APPROACH TO RASHES MACULOPAPU LAR RED ... - rEMERGs

APPROACH TO RASHES 

MACULOPAPU 

LAR RED RASH 

Viral exanthem 

NOS 

Rubeola 

Rubella 

Roseola 

Erythema 

Infectiosum 

Scarlet Fever 

RockyMtn 

Spotted F 

Hand-foot-mouth 

Kawasaki’s 

disesase 

Drug eruption 

Staph scalded skin 

Staph toxic shock 

Strep toxic shock 

Erythema 

Multiforme 

Steven’s - 

Johnson 

Psoriasis 

Urticaria 

Pityriasis Rosea 

Disseminated 

gonorr 

Scabies 

MACULOPAPU 

LAR RED AND 

SCALY RASH 

+/- Patches and 

Placques 

Pityriasis Rosea 

Atopic Dermatitis 

Contact 

Dermatitis 

Seborrheic 

dermatitis 

Tinea capitis 

Tinea corporis 

Tinea pedis 

Tinea versicolor 

Lichen plannus 

PAPULAR OR 

NODULAR 

RASH 

Pediculosis 

Scabies 

Molluscum 

Syphillus 

Warts 

Xanthomas 

Insect Bites 

Milia 

Mastocytomas 

Contact dermatitis 

Erythema 

Nodosum 

Erythema 

Multiforme 

VESICULAR/ 

BULLOUS 

Herpes simplex 

Varicella 

Herpes zoster 

Pemphigus 

Pemphigoid 

Bullous impetigo 

Staph Scalded 

Skin 

Epidermolysis 

bullosa 

TEN 

PUSTULAR 

Impetigo 

Folliculitis 

Carbuncle 

Hiradenitis 

Suppurati 

Gonococcal 

dermatitis 

PETECHIAL 

RASH/ 

PURPURIC 

RASH 

Vascular Integrity 

-Trauma: NAT, 

etc 

-Vasculitis: 

HSP,etc 

-Drugs 

-Infections: viral, 

mono, ricketsia, 

strep, endocarditis 

Platelet disorder 

-ITP 

-TTP 

-HUS 

-SEPSIS/DIC 

- 

Meningococcus,et 

c 

-Drug induced 

-BM infiltration 

-Liver failure 

-Congenital plt 

d/o 

Coagulation 

disorder 

-Congential: 

VWD, hemophilia 

A,B 

-Acquired: DIC, 

warfarin, Vit K 

deficient, liver dz, 

renal dz

DIFFERENTIAL DIAGNOSIS OF A RASH IN A TOXIC PATIENT 

Steven’s Johnson syndrome 

Staphylococcal toxic shock syndrome 

Staphylococcal scalded skin syndrome 

Streptococcal toxic shock syndrome 

Pemphigus/Pemphigoid 

Kawasaki’s syndrome 

Vasculitis 

Drug reaction 

Rocky Mountain Spotted Fever 

GENERAL NOTES 

Macular = red/pink color change < 0.5cm 

Patch = color change > 0.5 cm 

Papular = raised lesion 

Nodule = round elevated lesion > 0.5cm 

Plaque = elevated lesion >0.5 cm 

Finish definitions 

Approach to diagnosis 

Is the person toxic? 

Is the rash maculopapular, scaly, papular, nodular, vesicular, bullous, pustular, petechial 

or purpuric? 

Are there any recongnizable features of the rash or history? 

Is the rash acute or chronic? 

Is the rash associated with fever or infectious symptoms? 

Is the rash localized to an area of contact? 

Is the rash scaly? 

Common precipitants: drugs, infections, food, 

THE RED MACULOPAPULAR RASH +/- SCALES 

SCALES, PLAQUES, PATCHES 

FUNGAL INFECTIONS 

Principles 

Dermatophytoses = superficial fungal infections that are limited to skin 

Scaling, papules, plaques and patches are most common 

Grow best in heat and moistoure 

Only grow in keratin or outer layer of skink, nails, hair

Keratin accumulates in body folds 

Not very contagious (except Tinea capitis) 

KOH preparation: branching hyphae of the dermatophytes or the short, thick hyphae and 

clustered spores of tinea versicolor. 

Cultures of hair, nail, scales using Saboranund agar X 3 weeks 

Tinea Capitis 

Clinical Features 

Fungal infection of the scalp 

MC in preschoolers but increasingly common in adults etc 

More common in african americans 

Trichophyton tonsurans is cause of current epidemic (many have seborrheic-like scaling in the 

abscence of alopecia) 

Black dots representing hair broken off near the scalp 

Hair loss occurs b/c hyphae grow within the shaft thus the shaft is fragile and breaks off 1-2 mm 

from the scalp 

Circular patches of baldness may result 

Close personal contact spread 

Secondary bacterial infection as a complication 

Diagnosis and Differential Considerations 

Ddx of tinea capitis: alopecia areata, atopic dermatitis, nummular eczema, bacterial infections, 

apsoriasis, seborrheic dermaitits, tinea amiantacea, trichotillomania (hair pulling), histiocytosis 

KOH prep is not helpful; fungal culture should be obtained 

Bacterial culture if you think there is bacterial superinfection 

Management 

Griseofulvin 20 mg/kg od x 6 weeks (or fluconazole) 

Systemic therapy is required 

Refer for follow up and family should be evaluated 

Selenium sulfide shampooo 250 mg 2x/week decreases shedding 

Kerion 

Dermatophytic infection of the scalp that appears as an indurated, boggy inflammatory plaque 

studded with pustules 

Usually mistaken for bacterial infection 

Treat with Griseofulvin + prednisone for 2 weeks (decreases inflammation and scarring) 

Add keflex or clox if added bacterial infection occurs 

Tinea Corporis 

Classic “ring-worm” infection 

Arms, legs, trunk 

Sharply marginated, annular lesion with raised or vesicular margins and central clearing 

Single, multiple, or concentric lesions 

Tinea cruris:involves the groin, perineum, thighs, buttock (note that the scrotum is 

characteristically spared) 

Ddx: granuloma annular psoriasis, erythrasma, intertigo with secondary candidiasis 

Usually respond to topical therapy alone 

Many effective topical antifungal agents: Lotrimin, Tinactin, Micatin, terbinafine, griseofulvin, 

naftifine, etc

Apply to affected area tid X 2-3 weeks or until resolution 

Acute inflammatory blistering lesions: wet compresses of Burow’s solution: aluminum acetate 

solution that is useful for oozing, wet inflammatory lesions\ 

Tinea Pedis 

Athlete’s foot 

Scaling, maceration, vesiculation, fissuring between the toes and on the plantar surface of the 

foot 

Entire sole may be involved 

Secondary bacterial infections can occur 

Vesicular pustular form of tinea pedis should be considered with vesicles or pustules on inner 

aspect of foot 

Ddx: contact dermatitis and dyshidrotic eczema 

KOH prep helps differentiate 

Treatment: topical antifungal preparation until cleared (see above) 

Tinea Versicolor 

Superficial yeast infection caused by Pityrosporum ovale 

Superficial scaling patches occur mainly on the chest and trunk but may extend to the head and 

limbs 

Lesions are colorful: pink, tan, white 

May be itchy; patient may complain that the spots won’t tan 

Fine subtle scale is noted that may appear hypopigmented 

Pale yellow or orange florescence with Wood’s light 

Ddx: vitiligo, seborrheic dermatitis 

KOH prep: short hyphae mixed with spores (spagetti and meatballs) 

