Contents Chapter Topic Page Neonatology Respiratory Cardiology

Contents 

Chapter Topic Page 

1 Normal Values in Paediatrics………………………………… 1 

2 Immunisation………………………………………………….. 5 

3 Developmental Assessment…………………………………. 20 

4 Developmental Milestones Table……………………………. 28 

Neonatology 

5 Principles Of Transport Of The Sick Neonate……………… 32 

6 Neonatal Resuscitation……………………………………… 48 

7 The Premature Infant ……………………………………….. 57 

8 Enteral Feeding in Neonates ………………………………… 63 

9 Total Parenteral Nutrition in Neonates……………………… 69 

10 ICU/NICU: Guidelines……………………………………….. 76 

11 Surfactant Use Guidelines…………………………………. 83 

12 Newborn and Acid Base Balance……………………………. 86 

13 Birth Asphyxia…………………………………………………. 92 

14 Neonatal Seizures……………………………………………. 99 

15 Neonatal Hypoglycaemia……………………………………. 107 

16 Neonatal Jaundice …………………………………………… 111 

17 Exchange Transfusion for Neonatal Jaundice..……………. 120 

18 Prolonged Neonatal Jaundice……………………………… 123 

19 Apnoea in the Newborn…………………………………….. 126 

20 Neonatal Sepsis……………………………………………… 129 

21 Patent Ductus Arteriosus In The Premature…………………. 133 

22 Perinatally Acquired Varicella ………………………………. 137 

Respiratory 

23 Asthma………………………………………………………… 139 

24 Viral Bronciolitis………………………………………………. 151 

25 Croup………………………………………………………….. 154 

26 Pneumonia……………………………………………………. 157 

Cardiology 

27 Paediatric ECG Interpretation………………………………… 164 

28 Timing of Cardiac Surgery………………………………….. 168 

29 Cardiac Failure………………………………………………… 174 

30 Rheumatic Fever………………………………………………. 179 

31 Infective Endocarditis and Prophylaxis……………………… 182 

32 Kawasaki Disease…………………………………………….. 188 

33 Shock…………………………………………………………… 191

Neurology 

34 Febrile Convulsions……………………………………………. 192 

35 Epilepsy…………………………………………………………. 196 

36 Meningitis……………………………………………………….. 204 

37 Child with Altered Consciousness…………………………… 210 

38 Brain Death…………………………………………………… 217 

Endocrinology 

39 Diabetes Mellitus ……………………………………………… 223 

40 Congenital Hypothyroidism…………………………………… 234 

41 Ambiguous Genitalia………………………………………… 240 

42 Congenital Adrenal Hyperplasia……………………………. 246 

Nephrology 

43 Acute Glomerulonephritis…………………………………….. 251 

44 Acute Renal Failure………………………………………….. 257 

45 Acute Peritoneal Dialysis…………………………………….. 266 

46 Nephrotic Syndrome………………………………………….. 271 

47 Urinary Tract Infection……………………………………….. 279 

48 Vesico-ureteric Reflux………………………………………… 285 

49 Antenatal Hydronephrosis…………………………………… 288 

50 

Hematology / Oncology 

The Anaemic Child ……………………………………………. 294 

51 Haemophilia…………………………………………………….. 298 

52 Immune Thrombocytopenic Purpura………………………… 305 

53 Thalassaemia…………………………………………………… 311 

54 Oncologic Emergencies……………………………………… 317 

55 General Guidelines for Acute Lymphoblastic Leukaemia 

Maintenance Therapy…………………………………………. 328 

Gastroenterology 

56 Acute Gastroenteritis…………………………………..………. 332 

57 Acute Hepatic Failure………………………………………….. 343 

58 Gastrointestinal Bleed…………………………………………. 346 

Infections Diseases 

59 Sepsis / Septic Shock………………………………………….. 348 

60 Paediatric HIV………………………………………………….. 355 

61 Malaria…………………………………………………………… 369 

62 Tuberculosis……………………………………………………. 374 

63 BCG Lymphadenitis…………………………………………… 381 

64 Dengue Fever………………………………………………….. 384 

65 Congenital Syphilis…………………………………………….. 393 

66 Ophthalmia Neonatorum………….……................................ 396

Dermatology 

67 Atopic Dermatitis……………………………………………… 399 

68 Impetigo……………………………………………………….. 404 

69 Scabies…………………………………………………………… 405 

70 Steven-Johnson Syndrome…………………………………. 407 

71 

Metabolic / Genetics 

General Approach to Inborn Errors Of Metabolism……….. 410 

72 Algorithm For The Sick Infant to Screen for Treatable 

IEM……………………………………………………………… 

73 Approach to Hyperammonemia……………………………….. 419 

74 Approach to Hypoglycaemia…………………………………. 423 

75 Approach to Metabolic Acidosis…………………………….. 426 

76 Down Syndrome……………………………………………….. 430 

Surgical Topics 

77 Appendicitis……………………………………………………… 438 

78 Persistent Vomiting in the Neonate and Child………………. 442 

79 Intussusception………………………………………………… 448 

80 Inguinal Hernias, Hydroceles………………………………… 452 

81 Undescended Testis…………………………………………… 454 

82 The Acute Scrotum……………………………………………... 456 

83 Penile Conditions ……………………………………………… 459 

Rheumatology 

84 Juvenile Idiopathic Arthritis……………………………………. 461 

Poisons and Toxins 

85 Snake Bites……………………………………………………… 468 

86 Common Poisons………………………………………………. 476 

87 Anaphylactic Reactions………………………………………. 484 

Appendix 

88 Ward Procedures………………………………………………. 486 

Drug Dosages…………………………………………………. 513 

Growth Charts…………………………………………………. 565 

Pediatric Advanced Life Support Algorithms……………….. 577 

416

Dr. Angeline Wan 

Consultant Paediatrician 

Hospital Muar 

Ms. Anne John 

Consultant Paediatric Surgeon 

Sarawak General Hospital 

A/Prof Bina Menon 

A/Professor of Paediatrics 

Universiti Putra Malaysia 

Dr. Chan Lee Gaik 

Consultant Paediatric Neonatologist 

& Head, Dept. of Pediatrics 

Sarawak General Hospital, 

Dr. Chew Thean Meng 


Selayang Hospital 

Dr. Chieng Chae Hee 

Paediatrician, 

Hospital Sibu 

Dr. Chin Choy Nyok 


& Head Dept. of Pediatrics 

Hospital Kuantan 

Dr. Choy Yew Sing 

Consultant Paediatric Geneticist 

Hospital Kuala Lumpur 

Dr. Eni Juraida 

Consultant Paediatric Oncologist 


Dr. Fong Siew Moy 

Consultant Paediatric Infectious Disease 

Specialist 

Hospital Queen Elizabeth 

Kota Kinabalu 

Dr. Fuziah Md. Zain 

Consultant Paediatric Endocrinologist 


Hospital Putrajaya 

Contributors 

Dr. Hishamshah b. Mohd Ibrahim 

Consultant Paediatric Oncologist 


Dr. Hung Liang Choo. 

Consultant Paediatric Cardiologist 


Dr. Hussain Imam B. Hj Muhammad Ismail 

Consultant Paediatric Neurologist 

& Head Dept of Pediatrics 


Dr. Irene Cheah 



Datuk Dr. Jimmy Lee Kok Foo 



Hospital Kuala Terengganu 

Dr. Kamarul Razali 


Specialist 


Dr. Khoo Teik Beng 



Dr. Kok Juan Loong 



Dr. Lee Ming Lee 

Consultant Paediatric Nephrologist 

Hospital Seremban 

Dr. Leow Poy Lee 


Hospital Malacca 

Dr. Liew Siaw Phin 

Private Paediatrician 

Kuching 

Dr. Lim Chooi Bee 

Consultant Paediatric Gastroenterologist 

Hospital Kuala Lumpur

Dato’ Dr. Lim Nyok Ling 



Selayang Hospital 

Dr. Lim Poi Giok 



Dr. Lim Yam Ngo 



Dr. Lynster Liaw 


Department of Paediatrics 

Hospital Pulau Pinang 

Dr. Mardziah bt Alias 

Consultant Paediatric Dermatologist 


Dr. Mohd Hanifah bin Mohd Jamil 

Consultant Neonatologist 


Hospital Kota Baru 

Dr Neoh Siew Hong 


Hospital Taiping 

Dr. Ng Hoong Phak 

Consultant Paediatrician, 


Dr. Ngu Lock Hock 

Consultant Paediatrician, 


Dr. Nik Khairulddin 


Specialist 

Hospital Kota Baru 

Dr. Norzila Bt. Mohd Zainudin 

Paediatric Respiratory Disease Specialist 


Dr. Ong Gek Bee 

Consultant Paediatric Oncologist, 

Hospital Melaka 

Prof. Dr. Ong Lai Choo. 


Hospital University Kebangsaan Malaysia 

Dr. Revathy Nallusamy 


Specialist & Head Dept of Pediatrics 

Hospital Pulau Pinang 

Dr. Rosalie Yip CW, 

Lecturer in Paediatrics, 

Universiti Putra Malaysia 

Dr. Shirley Wong Siew Ling 

Private Paediatrician, 

Kuching 

Dr. Shyam Puthucheary 

Community Paediatrician 

Hospital Ipoh 

Dr. Susan Pee 


Hospital Sultanah Aminah, Johor Bharu 

Dr. Tan Kah Kee 


Specialist & Head Dept of Pediatrics 

Hospital Seremban 

Prof. Dr. Tang Swee Fong 

Consultant Paediatric Intensivist 

Hospital University Kebangsaan Malaysia 

Dr. Tang Swee Ping 

Consultant Paediatric Rheumatologist 

Hospital Selayang 

Dr. Teh Keng Hwang 

Consultant Paediatric Intensivist 


Hospital Alor Setar 

Dr. Wan Jazilah Wan Ismail 


Hospital Selayang 

Dr. Wilson Pau 

Paediatric Clinical Specialist 


Dr. Zuraidah Bt Abdul Latif 


Hospital Kuala Lumpur

Paediatric Protocols 

For Malaysian Hospitals 

1st Edition 2005 

Hussain Imam Hj Muhammad Ismail 

Ng Hoong Phak 

MINISTRY OF HEALTH MALAYSIA

ISSN 1823-3856 

Printed by: 

Perniagaan MMD 

No. 3A, Jalan Kenangan Utama, 

Taman Kenangan, Batu 6, Gombak, 

53100 Gombak, Selangor, 

Darul Ehsan. 

Tel: 03-6188 4419 Fax : 03-6188 4419 

Contect persons: 019-2766123

Foreword 

By Director General of Health, Malaysia 

MALAYSIA is a young country with a relatively young population. One third of 

Malaysians are under 15 years of age. While many children live in urban areas 

with ready access to specialist care, many still live in rural areas, where services 

are largely provided by medical officers. It is essential that these children receive 

timely and appropriate treatment when they present at government clinics and 

hospitals. 

