentation.• Skin pigmentation is reversible but may take up to 1 year for complete resolution after thedrug has been stopped.Source: New Zealand Dermatological Society Incorporated (2009).Box 13.6 Drugs that can causephotosensitisationAmiodaroneChlorpromazineNalidixic acidSulphonamidesLichen planusTetracyclinesThiazidesQuinineIn the USA, lichen planus (LP) has been reportedto affect 1% of new patients seen at health careclinics, with most patients being between the agesof 30 and 60, although it can affect any age. Theredoes not seem to be any gender differences. LP canbe described as a cell-mediated immune responseof unknown origin. The response may be provokedby a viral infection (and there may be a particularassociation with hepatitis C), by a drug orby a stressful event (Chuang and Stitle, 2008).Lichen planus represents a wide range ofclinical manifestations which are describedbelow. However, the disease is characterised bya number of histological features:■■■Marked liquefaction (conversion to liquid)of the basal layer;Expansion of the granular cell layer;Dense subepidermal infiltrate, predominantlyof T-lymphocytes.Clinically, patients may present with diseaselimited to one or two areas of skin, moreuncommonly the presentation may be extensiveaffecting both skin and mucous membranes(Figure 13.3). It is not uncommon for mucousmembranes to be affected without any symptoms

256 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalson the skin. In 85% of cases, the lesions willclear from the skin in 18 months time (NewZealand Dermatological Society Incorporated,2009) but where disease is more extensive andaffecting the mucous membranes it can takeconsiderably longer. In around 10% of patientsthere will also be nail changes.Classic presentationThe lesions are shiny flat-topped papules whichvary in size from being pin-prick to more thana centimetre. The shape of the lesion is oftendescribed as polygonal and they may be distributedclosely together or widely spread, in linearformation or in rings. They are purplish in colour(known as violaceous) and there are often greyor white lines and dots scattered over the surface;these are known as Wickham’s striae. Themost common locations for the lesions are wrists,lower back and ankles; however, they can occuranywhere on the body. For some people, scalppapules appear which may progress to atrophiccicatrical alopecia. Mucous membrane involvementis common; lesions are usually found onthe bucal mucosa and tongue, although they canaffect conjunctivae, the larynx, the tonsils, thebladder, the vulva, the GI tract and the anus. Thepresentation is white or grey streaks forming areticular pattern against a violaceous background.They may become ulcerative; this is linked to anincreased risk of malignant transformation, particularlyin men.Symptoms related to the skin lesions varyfrom nothing to severe pruritis. Scale may alsobe associated with LP and it tends to be thethicker, scalier areas which are most itchy. Asalready mentioned the lesions usually clearwithin 18 months, but during that time somelesions will disappear and other new onesappear. Hyperpigmentation can occur wherethe lesions have been and this seems to bemore common in darker skin colours. On themucous membranes, lesions can be accompaniedwith a stinging sensation; they maybecome painful should the lesions deteriorateand become erosive.Nail changes in LP occur because of nail platethinning; this results in longitudinal groovingand ridges. Other nail changes may includesubungual hyperkeratosis, onycholysis and longitudinalmelanonychia. Rarely the nails maydisappear altogether.Hypertrophic LPIt has already been mentioned that the lesionscan become thickened; in extreme cases, thisis known as hypertrophic LP and is characterisedby extreme pruritis. It usually occurs onthe lower limbs particularly around the ankles.These lesions are chronic in nature and cantake years to clear. When they do, scarring andhyperpigmentation can remain.Erosive LPFigure 13.3 Lichen planus. (Source: Reprinted fromGraham-Brown and Burns, 2006.)This type of LP affects mucosal surfaces, usuallythe mouth and genitals. It is painful and usuallychronic in nature. It may be associated with

Less common skin conditions 257classical cutaneous LP or it can occur alone.The main clinical features of oral erosive LP arelarge, painful ulcers which heal with scarring.Healing may take weeks. The lesions can occuron the sides of the tongue, insides of the cheeks,on the gums or inside the lips. It mainly affectsadults, usually women and children are rarelyaffected.Genital erosive LP in women can cause extensivechanges to the mucosa and structure of thegenitals. The labia minora and entrance to thevagina can become red and raw; more drasticallythe clitoral hood can disappear and thelabia minora stick to each other or the labiamajora. The subsequent scarring may causethe labia majora to close over the vagina. If LPaffects the inside of the vagina, it may bleed easilyon contact and there is a mucky discharge.Genital erosive LP is much less common in men;it causes redness and tenderness of the glans.These changes can be extremely painful particularlywhen passing urine or having sexualintercourse. The latter may become impossiblefor women who have considerable structuralchanges to their genitals.Bullous LPThis is a rare condition, blisters are seen formingeither within the LP papules or alone.Actinic LPLesions of LP are induced by exposure to sunlight.Treatment for LPThe mainstay of treatments for LP are topicalsteroids. The cutaneous form will need to betreated with potent or very potent topical products,usually for a 4- to 6-week course. Theresolving lesions will flatten to be the same asthe rest of the skin surface; it is important tomonitor this as the sign of clearance as somepigmentation may remain. If the disease persists,intermittent courses of topical steroidswill be needed. For more severe disease, particularlyerosive and hypertrophic variants,oral immunosuppressive therapy may berequired. This may be oral steroids, ciclosporinor methotrexate.For those with oral and genital disease, goodhygiene measures should be maintained. Soapsshould be avoided when washing the genitalarea; a soap substitute such as aqueous creammay be used instead. A petrolatum emollientointment may be helpful to provide some relieffrom general discomfort. Applying topical steroidsin the oral cavity will be enhanced by aninhaler spray or pastes. A number of smallstudies reviewed by Ruzicka et al. indicate thattopical calcineurin inhibitors, specifically topicaltacrolimus, are helpful for erosive genitaland oral LP (Ruzicka et al., 2003). Specificallya 2008 study considered 10 patients with erosiveoral LP, 7 of whom had no lesions after 30days of pimecrolimus compared to 2 with nolesions in the control group. A further 30 daysof treatment cleared the lesions in the patientswho did not respond in the first 30 days (Volzet al., 2008). This is, however, using the treatmentoff license.Pityriasis roseaThis rash of unknown origin can last up to 12weeks and then resolves spontaneously. It usuallyaffects teenagers and young adults. It maybe slightly itchy and scaly but is otherwiseasymptomatic. It is sometimes preceded by ageneralised viral infection.The presentation of pityriasis rosea developsover time starting with a single oval patchcalled a herald patch. This is usually 2–5 cm indiameter and precedes the rest of the rash by upto 20 days. Characteristically, it has a slightlyscaly trailing edge; this describes the edge justinside the patch. After the herald patch therest of the lesions, which are similar althoughusually smaller, appear mainly over the trunkbut also affecting the arms and legs. The distributionof these lesions is often compared toa fir tree, in that they follow the lines of theribs around the trunk. Lesions do not usuallyappear on the face.

258 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsNursing care will centre around helping toreassure the patient that what they have isself-limiting and non-contagious. Patients mayhave been wrongly diagnosed with either psoriasisor tinea corporis and it should be clarifiedthat pityriasis rosea is not related to eitherof these conditions. Good skin care such aswashing with a soap substitute and using atopical emollient may be helpful especially ifthe skin is itchy. For particularly itchy skin,a brief course of topical steroids (moderatepotency) may provide some relief. However, itis unlikely to make any difference to the courseof the condition.Table 13.3 Types of primary cutaneous T-cell lymphoma.IndolentMycosis fungoides (MF)MF variants• Fulliculotrophic• Pagetoid reticulosis• Granulomatus slack skinPrimary cutaneous CD30 + lymphoproliferativedisordersSubcutaneous panniculitis-likeT-cell lymphomasPrimary cutaneous CD4 +small/medium pleomorphicT-cell lymphomaAggressiveSezary syndromeAdult T-cellleukaemia/lymphomaExtranodal NK/T-celllymphoma, nasal typePrimary cutaneousperipheral T-cellPrimary cutaneous T-cell lymphomasLymphomas are tumours of the lymph nodesand lymphatic system. When the tumouroccurs in the skin with no sign of involvementelsewhere in the body, they are known as primarycutaneous lymphomas; of these 65% areT-cell type. The incidence of primary cutaneouslymphomas is about 0.4 per 100,000people per year and of these approximatelytwo-thirds are T-cell in origin (Whittakeret al., 2003). There appears to be a higherincidence in men. There are a number of typesof T-cell lymphoma which can be generallycategorised into indolent (or low grade, slowgrowing) types or the more aggressive lymphomas.These are listed in Table 13.3; however,in this section only the most common T-celllymphoma, mycosis fungoides (MF) (accountingfor 50% of all primary cutaneous lymphomas),is considered in any detail.Clinical staging for T-cell lymphomaBox 13.7 outlines how the disease develops indifferent parts of the body, T indicating the skin,N lymph nodes, M visceral involvement and Bhaematological involvement.Once the clinical level of involvement hasbeen established, this can be summarised usingthe grading system outlined in Box 13.8.Box 13.7 Summary of clinicalchanges seen in T-cell lymphomaT1: Patches or plaques 10% bodysurface areaT2: Patches of plaques 10% bodysurface areaT3: TumoursT4: ErythrodermaN0: No palpable nodesN1: 1 palpable node withouthistological involvement(dermatopathic)N2: Non-palpable nodes with histologicalinvolvementN3: Palpable nodes with histologicalinvolvementM0: No visceral diseaseM1: Visceral diseaseB1: No haematological involvementB2: Sezary count 5% of total peripheralblood lymphocytesSource: Whittaker et al. (2003).

Less common skin conditions 259Box 13.8 Burn and Lambertgrading systemStage IA: T1 N0Stage IB: T2 N0Stage IIA: T1/2 N1Stage IIB: T3 N0/1Stage III: T4 N0/1Stage IVA: T any N 2/3Stage IVB: T any N any M1Mycosis fungoidesDiagnosis of MF is made through an ellipticalbiopsy, particularly in the early stages it can bedifficult to distinguish from other chronic skinconditions such as psoriasis or discoid eczema.The initial patch stage of the disease occurs whenlymphocytes infiltrate the skin causing the patchesor lumps to appear. As this is a disease whichprogresses very slowly, it may take years beforethe individual moves into the next phase of thedisease (Figure 13.4). Table 13.4 is reproducedfrom the British Association of Dermatologistguidelines and indicates the survival rates fordifferent stages of the disease (Whittaker et al.,2003). As the disease progresses the skin signsFigure 13.4 Mycoses fungoides.change too, moving from patches to thickenedplaques and eventually on to skin tumours.Although the prognosis is generally good andtreatment can control symptoms, abnormal cellscan eventually infiltrate other organs includingblood, lymph nodes, heart, liver, lungs andspleen (New Zealand Dermatological SocietyIncorporated, 2009). It may not be necessary toinvolve the multidisciplinary team in the care ofsomeone who has very early MF, but throughoutTable 13.4 Survival rates for cutaneous T-cell lymphoma.IA IB IIA IIB III IVA IVBOS at 5 years (%) 96–100 73–86 49–73 40–65 40–57 15–40 0–15OS at 10 years (%) 84–100 58–67 45–49 20–39 20–40 5–20 0–5DSS at 5 years (%) 100 96 68 80 40 0DSS at 10 years (%) 97–98 83 68 42 20 0Disease progression at 5 years (%) 4 21 65 32 70 100Disease progression at 10 years (%) 10 39 65 60 70 100Source: Whittaker et al. (2003).OS – overall survivalDSS – disease specific survival