Mx: 2.5% selenium sulfide shampoo, imidazole creams or oral ketoconazole as a singel 400 mg 

dose or 200 mg po od X 5 days 

Recurrence rates are 30% 

Monthly prophylaxsis with selenium shampoos 

Tinea Unguium 

Fungal nail infection = opaque, thickened, cracked, crumbled nails 

Subungual debris; nail may have longitudingal yellow streaks 

Nail of great toe is MC location 

Mx: topical therapy rarely effective: Fluconazole, itraconazole, terbinafine are all acceptable 

options 

Recurrence common, may require nail removal 

CANDIDIASIS 

Perspective 

Infections more common in young, elderly, immunocompromised, diabetics, chronic steriods, 

endocrine disorders, cancers, antibiotics 

Oral Thrush

MC candidal infection 

MC in newborns 

Patches of white gray friable material covering an erythematous base on the buccal mucosa, 

gingiva, tongue, palate, or tonsils 

Fissures or crust at the corners of the mouth may be present 

AIDS defining illness 

Consider immunosuppression in abscence of abx use or dentures 

Dx is lichen planus (not easily scraped off as candida is) 

Mx 

Oral nystatin suspension (100,000 units/ml) qid 

Infants: 1ml painting the mouth qid 

Older children and adults: 4-6ml swish and swallow qid 

Treat for 7/7 or until lesions dissapear 

Clotrimazole troches dissolved in the mouth qid is an option in adults 

Oral ketoconazole or fluconazole is an option (some think this is the way to go) 

Soak dentures in sodium hypochlorite 1:10 solution at night 

Cutaneous Candidiasis 

Moist, warm areas of groin, axilla, folds, etc 

Moist lesions, bright-red macules rimmed witha collarette of scale which represents the pustule 

roof with scalloped borders 

Small satellite papules or pustules are just peripheral to the main rash 

Satellite lesions are the most typical indicators of candidiasis 

Intertirginous lesions prone to bacterial superinfection 

Candidal onychia and paronychia: hands frequently in hot water, thumb sucking 

Ddx: contact dermatitis, tinea cruris, intertrigo, malaria, folliculitis 

Candiasis: less sharply demarcated than tinea cruris and brighter red than intertrigo 

KOH prep from pustule and roof of the lesion will reveal hyphae and pseudohyphae 

Mx 

Clean mucky areas and expose to air (fan etc) 

Wet compresses with Burow’s solution for inflammatory lesion 

Imidazole cream to affected area qid (ketoconaloze, clotrimazole, miconazloe, econazole) 

Candidal paryonychia: protect hands from water, nystatin or clotrimazole cream to nail for for 8 

weeks 

PITYRIASIS ROSEA 

Mild skin eruption predominantly found in children and young adults 

Lesions are pink or pigmented oval papules or plaques 1-2 cm 

Primarily on the trunk and proximal extremities 

Mild scaling may be present 

Lesions are parallel to the ribs, form ing a Christmas tree-like distribution on the trunk 

Oral lesions are rare 

Papular or vesicular lesion variants occur in kids 

Herald Patch preceeds generalized eruption by one week in 50%

Herald Patch is a large 2-6cm patch 

Usually asymptomatic but may be mildly pruritic 

Self limited, resolves w/i weeks 

Viral cause suspected 

Ddx: tinea corporis, guttate psoriasis, lichen planus, drug eruption, secondary syphillus 

Recurrence rate 

Treatment only symptomatic for pruritis if present 

Eczema = dermatitis (constellation of disorders that include erythema, edema, vesiculation, 

scaling, pruritis) 

ATOPIC DERMATITIS 

Principles 

Cutaneous manifestation of atopic state 

Not an allergic disorder in itself 

Is associated with allergic disorders: asthma, allergic rhinitis 

Abnormalities of humoral and cell-mediated immunity 

Eosinophils, mast cells, and lymphocyte activation triggered by increased production of 

interleukin 4 by T-helper cells seems to be involved 

Increased IgE levels found in most but not all and levels do not correlate 

Course is remissions and exacerbations 


Inflammatory, thickened, papular or paulovesicluar lichenification 

May show hyperpigmentation of the skin 

Skin is typically dry and may be scaly 

Skin also can be vesicular, wet, weeping, oozing in the acute phase 

Infants: cheeks, extensor surfaces, diaper area 

Older children: antecubital and popliteal flexion areas, neck/face/chest 

Infantile atopic dermatitis usually begins at 4-6 months and imporves by 4-6yrs 

Childhood form: begins at a4-6 years and resolves or continues into adulthood 

INTENSE PRURTITIS is the hallmark of atopic dermatitis 

Itching can be focal or generalized, worse in the winter, triggered by increased body temp and 

stress, worse at night, excoriations common from scratching 

Secondary bacterial infection is common 

Repeat scratching and rubbing leads to lichenification (hyperpigmented, thick skin with 

accentuation of skin furrows) 

Differential Considerations 

Ddx: histiocytosis X, wiskott-aldrich syndrome, chronic seborrheic dermatitis, phenylkeotonuria, 

bruton’s x-linked agammaglobulinemias, psoriasis, scabies, drug eruption, contact dermatitis 

Complications: bacterial infection, otitis externa, cataracts, keratoconus, retinal detachment, 

cutaneous viral infections

Management 

Goals: control inflammation, dryness, itching 

Vaseline or Eucerin cream 10% (not lotion) to reduce dryness 

Exudative areas: apply wet dressing of gauze soaked in Burow’s solution; apply for 20 minutes 

qid 

Antihistamines 

Systemic steroids for very severe 

Cyclosporin, Ultraviolet B treatment, and other immunosuppressive are options for very severe 

disease 

Topical corticosteroids ointments are mainstay of treatment 

Mild disease: less concentrated ointment 

Face: triamcinolone 0.025% (milder) used b/c strong steroids can cause permanent cutaneous 

atrophy on the face 

Severe disease: florinated corticosteroid ointment (1/2 strength betamethasone valerate) to 

affected areas tid 

FIRST LINE TREATMENTS OF ECZEMA 

Antihistamines: gravol, benadryl, atarax 

Aveeno baths 

Bactroban ointment 

Celestoderm 

George’s cream 

Oatmeal baths 

Corticosteroid ointments 

SECOND LINE THERAPIES 

Protopic (Tacrolimus) 

Cyclosporine 

Prednisone 

Oral antibiotics 

RED MACULES 

DRUG ERUPTION 

Principles 

Different eruption of same drug in different individuals 

MC eruptions are urticarial and morbilliform rashes 

Tend to appear within a week after drug is taken (not necessarily right away) 

Reactions to semisynthetic penicillins tends to occur later 

May appear after drug has been discontinued 

Atopic patients with asthma, hay fever, eczema are at increased risk 

RARELY produce reactions: acetaminophen, codeine, digoxin, erythromycin, demerol, 

morphine, prednisone, maalox 

Clinical Features (see table 114-2) 

Exanthems: resemble viral and bacterial infections, usually widespread symmetric 

maculopapular eruptions

Eczematous drug rashes: resemble contact dermatitis but are more extensive; begin as 

erythematous or papular eruptions and become vesicular; prior sensitization is common with this 

type of reaction 

Vasculitis lesions: begin as erythematous papules or nodules but may ulcerate and become 

gangrenous. Purpuric drug eruptions may be the result of bone marrow supression, vasculitis, or 

platelet destruction. Platelet transfusion, plasmapharesis, steroids, splenectomy in severe cases 

Photosensitive druge reactions: require sunlight 

Phototoxic: more common; sulfa drugs/thiazides/tetracycline are common causes, not 

immunologic and can occur in any person; look like a sunburn but may have bullous or papular 

features; pruritis is minimal or absent 

Photoallergic: the result of antigen formation that results in sensitized lymphocytes (delayed 

immunoloci response); only occurs in sensitized individuals, usually 2 weeks after exposure to 

the drug and sunlight; not dose related, usually look eczematous and is intensely pruritic; 

chlorpromazine/promethazine/chlordiazepoxide are common sensitizers of photoallergic 

reactions; d/c drug and avoid sunlight/use sunscreen 

Fixed drug eruptions: appear and recur at the same anatomic site after repeateed 

exposures; sharply marginated and round/oval; may be pigmented, erythematous, or violaceous; 

may be pruritic 

Ddx 

Viral examthem, chronic exfoliative erythroderma: caused by psoriasis or eczema, sScarlet fever, 