Over the years the Ministry has taken many steps to ensure that doctors serving 

in the rural areas are prepared for their placement and have regular continuous 

professional development. Nonetheless, there are still some doctors who are 

posted to the rural area before completing their pediatric rotation. As specialist 

supervision is not always present, these doctors need ready access to treatment 

protocols covering pediatric conditions, especially emergencies, commonly 

encountered locally. Such protocols may have to be relatively didactic for use by 

those on the ground. 

Such a set of pediatric protocols has been available for some time for the state of 

Sarawak. Now pediatricians from all parts of the country have contributed to a 

more comprehensive manual, addressing topics covering the whole range of 

pediatrics. 

I hope that this manual will be widely circulated and utilized with the aim of 

improving the care of children through out the country. 

Thank you. 

Yours sincerely,

Foreword 

One of the maxims of science is that what is right today is wrong tomorrow. This seems 

to apply to clinical medicine more than many other areas of science. Hence one of the 

concerns of preparing a manual of clinical protocols is that some parts of the publication 

may well be outdated by the time the document finally sees the light of day. Nonetheless 

many institutions have found having a set of clinical protocols useful especially where 

the turnover of doctors is frequent. In Malaysia this was pioneered in Sarawak in the 

days when one pediatrician served the whole state, in an attempt to standardize practice 

in different hospitals. Pediatric service has come a long way since then. However now 

more than ever before is there a need to establish practice parameters based on current 

best practice and evidenced based medicine. Many young doctors are often 

overwhelmed by the myriad of options available when they search the internet and it is 

not always easy separating the wheat from the chaff. 

At a meeting of senior pediatricians in the MOH in February 2004, it was decided that we 

should all work together to produce a manual of pediatric protocols addressing clinical 

problems commonly encounter in local practice. The topics to be covered were proposed 

by those present and topics were allocated to various individuals to work on. We must 

say that everybody involved in the task has given their best. Many a time we have gone 

back to the authors of various section requesting modifications and the response has 

always been positive. 

After almost 11 months the final document was ready for printing. This has truly been a 

team effort involving colleagues from all over the country and we are very grateful to all 

the contributors who have made this manual a reality. 

This manual cannot cover all the problems we meet in our wards but we sincerely hope 

that we have covered the important ones. We hope, God willing, to revise this manual 

every 4 years and we welcome feedback and suggestions from all who happen to use 

this edition. 

We would like to thank Dr. Tan Poh Tin who started the first edition of the Paediatric 

Protocols for Sarawak Hospital; the third edition of which this manual was based. In 

addition to our local colleagues we would like to say a special word of thanks to Prof. 

Frank Shann of Melbourne for allowing us to incorporate part of his well established drug 

dosage booklet into our manual. 

This book is dedicated to the children of Malaysia and we pray it makes a difference to 

them. 

Hussain Imam Hj Muhammad Ismail 

Ng Hoong Phak

A. Vital Signs 

Normal Respiratory Rate 

Infant 30 - 40 

Toddler 24 - 40 

School Age 18 - 30 

Adolescent 12 - 16 

Normal Heart Rate (from Gillette 

1989) 2 

NORMAL VALUES IN PAEDIATRICS 

Awake 

Mean Sleeping 

< 3 months 85 - 205 140 80 - 160 

3 mo to 2 yr. 100 - 190 130 75 - 160 

2 yr. to 10 yr. 60 - 140 80 60 - 90 

> 10 yr. 60 - 100 75 50 - 90 

Any age HR > 220 consider SVT. 

Extra Tables for Abnormal Vital Signs: 

Normal Blood Pressure (from Hazinski MF 1992) 1 

Systolic Diastolic 

Day 1 (< 1000g)39 - 59 16 - 36 

Day 1 (> 3000g)50 - 70 25 - 45 

Neonate 60 - 90 20 - 60 

Infant 87 - 105 53 - 66 

Toddler 95 - 105 53 - 66 

> 7 years 97 - 122 57 - 71 

> 15 years 112 - 128 66 - 80 

Hypotension: Simple and rapid estimation to see if Hypotension is 

present: 

Age BP (Lower limit (5th centile) systolic value) 

0 - 1 month > 60 

1 mo - 1 yr. > 70 

Older > 70 + (2 x age in years) 

Blood Pressure in Hypertension 

Significant Hypertension Severe Hypertension 

1 week Systolic 96 Systolic 106 

7d - 1 mo Systolic 104 Systolic 110 

Infant Systolic 112 Systolic 118 

Diastolic 74 Diastolic 82 

3 - 5 years Systolic 116 Systolic 124 









Diastolic 92 Diastolic 98

B. Anthropometric Measurements 

a) Head Circumference 

Gestational Age Weekly increase cm/wk (1 - 8 wk) 

30 - 33 wk. 1.1 

34 - 37 wk. 0.8 

Rate of growth approximates that of term infant when chronological age reaches term. 

Term Increase in OFC 

< 3 mo. 2 cm per mo. First yr. 12 cm 

4 - 6 mo. 1 cm per mo. Second yr. 2 cm 

6 - 12 mo. 0.5 cm per mo. 

1 - 2 yr. 2 cm per yr. 

2 - 7 yr. 0.5 cm per yr. 

7 - 12 yr. 1/3 cm per yr. 

Age in months 1st 3 months 2nd 3 months Next 6 months 

Head growth (cm) 6 3 3 

Rate of CSF production : 0.35 ml/min = 500 ml/day 

b) Weight 

First 7 - 10 days lose 10 - 15% body weight. 

Regain birth weight by 7 - 10th day. 

First 3 month weight gain 25 gm/day. 

Double Birth Weight by 5 month. 

Triple Birth Weight by 1 year of age. 

As a rough guide: Year 0 1 5 10 

Wt in kg 3.5 10.0 20.0 30.0 

To calculate: 1 - 9 yr. Wt (kg) = (Age in yr. + 4) x 2 

7 - 12 yr. Wt (kg) = Age in yr. x 3 

b) Length and Height 

Length at birth 50 cm 

6 month 68 cm 

1 year 75 cm 

2 yr. 85 cm 

3 yr. 95 cm 

4 yr. 100 cm 

5-12 yr. 5 cm/yr.

C. Haematology 

a) Routine Haematological Values 

Age Hb (g/dL) PCV (%) Retics MCV (fL) MCH (pg/cell). TWBC Neu Lymp 

Lowest Lowest (x1000) (Mean) (Mean) 

Cord 

Blood 

13.7–20.1 45-65 5.0 110 9-30 61 31 

2 wk 13.0–20.0 42-66 29 5-21 40 63 

3 mo 9.5–14.5 31-41 27 6-18 30 48 

6 mo – 10.5–14.0 33-42 70-74 25-31 6-15 45 48 

6 yr 

1.0 

7-12 yr 11.0–16.0 34-40 

76-80 26-32 4.5-13.5 55 38 

Adult 14.0–18.0 42-52 27-32 

Male 

1.6 80 

5-10 55 35 

Adult 

Female 

12.0–16.0 37-47 

26-34 

Eosinophils: 2-3% 

Monocytes: 6-9 % 

Platelets are mildly decreased in 1st few months, by 6 months have reached 250 - 300 x 10 9 . 

ESR should be < 16 in childhood provided PCV at least 35%. 

b) Differential WBC 

< 7 days - neutrophils > lymphocytes 

1 w - 4 yr. - lymphocytes > neutrophils 

4 - 7 yr. - neutrophils = lymphocytes 

> 7 yr. - neutrophils > lymphocytes 

Hb electrophoresis – look under Thalassaemia protocol. 

D. Others 

Body Surface Area (BSA) (m 2 ) = Ht (cm) x Wt (Kg) 

3600 

Other normal values are found in the relevant chapters of the protocol. 

1 Nelson Textbook of Pediatric 15 th Edition 

2 Pediatric Advanced Life Support Textbook 1994.

Immunisation 

1. Immunisation schedule for Malaysia 

Immunisation 

Table 1: The current Immunisation Schedule 

Age (months) 

Age (Years) 

0 1 2 3 5 6 12 18 6 12 15 

BCG* 1 if no scar 

Hep B 1 2 3 

DPT 1 2 3 4 DT T 

OPV* 1 2 3 4 5 

Hib 1 2 3 

Measles* Sabah 

MMR* 1 2 

1.1 Vaccine/s available in KKM but not listed in the above schedule 

1.1.1 Pneumococcal vaccine : Pneumococcal polysaccharide vaccine - 

Protective efficacy ranges from 56 - 81%. Not recommended for children < 

2 years old as vaccine is not effective in this group (conjugate vaccine is 

immunogenic in these infants but currently not widely available). Single 

dose. Booster 3 - 5 years only for high risk persons. 

Category A (specialist prescription) 

1.1.2 Meningococcal A , C, Y & W-135 (Does not cover B). 

Polysaccharide vaccine : Immunogenic in children 2 years or older. 

Single dose. Immunity up to 3 years. 

Category C (medical officers) 

1.1.3 Cholera : Killed whole cell vaccine : 2 doses 4 weeks apart (minimum 1 

week). Booster every 6 months. Not highly effective & short duration of 

protection < 6 months. 

First dose given SC/IM; second dose and boosters given ID to reduce 

systemic side effects. Protects only 50% of vaccines (for 3 – 6 months). 

Vaccine is not recommended for infants < 6 months of age. 

Category B (MO) 

1.1.4 Japanese B encephalitis vaccine. 3 doses. Dose 1 and 2 at 2 – 4 weeks 

interval then Dose 3 at 1 year after that. This vaccine is given in Sarawak 

as part of the MOH vaccination program at 9, 10 and 18 months of age. A 

booster is then given at 4 year of age. 

1.1.5 Rabies: IM/SC (available in KKM as HDC~ human diploid cell vaccine) 

Pre-exposure immunisation: 3 doses at Day 0, 7 and 28. Then 

boosters every 2-3 years. 

Post-exposure treatment: 

o Fully immunised: 2 doses at Day 0 and Day 3 or 7. Rabies 

specific Ig unnecessary. 

o Unimmunised: 6 doses at Day 0, 3, 7, 14 and 30. Rabies 

specific Ig (20 IU/kg given half around the wound and the rest 

IM). 

Category B

1.1.6 Typhoid: a) Vi polysaccharide vaccine : Single dose. Seroconversion in > 

90% of vaccines and confers 60 – 80% protection commencing within 14 

days from vaccination. Boosters every 3 years. Immunogenicity < 2 years 

of age has not been established. 

b)Oral typhoid vaccine(Ty21a vaccine)* (three doses two days apart) and 

whole cell typhoid vaccines are also available. 

Category B 

1.2 Other Vaccines available in Malaysia but not yet in KKM’s program: 

1.2.1 Varicella zoster * 70 – 90 % effectiveness. 

From 12 months to 12 years: single dose. 

> 12 years old : 2 doses at least 28 days apart. 

Two vaccines are currently available in Malaysia: 

-Varivax (MSD) 

-Varilrix (GSK) 

Children who have not had chicken pox by 12 years of age are 

encouraged to receive the vaccine as the illness is more severe in 

older age groups. 