260 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsthe later stages the input from specialist cancerservices is vital.TreatmentsEarly stage MF (IA to IIA) can be treated conservativelywith emollients and moderatepotency topical steroids. However, dependanton the extent of skin signs and the thicknessof the plaques, phototherapy (in the form ofPUVA) and radiotherapy may need to be introduced.Resistant cases may need the addition ofα-interferon to PUVA therapy. Patients withmore advanced disease (IIB and above) will needto have systemic therapy which may includechemotherapy, immunotherapy or extracorporealphotophoresis (Whittaker et al., 2003). Novelretinoids are being developed for use in MF withthe hope that there will be fewer toxicities associatedwith these forms of treatment.As has already been mentioned, prognosis isgood in the early stages of MF. However, as thedisease progresses to later stages, treatment maybecome palliative and a key focus of care is tomaintain comfort and as much quality of life aspossible. If ulcerated lesions are present, thesewill require nursing intervention and considerationgiven to pain relief.RosaceaAlthough often considered alongside acne (andindeed has been called ‘acne rosacea’) rosaceais, in fact, a distinct condition with featuresthat set it apart from acne. It usually affectsthe older age group of 30- to 60-year olds andwomen are three times more likely than men toget it, although men tend to get it more severely.Rosacea is characterised by facial flushing andpustule formation (Figure 13.5). Unlike acnethere are no whiteheads or blackheads and thepustules tend to be domed in shape rather thanpointed. The skin is generally sensitive and facialoedema can occur. More severe cases can affectthe eyes. The course of the disease is unpredictable,with periods of remission followed byrelapse lasting for variable lengths of time.Four subtypes of rosacea exist (Layton, 2008).Figure 13.5 Rosacea.Erythematotelangiectatic rosaceaAs the name suggests, this type of rosacea ischaracterised by facial redness in the central zoneoften accompanied by telangiectasia (superficialblood vessels) and the patient usually experiencesstinging and soreness. There may be other typesof rosacea that accompany this subtype.Papulopustular rosaceaAgain facial redness is in evidence along withstinging and soreness but also accompanied bypustules. The skin may be extremely sensitive totopical products which generally aggravate thestinging sensations. Occasionally other parts ofthe body besides the face may be affected such asthe chest, ears and in bald men the scalp. When

Less common skin conditions 261these other areas are affected, it tends to indicatethat the condition will be resistant to treatment.Phymatous rosaceaThis type of rosacea is much more common inmen and may exist without any other signs ofthe disease. Excessive growth of sebaceous glandsand connective tissues leads to an enlarged, misshapennose which is often linked (wrongly) toexcessive drinking. Rhinophyma may start withpustules and redness in its early stages.Occular rosaceaEye symptoms include grittiness, redness andsoreness, conjunctivitis or blepharitis may occur.As a result, vision may be blurred and there canbe an increased sensitivity to light. In around 5%of cases, there may be more severe damage to theeyes. It should be noted that ocular problems mayoccur long before there are any skin symptoms.Whilst rosacea is a relatively common conditionaffecting around 10% of the population,there is little clarity about its pathophysiology.It is generally agreed that there is genetic predispositionwhich is aggravated by environmentalfactors with around 70% of cases reportingworsening when exposed to UV. Box 13.9 outlinessome of the trigger factors that can worsenrosacea. The facial flushing may be caused bydamage to the blood vessels which lead to vesseldilatation. There might be some association witha hair follicle mite called Demodex folliculorumas there is an increased incidence of these inrosacea papules in some people (New ZealandDermatological Society Incorporated, 2009). Itis well recognised that topical steroids aggravaterosacea and should not be used as part of thetreatment. Other oil-based skin applications canalso make the condition worse.TreatmentGeneral advice for patients with rosacea centrearound trying to keep the facial skin cool andavoiding the trigger factors listed earlier. ForBox 13.9 Trigger factors forrosaceaHeat: from ambient temperature, spicyfood, hot drinks, hot showers bathUV exposureTopical steroidsOil-based moisturisers and make-upproductsAlcoholsome direct cooling of the skin using an ice packor fan can be helpful. The rest of this sectionlooks at the various treatments that are availablefor treating rosacea.Rosacea can either be treated using oral antibioticsor topical therapies. A Cochrane reviewrevealed that the level of evidence for these treatmentswere generally poor, but that topical metronidazoleor azelaic acid were both effective withless evidence showing efficacy of the oral metronidazoleor tetracyclines (van Zuuren et al., 2005).Topical azelaic acidWhen topical azelaic acid applications are used,the face should be gently cleansed and then thetopical application applied to the dried skin.As a general guide, one finger tip unit (FTU)per two palms worth of area affected is a goodguideline, but it is advisable to follow manufacturer’srecommendations as different brands willvary slightly. For example Finacea recommends1 FTU for the face and Skinoren 2 FTU. (Furtherdetails about specific products can be foundfrom the Electronic Medicines Compendium –www.emc.medicines.org.uk). The treatmentshould be applied twice daily and gently massagedinto the face. After use the individualshould be instructed to wash their hands. Thepatient should expect to see significant improvementin 4–8 weeks, although it can be used overa prolonged period of many months if necessary.The most common side effect is skin sorenessand irritation and this can be minimised by reducingthe amount of treatment used each day (to justonce daily), before gradually building up to the

262 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionalsrecommended dosages. Because the productsare irritating, care should be taken to avoid contactwith the eyes and other mucous membranes.Should contact occur the areas should be washedwith large amounts of water. There is little evidencefor any ill effects that would mean the productsneeded to be stopped during pregnancy orbreast feeding; however, this should be discussedfor each individual case.Topical antibioticsThere are a number of different brands of topicalmetronidazole, some of which come in a gelformulation and others in cream. Again, theElectronic Medicines Compendium will givespecific advice about the use of each product.In general the method of application is similarto that of azelaic acid. The face should be gentlycleansed and dried before an application ofa thin layer of the product is gently massagedinto the face. It should be used twice daily, butunlike azelaic acid should not be used constantlyfor more than 9 weeks. Because metronidazolebecomes less effective when exposed to UV light,individuals should be warned not to go out inthe sunshine whilst using the product.It can act as an irritant and one of the sideeffects is skin burning and soreness. It may makethe eyes water if it is applied too closely or getsinto the eye by mistake. For some there are otherundesirable effects which include a metallic tastein the mouth, tingling or numbness of the extremities,nausea and exacerbation of the rosacea. It isrecommended that metronidazole should be discontinuedin pregnancy and whilst breast feeding.Oral antibioticsIf oral antibiotics are prescribed, they are usuallyfor a relatively prolonged course of around6–12 weeks, the dose depending on diseaseseverity. Metronidazole should be swallowedwith water before or after a meal whereas thetetracyclines should be taken on an empty stomachto aid absorption.Whilst the above treatments should be effectiveto some degree, none of them are curative.Once they have been discontinued, it is quitelikely that the rosacea will recur.Other treatmentsThere are a number of other treatments whichhave limited evidence related to their efficacybut which might be helpful in some cases.■■■■■Anti-inflammatories: It has already beenstated that topical steroids will aggravaterosacea; however, some have found the topicalcalcineurin inhibitors (tacrolimus andpimecrolimus) helpful. Oral non- steroidalanti-inflammatories such as diclofenac mightalso be helpful in reducing facial redness, butit is important to be aware of the potentialserious side effects (e.g. peptic ulceration).Isotretinoin: This drug was discussed extensivelyin the chapter on acne and its potentialside effects discussed at length. It maybe helpful particularly for those who do notrespond to antibiotics; however, a low doseover a prolonged period of time is likely tobe needed.Clonidine: This is an example of an alpha2 receptor antagonist which may reducevascular dilatation which leads to the facialflushing. Side effects are usually mild butmay include low heart rate and blood pressure,dry eyes, blurred vision and gastrointestinaldisturbance.Vascular laser: May be used to treat telangiectasiasuccessfully. Other methods if lasersare not available include sclerotherapy (injectionsof strong saline solution), diathermy orcautery. Intense pulsed light has been shown ina small study to have significant impact on theerythema and telangiectasia, an effect whichwas maintained at 6 months (Papageorgiouet al., 2008).Surgery: This may be necessary for people withrhinophyma in order to reshape the nose.UrticariaUrticaria describes a group of conditions inwhich itchy weals and red patches occur in theskin. They affect both children and adults. Theweals are caused by the release of histamine

Less common skin conditions 263or other chemicals from mast cells. These inturn increase the permeability of small bloodvessels which leak into the skin causing localisedswelling (Figure 13.6). Urticaria can beshort lived or long term and appear in smallpatches or large areas, map-like, across thebody. In some instances, urticaria is accompaniedby angioedema in which there is deeperswelling often of hands, eyelids or lips, but canoccur anywhere.There are many different classifications ofurticaria. Table 13.5 is taken from guidelinesfrom the British Association of Dermatologists(Grattan and Humphreys, 2007).Acute urticariaAcute urticaria can be classified further as eitherallergic or non-allergic. Allergic is less commonand may be an allergy to an ingested substance,e.g. a food or medicine, through a sting orthrough contact with a substance such as latex.Usually the allergic response will be mild requiringno emergency care; however sometimes theallergy may result in anaphylactic shock requiringemergency care and an injection of adrenaline.Table 13.5 Different types of urticaria.Overall clinicaldescription ofurticariaOrdinaryPhysical (reproduciblyinduced by thesame stimulus)Angiodema withoutwealsContact urticaria(with allergens orchemicals)Urticarial vasculitis(as defined by askin biopsy)AutoinflammatorysyndromesSubtypesAcute (up to 6 weeks continuousactivity)Chronic (6 weeks or more ofcontinuous activity)Episodic (acute, intermittent orrecurrent activity)Mechanical (e.g. delayedpressure, symptomatic dermographism,vibratory angioedema)Thermal (e.g. cholinergic, coldcontact, localised heat)Others (e.g. aquagenic, solar,exercise induced)IdiopathicDrug induced (e.g. ACEinhibitors)C1 esterase-inhibitor deficiencyHereditary (e.g. cryopyrinassociatedperiodic syndromes)Acquired (e.g. Schnitzlersyndrome)Non-allergic causes of acute urticaria are muchmore common and include:Figure 13.6 Urticaria.■■■Infections such as sinusitis, helicobacter,viral hepatitis;Serum sickness due to blood transfusions,viral illness or certain drugs (this is accompaniedby other symptoms including sickness,fever, joint pain and swollen lymphglands);Certain medicines such as morphine (andother opiates), codeine and radiocontrastagents can cause a non-allergic release of