Staphylococcal scarliatiniform eruption, Kawasaki’s syndrome 

Management 

D/c drug 

Warn that resolution will be slow 

Calamine lotion, cool compresses, tepid water baths with colloidal oatmeal (Aveeno) or 

cornstarch, antihistamines 

STAPHLOCOCCAL SCALDED SKIN 

Generally occurs in children < 6yo 

Erythema and crusting around the mouth 

Erythema then spreads to the body 

Bullae form and the skin desquamates 

Also called Stapylococcal Epidermal necrolysis 

Exfoliative toxin produced by phage groupt II, type 71 Stapylococci 

Toxin acts at the zona granulosa of skin to produce a superficial separation that results in 

widespread painful erythema, blisters 

Usually occurs in children 6 mo to 6 yrs 

Mortality 3% in kids but 50% in aldults and near 100% in adults with comorbidities 

Mucous membranes SPRARED (can have mild inflammation but not involved to the extent of 

Toxic Epidermal Necrolysis) 

Nikolski’s sign = the easy separation of the outer portion of the epidermis form the basal layer 

when pressure is exerted; often but not always present 

Vesicles and bullae are characteristic 

Loss of large sheet of superficial epidermis ----> Looks like SCALDED SKIN

Main ddx is Toxic Epidermal Necrolysis (TEN): usually cause by medications, mucous 

membranes are INVOLVED 

Dx can be confirmed by biopsy or frozen section demonstrating subglandular epithelial 

separation 

Lesions dry up after desquamation and resolution within 7 days 

Mx 

Most group 2 are penicillinase resistant 

Most recover without abx 

Naficillin, cloxacillin, dicloxacillin recomended 

TOXIC SHOCK SYNDROMES 

TSS = acute febrile illness characterized by diffuse desquamating erythroderma 

High fever, hypotension, constitutional symptoms, MSOF, rash 

Exotoxin-procuding S.aureus 

Post op setting is most common outside of tampon related 

Also associated with various staph/strep infections: cellulitis, erisepalis, PTA, sinusitis, burns, 

septic abortion, skin abscesses 

Stapylococcal and Streptococcal toxic shock syndromes 

STAPHYLOCOCCAL TOXIC SHOCK SYNDROME 

Perspective 

Often occurs in females related to tampons 

Incidence has decreased remarkable since high - absorbent tampons sere withdrawn from the 

market 

Now most cases related to focal soft tissue infections with staph 

Pathophys and Clinical Features 

Staph aureus isolated in 90% of cases related to tampons 

Results from TOXIN FROM PHAGE GROUP 1 S. aureus 

Fever, “sunburn” or sandpaper rash, hypotension, tackycardia and at least three organ system 

involvement 

Mucosal inflammation, myalgia, profuse watery diarrhea, mental status changes are common 

Differential diagnosis: streptococcal scarlet fever, stretococcal toxic shock syndrome, rocky 

mountain spotted fever, kawasaki syndrome, leptospirosis 

Managment 

Fluid resuscitation 

Vasopressors/ionotropes: need alpha and beta adrenergics 

IV antibiotics to cover penicillinase-producing staph: clox, naficillin, etc 

Clindamycin and vancomycin options for pen allergic 

Remove tampon 

Remove foreign bodies 

Drain abscesses 

Systemic steroids if given early may help 

CRITERIA FOR DIAGNOSIS (SSSTT) 

Skin Rash (diffuse macular erythema): sunburn or sandpaper looking –> resembles scarlet fever 

Skin Desquamation 1-2 weeks after onset 

SBP < 90 or orthostatic drop + symptoms 

Temp > 38.9 

Three organ systems (clinical or lab)

GI: N/V/D 

MSK: myalgias, CK doubled 

Mucous membranes: vaginal, oral, conjunctival 

Renal: BUN or Scr doubled or pyuria > 5 cells/hpf 

Hepatic: bili , AST/ALT doubled 

Hem: platelets < 100 

Neuro: altered LOC with no focality 

STREPTOCOCCAL TOXIC SHOCK SYNDROME (STSS) 

Perspective 

Described in 1987 

Predominantly caused by group A strains but can be caused by other groups 

Pathophysiology and Clinical features 

Predisposing factors: surgery, minor trauma, hematomas, muscle strain,m cellulitis, chicken pox; 

Mortality 30% 

MOST common cause in children is strep superinfection of chicken pos lesion 

Association with NSAID use which may mask presenting symptoms resulting in increased 

severity of disease 

Severe pain, abrupt onset 

Pain often present before physical findings 

Usually in extremities but may be pelvic, abdominal, chest, etc 

Minority have influenza like symptoms 

FEVER is the most common sign (can be hypothermic if sick) 

Tachycardia, hypotnesion, soft tissue infection signs, scarlet - fever like rash (sandpaper) are all 

common 

Renal failure, respiratory failure, DIC, MSOF, shock (septic and cardiogenic from cardiotoxic 

effects) are all complications 

NOTE: shock is predominantly cardiogenic: LOW CO and high SVR 

Streptococcal M and T serotypes 

Due to exotoxin A and B: toxins act as superantigens to activate T cells resulting in MASSIVE 

release of inflammatory mediators; fever, rash, hypotension, and MSOF 

Ddx: staph toxic shock, grm -ve sepsis, endotoxic shock 

Diagnosis 

Scr increase; Consider deeper infection if CK up 

Labs may show DIC; Blood cultures positive in 60%; Wound cultures positive in 95% 

DIAGNOSTIC CRITERIA (must meet both) 

Isolation of Group A strep 

From a normally sterile site (blood, CSF) is a definitive case 

From a normally non-sterile (sputum, skin) is a probable case 

Hypotension + at least two of.... 

Renal failure 

Coagulopathy 

Liver involvement

ARDS 

Generalized macular rash (may desquamate) 

Soft tissue necrosis 

Management 

Supportive, usually ICU 

Initial abx needs to cover staph and strep b/c hard to distinguish 

Penicillin + clindamycin 

Ceftriaxone + clindamycin 

Penicillin not great against a large inoculum with nec. fasc. 

Clindamycin advantages: not effected by large inoculum, kills cell wall-deficient streptococci, 

long post administration efficacy, enhances opsonization of streptococcal organisms when grown 

with low concentrations of penicillin 

Surgical consult for early surgical debridement 

IV gamma globulin may help: has antibodies against staphylococcal toxins which may cross 

react with streptococcal toxins 

Steroids: case reports indicate there may be benefit of dexamethasone if given with gamma 

globulin 

Antibiotic prophylaxis NOT recommended for household contacts 

TOXIC EPIDERMAL NECROLYSIS 

Principles 

Non-staphylococcal induced toxic epidermal necrolysis 

Hallmark = separation of large sheets of epidermis from underlying dermis 

Full thickness of epidermis is involved 

Skin biopsy easily distinguishes b/w TEN and staphylococcal scalded skin 

Moratility 20% 

Rarely associated with vaccinations (polio, measles, smallpox, td) 

Drugs 

Penicillin 

Sulpha 

Tegretol 

NSAIDs 

Allopurinol 

Barbituates 


Mucosal lesion common; may precede exanthem 

Nikolski’s sign: rubbing results in desquamation of underlying skin including the pigment (staph 

scalded skin ----> pigment remains) 