Considered for children with asymptomatic or mildly symptomatic 

HIV infection; two doses with a 3 month interval are recommended. 

Children with leukaemia & are in remission for at least 1 year, & 

have > 700/ml circulating lymphocytes may receive vaccination 

under supervision of the attending paediatrician 

1.2.2 Hepatitis A : 3 doses. Dose 1 and 2 at 2 - 4 weeks apart then Dose 3 at 6 

– 12 months later. Adults need 2 doses 6 – 12 months apart. 

Seroconversion rate almost 100%. Booster every 10 years. Approved for 

children > 1-2 years of age 

Missed second dose: If a child misses the second dose at 2 – 4 weeks 

then: 

If > 1 month and < 5 months from 1st dose just give the second 

dose. 

If > 5 months have elapsed from 1st dose repeat whole course. 

1.2.3 Influenza: Indications and recommended vaccine will vary between 

countries. Unprimed individuals will require a second dose 4 to 6 weeks 

after the first dose. Yearly revaccination with the latest recommended 

vaccine composition by WHO is required in countries at risk, e.g. 

temperate climate 

Recommendations: 

chronic decompensated disorders of respiratory or cardiovascular 

systems : e.g. cyanotic heart diseases, chronic lung diseases 

HIV infection. In advanced disease, vaccination may not induce 

protective antibody levels. 

* Live-vaccines – usually only one dose is required to produce long term immunity (except 

Yellow Fever for travel purposes (vaccination may be obtained at IMR & respective state health 

departments. An International Certificate of Vaccination will be issued, valid for 10 years 

commencing from 10 days after vaccination) and oral poliovirus vaccine which contains 3 

different components and more doses are required to ensure an adequate response to each 

component).

2 General Notes 

2.1 Many vaccines (inactivated or life) can be given together simultaneously (does not impair 

antibody response or increase adverse effect). But they are to be given at different sites unless 

given in combined preparations. Many vaccines are now packaged in combinations so that the 

child is not subjected to multiple injections. 

2.2 Site of administration 

2.2.1 Oral – OPV 

2.2.2 Deep SC & IM injections. (ALL vaccines EXCEPT BCG and OPV) 

a) anterolateral aspect of thigh – preferred site in children. 

b) upper arm – preferred site in adults 

c) upper outer quadrant of buttock - is associated with reduced antibody level production. 

2.2.3 Intradermal (ID) - BCG & rabies. Left deltoid area (proximal to insertion deltoid muscle) 

2.3 A person who has been immunised using OPV can subsequently use IPV for booster and vice 

versa. 

2.4 Repeat dose of OPV if child vomits soon after administration. 

2.5 PRP-T (Act Hib) and PRP-OMP (Pedvax) (H. influenzae b vaccines) used in the primary series 

are interchangeable. Children partially immunized in the private sector with one particular type 

may be immunized with another type in the KKM schedule. 

2.6 MMR can be given irrespective of previous history of measles, mumps or rubella infection. 

3 Immunisation : Contraindications 

3.1 Postponed during acute febrile illness. Minor infection without fever or 

systemic upset are NOT contraindication. Polio (OPV) postpone if severe 

diarrhoea and vomiting (to avoid decrease take). 

3.2 A relative contraindication: do not give a vaccine within 2 weeks of an elective 

surgery. 

3.3 Live vaccine: Absolute contraindication 

3.3.1 Immunosuppressed -malignancy; irradiation, leukaemia, lymphoma, 

primary immunodeficiency syndromes (but NOT asymptomatic HIV). 

3.3.2 On chemotherapy (< 6 months after last dose). 

3.3.3 High dose steroid: Prednisolone 2 mg/kg/day for > 7 days or low dose 

systemic > 2 wk.; (delay vaccination for 3 months). 

If tropical or inhaled steroids OR low dose systemic < 2 weeks or 

EOD for > 2 weeks can give live vaccine. 

3.3.4 If another LIVE vaccine including BCG had been given < 3 wk. ago. 

(Either give live vaccines simultaneously or if cannot then separately 

with a 3 week interval). 

3.3.5 Within 3 months following IV Immunoglobulin. (except yellow fever or 

oral polio).

3.3.6 Pregnancy (live vaccine theoretical risk to foetus) UNLESS there is 

significant exposure to serious conditions like polio or yellow fever in 

which case the importance of vaccination may outweigh the possible 

risk to the foetus. 

3.4 Killed vaccines are generally safe. 

The only Absolute contraindications are SEVERE local (induration involving > 

2/3 of the limbs) or severe generalised reaction in the previous dose (i.e. 

Temp > 39°C, anaphylaxis, persistent screaming, convulsions). 

3.5 Specific Contraindications 

3 Weeks 3 Months 

Live Vaccine HNIG Live Vaccine 

3.5.1 BCG - Not to be given to symptomatic HIV infected children. 

3.5.2 Hep B vaccine – Severe hypersensitivity to aluminium or thiomersal. 

(Not needed for HBsAg or Ab positive) 

3.5.3 Pertussis 

Progressive neurological diseases like infantile spasm, tuberous 

sclerosis. 

Severe reaction to previous dose i.e. 

a. Anaphylaxis b. Collapse or shock-like states 

c. Hyporesponsive states d. Fits and fever within 72 hr 

e. Fever > 40.5 C within 48 hours e. Encephalitis within 7 days 

f. Severe local reaction involving 2/3 of limbs. 

Static neurological diseases, developmental delay, personal or 

family history of fits are NOT contraindications. 

Severe hypersensitivity to aluminium and thiomersal. And point 3.4 

as above 

3.5.4 Diphtheria & Tetanus: Severe hypersensitivity to aluminium and 

thiomersal. And point 3.4 as above. 

3.5.5 Polio 

Diarrhoea & vomiting. 

Hypersensitivity to penicillin, neomycin, streptomycin or 

polymycin. 

Within 3 week from a proposed tonsillectomy (remote risk of 

vaccine induced bulbar polio). 

Polio (IPV) is to be used for immunocompromised children, their 

siblings and household contacts. OPV if given to 

immunosuppressed or HIV positive children tend to cause 

prolonged excretion of the OPV and be hazardous to care givers.

3.5.6 Rubella - Contraindicated in pregnancy (even though no reported cases 

of congenital rubella syndrome due to vaccine). 

3.5.7 Measles - If < 9 months old presence of maternal Ab may decrease 

immunogenecity. Avoid in persons hypersensitive to neomycin, 

polymyxin OR anaphylaxis to egg ingestion. 

3.5.8 MMR and Influenza – severe reaction to hen’s eggs or neomycin. 

3.5.9 Pneumococcal – children less than 2 years old; revaccination within 3 

years has high risk of adverse reaction; avoid during chemotherapy or 

radiotherapy and less than 10 days prior to commencement of such 

therapy – antibody response is poor. Pregnancy. 

3.5.10 Hepatitis A: Severe hypersentivity to aluminium hydroxide, 

phenoxyethanol or neomycin. 

3.5.11 Typhoid (whole-cell) and Cholera: patients with chronic illness such as 

multiple sclerosis, rheumatoid arthritis, diabetes and compensated 

cardiac conditions may suffer a relapse. 

3.5.12 Meningococcus A, C, Y & W-135: polysaccharide vaccine : Not useful 

in children < 2 years old. 

3.5.13 Japanese B: contraindicated in immunodeficiency and malignancy, 

diabetes, acute exacerbation of cardiac, hepatic and renal conditions. 

3.6 The following are NOT contraindications to vaccination in 

Children 

3.6.1 Mild illness without fever e.g. mild diarrhoea, cough, running nose. 

3.6.2 Asthma, eczema, hay fever, impetigo, heat rash, etc.(avoid injection in 

area of skin lesion). 

3.6.3 Treatment with antibiotics or locally acting steroids. 

3.6.4 Child's mother is pregnant. 

3.6.5 Breast fed child (does not affect polio uptake). 

3.6.6 Neonatal jaundice. 

3.6.7 Underweight or malnourished. 

3.6.8 Over the recommended age. 

3.6.9 Past history of pertussis, measles or rubella (unless confirmed 

medically). 

3.6.10 Non progressive, stable neurological conditions like Cerebral palsy, 

Down’s syndrome, simple febrile convulsions, controlled epilepsy. 

mental retardation. 

3.6.11 Family history of convulsions. 

3.6.12 History of heart disease, acquired or congenital. 

3.6.13 Prematurity (give immunisation according to schedule irrespective of 

gestational age).

4 Vaccination: Possible Side Effects 

4.1 Diphtheria and Tetanus vaccine. 

Swelling, redness and pain 

A small painless nodule may at injection site – harmless. 

Transient fever, headaches, malaise, rarely anaphylactic reaction. 

Neurological reactions rare. 

4.2 DPT 

Local swelling and redness within 24 – 72 hours lasting 1 – 2 weeks. 

Acute encephalopathy (0 – 10.5 per million) 

Shock and ‘unusual shock-like state (3.5 to 250 cases per 100 000) 

Anaphylaxis (2 per 100 000 doses) 

Protracted crying (0.1 to 6%) 

4.3 OPV 

Vaccine associated paralytic polio (VAPP) 

risk at 1 case/ 5.3 million doses 

highest risk after 1 st dose estimated at 1 case / 1 million contacts of first 

dose recipients. 

risk for subsequent doses is greatly reduced. It is important that contacts 

of children receiving OPV are themselves fully immunized. 

4.4 IPV 

No serious side effects have been documented, apart from local reaction. 

Indicated for children with severe immunocompromised conditions e.g. 

immunodeficiency states (1 o and 2 o such HIV infection, malignancy & organ 

transplantation) 

4.5 HiB (Haemophilus influenzae b) vaccine 

Local swelling, redness and pain soon after vaccination and last up to 24 

hours in 10% of vaccines 

Malaise, headaches, fever, irritability, inconsolable crying. Very rarely 

seizures. 

4.6 Measles: 

Transient rash in 5% of cases. 

Fever between D5 and D12 post vaccination lasting for 1-3 days (5 to 15% 

of doses of vaccines). 

URTI symptoms. 

Febrile convulsions (D6 to D14) in 1 in 1000 – 9000 doses of vaccine. 

(Natural infection 1:200) 

Encephalopathy within 30 days in 1 in 1,000,000 doses of vaccines. 

(Natural infection 1:1000 - 5000) 

SSPE may occur in 1 in 1,000,000 doses. (Incidence in natural infection is 

6 to 22 per 1,000,000). 

4.7 Mumps 

Rarely transient rash, pruritis and purpura. 

Parotitis in 1% of vaccines, 3 or more weeks after vaccination. 

Orchitis and retro bulbar neuritis very rare. 

Meningoencephalitis is mild and rarely occur. (1 in 800,000 doses). 

(Natural infection 1 in 400).

4.8 Rubella 

May have rash, fever, lymphadenopathy, thrombocytopenia, transient 

peripheral neuritis. 

Arthritis and arthralgia occurs in up to 3% of children and 20% of adults 

who receive the vaccine. 