264 Principles of Skin Care: A Guide for Nurses and Other Health Care Professionals■mast cell granules such as histamine. Aspirinand other non-steroidal anti-inflammatoriescan also produce urticaria but through theproduction of leukotrienes which are potentmediators of immediate hypersensitivityreactions and inflammation;Non-allergic food reactions can be causedby salicylates in fruit (which are highestin berry and dried fruits but occur in mostfruits), azo food dye benzoate preservatives(New Zealand Dermatological SocietyIncorporated, 2009).Chronic urticariaIn some instances, chronic urticaria is due toautoimmune disease and may be related to otherautoimmune conditions such as thyroid or coeliacdisease. In these cases autoantibodies willbe found. In other cases there are no circulatingautoantibodies and it is a more difficult conditionto determine a cause for, often impossible.This type of urticaria is known as chronic idiopathicurticaria.Physical urticariaFive minutes following physical contact, the skinproduces a weal that will last 15–30 minutes.Some people experience just the physical type ofurticaria and others have it in combination witha more chronic type. The cause is unknown.DermographismThis literally describes skin writing and theindividual experiences weals wherever the skinis touched be this through stroking the skin,touching it on furniture or the gentle pressure ofclothes. The weals are usually itchy and aggravatedwhen scratched, they can be worse whenthe individual is warm or upset.ThermalCertain temperature ranges can cause urticarialreactions. For example cholinergic describes thetiny red dots that appear on the skin followingsweating, these can be very itchy. Cold contacturticaria usually strikes when cold skin is warmingup after being exposed to cold outdoor temperatures.When the weals are widespread it can causefainting attacks. Localised heat and solar urticariaare less common but describe the development ofweals following exposure to said stimuli.Contact urticariaThis is caused by physical contact either throughthe skin or mucous membranes, with a substanceleading to either an allergic or non- allergicresponse. An IgE elicited response may be causedby a range of substances including white flour,latex, cosmetics or fish. A non- allergic reactionis caused by contact with substances such asnettles, certain insects (e.g. a hairy caterpillar).Weals may be limited to the contact area or maybecome more widespread.InvestigationsOn the whole, diagnosis is usually made throughclinical observation. Particularly for ordinaryurticaria there is usually no need to perform anyspecific investigatory tests. However in acuteand episodic cases allergic responses may be verifiedusing skin prick tests and CAP fluoroimmunoassaytests on blood. If patients with chronicordinary urticaria are not responding to antihistamines,it may be helpful to determine whetherthere are other autoimmune conditions present,e.g. check thyroid function. Long- standing urticariathat is not responding to treatment may bebiopsied to identify whether there is a vasculitispresent (Gittins, 2008).TreatmentsPrimarily treatment revolves around antihistamineuse and most people with urticaria do respondto these. However, some people do not respondand a few get worse. It is considered good practiceto give people a choice of two non-sedatingantihistamines to see which one they respond bestto and it may be necessary to prescribe in doses

Less common skin conditions 265which exceed the manufacturer’s recommendations(Grattan and Humphreys, 2007). In acutetype urticaria, oral steroids might be used for ashort course and there is some evidence to showthat ciclosporin can be helpful for those who arenon-responsive to antihistamines (Grattan andHumphreys, 2007).General advice to patients should alsoinclude avoiding things that appear to triggerthe urticaria, e.g. fruits which containsalicylates. Aspirin is also likely to be problematicfor those sensitive to salicylates andthis should be avoided as should non-steroidalanti-inflammatories. General measures whichmay be helpful include keeping the skin cool(e.g. applying ice packs) and avoiding alcoholwhich is a vasodilator and make the skinfeel hotter. Urticaria can be difficult to managesuccessfully and patients are likely to needongoing support.Figure 13.7 Vitiligo.VitiligoVitiligo may be thought of as an uncommoncondition, but in fact around 1% of the populationhas it. Vitiligo is characterised by areasof skin that lose their pigment (Figure 13.7).For reasons that are not entirely clear, melanocytes,which are the pigment making cells, aredestroyed. It is not certain what triggers this,although it may be related to an injury such assunburn or to psychological stress. There arethree possible theories as to why the melanocytesbehave in this way.(1) Abnormally functioning nerve cells injurethe melanocytes;(2) There is an autoimmune response in whichthe body’s own immune system attacks themelanocytes as they are viewed as foreignbodies;(3) The melanocytes destroy themselves.Whatever the mechanism may be, areas oftotally depigmented skin are created, often symmetricalin nature, in which there are few othersymptoms (e.g. no scaling or inflammation).Occasionally vitiligo will be segmental in naturewith asymmetric patches occurring on just onepart of the body.When the disease is seen in children, there isa much greater likelihood of spontaneous repigmentationthan in adults. Repigmentationstarts around the hair follicle and then spreadsacross the patch until the spots coalesce. Foradults the disease may be progressive withmore and more areas of skin becoming depigmented,for others the patches are more static.Many will notice cycles in which there are periodsof fairly rapid pigment loss, followed byperiods of stability, followed by further loss ofpigment, etc. Vitiligo is clearly more obvious inskin types 4 and above. But for all skin typesit can have a serious impact on the individual’spsychological well-being. Individuals alsohave to take a great deal of care when out inthe sun, as the areas of depigmentation aremuch more prone to burning than the rest ofthe skin.Pigment loss is not limited to the skin; forsome people there is also pigment loss fromthe hair leading to white or grey head hair, eyebrows,eyelashes or body hair.

266 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsTreatmentWhilst there are a number of treatments availablewhich may be of some help in the shortterm, there is very little evidence for their longtermefficacy or safety (Whitton et al., 2006).Potent topical steroids can sometimes inducerepigmentation and although it is not a licenseduse the calcineurin inhibitors have shown someeffect especially in areas such as the face wherepotent topical steroids may be particularly damaging.PUVA can also lead to repigmentation,although this may need to be long term. A coupleof studies have suggested that PUVA in combinationwith calcipotriol may be effective, butthe long-term results have not been evaluated.A 2008 guideline summarises the treatments forvitiligo along with the level of evidence associatedwith them (Gawkrodger et al., 2008).CamouflageUsing skin camouflage products can help to providea uniformity to skin tone and colour whichhides the depigmentation. There is a wide rangeof colours within the product palette and thecamouflage practitioner will mix no more thanthree of these together to make a skin tone colourthat suits the patient (Davies, 2007). Oncecover creams have been applied, they are fixedwith either a spray or powder which means theybecome fully waterproof. This allows the individualto leave the camouflage products on for up toa week and continue to wash as normal. In orderto remove the product, skin cleansers are used.Patients who are diagnosed with vitiligo mayneed significant levels of psychological support.Whilst treatment options are limited, it is nothelpful to say there is nothing that can be done.For some, repigmentation may occur with treatments,but it is important to be realistic aboutthe fact that these changes are unlikely to bepermanent. More importantly patients need toknow that they are not alone and the NationalVitiligo Society (http://www.vitiligosociety.org.uk/) may be able to provide invaluable support.Skin camouflage is always an option, some maychoose to see a practitioner privately; however,a referral from the GP should be an option.ConclusionThere are many hundreds of differential diagnosesin dermatology. This section has looked at:(a) Those conditions that are commonly seenbut yet do not fit neatly into any of the otherchapters, e.g. rosacea and pityriasis rosea;(b) Those common, uncommon conditions suchas bullous pemphigoid and vitiligo.Careful assessment of skin signs and symptomsis required to ensure correct diagnosis.This will increasingly become a nursing role asnurse practitioners and nurse prescribers becomemore common place.ReferencesChuang, T. and L. Stitle (2008). LichenPlanus. Retrieved 3 April 2009,from http://emedicine.medscape.com/article/1123213-overview.Davies, V. (2007). The use of camouflage in skinconditions. Dermatological Nursing, 6(4):16–20.Gawkrodger, D., A. Ormerod et al. (2008).Guideline for the diagnosis and managementof vitiligo. British Journal of Dermatology,159(5): 1051–1076.Gittins, S. (2008). Recognition and managementof urticarial vasculitis. DermatologicalNursing, 7(4): 20–27.Graham-Brown, R. and J.F. Bourke(1998). Mosby’s Color Atlas and Text ofDermatology. London: Mosby.Graham-Brown, R. and T. Burns (2006).Lecture Notes: Dermatology (9th edition).Oxford: Blackwell publishing.Grattan, C. and F. Humphreys (2007).Guidelines for the assessment andmanagement of urticaria in adults andchildren. British Journal of Dermatology,157(6): 1116–1123.Langan, S. and H. Williams (2009).A systematic review of randomised controlledtrials of treatment for inherited forms

Less common skin conditions 267of epidermolysis bullosa. Clinical andExperimental Dermatology, 34(1): 20–25.Layton, A. (2008). Clinical aspects andtreatment of rosacea. DermatologicalNursing, 7(2): 26–29.Ly, L. and J. Su (2008). Dressings used inepidermolysis blister wounds: A review. Journalof Wound Care, 17(11): 482, 484–486.New Zealand Dermatological SocietyIncorporated (2009). DermnetNZ. Retrieved25 March 2009, from www.dermnetnz.org.Papageorgiou, P., W. Clayton et al. (2008).Treatment of rosacea with intensedpulsed light: Significant improvement andlong lasting results. British Journal ofDermatology, 159(3): 628–632.Ruzicka, T., T. Assmann et al. (2003). Potentialfuture dermatological indications fortacrolimus ointment. European Journal ofDermatology, 13(4): 331–342.van Zuuren, E., M. Graber et al. (2005).Interventions for rosacea. Cochrane Databaseof Sytematic Reviews, (3). htt://www.cochrane.org/reviews/en/ab003262.htmlaccessed 8/12/09.Volz, T., U. Caroli et al. (2008). Pimecrolimuscream 1% in erosive oral lichen planus –A prospective randomised double-blindvehicle-controlled study. British Journal ofDermatology, 159(4): 936–941.Weller, R., J.A.A. Hunter, J. Savin andM. Dahl (2008). Clinical Dermatology(4th edition). Oxford: Blackwell Publishing.Whittaker, S., J. Marsden et al. (2003). JointBritish Association of Dermatologists and UKCutaneous Lymphoma Group guidelines forthe management of primary cutaneous T-celllymphomas. British Journal of Dermatology,149(6): 1095–1107.Whitton, M., D. Ashcroft et al. (2006).Interventions for vitiligo. Cochrane Databaseof Sytematic Reviews, (1). htt://www.cochrane.org/reviews/en/ab003263.htmlaccessed 8/12/09.Wojnarowska, F., G. Kirtschig et al. (2002).Guidelines for the management of bullouspemphigoid. British Journal of Dermatology,147(2): 214–221.