Onset: face and mucous membranes 

Ocular involvement can occur 

Erythema usually precedes the loosening of the epidermis 

Management 

D/c drug 

Fluid replacement as per burn 

Control infection 

Steroids controversial

Plasmapharesis experimental 

MAINSTAY of managment is wound care and prevention of secondary bacterial infection ------> 

should be managed in burn center 

ERYTHEMA MULTIFORME 

Etiology 

Drugs and HSV infections are the MCC 

Viral infections (heptitis, influenza) are next MCC 

Fungal infections: dermatophytosis, histoplasmosis, cocidiomyocosis 

Bacterial infections: strep and TB 

Collagen vascular disorders: RA, SLE, dermatomyositis, PAN 

Cancers 

Pregnancy 

DDX 

Urticaria 

Scalded skin syndrome 

Pemphigus 

Pemphigoid 

Viral exanthems 


Acute, self-limiting disease 

Erythematous or violaceous macules, papules, vesicles, or bullae 

Symmetrical distribution common 

Most common in PALMS and SOLES, back of hands or feet, extensor surfaces of the extremities 

Target Lesion with three zones of color is the hallmark: centra dark papule or vesicle, surrounded 

by a pale zone, a halo of erythema 

Steven - Johnson Syndrome = Toxic Exctodermal Necrolysis 

Severe form of EM 

Bullae, mucous membrane lesions, MSOF 

Chills, malaise, headache, fever, tachycardia, hypotension 

Purulent conjunctivitis may occur and be severe 

Management 

Look for underlying etiology 

Resolve spontaneously in 2-3 weeks in mild forms 

Severe cases: admit, iv hydration, burn unit care, systemic analgesia, systemic corticosteroids 

Wet compresses with dressing soaked in 1:16000 solution of potassium permanganate or 0.05% 

silver nitrate several times a day to bullous lesions 

Look for infection and hypovolemia 

URTICARIA 

Principles 

20% will eventually get urticaria 

Acute and chronic forms 

Chronic urticaria more common in women 

Histamine, bradykinin, kallikrein, acethycholine as mediatesors 

Immunologic reaction: anaphylaxis, serum sickness 

Nonimmunologic reaction: degranulation of mast cell by foods, drugs

Contact urticari: foods, textiles, animal dander and saliva, plants, topical medications, cosmetics, 

chemical 

Any drug can cause urticaria: penicillin and aspirin are most common 

Any food can cause urticaria: food allergy (fish, nuts, eggs) or non-immunologic histamine 

release (holbster, strawberries) 

Hereditary urticaria and angioneurotic edema exist 

Infections: common cause in children, less common in adults; hepatitis, mono, coxsackie more 

commonly produce urticaria 

Inhalation: pollens, mold, animal dander, dust, plant materials 

Stings and bites 

Other associations: SLE, lymphoma, carcinoma, rheumatic fever, hyperthyroid, JRA 

Dermatographism: urticarial wheal within 30 minutes after pressure 

Pressure urticaria: urticarial wheal forms 4-8 hours after pressure 

Cold urticaria: familial or acquired; associated with cryoglobulinemai, cryofibrogenemia, 

syphillus, connective tissue disorders: suppression with cyproheptadine 4mg tid, antihistamines 

before cold exposure; doxepin qhs 

Cholinergic urticaria: induced by heat, exercise, or stress; wheals of 1-2 mm surrounded by 

erythematous flares and occassionally satellite wheals; responds to hydroxyzine 

Heat and solar urticaria uncommon 

Chronic urticaria etiology often unknown 

DDX OF URTICARIA 

F Foods 

P Plants 

A Animals 

D Drugs 

I Infections 

C Contacts (cosmetics,etc) 

O Other:cold, cholinergic, chronic 

P Physical: dermatograph, pressure 


Edematous plaques with pale centers and red borders 

Individual hives are transient (lasting < 24hrs) 

New hives may continually develop 

Ddx: erythema multiforme, erythema marginatum (R.F.), erythema migrans (Lyme dz), JRA 

Management 

Remove inciting factor if possible 

H1 antagonists: benadryl, gravol, Hydroxyzine (Atarax, Vistaril): 10 - 25 mg (2 mg/kg/24hr in 

kids); supposed to be less sedating than benadryl, gravol 

H2 antagonists: actually good for skin, ranitidine/cimetidine 

Fexofenadine, astemizole, terfenadine are supposed to be even less sedating 

Prednisone X few days: effective utricaria can rebound after discontinuation 

When to use prednisone? Failed treatment with antihistamines, severe symptoms, anaphylaxisis

EXANTHEMS 

PRINCIPLES OF EXANTHEMS 

Exanthem = skin eruption that occurs as a symptom of a generalized disease 

Known infectious causes: 30+ enteroviruses (mostly coxsacki and echoviruses) as well as 

adenovirus have a particular nack to cause exanthems 

Most are maculopapular although scarlatiniform, erythematous, vesicular, and petechial rashes 

Usually nonpuritis, do not desquamate, and vary in extent 

Mucous membrane lesions may occur 

Echovirus type 9: meningitis, petechial exanthem resembling meningococcemia 

Echovirus type 16 (Boston exanthem): may resemble roseola 

Coxsackie group B type 5 may also resemble roseola in adults 

Coxsackie group A type 16: distinctive syndrome of vesicular stomatitis, oral vesicles, dorsum of 

hands and lateral borders of feet; may be associated with meningoencephalitis 

Classic viral exanthems 

Roseola Infantum = Exanthem subitum (HHV6) 

Rubella (German measles) 

Rubeola (measles) 

Erythema infectiosum = fifth disease (parvovirus B19) 

Enteroviruses: coxsackie, echo 

MEASLES (RUBEOLA) 


Highly contagious virus; droplet spread; incubation 10 days 

Now usually only seen in nonimmunized, immigrants 

Contagious from 2 days before symptoms until 4 days after rash appears 

Fever, malaise mark onset of symptoms; coryza, conjunctivitis, and cough begin within 24hours 

of the onset of symptoms 

Fever increases daily in a stepwise fashion until it reaches approximately 40.5 degrees celcius on 

the 4th - 5th day 

Koplick’s spots are pathognomonic: small, irregular, bright red spots with bluish-white centers 

that begin opposite the molars then spread to the adjacent oropharynx; usually appear on second 

day of illness 

Cutaneous eruption begins on th 3rd - 5th day of illness (rash BEFORE defervescence) 

Maculopapular erythematous lesions involve the forehead and upper neck then spread to the 

face, trunk, arms, and finally the feet (SPREADS TOP DOWN) 

Koplick’s spots disappear as the rash appears 

The rash begins to fade in the order of appearance (starts on 3rd day) 

Complications: OM (most common), encephalitis (1 in 1000), pneumonitis 

Management 

Antibiotics indicated for bacterial superinfections (OM, etc) only 

Supportive treatment only 

Isolation of limited value b/c not infectious by the time it is diagnosed 

Human immune globulin in a susceptible person within 6 days of exposure (0.25 ml/kg IM in 

children). 

Live virus vaccine given w/i 72 hrs of exposure may be effective in prevention 

Vitamin A shortly after exposures?? 