Rarely polyneuropathy (like Guillain-Barre syndrome can occur). 

4.9 BCG 

Local reaction :a papule at site of vaccination occurs within 2 to 6 weeks. 

This grows and flattens with scaling and crusting. Occasionally a 

discharging ulcer may occur. This heals leaving a BCG scar of at least 4 

mm in successful vaccination. 

BCG adenitis may occur. 

4.10 Influenza and Rabies 

Transient swelling, redness, pain and induration locally. 

Myalgia, malaise and fever for 1 – 2 days starting within a few hours post 

vaccination. Very rarely neurological or anaphylactic reaction occurs. 

4.11 Pneumococcal 

Local reaction. Fever and myalgia in less than 1% of vaccines. Rarely 

neurological disorder (Guillain-Barre), glomerulonephritis, ITP or 

anaphylaxis. 

4.12 Hepatitis A 

Local reaction. Flu-like symptoms lasting 2 days in 10% of vaccines. 

4.13 Hepatitis B 

Local reaction. Fever and flu-like symptoms in 1 st 48 hours. Rarely 

erythema multiforme or urticaria. 

4.14 Typhoid (Typhim Vi): 

Local reaction. Myalgia, malaise, nausea, headaches and fever in 3% of 

recipients. 

4.15 Cholera 

Local reaction. Headache, fever and malaise for 1 – 2 days. Rarely 

anaphylactic reaction, neurological symptoms including cerebral and 

meningeal irritation may occur. 

Repeated vaccination over a few years can result in hypersensitivity to the 

protein components. 

4.16 Meningococcus A, C, Y & W-135 

Local reaction. Irritability, fever and rigors for 1 – 2 days. Very rarely 

anaphylaxis.

5 Vaccination : Special Circumstances 

5.1 What to do if a measles case is admitted to the Paediatric Ward? 

5.1.1 Protect all immunocompromised children with immunoglobulin (HNIG) 

0.2 mls/kg (32 mg/kg). (Measles is the major cause of mortality in 

leukaemia in remission.) 

5.1.2 Check the status of the other children with regards with measles 

immunisation. If they are not immunised then give the measles 

monocomponent vaccine within 24 hours of exposure. Vaccination 

within 72 hours can abort clinical measles in 75% of contacts. 

5.1.3 Discharge uncomplicated measles case. 

5.2 Immunisation in HIV infected children 

5.2.1 With or without symptoms should receive : 

live vaccines (WHO recommends BCG for asymptomatic cases) 

Inactivated vaccines 

5.2.2 Give immunoglobulin if exposed to measles or chicken pox. 

5.2.3 IPV is to be used. 

5.3 In patients with past history or family history of fits, neurological or 

developmental abnormalities that would predispose to febrile fits :- 

5.3.1 Febrile fits can occur 5 – 10 days after measles (or MMR) vaccination 

or within the first 72 hours following pertussis immunisation. 

5.3.2 Give Paracetamol (120 mg or ¼ tablet) prophylaxis after immunisation 

(esp. DPT) 4 hourly for 48 hours regardless of whether the child is 

febrile or not. This can reduce the incidence of high fever, febrile 

convulsions, fretfulness, crying, anorexia and local inflammation. 

5.3.3 Rectal Diazepam may need to be given on stand by. 

5.4 Maternal Chicken Pox during perinatal period. Rash appearing within 5 days 

before and 2 days after delivery. 

5.4.1 Isolate mother from baby and other patients. Isolate baby. 

5.4.2 Immunoglobulin to be given :- 

Human immunoglobulin (400u/kg) OR 

ZIG (125µ/kg) within 48 hours 

5.4.3 Because severe varicella may develop in new-borns despite ZIG, some 

investigators recommend Acyclovir prophylaxis. Neonates with VZ 

infection should be treated with IV Acyclovir 10 mg/kg every 8 hrs for 

10 days.

5.5 Close contacts of immuno-deficient children and adults must be immunized, 

particularly against measles and polio (use IPV). 

5.6 In cases of contact with a patient with invasive Haemophilus influenzae B 

disease: 

5.6.1 Close contacts in a household, nursery or kindergarden under the age 

of 4 years should be immunised. 

5.6.2 Rifampicin prophylaxis should be given to all household contacts at 20 

mg/kg once daily (Maximum 600 mg) for 4 days (except pregnant 

women - one IM dose of ceftriaxone ) 

5.6.3 Index case should be immunised irrespective of age. 

5.7 Asplenia (Elective or emergency splenectomy; asplenic syndromes; sickle cell 

anaemia) – susceptible to encapsulated bacteria and malaria. 

5.7.1 Pneumococcal, Meningococcal A, C, Y & W-135 and Haemophilus 

influenza b vaccines should be given. 

5.7.2 For elective splenectomy (and also chemotherapy or radiotherapy); it is 

preferable to give the vaccines 2 or more weeks before the procedure. 

However they can be given even after the procedure. 

5.7.3 Penicillin prophylaxis should continue even after vaccination. Ideally for 

life. If not until 16 years old for children or 5 years post splenectomy in 

adults. 

5.8 Babies born to mothers who are HbeAg OR HbsAg positive should be given 

Hepatitis B immunoglobulin (200 IU) and vaccinated with the Hepatitis B 

vaccine at within 12 hours and not later than 48 hours. Given in different 

syringes and at different sites.

6. Recommended Immunisation Schedule for Infants and Children Not 

Immunised at the Recommended Time 

Time of Immunisation 

Age at first visit 

Between 6 weeks and 9 

months 

9 months and older 

1st visit BCG, DPT-Hib1, OPV1 & BCG, DPT1-Hib, OPV1 

HBV1 

measles in Sabah at 9 

months of age 

MMR at 12 months of age 

2nd visit (1 month later) DPT-Hib2, OPV2, HBV2 or DPT2, OPV2, HBV1 

3rd visit (1 month later) DPT-Hib3, OPV3, HBV2 DPT3, OPV3, HBV2 

1 month later HBV3 HBV3 

2-8 months later DPT & OPV (booster) 

measles in Sabah at 9 

months of age 

MMR at 12 months of age 

DPT & OPV (booster) 

Subsequent booster doses: follow "Recommended Immunisation Schedule for Infants & 

Children” 

For infants aged less than 6 weeks, use "Recommended Immunisation Schedule for Infants & 

Children". 

Note that measles vaccine should be given only after 9 months. 

Omit pertussis vaccine if child is aged 7 years or older at first contact. In this situation , adult 

dTap (lowered antigen) may be considered. 

For special groups of children with no regular contact with Health Services and with no 

immunisation records, BCG, OPV, DPT, HBV and measles can be given simultaneously at 

different sites at first contact. 

It is not necessary to restart a primary course of immunisation irrespective of the period 

that has elapsed since the last dose was given. Only the subsequent course that has 

been missed need be given. (Example. An infant who has been given OPV1 and then 9 

months later comes for follow-up, the OPV1 need not be repeated. Go on to OPV2.). Except 

Hepatitis A. 

Reference: 

1. Ministry Of Health Malaysia 

2. Immunization Precautions and Contraindications (2 nd Edition) – George C. Kassianos. Blackwell 

Scientific Publications. 1994. 

3. Health Technology Assessment Expert Committee report on immunisation (MOH Malaysia). 

4. Malaysian Immunisation Manual. College of Paediatrics, Academy of Medicine of Malaysia. 

2001 

5. Canadian Immunization Guide.(6 th Edition). 2002. 

6. Cholera vaccines. WHO position paper ; Weekly Epidemiol Rec 2001;76:117-124 

7. Typhoid vaccines. WHO position paper ; Weekly Epidemiol Rec. 2000;32:257-64.

Developmental Assessment 

Development is the progressive, orderly, acquisition of skills and abilities as a child grows. 

It is influenced by genetic, neurological, physical, environmental and emotional factors. 

Important points to note:- 

1. Child must be co-operative, not tired, fretful, hungry nor sick. 

2. Full allowance must be made for prematurity up to two years. 

3. Take note of parental account of what child can/cannot do. If parent says the child 

has a squint, there is a high chance that he has. Similarly, note comments on 

abnormal gait, speech defects, etc. 

4. Normal development is highly dependent on the integrity of child's hearing and 

vision. 

5. A normal pattern of speech and language development is essential for a normal 

social, intellectual and emotional development. 

6. Advanced motor development does not signify mental superiority, 

manipulative skills are a more reliable guide, as well as interest in surrounding, 

responsiveness, alertness and powers of concentration. 

7. Always assess vision, hearing, language and social development in addition to 

gross and fine motor skills. 

8. Retardation may be global i.e. affecting all areas equally, or otherwise normal 

except in specific areas e.g. speech (Always exclude deafness). 

9. Always rule out hypothyroidism in all cases of global retardation. 

Warning Signs 

A. General 

1. Head size out of proportion with length or crossing centile lines (too large or too 

small). 

2. Abnormal rates of growth in weight and height. 

3. Congenital anomalies, odd facies, symmetrical defects of hands and feet. 

4. Unusual hairs or hairline. 

5. Persistence of primitive reflexes after 6 months of age. 

6. Fisting or adducted thumb after the second month of age.

B. Gross Motor 

5 mo Does not roll over 

8 mo Does not sit without support 

10 mo Does not stand while holding on 

18 mo Not walking unaided 

2 yr Not climbing up or down stairs 

2 ½ yr Not jumping with both feet 

3 yr Unable to stand on one foot 

momentarily 

4 yr Not hopping 

5 yr Unable to walk a straight line 

back and forth or balance on one 

foot 

C. Fine Motor 

5 mo Unable to hold rattle 

7 mo Unable to hold an object in each 

hand 

12 mo Absence of pincer grasp 

15 mo Unable to put in or take out 

2 yr Not scribbling 

2 ½ yr Not turning a single page of a 

book 

3 yr Unable to draw a straight line 

4 yr Unable to copy a circle 

5 yr Unable to copy a cross 

D. Language 

6 mo Not babbling 

9 mo Not saying “da” or “ba” 

11 mo Not saying “dada” or “baba” 

18 mo Has < 3 words with meaning 

2 yr No two-word phrases 

2 ½ yr Speech unintelligible to parents 

3 yr Speech unintelligible to 

strangers. 

Gestures used instead of speech. 

4 yr No ‘Why?’ or ‘What?’ questions. 

Can’t tell a simple story. 

Poor social play. 

Poor word / sentence structures. 

5 yr Still gets words, sentences or 

ideas jumbled up. 

Articulation problems 

E. Psychosocial 

3 mo No social smile 

6-8 mo Not laughing in playful situation 

1 yr Hard to console, stiffens when 

approached 

18 mo Not pointing to indicate wants 

2 yr Kicks, bites, and screams easily 

and without provocation 

Rocks back and forth. 

No eye contact. 

3-5 yr In constant motion. 

Resists discipline. 

Does not play with other kids. 