AppendicesAppendix 1 – The psoriasis area severity index (PASI)This version of the PASI tool reproduced by kind permission of Shering-Plough Ltd (UK), copyrightreserved.Score0123456NoneSlightModerateSevereVerySevereErythemaNoneScaleNoneIndurationNothingpalpableSlight butdefinite tothe touchEasilypalpableRoundedor slopededgesDefinitelyelevatedHard sharpboardersMarkedelevatedVery visiblehard sharpboardersArea % 0

270 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsDate Patient name Hospital numberHeadUpperlimbsTrunkLowerlimbsErythema (E)Induration (I)Scaling (S)Sum (EIS)Area scoreSum Area0.1 0.2 0.3 0.4Total PASI scoreHead(includes neck)Upper limbs(includes hands)Trunk(includes axillae and groin)Lower limbs(includes buttocks)

Appendices 271Appendix 2 – The SCORAD indexPermission kindly received from Dr Stalder on behalf of the European Task Force on AtopicDermatitis.Last NameFirst NameEUROPEAN TASK FORCEON ATOPIC DERMATITISDate of Birth:Date of Visit:DD/MM/YY4.54.5(8.5) (8.5)4.5 4.5184.5 4.5189 9(6) 9 9 (6)Figures in parenthesisfor children under two yearsA: EXTENT Please indicate the area involvedB: INTENSITYA/5 + 7B/2 + CC: SUBJECTIVE SYMPTOMSPRURITUS + SLEEP LOSSCRITERIAErythemaOedema/PapulationOozing/crustExcoriationLichenificationDryness*INTENSITY* Dryness is evaluatedon uninvolved areasMEANS OF CALCULATIONINTENSITY ITEMS(average representative area)0=absence1=mild2=moderate3=severeVisual analog scale(average for the last3 days or nights)PRURITUS (0 to 10)SLEEP LOSS (0 to 10)0 10

272 Principles of Skin Care: A Guide for Nurses and Other Health Care ProfessionalsAppendix 3 – Examples of emollients with excipientsLess greasy for dry skinMost greasy for very dry skinLotions Creams and gels OintmentsEucerin lotion (10% urea)(benzyl alcohol, isopropyl palmitate)Balneum plus (contains urea and anti-pruritic)(benzyl alcohol, polysorbates)Unguentum M(cetostearyl alcohol, polysorbate,propylene glycol, sorbic acid)Double base 50% white soft paraffin 50%liquid paraffinE45 lotion E45 cream White soft paraffin(cetyl alcohol, hydroxybenzoate) (cetyl alcohol, hydroxybenzoate, isopropylpalmitate)Dermol 500 lotion (containsantiseptic)(cetostearyl alcohol)Eucerin cream (10% urea)(benzyl alcohol, isopropyl palmitate, wool fat)Emulsifying ointment(cetostearyl alcohol)Aveeno Diprobase cream Yellow soft paraffin(benzyl alcohol, cetyl alcohol,isopropyl palmitate)(cetostearyl alcohol, chlorocresol)Dermol cream (contains antiseptic)Diprobase ointment(cetostearyl alcohol)Vaseline Dermacare Lipobase Hydrous ointment(cetostearyl alcohol, hydroxybenzoate) ( phenoxyethanol)OilatumEpaderm(benzyl alcohol, cetylstearyl alcohol)(cetostearyl alcohol)UltrabaseHydromol ointment(fragrance, hydroxybenzoate, disodium (cetostearyl alcohol)edentate, stearyl alcohol)ZerobaseAquaphor(cetostearyl alcohol, chlorocresol)Aquadrate (contains urea)Decubal(cetyl alcohol, hydroxybenzoate)Calmurid (contains urea)Nutraplus (contains urea)(hydroxybenzoate, propylene glycol)Cetraben(cetostearyl alcohol, hydroxybenzoate)Hydromol cream(cetostearyl alcohol, hydroxybenzoate)Sensicare emollient(cetostearyl alcohol)Aqueous cream (soap substitute)(phenoxyethanol, cetostearyl alcohol)

IndexNote: Page numbers in bold refer to themain sources of information5-year survival rates, 2068 methoxypsoralen (8MOP), 138AABCDE guidance formula, 204ablative methods, 6abscess, 224abuse and discrimination, of skin, 3–4acetyl CoA, 21aciclovir, 167, 227, 228acid mantle, 24, 52acitretin, 135, 140, 141acne, 18, 26, 29, 39, 54, 88,179–93bacterial activity and resultinginflammation, 181–2with comedones, 181conglobata, 182–3with cysts, 182and distribution, 184genetics, impact of, 184infantile acne, 184middle age, acne in, 184follicular plugging, 181fulminans, 182–3meaning of, 179pathogenesis, 180psychological impact, 192–3rosacea, see rosaceascarring, 183–4sebum, production of, 180–81treatmentsgeneral guidance, 185photodynamic therapy, 192severe acne, 189–92topical treatments, 186–9acquired immune deficiency syndrome(AIDS), 242acral lentiginous melanoma, 203actinic keratosis (AK), 196diagnosis, 197treatment, 197actinic LP, 257active ingredients, 72active listening, 93acute dermatitis, 162acute eczema, 151–2, 157acute inflammation, 50acute lesion, 32acute staphylococcal infections, 224acute urticaria, 263adalimumab, 142adapalene, 186Addison’s disease, 13adherence, 110, 243to therapies, 221adjuvant treatments, 204adolescents, 208adornment, of skin, 3adrenaline, 263adrenocorticotrophic hormone,13, 89adulthood eczema, 160–61adverse drug reactions (ADRs), 44,54–5prevention, 59advice, 93aesthetic considerations, of skinhealth, 5aesthetic knowledge, 43Afro-Caribbean hair, 17Afro-Caribbean skin, 16, 183ageing, 5, 24ageing and skin, 24, 27at birth, 24old age, 27post-birth/early months, 25arterial naevi, 25–6benign acquired melanocyticlesions, 25congenital melanocytic naevi, 25milia, 25mongolian blue spot, 25physiological jaundice, 26vascular naevi, 25pre-birth, 24pregnancy, 26–7puberty, 26air pressure alleviating mattresses, 57airborne contact dermatitis, 157Ajzen’s Theory of Planned Behaviour,209albinism, 3, 201alcohol abuse, 123alkaline skin, 55allergen load, 56allergenic, 72allergens, 20, 163allergic contact dermatitis, 52, 152,155, 162–3allergic reaction, 73allergy testing, 155

274 Indexalopecia areata, 233amelanotic melanoma, 197amino acids, 12ammonia, 53amniotic fluid, 24anagen, 17anaphylactic shock, 74, 263androgens, 18, 26, 179angioedema, 263anogenital warts, 232anoxia, 52anthralin, see dithranolantibacterial product, 187, 186antibacterial therapy, 164antibiotics, 44, 167antibiotic therapy, 164, 226antibodies, 50anticipatory grief, 207antifungal drugs, 44antigen-presenting cells, 14antihistamine, 46, 164, 264anti-infective agents, 81–2anti-inflammatories, 262anti-inflammatory propertiesof emollients, 81of retinoids, 186antimicrobials, 167antipruritic agents, 82antiviral agents, 44antiviral drugs, 44anxiety, 92, 96, 211anxiety management, 108apocrine sweat glands, 19–20, 26appendageal structures, of skin, 17–20hair, 17growth, 17types, 17–18nails, 18–19sebaceous glands, 18sweat glands, 19apocrine sweat glands, 19–20eccrine sweat glands, 19appendages, of skin, 35appraisal, 96aqueous cream, 74arrector pili muscle, 18arterial naevi, 25–6arthritis, 123arthritis mutilans, 129assessment, of skin, 29, 30–42, 38examination, of skin, 35history taking, 35–7lesions, understanding anddescribing, 31rashes, 32–5normal skin, 30body surface area, 30–31racial variations, 30nursing diagnoses, 37–8technological aids, 41–2tools, 38disease-related quality of life, 40severity tools, 38–40asteatotic eczema, 152, 158, 161, 170ataxia, 228athlete’s foot, 235atopic dermatitis, see atopic eczemaatopic eczema, 4, 14, 29, 50, 88, 152,154–157, 158, 222climate for, 156clinical signs, 154–5environmental factors increasingprevalence of, 156epidemiology, 154holistic assessment for, 159significance and impact of, 156–7treatment, 166–173bacterial infection, managementof, 167behavioural management, 168complementary therapies, 169–70oral immunosuppressant therapies,169phototherapy, 168–9seborrhoeic eczema, managingfungal infections in, 167–8sedating antihistamines, 168topical calcineurin inhibitors, 168viral infection, management of,167trigger factors, 155–6atrophic cicatrical alopecia, 256atrophic macular scars, 183atrophic scars, 183atrophied skin, 12atrophy, 24, 32attachment styles, 112attachment theory, 112attitudes, 61and behavioural change, 208audiovisual materials, 106Auspitz sign, 122autoantibodies, 264autonomic nervous system, 89autoregulatory systems, 52axillary hair, 26azathioprine, 143, 169azelaic acid, 187, 261–2BB2 (riboflavin), 62B3 (niacin), 62B6 (pyridoxine), 62bacterial activity and inflammation, inacne, 181–2bacterial contamination, 76bacterial infection, managing, 167bacterial resistance, 167risk factors, 188bacterial skin infections, 221cellulitis and erysipelas, 225–6folliculitis and related conditions,224impetigo, 222–4staphylococcal scalded skinsyndrome, 224–5bacterial swab, 223bactericidal effect, 187bacteriology, 42bad hair day, 24BAD Therapy Guidelines and AuditCommittee, 173bald patches, 92bandages, 44bandaging techniques, 56–7Bandura’s Self-efficacy Construct, 61barrier cream, 55barrier dysfunction, 80barrier function, of skin, 20, 49, 72,90, 153chemical protection, 20immunological surveillance, 20–21physical protection, 20basal cell carcinoma (BCC), 27, 198clinical presentations, 199definition, 198high- and low-risk BCCs, 198–9prevention, 200–201treatment, 200types, 198basal lamina, 14basal layer, 12–13basalioma, 198basement membrane zone, 14–15basisquamous BCC, 199Bateman, Thomas, 121bath additives, 75bath oils, 167BCC, see basal cell carcinomaBDNG (British Dermatological NursingGroup), 57beauty industry, 5beauty treatments, 5Beck Anxiety Inventory, 97behaviour change, 60, 61, 95, 209behavioural management, 63–4, 171beliefs, 61benign acquired melanocytic lesions, 25benign melanocytic naevi, 41benign tumours, 29benzoyl peroxide (BPO), 186, 187benzylkonium chloride, 82beta-blockers, 131betamethasone valerate, 165

Index 275bevacizumab (AVAST-M)., 204bilirubin, 26biochemical reactions, in skin, 23biofeedback, 172biologic drugs, 141–3potential side effects of, 145and prescribing regimes, 142biologic monitoring, 45biological barriers, 88biological therapy, 44, 124biology, of skin, 11–28ageing and skin, 24–7functions, of skin, 20–24structure, of skin, 11–20biopsy, 41–2, 44, 208, 250black eschar, 52blackheads, 181bleaching creams, 183bleeding, 86blepharitis, 261blistering conditions, in skin, 29, 247epidermolysis bullosa, 248–9immunobullous diseases, 249–51blood cultures, 223blood pressure, 250blood vessels, 16body image, 87body language, 93body lice, 241body map, 30body odour, 20body surface area (BSA), of normalskin, 30–31boils, 224bonding, 22bony prominences, 57Borders’ classification system, 201Botox, 6botulinum toxin, 6Bowen’s disease, 196, 197Braden Scale, 58bradykinin, 50brain–skin axis, 85, 131breakdown of skin, causes of, 50–55dry skin, 50–51inflammation, 50poor perfusion and disruptedmicrocirculation, 51–2skin breakdown, factors affecting,54–5urine and incontinence, effects of,53–4washing (skin hygiene) practices,effects of, 52–3breast feeding, 156, 249breathing exercises, 59Breslow thickness, 202brick wall, 80British Association of Dermatologists,141, 168British Association of DermatologistsDiagnostic Index, 29British Dermatological Nursing Group,113British National Formulary (BNF),113, 134, 164British National Health Service, 3brown fat, 21bullae, 32, 34, 160, 162, 223bullous impetigo, 223bullous LP, 257bullous pemphigoid, 15, 247, 249burning, of skin, 60burrows, 240CC fibres, 22cadherins, 13calcineurin inhibitors, 262, 266calcipotriol, 135and betamethasone diproprionate,134–5calcitriol, 132calcium, 23camouflage, 208, 266camouflage techniques, 183–4Cancer Help, 207cancer, in skin, see skin cancerCancerbacup, 207Candida, 237Candida albicans, 238, 239candidiasis, 41CAP fluoroimmunoassay tests, 264carbohydrate, 62carbomer gelling agent, 76carbon dioxide laser, 200carbuncles, 224carcinogenic substances, 135cardiovascular disease, 51care consultation, 110catagen, 17catecholamines, 89Caucasian hair, 17Caucasian skin, 16cautery, 44, 200, 201, 262cell-mediated immune response, 123,254, 255cellulitis, 44, 223, 225, 226cellulitis erysipelas, 51Centella asiatica, 27ceramides, 14ceruminous glands, 20cetostearyl alcohol, 72chemical irritation, 53chemical peels/dermabrasion, 184chemical protection, of skin, 20chemotherapy, 202chest X-ray, 143chickenpox, see varicella zosterchildhood eczema, 160childhood sun exposure, 208Children’s Dermatology Life QualityIndex (CDLQI), 99, 159chiropodists/podiatrists, 114chloasmal pigmentation, 26chlorhexidine hydrochloride, 82chloroquine-based anti-malarials, 131cholesterol, 14cholinergic urticaria, 264chronic actinic dermatitis, 157chronic dermatitis, 158chronic disease management, 104, 172chronic eczema, 152, 158chronic illness management, 103–4chronic irritant eczema, 158chronic lesions, 32chronic oedema, 51chronic plaque psoriasis (CPP), 124–5chronic skin severity tools, 39–40chronic urticaria, 264ciclosporin, 140, 169classical conditioning, 63cleansers, 52, 55, 75–6clindamycin, 187clinical decision-making, concepts andtheories of, 43–4clinical images, 8Clinical Knowledge Summaries (CKS),114clinical management plan (CMP), 114clinical nurse specialist, role of, 206clinical psychologist, 92, 207clinical severity, of skin assessment, 38clobetasol proprionate, 250clonidine, 262closed comedones, 181clotrimazole, 236clubbed nails, 35coal tar, 135method of application, 135–6cocoamido-propyl betaine, 52cognitive behavioural approaches, 63cognitive behavioural therapy, 93cold sores, 223collagen, 16, 15synthesis, 62colonisation, of skin, 52colour, of skin, 29, 32combing, 242comedones, 26, 181commensal bacteria, 24commensal organisms, 20, 238common skin disorders, classic lesiondistribution in, 36