? indications for immune globulin

ROSEOLA INFANTUM = EXANTHEM SUBITUM = SIXTH DISEASE 

Caused by Human Herpes Virus 6 

Fever and skin eruption 

95% occur in 6mo to 3yrs and most are < 2yo 

Febrile seizures may occur 

Abrupt onset fever, rising rapidly to 40 degreees 

Temperature continues for 3-4 days (constant or fluctuant) then rapidly decreases to normal 

Rash appears with defervescence 

Pink or rose colored macules or maculopapules 2-3 mm diameter which blanch on pressure and 

rarely coalesce; trunk initially the SPREAD PERIPHERALLY to neck and extremities 

Rash clears over 1-2 days without desquamation 

LOOKS WELL despite high fever 

Encephalitis rare, very few complications 

Excellent prognosis, no treatment 

RUBELLA = GERMAN MEASLES 

Fever, skin eruption, generalized lymphadenopathy 

Spread by droplet contact; peak in winter and spring 

Incubation 14 - 21 days: contagious few days before rash and 7 days after onset 

Infants with congenital exposures can shed virus for more than a year 

Adults: 1-6 day viral prodrome, symptoms dissapear w/i 24 hours after rash develops 

Pink to red maculopapules; first on face then spreads rapidly DOWN to the trunk and extremities 

Lesions on the trunk tend to coalesce but those on extremities do not 

Rash remains for 1-5 days classically disappearing on the 3rd day 

Clearing may be accompanied by fine desquamation but usually not 

Lymphadenopathy begins days before the rash: suboccipital, postauricular, posterior cervical 

No specific treatment 

Complications 

Encephalitis 

Thrombocytopenia 

Arthritis 

Congential Defects 

24% of infected fetuses have a congenital defect 

Maternal infection may be determined by serology: acute and convalescent increase in titers 4 

fold is diagnostic 

Routine use of PEP in an unvaccinated women in early pregnancy is not recommended 

ERYTEHMA INFECTIOUSUM = FIFTH DISEASE = SLAPPED-CHEEK RASH 

Parvovirus B19 infection 

Mild systemic symptoms, fever in 15%, characteristic rash 

Arthralgias and arthritis common in adults, rare in kids 

Slapped - cheek rash b/c of intensely red face with circumoral pallor 

Maculopapular lacelike rash in the arms, trunk, buttocks, and thighs 

Rash may recur with temperature changes

Incubation is 4 - 14 days 

Parvovirus: may also cause URTI, atypical rash, arthritis without rash 

Hepatitis can occur (rare) 

Aplastic crisis associated with parvoB19 and hemolytic anemias an sickle cell dz 

Pregnancy infection: fetal hydrops and death 

No treatment 

SCARLET FEVER 


Recent decline in incidence 

Abrupt onset with fevers, chills, malaise, sore throat followed within 12-48hrs of distinctive rash: 

begins on chest and spreasds rapidly 

Circumoral pallor, sandpaper-like texture b/c of the rough feel of the skin due to the multitude of 

pinhead size lesion 

Pharyngitis +/- erythematous or petechial lesions on the palate 

After resolution of the symptoms, desquamation of the inovlved areas is characteristic 

Complications: abscess, OM, pneumonia, rheumatic fever, post strep GN 

Management 

Antistrep abx: penicillin V 50 mg/kg/day dividied qid in kids 

Pen V 250 po qid in adults 

Benathine IM injection X 1 is an option 

Erythromycin 250 mg (or 40 mg/kg) po qid if pen allergic X 10 days 

Need full 10 days b/c only literature to show prevention of rheumatic fever is with a 10 day 

course 

KAWASAKI DISEASE 

Acute vasculitis primarily of infants and children 

Previously named Mucocutaneous lymph node syndrome 

Peak incidence in spring and winter 

Majority occur < 5 yo; 1-2 yo is most common; RARE in adults 

Etiology unknown 

Immune system activation wth vascular injury as the result 

Myocarditis is the most common cause of death 

Fever, conjunctivits, rash, mucous membrane lesions, extremity changes, cervical 

lymphadenopathy 

Cervical adenopathy: 50%, may be presenting feature 

Fever: high, spiking, persistent for 1-3 weeks 

Conjunctivitis: bilateral, bulbar > palpebral, no exudate, mild uveitis 

Mucous membrane lesions: injected or fissured lips, injected pharynx, or strawberry tongue, no 

ulcerations 

Extremity changes: painful, erythematous, swollen hands and feet (may not be able to walk, may 

present with limp); desquamation of finger and toes begins 10-20 days after fever; Beau’s lines 

are transverse grooves of the nail months after fever 

Rash: highly variable, appears within 5 days of fever, generally a maculopapular rash that may 

look like scarlet fever, urticaria, erythema multiforme, or morbiliform rash; may have small 

vesicles but no pustules or bullae

Arthritis common 

MCC of pediatric acquired heart dz: coronary artery aneurysms, coronary vasculitis, myocarditis, 

pericarditis, CHF, pericardial effusions, valve dz, arrtyhmias 

Coronary aneurysms: 20%; prone to MI or coronary rupture and tamponade; treatment with 

IVIG and high dose aspirin decreases incidence of coronary aneurysms to 3-5% 

Natural History 

Phase I: acute phase (1-2wks); fever, myocarditis, pericaridal effusions, other diagnostic signs 

Phase II: subacute phase (1-4 wks): fever/rahs/lymph nodes resolve and conjucntivitis persist; 

desquamation/arthritis/myocardial dysfunction occurs; highest risk of death 

Phase III: convalescent phase; clinical findings resolve, continues until ESR is normal 6-8 weeks 

after onset 

CDC Diagnostic Criteria = Unexplained fever for 5 days + 4/5 criteria 

C - Conjunctivitis: bilateral w/o exudate 

R - Rash 

E - Extremity changes (red, swollen, desquamating) 

A - Adenopathy (cervical ln, at least one > 1.5 cm) 

M - Mucous membrane lesions (injected lips/pharynx, tongue) 

Atypical Kawasaki’s 

Cases that don’t meet the CDC case definition 

More common in those < 6 months were diagnosis is more difficult 

Investigations 

Admit for echo 

Do ECG 

May need coronary angiogram 

CBC, lytes, creatinine, ESR, CXR, blood culture, urinalysis, ASOT titer, throat swab, LP if signs 

of aseptic meningitis 

Differential Diagnosis 

Rash: measles, toxic shock syndrome, Stevens-Johnson, RMSF, JRA, drug reaction, viral 

exanthem, scarlet fever 

H/N manifestations: RP abscess, GAS pharynitis, Mono 

Measles: severe cough, Koplik’s spots 

Managment 

IV gamaglobulin: 2 g/kg over 12 hours (may need further treatments) 

High dose ASA: 100 mg/kg/day divided into q6hr dosing 

Therapy decreases incidence of coronary aneurysm 

ROCKYMOUNTAIN SPOTTED FEVER 

Rickettsia rickettsii 

Transmitted to humans through tick bites (saliva at time of bite) 

Reported in North, South, and central america 

Most cases reported form SOUTHEASTERN USA 


Abrupt onset of headache, N/V, chills, fever to 40 degrees 

Ocassionally onset is more gradual with anorexia, malaise, fever 

May be prolonged (3 weeks)

May be severe (CNS, cardiac, pulomonary, GI, renal complications) 

Rash develops on 2nd - 4th day 

Erythemaous macules that blanch on pressure, appearing first on wrists and ankles then 

spreading up the extremities to the face and trunk w/i hours 

Lesions may become petechial or hemorrhagic 

Lesions on the palms and soles are particularly characteristic 

Increased capillary fragility and splenomegaly may be present 

Diagnosis 

Weil-Felix reaction (serology) 

Other immunologic flourescent procedures exist 

Treat based on suspicion b/c lab will be slow 

Management 

Tetracycline 25 mg/kg/day is the antibiotic of choice (po or iv) 

Doxycycline and chloramphenicol may be used as options 

Usual course is 10 days 

Avoid sulpha drugs which can exacerbate the illness 

Rickettsiae routinely resistant to penicillins, cephalosporins, aminoglycosides, and erythromycin 

PAPULAR AND NODULAR LESIONS 

CONTACT DERMATITIS 

Non - Allegic Contact Dermatitis 

Inflammatory reaction to chemical, physical, or biological agent 

Caustics, solvents, detergents cause irritant dermatitis 

Allergic contact dermatitis 

Delayed hypersensitivity reaction mediated by lymphocytes sensitize by the contact of the 

allergen to the skin 

Less common than (non-allergic) irritant contact dermatitis 

Clothing, jewelry, soaps, cosmetics, plants, medications contain allergens that commonly cause 

allergic contact dermatitis 

Rubber, poison ivy/oak/sumac (Rhus genus plants), paraphenyldenediamine (hair dyes and 

industrial chemicals), ethylenediamine (topical medication ingrediant) are the MCC of allergic 

contact dermatitis 

Sensitization to poison ivey results in sensitization to other similar plants: cashew, mango, 

lacquer, ginkgo trees 

Management 

Avoid irritant or allergen 

Treat secondary bacterial infections 

Wet compresses of Burow’s solution for oozing or vesicular lesions (qid) 