F. Cognitive 

3 mo Not alert to mother 

9 mo No interest in peek-a-boo 

12 mo Does not search for hidden object 

18 mo No interest in cause-and-effect 

games 

2 yr Does not know categories 

3 yr Does not know own full name 

4 yr Cannot pick shorter or longer of 

two lines 

4 ½ yr Cannot count sequentially 

5 yr Does not know colours or any 

letters

Hearing Assessment 

Warning signs for hearing 

Child appears not to hear or 

does not attempt to listen. 

Child by 12 months of age 

does not respond to his name 

or understand "No" or make 

response to clue words like 

"Shoe" 

Also those with warning signs 

for speech / language delay 

Normal Hearing 

Auditory Tests 

At Risk Groups 

Prematurity. 

Intrauterine Infection (TORCHES) 

Severe Neonatal jaundice 

Use of ototoxic drugs e.g. gentamicin. 

Meningitis, HIE 

Trauma. 

Chronic Secretory Otitis Media 

Family history of deafness (exclude Otitis media) - 

at least 10 different genes are responsible for 

deafness. 

Abnormal looking babies, abnormal external ears. 

Newborn Sudden loud noise induces blinking, startle or cry. 

Stilling to voice, change in breathing pattern 

4 months Consistent head turning towards sound. 

5-6 months Turns head to sound at level of ears. 

7 months Turns to sound source below ear level 

8 months Turns to sound source above ear level. 

12 months Looks up to sound above head 

7 - 9 months Distraction Tests. Baby held sitting facing forwards on mother's lap. A 

toy is held in front by one team member to give visual distraction. Second 

team member makes soft sounds 2-3 feet from either ear. The first team 

member decides on the child’s response. 

21mths - Voice Triggered Conditioning Test. Child conditioned to do a task 

2 yr. when a sound is heard i.e. put a brick in the container. Voice sounds 

or an audiometer are used. 

> 18 mths Toy Tests. Child identifies toys when their names are spoken quietly. 

4 yr. Pure tone audiometry. (Requires cooperation). 

All ages Brainstem Auditory Evoked Response (BAER).

Visual Assessment 

Warning signs for Poor Vision 

Does not fix on face of mother while 

feeding by 6 weeks. 

If the child's eyes wander from one corner 

of the eye to the other after 6 weeks. 

If leukocoria (white eye reflex) is noted at 

any age. 

Child holds objects very close to eye. 

Squint in one of his eyes after 6 months of age. 

Strong objection to covering one eye (good eye), but not the other (bad eye). 

Blind mannerisms, abnormal head postures. 

Development of Vision 

When assessing vision in a young baby it is important to know the normal visual 

attainment that can be expected at each age. 

At birth Turn head towards source of light, follow face of mother if very 

close, optokinetic nystagmus. 

At 4 weeks Should follow light, dangling object < 90 o , visual acuity 6/60 at this 

stage. 

8 weeks Fixation, convergence, focusing. 

12 weeks Hand regard. Dangling object 180 o . Visual acuity 6/18 - 6/12. 

16 weeks Reach for any object in its view. 

20 weeks Smile at mirror image. 

8 months See Smartie or raisins, look for fallen toy. 

10 months 100s and 1000s. 

> 18 months Picture charts. 

21mths/2 yr. Sheriden letters. 

41mths/2-5yrs Snellen chart 

At risk 

Prematurity. 

Small for Gestation. 

Family history of cataract, retinoblastoma, 

squint. 

NB. If vision improves when child reads through pinhole, refer to optician for 

spectacles. 

Corneal reflection test for squint 

Refer funny looking eyes, abnormal eye movements/head posture.

Global Developmental Delay 

History 

Consanguinity 

Pregnancy: Drugs, Alcohol or Illnesses. 

Delivery: Premature or Birth Asphyxia 

Neonatal: Severe NNJ or Hypoglycaemia 

Family History 

Do 

Refer for eye and hearing test. 

T4 / TSH 

Chromosomal Analysis 

MRI brain 

(if not available, CT scan) 

KIV 

o Other genetic studies if available (Methylation PCR for PWS / Angelman, 

Subtelomeric rearrangements, Fragile X screen, MECP2) or get a genetic 

consultation. 

o Metabolic screen (VBG, serum lactate, ammonia, serum amino acids, urine 

organic acids screen) 

o Serum CPK in boys 

o EEG if history suggestive of possible seizures 

Isolated Speech Delay 

History 

Congenital Rubella 

Perinatal Drugs 

Severe Neonatal Jaundice 

Family History 

Ear Infection 

Ask for Quality and Quantity of speech 

Consider 

1. Hypothyroidism 

2. Chromosomal anomaly e.g. Down or 

Fragile X 

3. Structural Brain Disorder 

4. Cerebral Palsy 

5. Congenital Infection 

6. Specific Syndromes including tuberous 

sclerosis or neurofibromatosis. 

7. Inborn error of metabolism 

8. Postnatal causes like head injury, 

intracranial bleed, CNS infections. 

9. Muscular Dystrophies 

10. Autism 

Consider 

1. Hearing Impairment 

2. Familial or Genetic causes 

3. Social Cultural Deprivation 

4. IQ Low (Mental Retardation) 

5. Language Confusion 

6. Autism 

7. Hypothyroidism 

Do 

Check ears and tonsils 

Distraction Test 

T4 / TSH 

Referral to ENT / Audiologist for formal hearing test 

Referral to Speech therapist 

KIV 

o Chromosomal Analysis and other genetic testing. 

o Metabolic screen 

o EEG if there is language regression (Landau Kleffner syndrome)

Delayed Motor Development 

Consider 

1. Normal or Familial variation 

2. Previous Chronic Illness 

3. Cerebral Palsy 

4. Neuromuscular Diseases e.g. 

Duchenne Muscular Dystrophy 

5. Orthopaedic Problems 

6. Emotional Neglect 

Learning Difficulties In School 

Consider 

1. Previous developmental delay 

2. Medical Problems 

Hypothyroidism 

Iron deficiency anaemia 

Chronic lead poisoning 

Epilepsy (eg Absence Seizures) 

3. Specific Learning Difficulty (Dyslexia) 

References:- 

1. RS. Illingworth. The Development of the Infant and Young Child. 

2. Nelson’s Textbook of Pediatrics. 

3. First LR, Palfrey JS. The infant or young child with developmental delay. NEJM 1994;330:478-483 

4. Shevell M et al. Practice parameter: Evaluation of the child with global developmental delay. 

Neurology 2003;60:367-380

Developmental Milestones Table 

AGE Gross Motor Vision & Fine Motor Speech & Language Personal Social 

6 weeks Pull to sit: Head lag and rounded back. Fixates and follows to 90 Vocalising by 8/52 Smiles responsively. 

Ventral Suspension: Head momentarily in 

Quiets to sound. Startles 

same plane as body. 

Prone: Pelvis high but knees no longer 

under abdomen. Chin raised occasionally. 

to sound. 

3 months Pull to sit: Only slight head lag. Head Hand regard. 

Squeals with delight. Laughs. 

occasionally bobs forward. 

Follows object from side to Turns head to sound. 

Ventral Suspension: Head above plane of side (180°) 

body. 

Hands held loosely. 

Prone: Pelvis flat. Lifts head up 45° - 90°. Grasp object placed in 

hand. Not reaching out. 

5 months Pull to sit: NO head lag and sits with Reaches for objects. 

Mouthing. 

straight back. 

Lying supine : Feet to mouth. 

Plays with toes. 

6 months Pulls to sit: Lifts head off couch in 

Palmar grasp of cube with 

anticipation. 

ulnar approach. 

Sits with support. 

Moves head and eyes in all 

Bears full weight on legs. 

directions. 

Prone: Supports weight on hands with 

chest and upper abdomen off couch. 

Rolls prone to supine. 

No squint (after 4 months). 

7 months Sits with hands on couch for support. 

Rolls from supine to prone. 

Feeds self with biscuits. 

Transfers objects form hand 

to hand. 

Rakes at pea. 

Babbling in single 

syllables. 

Babbling in combined 

syllables at 8 months. 

Distraction Test. 

Stranger anxiety.


9 months Sits steadily. Leans forward but cannot 

pivot. 

Stands holding on. 

Pulls self to stand. 

10 months Crawls on abdomen. 

Pull self to sit. 

11 months Creeping on all FOURS 

Pivoting. 

Cruising. 

Walks with 2 hands held. 

1 year Gets from lying to sitting to crawling to 

standing. 

Walks like a bear. 

Walks with ONE hand held. 

Walks well (13 months). 

Stands alone. 

15 months Creeps upstairs. 

Stoops for toy and stands up without 

support. (best at 18 months) 

18 months Gets up and down stairs holding on to 

rail or with one hand held. 

Pulls toy or carries doll. 

Throws ball without falling. 

Sits on a chair. 

Inferior pincer grasp. 

(Scissors grasp). 

Index approach. Uses index 

finger to poke at pea. 

Able to let go of cube in 

hand. 

Neat pincer grasp. 

Bangs 2 cubes. 

Sees and picks up 

hundreds and thousands. 

Tower of 2 cubes. 

Scribbles spontaneously 

(15-18 months) 

Tower of 3 cubes. 

Scribbles spontaneously. 

Visual test: Picture charts. 

Handedness (18 - 14 

months). 

Localises sound at 3 feet, 

above and below the ear 

level. 

Feeds with spoon 

occasionally. 

Looks for fallen toys. 

Understands “NO!” 

Waves “Bye bye” 

Plays “Pat-a-Cake” 

ONE word with meaning. Plays “peek-a-boo” 

Understands phases. 

(e.g. where is your 

shoes). 

2 - 3 words with 

meaning. 

Localising sound above 

head. 

More words. 

Points to objects he 

wants. 

Continual jabber and 

jargon. 

Points to 2 - 3 body parts. 

Picture Cards - identify 

one. 

Casting (13 months) 

Less mouthing. 

Shy. 

Takes off shoe. 

Feeds self with cup (able 

to pick up and put down) 

and spoon (but spills). 

Mouthing stops. 

Imitates housework. 

Toilet trained. 

Uses spoon well. 

Casting stops.


2 years Goes up and down stairs alone, 2 feet per 

step. 

Walks backwards (21 months) 

Runs. 

Picks up toy without falling. 

Able to throw and kick ball without falling. 

2 1/2 

years 

Jumps on both feet. 

Walks on tip toes. 

3 years Goes up stairs one foot per step. 

Down stairs 2 feet per step. 

Jumps off bottom step. 

Stands on 1 foot for seconds. 

Rides tricycle. 

3 1/2 

years 

4 years Goes up and down stairs one foot per step. 

Skips on one foot. 

Hops on one foot. 

4 1/2 

years 

Tower of 6 cubes 

Imitates cube of train with 

no chimney. 

Imitates straight line. 

Visual test: Snellen chart. 

Tower of 8. 

Imitates train with 

chimney. 

Holds pencil well. 

Imitates and . 

Tower of 9. 

Imitates bridge. 

with cubes: 

Copies 

Imitates 

Draw a man test. (3 - 10y) 

Copies bridge. 

Imitates gate with cubes. 