276 Indexcommon warts, 231communication skills, 93comorbidities, 123associated with psoriasis, 123–4complementary therapies, 167, 169–70compliance, 109concordance, 188concordance process, 109, 110, 115conduction, 21confidence, 107congenital melanocytic naevi, 25conjunctivitis, 232, 261connective tissue, 15connective tissue disorders, 251systemic lupus erythematosus, 251–2systemic sclerosis, 252consultation skills, 36consultations, 110contact allergic dermatitis, 151, 170contact dermatitis, 29, 73–4, 152,161–3allergic contact dermatitis, 162–3irritant dermatitis, 162prevalence and incidence, 161contact eczema, 151contact urticaria, 264contraceptive advice, 192controlled drugs, 114convection, 21coping, 85, 90, 109external factors related to, 90–91internal factors related to, 90mechanisms, 112strategies, 108styles, 207copper, 62corneocytes, 12, 80, 153corneodesmosomes, 90cortex, 18corticosteroids, 136, 250corticotrophin releasing hormone, 89cortisol, 89cosmesis, 5cosmetic considerations, of skinhealth, 5cosmetic dermatology, 5–7cosmetic emollients, 71, 72–3cosmetic procedure, for skin, 5counselling skills, 209coxsackie A16 virus, 232cradle cap, 160, 167cream emollients, 79creams, 76CREST, 252Crohn’s disease, 123crude touch, 22crust, 32, 222crusted (Norwegian) scabies, 240crusting, 225cryotherapy, 197, 200, 201, 230, 232crystacide cream, 230CTCL, see cutaneous T-cell lymphomascultural influences, of skin, 2curettage, 44, 200, 201, 232cutaneous itch, 22cutaneous lymphatics, 16cutaneous melanomas, 202cutaneous T-cell lymphomas (CTCL),54, 201mycosis fungoides, 201primary cutaneous CD30+lymphoproliferative disorders,202Sézary syndrome, 202treatment, 202cuticle, 18cysteine, 12cystic lesions, 182cytokines, 20, 22, 123, 154production, 90cytoplasm, 12cytotoxic agents, 45Ddactylis, 129daughter cells, 12debris, 75decision-making, 110decoration, of skin, 3deep breathing exercises, 96dehydration, 21, 228delusional parasitosis, 92Demodex folliculorum, 261dendritic cells, 14Department of Health (DH) website,114depression, 86, 96dermabrasion, 184dermal necrosis, 52dermal papilla, 15, 18dermatitis, 151dermatitis artefacta, 92Dermatitis Family ImpactQuestionnaire, 38, 159dermatitis, see eczemadermatological diagnoses, 29, 43dermatological emergency, 127dermatological ‘red flag’ conditions, 44dermatology consultation, 111Dermatology Life Quality Index(DLQI), 98dermatomal distribution, 228dermatomes, 229dermatomyositis, 251dermatophyte infections, 41, 233dermatoscope, 41, 198dermis, 15–16dermographism, 264dermoscope, see dermatoscopedescaling agents, 82desmoglein, 224desmosomes, 13desquamation, 12, 54, 60, 80detergents, 164developmental stage, 35of child, 171diathermy, 262diclofenac gel, 197diet, 156direct immunofluorescence, 250disability, 97and impairment, 86–7discoid eczema, 151, 158,160, 170discomfort, 91discrimination, 3, 88disease, typology of, 90disease severity, 97, 157display, of skin, 3disseminated herpes simplex, 227disseminated herpes zoster, 229distal and lateral subungualonychomycosis (DLSO), 236distal interphalangeal joint arthritis,129dithranol, 44, 132, 136method of application, 136doctor/patient relationship, 222doxycycline, 188dressings, 44, 249drug administration, 112–13drug hypersensitivity syndrome, 253drug induced dry skin, 50drug reactions, 252–3drug hypersensitivity syndrome, 253drug-induced photosensitization,254, 255drug-induced skin pigmentation,253–4fixed drug reactions, 253toxic erythema, 253dry skin, 50–51, 54dry wraps, 56drying, 55, 236, 238drying practices, 55dryness, problem of, 29dystrophic type of EB, 248dysuria, 227EEB simplex, 248eccrine sweat, 21eccrine sweat glands, 19economic pressures, 87ectoderm, 24eczema, 29, 78, 90, 110, 151–73adulthood eczema, 160–61

Index 277atopic eczemaclinical features and epidemiology,154–7behavioural treatments, 170caring for children with, 159–60childhood eczema, 160classification, 152contact dermatitis, 161–3diagnosis, 157–8differential diagnoses, 157–8, 173economic cost, 156meaning of, 151–3biology and pathophysiology of,153–4severity assessment, 158–9treatment for 163atopic eczema, see atopic eczema:treatmenteducational interventions, 171–3psychological interventions,170–71topical treatments, 164–6eczema craquele, 161eczema herpeticum, 167, 227Eczema School model, 106eczema schools, 172eczema severity assessment, 158–9eczema variant, 157education, 243importance, 171and support, 103educational intervention, 29, 106for treating eczema, 170, 171educational resources, 105awareness of, 105–7efalizumab, 141efficacy, 72elastic fibres, 16elasticity, of skin, 35, 60elastin, 15elephantiasis, 5Elidel ® , 168elliptical biopsy, 259embryogenesis, 24emetophobia, 92emollients, 56, 71–83, 132antimitotic properties, 81antipruritic properties, 81constituents, 72–3definition, 71–2of eczema, 164formulations, 75bath additives, 75leave-on topical emollients,76–80skin cleansers, 75–6how to apply, 77–8potential side effects, 73contact dermatitis, 73–4occlusive nature, adverse effectscaused by, 74–5safety concerns, 75therapy, 55–6, 164usage, factors affecting, 82–3when to apply, 78–9where to apply, 79–80working mechanism, 80–82emotional behaviour, regulation of,108–9emotional importance, of skin, 1emotional involvement, 111emotional response, 206empathy, 111empirical knowledge, 42–3emulsifiers, 76emulsifying wax, 72emulsion, 72, 76encephalitis, 228endogenous eczema, 151endonyx onychomycosis, 237endoplasmic reticulum, 12endothrix infection, 233energy storage, 21entonox, 249environmental changes, affectingskin, 4epidermal necrosis, 52epidermal proliferation, 90epidermis, 11–12basal layer, 12–13granular layer, 14horny layer, 14prickle cell layer, 13–14epidermolysis bullosa, 15, 44, 248autosomal dominant forms of, 248autosomal recessive forms of, 248Epidermophyton, 233Epidermophyton floccosum, 235eponychium, of nail, 19erosion, 32erosive LP, 256erysipelas, 225erythema, 30, 39erythema multiforme, 54, 227erythema nodosum, 54erythematotelangiectatic rosacea, 260erythematous skin, 32erythrasma, 41erythroderma, 54erythrodermic psoriasis (EP), 44, 127erythromycin, 187, 188essential fatty acids (EFAs), 62etanercept, 142ethnic differences, in skin structure, 16European Medicines Agency, 141European Pressure Ulcer AdvisoryPanel (EPUAP), 52European standard battery, 163European Task Force on AtopicDermatitis, 39evaporation, 21, 52examination, of skin, 35excipients, 72excision, 44excisional biopsies, 42excoriated lesion, 32excoriation, 32, 241exfoliation, 6exfoliative dermatitis, 54exocytosis, 14exogenous eczema, 151exothrix infection, 233extrinsic ageing, 27Ffacial flushing, 260faecal incontinence, 53faeces, 53famciclovir, 227, 229fast pain, 23fats, 72fatty acids, 14fauna, 24feet, 235female genital mutilation, 3fibrin, 50fibroblasts, 15fibrosis, 51filaggrin, 14filaggrin mutations, 153filiform warts, 232fillers, 6fine touch, 22finger nails, 236Finger Tip Unit (FTU), 166finger/toenail, 237fingerprint, 16Finn chambers, 42, 163fissures, 32, 53, 50, 160fixed drug reactions, 253flammability, 75flare-ups, 166flat lesion, 32fleas, 222flexural areas, 154flexural dermatitis, 154flexures, 125flora, 24fluid-filled lesion, 32fluorouracil, 197foetus, 27fold, of skin, 238follicle, 181follicular keratinocytes, 180follicular macular atrophy, 183follicular plugging, 180, 181follicular pustules, 224