Topical baths OTC 

Prednisone 50 mg po od if severe: taper over 14 days (21 for poison ivy) 

Taper of steroid needed to prevent relapse 

Antihistamines for pruritits 

Wash all clothes to remove offending agent that could be contaminated

DIAPER DERMATITIS 


Occlusive diapers and clothing, heat, moisture, friction, urine and feces all contribute 

Tends to SPARE CREASES 

Erythematous plaques in the genital, perianal, gluteal, and inguinal areas 

May extend elsewhere with more severe cases 

May be superinfected with candida: moist, red patches with well demarcated borders and papular 

or pustular satellite lesions 

May reflect atopic or seborrheic dermatitis in infants (especially if lesions are found elsewhere in 

the body) 

Management 

Remove excess clothing 

Remove occlusive diapers 

Frequent diaper changes 

Leave diapers off long enough to dry area 

Sterilized cloth diapers preferred 

Exudative lesions: wet compresses with saline or Burow’s solution for 3/7 

Zinc oxide (Desitin) may dry the area 

Hydrocortisone 1% cream in severe cases 

Avoid ointment based topical medications for treatment b/c their occlusive nature enhances 

moisture retention (use cream, not ointment) 

Nystatin cream or powder if Candida superinfection 


Etiology 

Drugs and HSV infections are the MCC 

Viral infections (heptitis, influenza) are next MCC 

Fungal infections: dermatophytosis, histoplasmosis, cocidiomyocosis 

Bacterial infections: strep and TB 

Collagen vascular disorders: RA, SLE, dermatomyositis, PAN 

Cancers 

Pregnancy 

DDX 

Urticaria 

Scalded skin syndrome 

Pemphigus 

Pemphigoid 

Viral exanthems 


Acute, self-limiting disease 

Erythematous or violaceous macules, papules, vesicles, or bullae 

Symmetrical distribution common 

Most common in PALMS and SOLES, back of hands or feet, extensor surfaces of the extremities 

Target Lesion with three zones of color is the hallmark: centra dark papule or vesicle, surrounded 

by a pale zone, a halo of erythema 

Steven - Johnson Syndrome = Toxic Exctodermal Necrolysis 

Severe form of EM

Bullae, mucous membrane lesions, MSOF 

Chills, malaise, headache, fever, tachycardia, hypotension 

Purulent conjunctivitis may occur and be severe 

Management 

Look for underlying etiology 

Resolve spontaneously in 2-3 weeks in mild forms 

Severe cases: admit, iv hydration, burn unit care, systemic analgesia, systemic corticosteroids 

Wet compresses with dressing soaked in 1:16000 solution of potassium permanganate or 0.05% 

silver nitrate several times a day to bullous lesions 

Look for infection and hypovolemia 

PEDUNCULOSIS 


Nits or adult lice seen on microscopic examination of hair from symptomatic areas: nits are more 

common than the aduult louse form 

Nits attach tot eh bases of hair shafts looking like white dots 

Adult louse look like blue or black grains 

Severe itching and scratiching 

Secondary infections can occur 

Pediculosis corporis: lice live in clothing, bedding and feed on the host; the parasites are usually 

absent from the body except in very severe cases; Erythematous macules or wheals may be 

present with intense itching: Treatment consists of luandering or boiling the clothes and linen; 

may add lindane lotion if nits are found in the hair but this is usually not neccessary 

Pediculosis capitits: more common in small children; pruritis is the major sympom and may be 

confined to the scalp; excoriations and secondary bacterial 

Management 

Permetrhin (Nix) is the recommended treatment 

Lindand (Kwell) lotion or cream is no longer preferred 

Nix remains active for 2 weeks 

Avoid shampoos and conditioners for 2 weeks b/c it coats and protects the lice 

Nix: shampoo hair, dry, apply Nix, wash out after 10 minutes (MUST be applied when the hair is 

dry b/c lice don’t breath for 30 min when immersed in water!); repeat dose one week after initial 

use 

Treat sexual partners 

Treat only symptomatic household members 

Wash clothes, sheets, pillow cases in hot water and dry in hot cycle 

Ivermectin 200 ug/kg and repeat in 10 days has been shown to eradicate lice 

SCABIES 


Mite infestation with severe itching 

Interdigital web spaces, flexion area of wrists, axillae, buttocks, lower back, penus, scrotum and 

breasts are the most common locations 

Infants have a more generalized involvement 

Reddish papules/vesicles surrounded by erythematous border and scratch marks 

Infants and young children often have generalized skin involvement includine scalp, palms, 

soles, face: most common presenting lesions are papules and vesiculopustules

Norwegian scabies: extensive hyperkeratosis and crusting of the hands, feet, and scalp; 

immunosuppressed patients; highly contagious 

Close personal contact transmission; multiple family members will usually have 

Management 

Permetrin 5% cream (Elimite) or crotamiton (Eurax) cream 

Lindane is no longer the preferred treatment 

Elimite: applied overnight once weekly for 2 weeks; cover the entire body (preferred treatment 

for infants and small children) 

Post scabietic nodules and pruritis may persist for months after sucessful tx 

Norwegian scabies requires repeated treatment 

Treat all family members and sexual contacts 

Wash and dry in hot temperatures the linens and underwear 

SYPHILLUS 


Treponema pallidum 

Incubation 10 - 90 days 

Primary lesion: chancre, usually single lesion, lasts 3-12 weeks and heals spontaneously, appear 

at site of inoculation (genitalia or mucous membranes), chancre begins as a papules and 

characteristically develops into an ulcer approximately 1cm in diameter with a clean base and 

raised borders; painless chancre unless secondary infection; lymphadenopathy 

Secondary stage: 

6weeks to 6 months with various different lesions 

Erythematous or pink macules or papulues, usually with a generalized symmettrical distribution 

Pigmented macules and papules classically appear on the palms and soles; may be scaly but 

rarely pruritic 

Papular, annular, circinate lesions are more common ion nonwhites 

Generalized lymphadenopathy and malaise accompany the lesions 

Irregular patchy alopecia 

Moist, flat, verucous condyloma latum may appear on genitals 

Diagnosis 

Primary: darkfield microscopy for spirochetes; not available in ED thus suspect and treat based 

on clinical suspicion and refer to STD clinic 

VDRL not very sensitive or specific in primary syphillus 

VDRL is better with secondary syphillus 

FTA-ABS serology is better (Florescent Treponema antibody absorption) 

Many causes of false +ve VDRLs: vaccines, mono, mycoplasma, etc 

Management 

Incubating syphillus (before chancre): 1gm of probenecid po then 4.8 million units of procain 

penicillin IM 

Primary and secondary: benzathine penicillin G 2.4 million units IM 

Doxycycline or tetracycline for pen allergic for 14 days 

Jarisch-Herxheimer reaction: febrile reaction and diffuse rash 12 hours after receiving treatment 

for syphillus, resolves spontaneously in 24hrs

ERYTHEMA NODOSUM 


Inflammation of the dermis and adipose tissue 

Painful red to violet nodules 

Nodules are elevated skin lesions located deep in the skin thus the overlying skin can be moved 

on palpation 

MC over anterior tibia but may be on arms or thrunk 

Fever and arthralgia of ankles may preceed the rash 

Lesions may turn yellow-purple and resemble bruises with evolution 

Most common in women in 20 - 50s 

Associations 

Infections: TB, sterptococci, yersinia, chlamydia, coccidio, histoplasmosis 

Sarcoidosis 

Ulcerative colitis and regional enteritis 

Pregnancy 

Idiopathich 

Drugs: OCP is the MCC 

Management 

Treat underlying condition 

CXR for ? sarcoidosis or TB should be considered 

Bed rest, elevate legs, wear stocking 

ASA 600 mg q4hr 

Resolves spontaneously in 4-6 weeks 

Potassium iodide 360 - 900 mg po od for 3-4 weeks if severe (? May act through an 

immunosuppressive mechanism mediated via heparin release from mast cells) 