Copies 

Goodenough test 4. 

Copies gate with cubes. 

Copies square. 

Draws recognisable man 

and house. 

Joins 2 - 3 word in a 

sentence. 

Uses ‘you’ ‘me’ ‘I’. 

Picture cards - Names 3 

objects.- Points to 5. 

Obeys 4 simple 

commands. 

Points to 4 body parts. 

Knows FULL name and 

sex. 

Names one colour. 

Can count to 10 

Names 2 colours. 

Nursery rhymes. 

Understands “on”, “in”, 

“under”. 

Names 3 colours. 

Fluent conversation. 

Understands “in front of”, 

“between”, behind”. 

Puts on shoes, socks, 

pants. 

Dry by day. 

Play near other children 

but not with them. 

Unbuttons. 

Dresses and undresses 

fully if helped with buttons 

and advised about correct 

shoe. 

Dry by night. 

Plays with others. 

Buttons clothes fully. 

Attends to own toilet 

needs.


5 years Skips on both feet. 

Copies ‘X’ (5 years) 

Knows AGE. 

Ties shoelaces. 

Runs on toes. 

Names 4 colours. Dresses and undresses 

Copies (5½ years) triangle. Triple order preposition. alone. 


Tell time. 

6 years Walks heel to toe 

Kicking, throwing, climbing. 

Copies 


Imitates or copies 

steps with 10 cubes: 

1. Goodenough test: 3 + a/4 years (a = each feature recorded in his picture). 

2. 10% still not dry by day or night at 5 years. 

3. Draw the following: 8 years 10 years 12 years.

Principles of Transport of the Sick Neonate 

• Transport of neonates involves pre-transport intensive care level resuscitation 

and stabilisation and continuing intra-transport care to ensure that the child 

arrives in a stable state. 

• Organized neonatal transport teams bring the intensive care environment to 

critically ill infants before and during inter-hospital or intra-hospital transport. 

• The basis of a safe and timely transport is good communication and 

coordination between the referring and receiving hospital to ensure adequate 

stabilisation pre-transport and continuing intra-transport care. 

• There is a rare need for haste. 

• There must be a balance between anticipated clinical complications that may 

arise due to delay in definitive care and the benefits of further stabilisation. 

1. Special Considerations in Neonates 

Apnoea – Premature and septic babies are especially prone to apnoea 

Bradycardia – In the newborn, hypoxia causes bradycardia followed by heart block and 

asystole 

Oxygen toxicity to the lungs and retina - especially important in the premature baby 

Reversal to fetal circulation (Persistent pulmonary hypertension of the neonate PPHN) 

– Can be precipitated by hypoxia, hypercarbia, acidosis and sepsis 

Hypothermia – The mechanisms of thermoregulation are less developed and the child 

has a larger body surface area: mass ratio. Non shivering thermogenesis is induced by 

the oxidation of brown fat. If the bowels are exposed, the heat and fluid loss are 

compounded by evaporation. The effects of hypothermia are acidosis and subsequent 

Primary Pulmonary Hypertension, impaired immune function and delayed wound 

healing. 

Hypoglycemia – The neonate lacks the glycogen store in the liver and fat deposits. 

Jaundice – worsen in the baby with sepsis or intestinal obstruction. 

2. Mode of transport 

Careful consideration must be made as to the mode of transport. 

• The best mode of transfer is “in utero” as far as possible. E.g. a mother in 

premature labour should be managed in a centre with NICU facilities or if a 

surgical anomaly has been detected antenatally, the mother should be advised to 

deliver at a centre with paediatric surgical facilities. 

• For post natal transfers, the advantages and disadvantages of road, air 

(helicopter / commercial airlines) and riverine transport must be considered in 

each child. If air transport is chosen, then the effects of decreased atmospheric 

pressure on closed cavities and the lack of working space must be taken into 

account. Transport incubators with monitors, ventilators and suction equipment 

are ideal. 

2.1 Air Transport 

A number of patients are transported by either the commercial airlines with 

pressurised cabins flying at higher altitudes or by helicopters flying at lower altitudes 

but without pressurised cabins. There are special problems associated with air 

transport:

• Changes in altitude – Physiologic changes associated with altitude are due 

to the decreased atmospheric pressure causing a decreased oxygen 

concentration and expansion of gases. This becomes especially important in 

children with air trapped in closed cavities e.g. pneumothorax, 

pneumoperitoneum, volvulus and intestinal obstruction. These cavities must 

be drained before setting off as the gases will expand and cause 

respiratory distress. Children requiring oxygen may have an increased 

requirement and become more tachypnoeic at the higher altitude. 

Assessment of hypoxia can be difficult due to poor lighting. 

• Noise and Vibration – In addition to causing stress to the baby and the 

transport team, there is usually interference with the monitors especially 

pulse oximeters. It is also impossible to perform any procedures. 

• Limited cabin space – Prevents easy access to the baby especially in the 

helicopters. The commercial aircraft and current helicopters also are not able 

to accommodate the transport incubators. The baby is thus held in the arms 

of a team member. 

• Weather conditions and availability of aircraft – Speed of transfer maybe 

compromised “waiting” for the availability of aircraft/flight or for the weather to 

change. Stress and safety to the baby and team during poor weather 

conditions needs to be considered. 

• Take off and landing areas – special areas are required and there will be 

multiple transfers, e.g. hospital – ambulance – helicopter – ambulance - 

hospital 

• Finances – Air transport is costly 

3. Pre-transport Stabilisation 

Transport of the neonate is a significant stress on the child and they can easily 

deteriorate during the journey. The presence of hypothermia, hypotension and 

metabolic acidosis has a significant negative impact on the eventual patient 

outcome. It is also almost impossible to do any significant procedures well during the 

actual transport. Therefore, stabilisation pre-transport is critical to ensure a good patient 

outcome. 

The principles of initial stabilisation of the neonate follow the widely recognised ABC’s of 

resuscitation. 

Airway 

Breathing 

Circulation/ {Communication} 

Drugs/ {Documentation} 

Environment/ {Equipment} 

Fluids – Electrolytes/ Glucose 

Gastric decompression

3.1 Airway Management 

Establish a patent airway 

Evaluate the need for oxygen, frequent suction (Oesophageal atresia) or 

an artificial airway (potential splinting of diaphragm). 

Security of the airway – The endotracheal tubes (ETT) must be secure to 

prevent intra-transport dislodgement 

Chest X-ray – to check position of the ETT 

3.2 Breathing 

The need for intra-transport ventilation has to be assessed: 

• Requires FiO2 60% to maintain adequate oxygenation 

• ABG – PaCO2 >60mmHg 

• Tachypnoea and expected respiratory fatigue 

• Recurrent apnoeic episodes 

• Expected increased abdominal/bowel distension during air 

transport 

If there is a possibility that the child may require to be ventilated 

during the transfer, it is safer to electively intubate and ventilate 

before setting off. 

However, there may be certain conditions where it may be preferable not 

to ventilate if possible, e.g. tracheo-oesophageal fistula. If in doubt, the 

receiving surgeon should be consulted. If manual ventilation is to be 

performed throughout the journey, due consideration must be taken about 

fatigue and possible erratic nature of ventilation. 

3.3 Circulation 

Assessment: 

Heart rate and perfusion (Capillary refill) are good indicators of the 

hydration status of the baby. The blood pressure in a neonate drops just 

before the baby decompensates. The urine output should be a minimum 

of 1-2 mls/kg /hr. The baby can be catheterised or the nappies weighed 

(1g = 1 ml urine) 

A reliable intravenous access (at least 2 cannulae) must be ensured 

before setting off. 

If the child is dehydrated, the child must be rehydrated before 

leaving. 

3.3.1 Fluid Therapy 

Resuscitation Fluid 

Rate – 10 – 20 mls/kg aliquots given as boluses over up to 2 

hours according to the clinical status 

Type – Hartmann’s solution 

5% Albumin in Normal saline 

Fresh Frozen plasma 

Blood

This fluid is also used to correct ongoing measured (e.g. 

orogastric) or third space losses as required. The perfusion and 

heart rates are reliable indicators of the hydration. 

Maintenance Fluid 

Rate – D1 – 60 mls/kg 

D2 – 90 mls/kg 

D3 – 120 mls/kg 

D4 onwards – 150 mls/kg 

Type – In the surgical neonate, the recommended solution is ½ 

Saline + 10% D/W. 

Watch out for hyponatraemia and hypoglycemia. 

3.4 Communication 

Good communication between the referring doctor, transport team and the 

neonatologist / paediatric surgeon will help better coordination of the transfer, 

stabilisation of the baby before the transfer and the timing of the transfer, and 

preparedness of the receiving hospital. 

• Inform the receiving specialist and the emergency department of the 

receiving hospital 

• Name and telephone contact of the referring doctor and hospital 

• Patient details 

• History/ physical findings/provisional diagnosis/investigations 

• Current management and status of the baby 

• Mode of transport/ Expected Times of Departure and Arrival at referral 

centre 

• Destination of the patient (e.g. A&E, NICU, Ward) 

3.5 Drugs as required 

• Antibiotics – Most sick neonates will require antibiotics 

• Analgesia/ Sedation – especially if the baby has peritonitis or is intubated 

• Inotropes 

• Vitamin K 

• Sodium bicarbonate 

3.6 Documentation 

History including antenatal and birth history/ Physical Findings/ Diagnosis 

Previous and current management 

Previous operative and histopathology notes, if any 

Input/output charts 

Investigation results/ X-rays 

Consent – informed and signed by parents especially if high risk 

and parents are not escorting 

Parents’ contact address and telephone numbers, if not escorting 

Mother’s blood – about 5-10 mls for cross match, if the mother cannot 

escort the child

3.7 Environment 

Neutral Thermal Environment – environmental temperature at which an 

infant can sustain a normal temperature with minimal metabolic activity 

and oxygen consumption. 

Optimal temperature for the neonate (axilla) – 36.5 – 37.0 C 

Prevention of heat loss 

As the mechanisms of heat loss are radiation, conduction, convection 

and evaporation, prevention of heat loss involves maintaining an optimal 

ambient temperature as well as covering the exposed surfaces. 

• Transport Incubator – would be ideal 

• Wrap the body and limbs of the baby with cotton, metal foil or plastic. 

• Do not forget a cotton-lined cap for the head. 

• Care of the exposed membranes (See section on Abdominal wall 

Defects) 

• Warm the intravenous fluids 

3.8 Equipment 

(Please see table at the end of chapter) 

Check all equipment - their completeness and function before leaving the 

hospital 

• Monitors- Cardiorespiratory monitor/ Pulse oximeter for transport would 

be ideal. However, if unavailable or if affected by vibration, perfusion, a 

praecordial stethoscope and a finger on the pulse will be adequate. 