278 Indexfolliculitis, 74, 135, 224, 242foot and nail care, 238foot hygiene, 236footwear, 236fragrance, 82fragrance free, 74freckles, 25, 41free nerve endings, 22friction, 53, 58friction coefficient, 53frictional damage, 55fumarates, 143fumaric acid esters, 143functions, of skin, 20barrier function, 20–21biochemical reactions, in skin, 23heat loss, 21psychosocial, 23–4sensation, 21–3storage, 21temperature regulation, 21fungal infections, 221, 223, 233dermatophyte (ringworm) infections,233–8pityriasis versicolor, 239–40in seborrhoeic eczema, 167–8yeast infections, 238–9furuncle, 224fusidic acid, 224Ggabapentin, 229gangrene, 24gastrostomy, 249gel emollients, 76–7generalised pustular psoriasis (GPP),126, 127genes, 121genetic counsellor, 249genetics, 27impact of, 184genital erosive LP, 257genital thrush, 238genital warts, 231genuine, being, 111germ cells, 24gingivostomatitis, 226glabrous skin, 17glomerulonephritis, 240glucose, 250glycerine, 81glycol, 72glycoproteins, 13glycosaminoglycans (GAGS), 15Goeckerman regime, 135Golgi complex, 12grafting, of skin, 44granular layer, 14gravitational eczema, see varicose eczemagriseofulvin, 234, 237ground substance, 15group support, 106guilt, 86gustatory sweating, 19guttate psoriasis (GP), 125–6, 223Hhabit reversal, 63haemorrhagic blisters, 250haemosiderin, 35hair, 2, 17, 35, 41debris, 234ethnic groups, 17follicle, 17, 22, 26growth, 17shaft, 18structure of, 18types, 17–18hair-root plexuses, 22hand, foot and mouth disease, 232hand protection, 238hand washing, 161, 222, 223handicap, 87head lice, 242infestations, 242health behaviour, 104Health Care Commission, 3health education, 30, 61health/patient education, 172health promotion, 109healthy skin, 1, 2heat loss, from skinconduction, 21convection, 21evaporation, 21radiation, 21hemidesmosomes, 14, 15hepatitis, 228herald patch, 257herpes encephalitis, 227herpes infections, 223herpes simplex, 44, 167, 226, 242herpes simplex virus (HSV), 88,226–7herpes zoster, 44, 228, 242herpetic whitlow, 227heuristics, 43histamine, 16, 22, 50, 262histocytes, 16history taking, 35–7HIV, 237, 242infection, 4, 230, 240Holt, L.E, 22home environment, 156hormonal therapies, 189horny layer, 14house dust mites, 155, 156human genome, 121human immunodeficiency virus (HIV),222, 253human papilloma virus, 231humectant, 72, 80, 81humid environments, 238hyaluronic acid, 15, 60hydration, of skin, 55, 56promotion, 55–7hydrocoele, 4hydrocortisone, 165hydroxyurea, 143hygiene, 52, 238hypothesis, 4, 155self-care, 37hyperaemia, 50hyperkeratinisation, 180hyperkeratosis, 51, 122hyperkeratotic lesion, 32hyperpigmentation, 16, 61hyperplasia, 24hyperproliferation, 21, 122hypersensitivity reactions, 42hypertrichosis, 165hypertrophic LP, 256hypertrophic scars, 183hypertrophy, 24hypnotherapy, 172hyponychium, of nail, 19hypothalamic–pituitary–adrenal axis,88hypothalamus, 21hypothetico-deductive theory, 43Iiatrogenic effects, 54ice-pick scars, 183ichthyoses (inherited), 50icterus neonatorum, see physiologicaljaundiceicthyosis, 14id response, 233IgE-mediated response, 74IL-1α, 81Imiquimod, 197, 200, 230immune system, 1, 153immune-mediated response, 74immunity, 20–21immunocompromised patients, 228immunodeficiency, 224immunoglobulin (Ig) E, 153immunological surveillance, of skin,20–21immunomodulators, 164immunosuppressed patients, 238immunosuppression, 169, 240, 250immunosuppressive agents, 44impaired skin integrity, risk for, 38impairment, 86, 87impetigo, 221, 222–4

Index 279impetigo contagiosa, 222incisional biopsies, 42, 44incontinence, 55, 58assessing and limiting effects of,58–9independent prescribing, 113–14Indo-Chinese hair, 17induration, 39due to hyperkeratosis, 122of plaque, 129infantile acne, 184infantile seborrhoeic dermatitis, seecradle capinfantile seborrhoeic eczema, 156infants, 156Infants Dermatology Life QualityIndex, 159infections, of skin, 221infective disorders, 29infective skin conditions, 221–43bacterial skin infections, see bacterialskin infectionsfungal infections, see fungalinfectionsviral infections, see viral infectionsinfestations, 221, 240–42lice, see licepubic lice, 242scabies, 240–41diagnosis, 241management, 241inflammation, 21, 50, 56, 130and skin breakdown, 50inflammatory acne, 185inflammatory agents, 81inflammatory changes, in skin, 35inflammatory episodes, 59inflammatory lesions, 187inflammatory mediators, 164inflammatory process, 50inflammatory response, 50, 154infliximab, 45, 142information leaflets, 105information sources, 105inherited blistering disorders, 248innate defence system, 20innate nonspecific resistance,20–21inositol, 131insect, 240insect bites, 44, 222insensible water loss, 19integrity, of skin, 37maintenance, 57–60intense pulsed light, 262interferon levels, 153interferons, 202interleukin levels, 153interleukins, 20International Classification for NursingPractice (ICNP ® ), 37International Classification ofDisease, 29International Council of Nurses (ICN),37intertrigo, 78, 239intracellular proteins, 251intrinsic ageing, 27intrinsic capability, 90invasive melanoma, 202inverse psoriasis, 125iontophoresis, 44iron, 62irritant and contact dermatitis,diagnosis of, 162irritant contact dermatitis, 161irritant dermatitis, 162, 170irritant reaction, 73irritants, 162isotretinoin, 186, 189–90, 262drying effects of, 191monitoring, 190–91relapse, 191side effects, 190supporting patients, 191–2itch, 22, 91, 156, 160, 230itch–scratch cycle, 63, 154, 171itraconazole, 237, 240Jjobs, 88junctional type of EB, 248juvenile plantar dermatoses, 160, 170KKawasaki disease, 232–3keloid scars, 16, 183steroid injections for, 184keratin, 12, 14, 52keratinocytes, 12, 122keratohyalin, 13, 14keratolytic agents, 44kerions, 233, 234ketaconazole shampoo, 235ketoconazole, 167kinins, 23knowledge of self, see personalknowledgeknowledge, types of, 42Koebner phenomenon, 130Krebs cycle, 21kwashiorkor, 61Llactic acid, 14lamellar bodies, 90lamellated corpuscles, 22lamina lucida, 14, 248laminin, 14Langerhans cells, 12, 14, 20, 153lanolin, 71, 72lanugo hairs, 17, 24laser resurfacing, 6laser therapy, 44, 192lasers, 44, 184lauromacrogols, 82leave-on topical emollients, 76–80leg oedema, 226leg ulceration, 29leg ulcers, 226lentigo, 25lentigo maligna melanoma, 203leprosy, 23, 50, 121lesions, 29differential diagnosis of, 32distribution of, 31understanding and describing, 31–5leukoplakia, 239leukotrienes, 264lice, 222, 241–2lichen planus (LP), 88, 237, 255actinic LP, 257bullous LP, 257classic presentation, 256erosive LP, 256–7hypertrophic LP, 256lichen simplex, 160, 170lichenification, 32, 39, 152, 153, 241lifestyle, 208lifestyle choice, 123lightening, of skin, 3limb elevation, 59lipid bilayer, 14lipid lamellae, 153lipids, 14, 53, 72liquefaction, 255listening, 110, 207lithium, 131liver function tests (LFTs), 190local skin reactions, 200locus of control, 108long-term condition, 103people with, 104lotions, 76low self-esteem, 103lunule, 18, 19lupus erythematosus-type reaction, 188lymecyline, 188lymph flow, 59lymph nodes, 205, 212metastasis, 206lymphadenectomy, 204lymphadenopathy, 205, 233lymphangiectasia, 51lymphangioma, 51lymphangitis, 223

280 Indexlymphatic filariasis, 4, 5, 59lymphatic impairment, 51lymphatic vessels papillomatosis, 51lymphocyte, 123trafficking, 90lymphocytosis, 90lymphoedema, 4, 51, 226management, 59services, 208lymphomas, 201, 258lymphomatoid papulosis, 202lymphorrhoea, 51lysosomal activity, 14lysosomes, 14Mmaceration, 53Macmillan Cancer Support, 207macrophages, 16macule, 34major histocompatibility complexmolecules, 14Malassezia, 167Malassezia furfur, 160maliathon, 241, 242malignant melanomas, 25, 27malignant skin cancers, 3malnutrition, 62mammary glands, 20Marc’s Line, 207masking fragrances, 74mast cells, 263mattresses, 58maturity of skin, 51measurements of skin barrier function,55mechanical barrier, 56medicated paste bandages, 56–7medication, managing, 105Medicines and Health care productsRegulatory Agency (MHRA),114medicines education, 112skin-related products andopportunities for, 112–13independent prescribing, 113–14patient group directions, 113patient-specific direction, 113supplementary prescribing,114–15medulla, 18Meissner’s corpuscles, 16, 22melanin, 13, 20, 23, 30, 35, 202melanocyte stimulating hormone(MSH), 13melanocytes, 12, 13, 25, 265melanoma, 41, 195, 202ABCDE guidance formula, 204adjuvant treatment, 204diagnosis, psychological impact of,206–7distribution, 203follow-up, 204–5incidence, 196metastatic melanoma, 205prevalence, 196primary melanomadiagnosis, 203–4treatment, 204risk factors, 203survival, 205–6type, 203melanoma staging system, 205melanonychia, 256melanosomes, 13, 30menstrual cycle, 26mental health problems, 23mental health well-being, 91mental well-being, 85Merkel discs, see Type I receptorsMerkell cells, 13mesoderm, 24metabolic syndrome, 124metastatic BCC, 198metastatic disease, 205self-examination teaching for, 212teaching of self-examination for, 212metastases, of skin, 205metastatic melanoma, 205methicillin resistant staphylococcusaureus (MRSA), 223, 224methotrexate, 45, 139–40microcirculation, 35microcomedone, 180microdermabrasion, 6microfilariae, 5microscopy, 41, 223microsphere, 186Microsporum, 233Microsporum audouinii, 41Microsporum canis, 41, 235middle age, acne in, 184mild to moderate acne, 186azelaic acid, 187benzoyl peroxide (BPO), 187nicotinamide, 187retinoid product, application of,186–7topical antibiotics, 187–8topical retinoids, 186milia, 25Milroy’s disease, 51mind, 85mindfulness-based stress reductiontechniques, 109minerals, 62minimal erythema dose, 45, 138minocycline, 188mite allergens, 156mites, 222mitochondria, 12mitosis, 18moderate acne, 188hormonal therapies, 189oral antibiotics, 188–9moisture, 78moisturisers, 71–2moisturising, 238moles, 41mollusca, 242molluscum contagiosum, 167, 230mongolian blue spot, 25monocyte, 90monotherapy, 187morality, 86morbilliform, 253morphea, 251morphoeic BCC, 199motivation, 103motivational training, 64mucous membranes, 250multidisciplinary approach, for atopiceczema, 164mycology, 41mycosis fungoides (MF), 54, 201, 258,259–60myelinated A fibres, 23Nnail, 2, 17, 18–19, 35, 41, 224anatomy, 19structure, 19nail bed, 19nail, body of, 19nail fold, 19nail, free edge of, 19nail infections, 35nail involvement, 128nail matrix, 18, 19nail plate, 18, 19, 236nail psoriasis, 126narrowband UVB, 169National Cancer Plan, 204National Eczema Society, 108, 169,173National Institute for Health andClinical Excellence (NICE), 143National Pressure Ulcer Advisory Panel(NPUAP), 57natural moisturising factor (NMF), 14,81, 153necrosis, 24negotiation, 110neonatal bullous impetigo, 223neonates, 227neoplasia, 24nerve growth factor, 89