VESICULAR AND BULLOUS LESIONS 

PEMPHIGUS VULGARIS 


Vesicles = elevated lesions that contain clear fluid 

Bullae = vesicles > 1 cm 

Pemphigus vulgaris is an uncommon but severe disorder 

Bullous disease most common in 40 - 60yo 

Small, flaccid bullae that break easily forming superficial erosions and crusted ulcerations are the 

typical lesions 

Any area of the body may be involved 

Nikolsky’s sign is present 

60% have mucous membrane lesions 

Oral lesions typically preceed the cutaneous lesions by months 

Gums and vermilion borders of lips are particularly common 

Oral lesions are bullous but break easily thus superficial ulceration is seen 

Cause unkonwn 

Has been seen rarely with captopril and penicillamine 

Tzanck cytologic test suggest the diagnosis (finding acanthyolytic cells, degenerated rounded 

epithelial cells with amorphous nuclei) 

Acantholytic cells are not specific for pemphigus 

Serum immunofluorescence confirms the diagnosis

Ddx: bullous pemphigoid, epidermolysis, dermatitis herpetiformis, TEN, bullous scabes, bullous 

SLE 

Management 

Pain control 

Local wound care 

Steroid: 100 - 300 mg prednisone 

Consult dermatology 

Other immunosuppressants sometimes used 

Mortality very high without steroids 

Superinfection and complications of steroids are problematic 

PEMPHIGOID 

HERPES SIMPLEX 

HSV 1: primarily nongenital areas 

HSV 2: primarily genital areas 


HSV 1 most common in mouth, more common in children 

Cluster ov vesicles that appear, break and leave crusted erosions 

Can have very severe gingostomatitis with dehydration 

Secondary infection with staph and strep can occur 

Hallmark = painful group of vesicles on erythematous base 

Usually nondermatomal distribution 

Avoid contact with atopic dermatitis kids b/c of severe generalized HSV can develop in kids 

with atopci eczema and other dermatosis 

HSV2: single or grouped vesicles on penis, prodrome of local pain and hypesthesia common, 

constitutional symptoms and L.N. common 

Versicles erode over few days, become crusted, and heal over 2 weeks 

Located to cervix, vagina, or introitus in women 

Herpes cervicitis may cause severe pelvic pain in women 

Managment 

First episode of gential herpes: acyclovir (Zovirax) 200mg po 5X/day X 10/7 

Famciclovir or vancyclori are options 

Treat until resolution of lesions if not gone by 10 days 

Improve healing and decrease spread with treatment but do NOT prevent recurrences (acyclovir 

prophylaxis may help suppress herpes) 

Acyclovir can be started at first sign of recurrence 

Immunocompromised: admit for iv acyclovir 

Pain control important 

Treat partner 

Stomatitis: Maalox and benadryl (?treat primary gingivostomatitis with acyclovir)

VARICELLA 


Chickenpox; Varicella-zoster virus 

Incuation 2-3 weeks 

Begins with low fever and constitutional sympomts 

Exanthe4m conincides with these sympomts in children but follows them in adults by 1-2 days 

Lesions rapidly progress from macules to papulues to vesicles to crusting lesion sometimes 

within hours; vesicles are 2-3 mm and surrounded by erythematous border (can have larger 

bullae) 

Drying vesicles produce scabs which fall off in 5-20 days 

Highest concentration in trunk 

Hallmark = lesions in all stages (macules, papules, vesicles, crusts) 

Complications 

Bacterial superinfection of lesions 

Secondary bacterial pneumonia 

Encephalitis 


Arthritis 

Hepatitis 

Glomerulonephritis 

Management 

Symptomatic treatment 

AVOID ASA (Reye’s syndrome) 

Oral acyclovir may be effective if started within 24hours of rash for patients with chronic 

respiratory or skin diseases; may decrease duration and symptoms 

Isolation usually futile b/c spread before diagnosis: keep at home though becouse spread 

continues until all vesicles have crusted over and dried up 

Varicella vaccination exists 

Maternal varicella 5 days before and 2 days after delivery can result in disseminated herpes in 

the newborn 

Pregnant women and immunocompromised exposed to chicken pox 

Check varicella-zoster titers 

VZIG must be given to those with negative titers who are exposed 

Congenital anomalies if exposed in first or early second trimester: embryopathy, limb atrophy, 

scarring extremities, CNS and ocular manifestations 

HERPES ZOSTER 


Shingles is an infection caused by varicella zoster virus 

Virus lives in dorsal root ganglion and is reactivated 

Pain in dermatome prior to appearance of rash by 1-10 days 

Grouped vesicles on erythematous base in dermatomal pattern 

Thorax and trigeminal nerves are the MC location 

Vesicles appear then b/cm cloudy and progress to crusts and scabs 

Crusts fall off at 2-3 weeks 

Peak incidence in 50 - 70yo (rare in children) 

Associations: leukemia, Hodgkin’s, other cancers (don’t need to hunt for) 

You CAN acquire chicken pox from exposure to shingle but uncommon

Can be a disseminated infection 

Complications: ocular infection, postherpetic neuralgia, meningoencephalitis, myelitis, 

peripheral neuropathy 

Ocular: 20 - 70% involve the opthalmic division of trigeminal nerve (V1); can be vision 

threatening; anterior uveitis, conjunctivitis, secondary glaucoma, corneal scarring can all occur; 

tip of the nose means that the nasociliary nerve is involved and predicts eye involvement 

More severe in immunosuppressed especially AIDS, Hodgkin’s, other lymphoma; cutaneous and 

CNS dissemination more common in these groups 

Postherpetic neuralgia 

More common in elderly and immunocompromised 

May lasts months to years 

Management 

Analgesia 

Other treatment rarely necessary 

Burow’s solution may be applied to hasten drying 

Steroids: may shorten duration of postherpetic neuralgia but does not lesson the severity of pain 

or affect the rate of healing 

Acyclovir, famciclovir, valacyclovir etc: have been shown to be effective for 

immunocompromised patients 

Capsaicin cream can be used on areas with postherpetic neurlagia\ 

Severe ocular zoster: iv acyclovir may be of some benefit, topical steroids (is used with zoster; is 

NOT used with herpes simplex conjunctivitis) 

PUSTULAR LESIONS 

IMPETIGO 

Principles 

Slowly resolving pustular eruption most common in preschool children 

Staph aureus is the most common cause currently 

Group A strep is the second MCC 

Predispositions: eczema, poor hygeine, malnurished, other skin conditions 


Streptococcal impetigo (ECTHYMA) 

Most common on the face 

Begins as a single pustule but then develops into multiple lesions: 1-2mm vesicles with 

erythematous margins; when they break they leave red erosions covered with a golden yellow 

crust 

Can be pruritic but are not paiful 

Regional lymphadenopathy common 

Very contagious among infants and children (less in older) 