• Syringe and/or infusion pumps with adequately charged batteries 

• Intubation and ventilation equipment and endotracheal tubes of varying 

sizes 

• Oxygen tanks – ensure adequacy for the whole journey 

• Suction apparatus and catheters and tubings 

• Anticipated medication and water for dilution and injection 

• Intravenous fluids and tubings. Pre-draw fluids/ medication into syringes if 

required during the journey 

3.9 Gastric Decompression 

An orogastric tube will be required in nearly all surgical neonates 

especially if the baby has intestinal obstruction, congenital diaphragmatic 

hernia or abdominal wall defects. The oral route is preferred as a larger 

bore tube can be inserted without compromising the nasal passages 

(neonates are obligatory nasal breathers). However, the orogastric tube 

can easily dislodge and the position needs to be checked regularly. 4 

hourly aspiration and free flow of the gastric contents is recommended.

4. Immediately Before Departure 

Check vital signs and condition of the baby 

Check and secure all tubes 

Check the completeness and function of equipment 

Recommunicate with receiving doctor about the current status and the expected time of 

arrival 

5. Intra-transport Care 

• Staff –Ideally, there should be a specialised neonatal transport team. If not, the 

medical escort should be a neonatal trained doctor with/without a neonatal 

trained staff nurse. A minimum of 2 escorts will be required for the 

ventilated/critically ill baby. The team should be familiar with resuscitation and 

care of a neonate. They should also be able to handle critical incidents. The team 

members should preferably not be prone to travel sickness! 

• Safety of the team must be a priority. Insurance, life jackets and survival 

equipment should be made available for the escort team and parents. 

• Monitoring – Regular monitoring of the vital signs, oxygenation and perfusion of 

the should be performed 

• Fluids – Intravenous fluids must be given to the ill child to prevent dehydration 

and acidosis during the transport. Boluses need to be given as necessary 

depending on the assessment of the perfusion and heart rate of the child. If 

catheterised, the urine output can be monitored. The orogastric tube should be 

aspirated as required. 

• Temperature Regulation – A check on the baby’s temperature should be made. 

Wet clothes should be changed if required especially in the child with abdominal 

wall defects. Disposable diapers and one way nappy liners can be very useful 

here. 

• Critical Incidents – Preoperative preparation is to minimise the critical incidents 

as these can cause loss of life and stress to the transport team. 

Edge et al (Critical Care Medicine, 1994) showed that the number of critical incidents 

that occurred during the transport by a nonspecialised team was 10 times the 

occurrence when transported by a specialised team. E.g. 

Airway – Blocked /dislodged endotracheal tube 

Oxygen Supply – exhausted 

Loss of IV Access 

Deterioration in patient’s condition 

Loss of life or injury to patient /co-worker 

6. Arrival at the Receiving Hospital 

Reassessment of the baby 

Handover to the resident team

7. Special Surgical Conditions 

7.1 Oesophageal Atresia with /without Tracheo-oesophageal fistula 

(These babies have a risk of aspiration of saliva as well as reflux of the gastric contents 

through the distal fistula) 

• Evaluation for other anomalies e.g. cardiac, pneumonia, intestinal atresias 

• Suction of the upper oesophageal pouch – A Replogle (sump suction) tube 

should be inserted and continuous low pressure done if possible. Otherwise, 

frequent intermittent (every 10-15 mins) suction of the oropharynx is done 

throughout the journey to prevent aspiration pneumonia. 

• Ventilation only if absolutely necessary if there is a tracheo-oesophageal fistula 

as it may lead to intubation of the fistula, insufflation of the GI tract, and possible 

perforation if there is a distal atresia of the bowel. 

• Warmth 

• Fluids - Maintenance fluids and resuscitation fluids as required 

• Position - Lie the baby lateral or prone to minimise aspiration of the saliva and 

reflux 

• Monitoring – Pulse oximetry and cardiorespiratory monitoring 

7.2 Congenital Diaphragmatic Hernia 

• Evaluation for associated anomalies and persistent pulmonary hypertension of 

the newborn (PPHN) 

• Ventilation - Intubation and ventilation may be required pre-transport. Ventilation 

with a mask should be avoided and low ventilatory pressures used. A 

contralateral pneumothorax or PPHN need to be considered if the child 

deteriorates. If the baby is unstable or on high ventilatory settings, the baby 

should not be transported. Frequent consultation with a Paediatric Surgeon will 

be helpful to decide when to transport the baby. If a chest tube has been 

inserted, it should not be clamped during the journey 

• Orogastric Tube –– Gastric decompression is essential here and a Size 6 or 8 Fr 

tube is inserted, aspirated 4 hourly aspiration and placed on free drainage. 

• Fluids – Caution required as dehydration and overload can precipitate PPHN 

• Monitoring 

• Warmth 

• Consent - High risk 

• Position – lie baby lateral with the affected side down to optimise ventilation 

• Air transport considerations 

7.3 Abdominal Wall Defects 

Exomphalos and Gastroschisis are the more common abdominal wall defects. 

Fluid loss and hypothermia are important considerations in these babies. 

Gastroschisis - defect in the anterior abdominal wall about 2-3 cm diameter to the 

right of the umbilicus with loops of small and large bowel prolapsing freely 

without a covering membrane. 

Exomphalos -Defect of anterior abdominal wall of variable size (diameter of 

base) It has a membranous covering (amnion, Wharton’s jelly, peritoneum) and 

the umbilical cord is usually attached to the apex of the defect. The content of the

large defect is usually liver and bowel but in the small defect the content is just 

bowel loops. 

• Evaluation – for associated syndromes and cardiac anomalies (more 

commonly in babies with exomphalos. 

• Fluids – Intravenous fluids are essential as the losses are tremendous 

especially from the exposed bowel. Boluses (10-20 mls/kg) of normal saline/ 

Hartmann’s solution must be given frequently to keep up with the ongoing 

losses. A maintenance drip of ½ Saline + 10% D/W at 60 – 90 mls/kg (Day 1 

of life) should also be given. Hypoglycemia can occur in about 50% of babies 

with Beckwith-Wiedermann’s Syndrome (exomphalos, macroglossia, 

gigantism). 

• Orogastric tube – Gastric decompression is essential here and a Size 6 or 8 

Fr tube is inserted, aspirated 4 hourly and placed on free drainage. 

• Warmth – Particular attention must be paid to temperature control because of 

the increased exposed surface area and the fluid exudation causing 

evaporation and the baby to be wet and cold. Wrapping the baby’s limbs with 

cotton and plastic will help. 

• Care of the exposed membranes – The bowel/membranes should be 

wrapped with a clean plastic film (Clingwrap/Gladwrap) without 

compressing, twisting and kinking the bowel. Please do not use a “warm, 

saline soaked gauze” directly on the bowel as the gauze will get cold and 

stick to the bowel/membranes. Disposable diapers or cloth nappies changed 

frequently will help the keep the child dry. The baby may need to be 

catheterised to monitor urine output. 

• Position – The baby should be placed in a lateral position to prevent tension 

and kinking of the bowel. 

7.4 Intestinal Obstruction 

May be functional e.g. Hirschsprung’s disease or mechanical e.g. atresias, volvulus. 

Fluid loss with dehydration and diaphragm splinting needs to be assessed for. 

• Evaluation – for associated syndromes and cardiac anomalies. 

• Fluids – Intravenous fluids here are essential, too. 

Boluses - 10-20 mls/kg Hartmann’s solution/normal saline to correct 

dehydration and replace the measured orogastric losses. 

Maintenance - ½ Saline + 10% D/W. 

• Orogastric tube – Gastric decompression is essential here and a Size 6 or 8 Fr 

tube is inserted, aspirated 4 hourly and placed on free drainage. 

• Warmth 

• Monitoring – vital signs and urine output 

• Air transport considerations 

7.5 Necrotising Enterocolitis 

• Evaluation – These babies are usually premature and septic with severe 

metabolic acidosis, coagulopathy and thrombocytopenia. There may be an 

associated perforation of the bowel or gangrenous bowel, initiating the referral to 

the surgeon.

• Ventilation – Most of the babies may require intubation and ventilation before 

setting out especially if are acidotic. 

• Fluids – Aggressive correction of the dehydration, acidosis and coagulopathy 

should be done before transporting the baby 

• Orogastric tube – Essential 

• Drugs – Will require antibiotics and possibly inotropic support that needs to be 

continued during the journey 

• Peritoneal Drain – If there is a perforation of the bowel, insertion of a peritoneal 

drain with/without lavage with normal saline or dialysate solution should be 

considered. This can help to improve the ventilation as well as the acidosis. 

8. Intrahospital Transport 

Supine abdominal X-ray showing free 

intraperitoneal gas – loss of liver 

shadow, falciform ligament seen and 

Wrigler’s sign 

Loss of Liver shadow 

Falciform ligament seen 

Wrigler’s sign 

• Use transport incubator if available 

• Ensure all parties concerned are ready before transfer 

• Send team member ahead to commandeer lifts, clear corridors 

• Ensure patient is stable before transport 

• Skilled medical and nursing staff should accompany patient 

• Ensure adequate supply of oxygen 

• Prepare essential equipment and monitors for transport 

• Ensure venous lines are patent, well secured 

• Infusion pumps should have charged batteries. To decrease bulk of equipment, 

infusions like insulin, relaxants maybe ceased temporarily

Pre-departure checklist 

Equipment Medication 

• transport incubator ( if available ) 

• airway and intubation equipment are all available and working 

( ET tubes of appropriate size, laryngoscope, Magill forceps, 

• batteries with spares 

• manual resuscitation (Ambu) bags and masks of appropriate 

size are available and functions properly 

• suction device functions properly 

• oxygen cylinders are full 

• a spare oxygen cylinder is available 

• oxygen tubing 

• infusion pumps are functioning properly 

• intravenous cannulae of various sizes 

• needles of different sizes 

• syringes and tubings 

• suture material 

• adhesive tape, scissors 

• gloves, gauze, swabs (alcohol and dry) 

• stethoscope, thermometer 

• nasogastric tube 

• pulse oximeter ( if available ) functions properly, set alarm 

limits 

• cardiac monitor if indicated 

• chest clamps ( if an underwater chest drain is present ) 

Patient status Document 

• airway is secured and patent ( must do post intubation chest 

X-ray before departure to make sure ET tube is at correct 

position ) 

• venous access is adequate and patent ( at least 2 iv lines ) 

• iv drip is running well 

• patient is safely secured in transport incubator or trolley 

• vital signs are charted 

• all drains ( if present ) are functioning and secured 

• Intravenous fluids 

- normal saline 

- Hartmann’s solution 

- 5% albumin 

- 1/5 D/S 

- dextrose 10% 

• Inotropes 

- dopamine 

- dobutamine 

- adrenaline 

• Sedative 

- morphine 

- midazolam 

• Blood product if indicated 

• Others 

- Atropine 

- Sodium bicarbonate 

- sterile water for injection 

- normal saline for injection 

• Patient notes / referral letter 

• X-rays 

• Consent form 

• Vital signs chart 

• Input/Output charts 

• Maternal blood (for infant) 

References 

1) Hatch D, Sumner E and Hellmann J: The Surgical Neonate: Anaesthesia and Intensive Care, Edward 