Index 281neurodermatitis, see lichen simplexneuropeptides, 22newborn, 24nicotinamide, 187nociceptors, 23nodular BCC, 199nodular lesions, 182nodular melanoma, 203nodule, 32, 35, 190, 205formation, 26non-ablative methods, 6non-accidental injury, 25non-blanchable oedema, 59non-bullous impetigo, 222non-comodogenic products, 185non-erythematous skin, 32non-immune-mediated reaction, 74non-inflammatory acne, 185non-inflammatory lesions, 187non-malignant skin cancers, 3non-medical prescribing, 115non-medical prescribing, informationsources on, 114–15non-melanoma skin cancer (NMSC),195non-melanoma skin lesions, 195basal cell carcinoma, 198–201squamous cell carcinoma, 201normal skin, 30body surface area (BSA), 30–31racial variations, 30North American Nursing DiagnosisAssociation (NANDA), 37nucleus, 12nurse-independent prescribing, 113,114nurse-led dermatology services, 173nurse-led prevention, 61nurse-led services, 173nurse–patient relationship, 111–12nurse–prescriber–patient consultations,111nursing diagnoses, 37–8nursing intervention, 92, 209active listening, 93–5cognitive behavioural therapy, 95–7skin disease impacts, measurementof, 97–100to support behavioural change,60–61nutritional support to skin integrity,61–3Oobesity, 53, 62, 226, 238obsessive/compulsive disorder, 96occlusion, 52, 57, 72occlusive bandages, 79occlusive body bandages, 166occular rosacea, 261occupational dermatoses, 161oedema, 26, 39, 51oils, 72ointments, 76oligoarticular arthritis, asymmetric, 129onycholysis, 126, 254onychomycosis, 236, 238open comedones, 181optometrists, 114oral antibiotics, 188–9oral fluconazole, 239oral immunosuppressant therapies, 169oral retinoids, 202osteolysis, 129over-hydrated skin, 54over-washing, 50ovulation, 26oxytetracycline, 188ozone protection, 4Ppain, 22, 23, 130and pruritus, 130relief, 249palmar plantar pustulosis (PPP), 126palmar psoriasis, 125palmoplantar psoriasis, 123palmoplantar pustulosis, 158palpation, 32, 35papillary layer, 16papillomatosis, 51papular lesions, 188papules, 32, 34, 182papulopustular rosacea, 260parasites, 222parasympathetic nervous system, 89parental education, 157parental self-efficacy, 108paronychia, 35PASI score, 45paste bandages, 57patch testing, 42, 74, 162–3patches, 32pathogenic microorganisms, 52pathogens, 1, 20, 221patient education, 43, 111patient group directions (PGD), 113patient history, 35patient involvement, 111patient-orientated eczema measure,158–9patient participation, 111patient repositioning, 57patient-specific direction (PSD), 113patient support, 103patient teaching, 172peanut allergy, 190pediculicide, 242peeling, 54peels, 7pellagra, 61pemphigus vulgaris, 88, 251Penn State Worry Questionnaire, 97perceived self-efficacy, 108perfumes, 74perineal dermatitis, 53perioral dermatitis, 165periorbital cellulites, 226peripheral nervous system, 88permethrin, 241personal accomplishment, 108personal knowledge, 43petrolatum, 72pH level, 55pharmaceutical industry, 82pharmacist-independent prescribing,113, 114pharmacists, 114phosphorous, 23photo-ageing, 27photo allergic dermatitis, 163photoallergic sensitisation, 254photochemotherapy, 169photodynamic therapy (PDT), 44, 192,197, 200photo-patch testing, 163photophoresis, 202photosensitisation, 254photosensitising agent, 162photosensitivity, 54, 157, 186phototherapy, 44, 50, 137, 168–9, 202assessment, 45and oral immunosuppressants, 168phototoxic reactions, 162, 254phymatous rosacea, 261physical examination, 205physical protection, of skin, 20physical urticaria, 264physiological jaundice, 26physiotherapists, 114physiotherapy, 249piercing, 3pigment, of skin, 3pigmentation, of skin, 30pigmented BCC, 199pilosebaceous gland, 179pimecrolimus (Elidel ® ), 168pituitary gland, 13, 89pityriasis rosea, 257–8pityriasis versicolor, 41, 239Pityrosporum orbiculare, 239Pityrosporum ovale, 160pityrosporum yeast, 41plane warts, 231planning care, 42–4clinical decision-making, conceptsand theories of, 43–4

282 Indexplanning care (contd.)clinical judgements, 42–3dermatological ‘red flag’ conditions,44evaluation, 45intervention, 44–5plantar psoriasis, 125plantar warts, 231plaque, 13, 34plucking, 17pneumonia, 228podiatrist, 238podophyllotoxin cream, 230polysaccharides, 15polysiloxane, 72pompholyx (pompholyx eczema), 158,160–61, 170, 171poor nutrition, 51poor perfusion, 50and disrupted microcirculation, 51–2port wine stains’, 25positioning, 58postherpetic neuralgia, 229post-inflammatory pigmented lesions,183post-traumatic stress disorders, 96potassium, 23potassium permanganate solution, 226potency, 165poverty, 4skin diseases of, 4–5pox virus, 230practical demonstrations, 171practitioner–patient relationship, 111prednisolone, 250pregnancy, 26pregnant women, 228pre-malignant skin lesions, 195actinic keratosis, 196treatment, 197Bowen’s disease, 196, 197diagnosis, 197prevention, 198prescriptions, 88, 112preservatives, 74, 76pressure, 51alleviating, 57effects, 50, 51–2sores, 53pressure-relieving beds, 57PRESSURE trial, 57–8pressure ulcer, 52aetiology, 52prevention, 57, 58prickle cell layer, 13–14Primary Care Dermatology Society(PCDS), 168primary cutaneous CD30+ lymphoproliferativedisorders, 202primary cutaneous lymphomas, 258primary cutaneous T-cell lymphomas,258primary impetigo, 222primary irritant contact dermatitis, 152primary lesions, 32primary melanoma, diagnosis of, 203primary T-cell lymphomas, 201printed materials, 106prodromal phase, 226professional support, 104progesterone levels, 26progressive disease, 90progressive muscle relaxation, 96prolactin, 89propellants, 76Propionibacterium acnes, 52, 180colonisation by, 185propylene glycol, 52prostaglandins, 22Protection Motivation Theory, 109protection, of skin, 49–64breakdown, causes of, 50–55damage by scratching, preventing,63–4nursing intervention, to supportbehavioural change, 60–61nutrition to support skin integrity,61–3preventative practices, 55promoting skin hydration, 55–7skin integrity, maintaining, 57–60skin washing and drying, 55vulnerability, 49protein, 15malnutrition, 61proximal subungual onychomycosis(PSO), 237pruritic skin, 57pruritus, 40, 130pseudofolliculitis barbae, 16psoralens, 169psoriasis, 29, 50, 79, 86, 88, 90, 110,121–47, 237biology, 122–3clinical variantschronic plaque psoriasis, 124–5erythrodermic psoriasis, 127guttate psoriasis, 125–6nail psoriasis, 126psoriatic arthritis, 127–8pustular psoriasis, 126–7comorbidities associated with, 123–4differential diagnoses for, 128history, 121–2physical symptoms, 128inflammation, 130pain and pruritus, 130scaling, 128–30proportions of populations having,122quality of life, measurement of,145service provision, 143–5systemic drugs for, 143treatments for, 131systemic therapies, see systemictherapies, for psoriasistopical therapies, see topicaltherapies, for psoriasistrigger factors in, 130drugs, 131koebner phenomenon, 130streptococcal throat infection, 131stress, 131ultraviolet light exposure, 131Psoriasis Area Severity Index (PASI),31, 99, 135Psoriasis Association, 108Psoriasis Disability Index, 86psoriasis vulgaris, 124psoriatic arthritis (PSA), 123, 127–8clinical presentations of, 129psoriatic arthropathy, 104psychological aspects, of skin care, 85,88–92brain–skin axis, 88–90coping, 90–91mental health well-being, 91–2psychological assessment, of skin, 38psychological functions, for healthyskin, 2psychological impactsof acne, 192–3of chronic skin conditions, 40of skin disease, 2, 85psychological importance, of skin, 1psychological interventions, for treatingeczema, 170psychological stress, 131psychological support, 103psychological well-being, of skinhealth, 5psychorheology, 82psychosocial impact, of skin disease, 38psychosocial phases, 207psychosocial well-being, for atopiceczema, 159puberty, 26pubic hair, 26pubic lice, 242pulsed laser therapy, 44pump dispensers, 79punch biopsies, 42, 44, 198, 201purpura, 61purpuric eruptions, 54purpuric rash, 44pustular psoriasis, 126–7

Index 283pustules, 32, 182, 186PUVA, 138–9, 169, 266pyrrolidonecarboxylic acid, 14Qquality of life, 30, 97, 104impact of skin, 40measurement, 145skin disease, impact of, 157quantities of emollients, 77quasi-continuous wave laser therapy,44Rracial variations, 30racism, 3radiation, 21radiographers, 114radiotherapy, 54, 59, 200, 201, 202raised lesion, 32rashes, 30, 32–5diagnosis of, 32reactive hyperaemia, 52reasoning, 43red blood cells, 26red flag conditions, 42, 44red man syndrome (Sezary syndrome),202re-epithelisation, 72reframing, 96rejection, 86relaxation methods, 109, 172religious observance, of skin, 3remission, 91reperfusion, abrupt, 52repigmentation, 265reproductive organs, 26resistance, in acne, 188resistance patterns, 223rete ridges, 15reticular layer, 16retinoid product, application of,186–7retinoids, 44, 140–41retinol, 7rhesus, 26rhinophyma, 261ribosomes, 12ringworm, 237infections, see dermatophyteinfectionsrisk and trigger factors, of contactdermatitis, 161rodent ulcer, 198root, of nail, 19rosacea, 260erythematotelangiectatic rosacea,260occular rosacea, 261papulopustular rosacea, 260–61phymatous rosacea, 261treatment, 261–2rough drying technique, 55rubbing, 55rule of nines, 31Ssacroiliitis, 129Salford Psoriasis Index (SPI), 99–100salicylic acid, 197, 232samples, 82SAPHO, 182Sarcoptes scabeii mite, 240scabicides, 241scabies, 4, 222, 240, 242scale, 32scaling, 39, 54, 128–30, 225scalp, 35infections, 237psoriasis, 125scaling, 35scaly lesion, 32scar, 32scarring, 182, 183, 230, 248camouflage techniques, 183–4chemical peels/dermabrasion, 184keloid scars, steroid injections for,184lasers, 184silicon sheets, 184SCC, see squamous cell carcinomasclerotherapy, 262SCORAD, 39, 159scrapings, 234, 241scratch–itch cycle, 56breaking and behaviouralmanagement, 63–4scratching, 18, 56, 86, 156season ticket, 88seat cushions, 57sebaceous glands, 17, 18, 26,179, 261sebocytes, 180seborrhoeic dermatitis, 157, 160, 170seborrhoeic eczema, 151, 152seborrhoeic keratosis, 41sebum, 18, 24, 26, 51, 56, 60, 81, 179,185production, 180–81secondary impetigo, 222secondary lesions, 32secondary sexual characteristics, 26sedating antihistamines, 168selenium sulphide, 235self-awareness, 111self-care, 104self-care management, 49self-care strategies, 60self-care support, 104self-cognitive theory, 109self-efficacy, 61, 90, 107–9self-efficacy theory, 209self-esteem, 23self-examination, 61, 209, 211promotion, 209teaching, for metastatic disease, 212self-harm, 92self-help groups, 207self-management, 45, 103, 109, 172self-management and patient support,103–5educational resources and strategies,105–7social learning theory andself-efficacy concept, 107–9sensation, 21–3cutaneous itch, 22pain, 23touch, 21–2sensitisers, 72sensory neuropathy, 59sentinel lymph node biopsy (SLNB),204, 208septicaemia, 223, 225serotonin, 50serum lipid, 190service delivery, models of, 172service provision, 143–5severe acne, 189isotretinoin, 189–92severe sunburn, 54severity reaction, 60sex hormones, 26sexual abuse, 232Sézary syndrome, 202shame, 86shave, 44shea butter, 60shear forces, 58shingles, 44, 223, 227, 228–9shoes, 236signalling molecules, 20silicon sheets, 184skin, definition of, 1skin barrier, 24, 29, 44, 49disruption, 53function, 55skin cancer, 4, 27, 29, 195–213causation, risk prevention and earlydetection, 208attitudes and behavioural change,208–9epidemiology, 195–6incidence, 195melanoma, 202–7non-melanoma skin lesions,198–202