Post strep glomerulonephritis as a complication 

Staphlococcal impetigo 

Little surrounding erythema compared to strep 

Staph is a more superficial infection 

Bullous impetigo 

Caused by staph phage group 2 

Primarily in infants and young children

Initial lesions are thin walled 1-2cm bullae; they rupture to leave a thin serous crust and 

collarette-like remnant of the blister roof at the rim of the crust 

Face, neck, extremities are most common 

Ddx: dermatitis, HSV infection, fungus, pemphigus vulgaris 

Gram stain of fluid from bullae: Gram+ve cocii 

Management 

Systemic and topical antibiotics are equally effective 

More extensive lesions should be treated systemically 

NO evidence that antibiotics prevent post strep GN 

Mupirocin 2% ointment tid 

Erythromycin qid X 10/7 or Keflex are options 

Bullous impetigo: penicillinase resistant semisynthetic penicillin (dicloxicillin) or erythromycin; 

add mupirocin 2% ointment to area as well 

FOLLICULITIS 

Inflammation of the hair follicle 

Usually caused by staph aureus 

Lesions are on usually on buttocks, thighs, and occasionally scalp/beard 

Ddx: acne, keratosis pilaris, fungal infection 

Pseudomonas associated with hot tubs, pools, antibiotic use for acne 

Gram stain of lesion can tell pseudomonas from staph 

Mx: antiseptic cleaner (chlorhexidine) daily until cleared 

Extensive involvement: erythromycin, dicloxacillin may be added 

CARBUNCLE 

Large abscess that develops in thick inelastic skin of back of neck, back, thighs 

Severe pain, fever, sepsis possible 

Local heat 

I&D when fluctuance present 

Abx only necessary if cocomitant cellulitis or sepsi 

HIRADENITIS SUPPURATIVA 

Apocrine sweat glands 

Recurrent abscess formation in axilla and groin resembles furunculosis 

Recurrence common; often resistant to therapy 

Need to I&D abscesses 

Antistaph abx useful if early and long course used 

Many require local incision and skin grafting 

Antiandrogen therapy is an option in resistant cases 

GONOCOCCAL DERMATITIS 

Arthritis - dermatitis syndrome 

MC presentation of disseminated gonococcal disease 

2% of patients with gonnococcus (MC in women) 

Fever, migratory polyarthralgias, skin lesions 

Multiple lesions with predominance for periarticular regions of distal extremities

Erythematous or hemorrahgic papules that evolve into pustules and vesicles with an 

erythematous halo (look like meningococcemia). They are tender and may have a gray necrotic 

hemorrhagic center. Healing with crust formation usually occurs w/i 4-5 days 

Recurrent crops of lesions can occur even after antibiotics started 

Gultures and gram stains of lesions usually negative 

Immunofluorescent antibody staining of direct smears from pustules more reliable 

Diseminated gonococcal infection 

Ceftriaxone 1gm iv/im q24hrs OR cefotaxime 1gm q8hr 

Allergic to Blactams: spectinomycin 2 gm im q12hrs 

Switch to po cefixime, cefuroxime, cipro, or ofloxacin 

Total treatment of 7 days 

Hospitalization for septic arthritis, meningitis, endocarditis 

PETECHIAL AND PURPURIC LESIONS 

INTRODUCTION 

Purpura = blood in the skin or mucous membrane; divided into petechiae and echymosis 

Petechia = small, golden-brown -> yellow 

DIFFERENTIAL DIAGNOSIS OF PURPURIC RASH 

VASCULAR INTEGRITY PROBLEM 

Trauma: normal and Non-Accidental trauma must be thought of 

Infections: meningococcus, viral NOS, mono, endocarditis, ricketssia, strep 

Drugs 

HSP and other vasculitidies (kawasaki’s, serum sickness, cryoglobulinemia, vasculitis with 

SLE/lyme/IVDA/PBC) 

Vit C deficient 

Ehlers-danlos etc 

PLATELET PROBLEM 


Decreased production 

Sepsis: esp meningococcus 

Drug suppression 

Aplastic anemia 

BM infiltration 

Increased destruction 

Sepsis/DIC 

Drug 

HUS 

TTP 

ITP 

Increased sequestration 

Liver dz

Splenomegaly 

Platelet Dysfunction 

Chronic renal failure, aspirin and other drugs 

Congenital platelet disorders 

COAGULATION FACTOR PROBLEM 

Congenital 

Hemophilia A/B 

Von-Willebrand factor 

Christmas tree factor def 

Acquired 

DIC 

Warfarin 

Vit K deficiency 

Liver dz, renal dz 

APPROACH TO THE PURPURIC RASH 

MUST consider non-accidental trauma 

Other causes of sepsis actually more common than meningococcus for the sick purpuric rash 

The well looking person/child with a petechial rash? Is it meningococcemia???? 

Many infections can cause petechiae or ecchymosis in absence of platelet or 

coagulation disorder 

Capillary damage from the infection 

Rubeola, mono, ricketsia, streptococcal, RMSF, endocarditis can all present 

Keep in mind the above ddx: vascular integrity problem, thrombocytopenia, coagulation factor 

problem 

Approach 

Toxic appearing: monitored bed, iv access, draw labs, fluid bolus, draw cultures, start antibiotics, 

resuscitate as needed 

History and Physical: drugs, infectious symptoms, bleeding history, easy bleeding or brusing, 

lumps or bumps, weight loss or systemic symptoms, full review of symptoms 

Order: CBC, diff, platelet count, retic count, PTT, INR, bleeding time 


Prolonged INR/PTT: sepsis and DIC 

Normal INR/PTT: ITP, TTP, HUS, bone marrow suppression, bone marrow infiltration, platelet 

sequestration 

Platetlets normal, INR/PTT prolonged 

Hemophilia 

Liver dz 

Warfarin 

Platelets normal, INR/PTT normal, Bleeding Time prolonged 

Von-Willebrand disease 

Aspirin or other platelet inhibitors 

Platelets normal, INR/PTT normal, Bleeding Time normal 

Vasculitis: HSP, serum sickness, cryoglobuinemia, IVDA, kawasaki’s 

Trauma 

Infections

Drugs 

Connective tissue disease 

MALIGNANCY AND DERMATOLOGY 

ACANTHOSIS NIGRANS 

Most do NOT have tumors but some do 

Malignant acanthosis nigrans: = associated with cancer (skin lesion itself is NOT cancer) 

Hyperpigmented verrucous velvet - like hyperplasia and hypertrophy of the skin with 

accentuated skin markings: body folds, especially axillae, antecubital fossae, neck and groins 

MC is adenocarcinoma of the stomach 

Others: breast, ovary, pancreas, colon, uterus 

Tumor produces insulin-like growth factor which stimulates the skin 

DERMTOMYOSITIS 

Some will have underlying malignancy 

Breast, ovary, GI, uterus 


Associated with leukemia 

Also Hodkin’s 

ERYTHRODERMA 

Almost pathognomonic of Hodgkin’s lymphoma 

Also occurs with lymphocytic leukemia 

ACQUIRED ICHTHYOSIS 

Generalized dryness of skin, scalin, superficial cracking, or hyperkeratosis of soles and palms 

Hodgkin’s is MCC 

Other cancers also 

PRURITIS 

Hodgkin’s lympoma, leukemia, adenoCa, Sqcell Ca, carcinoid, multiple myeloma 

Hodgkin’s may have severe itching and burning sensations 

Standard treatments ineffective 

PURPURA 

MC manifestation of acute granulocytic and monocytic leukemia 

Also myeloma, lymphoma, polycthemia vera 

Thrombocytopenia secondary to BM suppression is the mechanism 

Non-thrombocytopenic forms do occur 

URTICARIA 

Hodgkins 

Leukemia 

Internal carcinomas

NARCOTIC ADDICTION 

Skin needle tracks: indurated linear hyperpigmented streaks 

Skin popping: subcutaneous injections result in round or oval hyperpigmented atrophic 

depressed scars 1-3 cm in diameter 

Skin abscesses 

Hypertrophic keloid scars 

Increased pigmentation at site of tourniquet use

APPROACH TO RASHES MACULOPAPU LAR RED ... - rEMERGs

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