284 Indexskin cancer (contd.)nursing intervention andself-examination promotion,209–13pre-malignant skin lesions, 196–8prevention, 195psychological impact of diagnosis,206public awareness of, 196surgery, 207–8Skin Care Campaign, 82skin cleansers, 75–6skin knowledge, 22skin prick tests, 264skin self-examination (SSE), 201,209–10socio-demographic factors, 210teaching for metastatic disease, 212skin tag, 5skin turgor, 35skin typing, 30sleep, 56disturbance, 160loss, 156slippery feeling, 75slow pain, 23smell, 82smoking, 123soap, 52, 55, 59, 75, 164, 238physico-chemical effects of, 52soap substitutes, 55, 74, 75, 167social aspects, of skin care, 85body image, 87disability and impairment, 86–7economic pressures, 87–8historical context, 85–6social pressures, 87stigma, 86social confidence, 103social functions, for healthy skin, 2social impacts, 85–8of chronic skin conditions, 40of skin disease, 2, 85social influences, of skin, 2social interactions, 86social learning theory, 61, 107–9society, 85socioeconomic status, 210sodium lauryl sulphate, 52soft cotton clothing, 56superficial white onychomycosis(SWO), 236–7SPF, see sun protection factorspider naevi, 26spondylitis, 129spoonfuls, 78sprays, 76squamous cell carcinoma (SCC), 27,196, 197, 201diagnosis, 201grading, 201prevention, 201treatment, 201staining, 136standard battery, 42Staphylococcal scalded skin syndrome,224Staphylococcus aureus, 52, 153, 154,167, 190, 222, 223starvation, 21stasis eczema, 161stem cells, 12Stemmer’s sign, 51steroid injections, 184steroids, 3, 44Stevens–Johnson syndrome, 54, 223stigma, 86stinging, 73stratum basale, 12–13stratum corneum, 14, 49, 53, 72, 80,153see also horny layerstratum germinativum, 12–13stratum granulosum, 14stratum spinosum, 13–14strawberry birth marks, see arterialnaevistreptococcal throat infection, 131Streptococcus pyogenes, 222, 223stress, 88, 131management, 108stretch marks, 27striae atrophicae, 165structure, of skin, 11appendageal structures, 17–20basement membrane zone, 14–15dermis, 15–16epidermis, 11–14ethnic differences in, 16subcutis, 16subcutaneous fat, 15subcutaneous tissues, 52subcutis, 16substance P, 89, 90subungual hyperkeratosis, 256sulphasalazine, 143sulphur, 241sun avoidance, 60sun beds, 213sun block, 197sun prevention activities, 212–13sun protection, 200, 254sun protection factor (SPF), 212–13sun-tan, 3sun/ultraviolet (UV) damage, 30sunscreen/clothing use, 209sunscreen, 198, 200, 212, 213effective, 60SunSmart, 212, 213SunSmart campaign, 208superantigens, 154superficial angiomatous naevi, seearterial naevisuperficial basal cell carcinoma, 197,199superficial fungal skin infections, 233superficial spreading melanoma, 203superficial white onychomycosis(SWO), 236supplementary prescribing, 113,114–15support needs, 104surface area, of skin, 30surface features, of skin, 29, 32surfactants, 52surgery, for melanoma, 207survival, 205swabs, 224sweat glands, 17, 19apocrine sweat glands, 19–20eccrine sweat glands, 19symmetric polyarthritis, 129sympathetic nervous system, 20, 89systemic lupus erythematosus (SLE),251systemic sclerosis, 251systemic therapies, for psoriasis,137–43biologics, 141–3ciclosporin, 140methotrexate, 139–40nursing care, 143phototherapy, 137PUVA, 138–9retinoids, 140–41UVB, 137–8systemic therapy, 45systemic treatments, in children, 168TT-cell lymphoma, 258T-cell-mediated response, 74T-cells, 14, 123T-helper (TH) lymphocytes, 153T-lymphocytes, 154, 255tacalcitol, 132Tacrolimus (Protopic ® ), 168talking therapy, 95tars, 44, 45tattooing, 3technological aids, 41bacteriology, 42biopsy, 41–2dermatoscopy, 41mycology, 41patch testing, 42Wood’s light, 41

Index 285telangiectasia, 165, 260, 262telephone consultations, 105telogen, 17temperature regulation, 21tension lines, 15teratogenicity, of isotretinoin, 190Terbenafine cream, 235terbinafine, 167, 234, 236, 237terminal hairs, 17, 24test patch, 74testosterone, 179tetracycline, 187TEWL, see transepidermal water losstexture, of skin, 29theory of planned behaviour, 61therapeutic consultation, 111–12therapeutic-helping relationships,features of, 111therapeutic professional relationships,111therapeutic relationship, 37, 111thermoregulation, 75thick skin, 12thin skin, 12thread face-lift, 7tickle, 22tinea, 221, 233, 238, 242Tinea capitis, 41, 233, 234Tinea corporis, 233, 235Tinea cruris, 233, 235Tinea incognito, 238Tinea pedis, 233, 235, 236, 237Tinea unguium, 233, 236tissue loading, 57TNF inhibitors, 45toe web intertrigo, 226toenails, 35, 236, 237, 238tonofilaments, 13topical antibiotics, 187–8, 224topical antifungals, 167topical calcineurin inhibitors, 168, 257topical corticosteroids, 164, 238application, 166and potencies, 165side effects from, 165topical emollients, 75topical imidazoles, 239topical immune-modulators, 44topical immunotherapy, 200topical nitrogen mustard, 202topical non-steroidal anti-inflammatoryagents, 197topical retinoid, see Vitamin Atopical steroid, 56, 250topical tacrolimus, 257topical therapies, for psoriasis, 132–7calcipotriol and betamethasonediproprionate, 134method of application, 134–5calcipotriol combined with othertherapies, 135coal tar, 135method of application, 135–6corticosteroids, 136dithranol, 136method of application, 136emollients, 132vitamin A, 137method of application, 137vitamin D analogues, 132method of application, 132–4topical treatments, for acne, 186–9mild to moderate acne, 186azelaic acid, 187benzoyl peroxide (BPO), 187nicotinamide, 187retinoid product, application of,186–7topical antibiotics, 187–8topical retinoids, 186moderate acne, 188hormonal therapies, 189oral antibiotics, 188–9topical treatments, for eczema, 164emollients, 164topical corticosteroid application,166topical corticosteroids, 164–5total emollient therapy, 75touch, 21–2toxic epidermal necrolysis (TEN), 44,54, 55, 225, 253toxic erythema, 54, 253toxicity, of skin, 60transepidermal water loss (TEWL), 50,55, 72, 81transmission, 222treatment adherence, 109, 110, 112,115promotion, challenge of, 109concordance process, importanceof, 109–10therapeutic consultation, 111–12treatment beliefs, 105treatment choice, 110treatment decisions, 103–15treatment effectiveness, 103treatment expectations, 109tretinoin, 186tribes, 3Trichophyton, 233Trichophyton interdigitales, 236Trichophyton rubrum, 235, 236Trichophyton tonsurans, 234trichotillomania, 92trigeminal nerve, 229trigger factorsin atopic eczema, 155in psoriasis, 130trimethoprim, 188trust, 111developing, 93Tubifast, 56tubular bandages, 56tumour necrosis factor α, 90tumour thickness, 205Type 1-mediated response, 74Type 4-mediated response, 74Type I receptors, 22Type II (Ruffini corpuscles), 22type IV hypersensitivity reaction, 42tyrosinase, 13tyrosine, 13Uulcers, 32ultraviolet light, 163exposure, 13, 45, 131narrow band (A and B), 44risk behaviour, 61unconditional positive regard, 111United Nations Environmentprogramme, 4unlicensed medicines, 114unmyelinated A fibres, 23urea, 14, 72, 81urinary incontinence, 50, 53effects of, 53–4urticaria, 45, 88, 90, 262–5acute, 263–4chronic, 264investigations, 264physical, 264treatments, 264–5ustekinumab, 141UV Index, 213UV-protective behaviour, 208UV radiation, 4, 26, 212UVB, 45, 137–8Vvalaciclovir, 227varicella (chicken pox), 167, 227, 228vaccines, 228varicella zoster, 227–8varicella-zoster immunoglobulin(VZIG), 228varicella zoster virus (VZV), 227varicose eczema, 151, 158, 161, 170,225–6varicose veins, 26vascular laser, 262vascular lesions, 29vascular naevi, 25vascular tracking, 44vasculitis, 54vasculopathy, 252

286 IndexVaseline, 71vasoactive chemicals, 16vasoconstriction, 21vasodilation, 21vector borne diseases, 4vellus hairs, 17, 24venous disease, 35venous eczema, see varicose eczemavenous insufficiency, 226venous pressure, 27verbal persuasion, 108vernix caseosa, 24vesicles, 34, 162, 223, 226vicarious experience, 108video-assisted education, 107video-based education, 172violaceous, 256viraemia, 228viral rashes, 44viral infections, 221, 230hand, foot and mouth disease,232herpes simplex, 226–7herpes zoster, 228–9Kawasaki disease, 232–3management, 167molluscum contagiosum, 230varicella zoster, 227–8warts, 230–32viral warts, 29, 167, 242visual analogue scales, 159vitamin A, 62, 137, 186method of application, 137vitamin B complex, 62vitamin C, 61, 62vitamin D, 23, 62, 213vitamin D analogues, 44, 132application method, 132–4vitamin deficiency, 61vitiligo, 41, 88, 90, 265–6von Hebra, Ferdinand, 121vulnerability of skin, 49, 53vulvovaginitis, 238Wwarts (verrucae), 230–32warty lesion, 32wash product, 74washcloth, 76washing, of skin, 52, 53, 55and drying practices, 55effects of, 52–3practices, 50, 59water, 72saturation, 51Watson, R., 22waxes, 72waxing, 17webbing, 248websites, 106, 114–15wet-wrapping technique, 56, 108white blood cells, 50white soft paraffin, 249whiteheads, see closed comedonesWickham’s striae, 256Willan, Robert, 121Willan’s lepra, 121Wood’s light, 41examination, 234wool alcohol, see lanolinwool wax, see lanolinworm parasites, 240wound, 50healing, 62, 249wrapping technique, 56, 166written information, 207Xxeroderma pigmentosum, 201xerosis, 29, 50see also dry skinYyeast infections, 238, 239yeasts, 233yoga, 109Zzinc, 62

Principles of Skin Care: A Guide for Nurses and Health Care ... - Ola.tm

Transform your PDFs into Flipbooks and boost your revenue!

Principles of Skin Care: A Guide for Nurses and Health Care ... - Ola.tm

Transform your PDFs into Flipbooks and boost your revenue!

Delete template?

Save as template ?