Arnold, 1995 

2) McCloskey K, Orr R: Pediatric Transport Medicine, Mosby 1995 

3) Ferrara A: Evaluation of efficacy of regional perinatal programs Seminar Perinatol. 1: 303-308, 1977 

4) Chance GW, O’ Brien MJ, Swyer PR: Transportation of sick neonates 1972: An unsatisfactory aspect 

of medical care. Can Med Assoc J 109:847-852, 1973 

5) Chance GW, Matthew JD, Gash J et al: Neonatal Transport: A controlled study of skilled assisstance J 

Pediatrics 93: 662-666,1978 

6) Vilela PC, et al: Risk Factors for Adverse Outcome of Newborns with Gastroschisis in a Brazilian 

hospital. J Pediatr Surg 36: 559-564, 2001 

7) Pierro A: Metabolism and Nutritional Support in the Surgical neonate. J Pediatr Surg 37: 811-822, 2002 

8) Lupton BA, Pendray MR: Regionalized neonatal emergency transport. Seminars in Neonatology 9:125- 

133, 2004 

9) Insoft RM: Essentials of neonatal transport 

10) South Carolina Guidelines for air and ground transport 

11) Holbrook PR: Textbook of Paediatric Critical Care, Saunders, 1993

Neonatal Resuscitation 

High Risk Deliveries 

A person trained in neonatal resuscitation is usually called to be present for the following 

deliveries: 

1. Antepartum factors 

• Maternal diabetes 

• Pregnancy induced hypertension 

• Chronic hypertension 

• Anaemia or Rhesus isoimmunisation 

• Previous fetal or neonatal death 

• Bleeding in second or third trimester 

• Maternal infection 

• Maternal cardiac, renal, pulmonary, 

thyroid or neurological disease 

• Oligo/polyhydramnios 

• Prolonged rupture of membranes 

• Premature rupture of membranes 

2. Foetal factors 

• Emergency Caesarean section 

• Breech or other abnormal presentation 

• Premature labour 

• Precipitous labour 

• PROM > 18 hrs. before delivery 

• Prolonged labour (>24 hours) 

• Prolonged second stage of labour (>2 

hours) 

• Fetal bradycardia 

Apgar Score 

Apgar score 

Colour 

(Appearance) 

0 1 2 

Blue or 

Pale 

Pink centrally. 

Blue 

extremities 

Completely 

Pink 

Heart Rate Absent < 100/min > 100/min 

Response to nasal No Grimace Cough or 

stimuli (Grimace) 

sneeze 

Tone (Activity) Limp Some flexion Active 

movement 

Breathing 

Absent Slow, 

Vigorous 

(Respiration) 

irregular Cry cry 

• Post-term gestation 

• Multiple pregnancy 

• Size-dates discrepancy 

• Drug therapy 

• Maternal substance abuse 

• Fetal Malformation 

• Diminished fetal activity 

• No prenatal care 

• Maternal age < 16 or > 35 years 

• Non-reassuring FHR patterns 

• Use of general anaesthesia 

• Uterine tetany 

• Narcotics to mum within 4 hours of 

delivery 

• Meconium-stained liquor 

• Prolapsed cord 

• Abruptio placentae 

• Placenta praevia 

While the Apgar score at birth may not be useful for decision-making at the 

beginning of resuscitation, it is helpful for assessing the infant’s condition and 

identifying the infant with a problem. Subsequent Apgar scores help in the 

assessment of the effectiveness of the resuscitative effort.

5 minutes Apgar score is useful to indicate response to resuscitation and is a rough prognostic indicator. If a 

baby scores 100 mmHg) 

10. Suction catheters (F5 - F12) 

11. Stethoscope – paediatric/ neonatal 

12. Umbilical catheterization set with F3.5 and F5 catheters. 

13. Endotracheal tubes, size 2.5, 3.0, 3.5, 4.0 mm internal diameter 

14. Meconium aspirators 

15. Sterile syringes and needles: 1, 2, 5, 10 mls, G21, G23, G25, G19 

16. Drugs: 

• Volume Expanders (Normal Saline or Ringer’s lactate) 

• Adrenaline 1:10000 ( dilute with distilled water 1ml of 1:1000 

adrenaline to 10 ml) 

• NaHCO3 4.2% ( dilute 8.4% NaHCO3 with equal volume of distilled 

water) 

• Naloxone (0.4mg/ml preparation) 

17. Prewarmed dry towels ( put under radiant warmer) 

18. Sterile umbilical catheterisation tray 

Before each resuscitation, ensure the following (which would depend on the 

estimated size or gestation of the baby): 

• Heater is switched on, 

• Warm towels have been prepared. 

• Oxygen tank is full or nearly full. 

• Suction apparatus is working. 

• Proper sized masks, ETT tubes, suction catheters are prepared 

• Correct sized laryngoscope blade is chosen and the laryngoscope is working. 

• Check that the resuscitation bag-valve mask device is functioning properly 

including the pop-off valve.

• Drugs are available (and prepared if history suggestive of need). (See the 

preparations used in section of drugs) 

RESUSCITATION 

1. Place infant on preheated radiant warmer 

2. If thick or particulate meconium is in the amniotic fluid, perform a tracheal suctioning. 

(See notes on Meconium stained liquor). 

3. Position the infant with neck slightly extended and suction the mouth first and then 

the nose. Suction should be gentle, brief and not too deep (may cause reflex 

bradycardia). 

4. Dry amniotic fluid thoroughly from the baby and remove the wet linen from contact 

with infant. 

5. Evaluate the respiration, heart rate and colour. 

6. NG tube insertion after 2 minutes of Bag-valve-mask PPV. 

7. Indications for Endotracheal Intubation: 

When prolonged PPV is required. 

When bag-and mask ventilation is ineffective 

When tracheal suctioning is required. 

When diaphragmatic hernia is suspected. 

8. It is important to minimise hypoxia during intubation. Steps to do so include: 

Providing free-flow oxygen during intubation without interfering with the 

procedure. 

Limiting intubation attempts to 20 seconds. 

Providing appropriate ventilation with bag and mask using 100% O2 before and 

between intubation attempts. 

9. Vascular Access – peripheral IV line; umbilical vein or intraosseous.

Can attempt tactile stimulation 

once only and briefly. Slap foot, 

flick heel, or rub back. 

None or gasping 

Bag-mask-valve PPV with 100 % O2 for 30 

seconds. O2 at 5 L/min. Rate of 40-60/min 

(10-15 in 15 sec). 

• Infant's neck slightly extended to 

ensure open airway. 

• Ensure gentle chest rise with bagging. 

• If no chest rise: 

• Reapply mask 

• Reposition head 

• Check for secretions, suction if 

present. 

• Ventilate with mouth slightly open 

• Increase pressure slightly 

After 30 secs of PPV with 100 % O2 

Evaluate Heart Rate 

Below 60 

• Continue 

ventilation 

• Chest 

Compressions 

Initiate medications if 

HR below 60 after 30 

secs of PPV with 

100% oxygen and 

chest compressions. 

Reevaluate every 30 secs 

1. Evaluate Respiration * 

< 100/min 

60-100 

⇒ Discontinue chest compressions 

⇒ Continue ventilation 

Pink or peripheral 

cyanosis 

Spontaneous 

2. Evaluate Heart Rate 

(Count for 6 seconds,X10) 

Observe and 

monitor 

> 100/min 

3. Evaluate Colour 

Blue 

Provide free flow 

O2 by using 

oxygen tubing 

and cupped hand 

method with flow 

rate of at least 5 

L/min until pink. 

Withdraw slowly. 

Above 100 

• Watch for spontaneous 

respiration (and do 

appropriate bagging if nil) 

• Once spontaneous 

respiration is established 

discontinue ventilation. 

Notes on Chest Compressions: 

• Provide firm surface or support for the back. 

• Locate compression area. It is at the lower third of the sternum 

just below an imaginary line drawn between the nipples. 

• Compress sternum at a rate of 3 compressions and 1 

ventilation per 2 secs, giving 90 compressions and 30 

ventilations in 1 minute. 

• Compression depth is 1/3 of AP diameter. 

• After 30 seconds, stop compressions and check HR for 6 

seconds X10 

• Complications can occur if technique of chest compressions is 

poor e.g. broken ribs, lacerated liver and pneumothorax.

Meconium stained liquor: 

Meconium in amniotic fluid 

Suction the mouth, pharynx and nose at delivery of 

the head (before delivery of shoulders) using a 10F 

or larger suction catheter. 

Tracheal suctioning can be done by 

Infant vigorous? 

- Good respiration 

- HR > 100/min 

- Good muscle tone 

NO 

As soon as the infant is on radiant warmer and 

before drying: 

• Residual meconium in the hypopharynx 

should be removed by suctioning under direct 

vision. 

• The trachea must be intubated and meconium 

suctioned from the lower airway and repeated 

until clear. 

Resuscitate as 

needed 

a) Applying suction (100 mmHg) directly to the ET tube with a meconium 

aspirator adapter. Continuous suction is applied to the tube as it is 

withdrawn. Reintubation followed by suctioning should be repeated until 

returns are nearly free of meconium. DO NOT attempt to suction thick 

meconium with a suction catheter through an ET tube (catheter size too 

small). 

b) Alternatively use a large bore suction catheter (at least 12F) with an end 

hole and side hole inserted directly into the trachea. The catheter is rotated 

and continuous suction applied as it is being withdrawn. This is the 

recommended method in places with no meconium aspirator adapter. 

Continuous suction should not be applied for longer than 3 – 5 seconds. 

If baby is severely depressed with heart rate < 60/min., positive pressure 

ventilation may be needed even if some meconium remains in the airway. 

After tracheal suctioning, the stomach should be suctioned to prevent aspiration of 

meconium containing gastric contents. This should be done when the child is fully 

resuscitated and vital signs are stable. 

YES

Medications used in Neonatal Resuscitation: 

Type Indications Concentration 

to Administer 

Adrenaline 1) HR < 60/min 

despite a 

1:10 000 

minimum of 30 (The only 

seconds of preparation 

adequate available is 

ventilation with 1:1000. Dilute 

100 % O2 and 1ml of 

chest 

Adrenaline 

compressions. 1:1000 with 

2) Heart rate is distilled water 

zero. 

to 10ml) 

Volume 

Expanders 

Sodium 

Bicarb. 

Naloxone 

HCl 

1) Prolonged arrest 

not responding to 

resuscitation 

2)Evidence or 

suspicion of acute 

blood loss with signs 

of hypovolaemia 

1)Severe metabolic 

acidosis is 

suspected or 

proven by blood 

analysis; 

2)Prolonged arrest 

not responding to 

resuscitation 

Severe respiratory 

depression and a 

history of maternal 

narcotics 

administered within 

the past 4 hours. 

Normal Saline 

Ringer's lactate 

0.5 mEq/ml 

(4.2% solution) 

0.4 mg/ml 

(dilution that is 

usually 

available) 

1.0 mg/ml 

Prepara- Dosage/ 

tion Route 

1 ml 0.01-0.03 

mg/kg. 0.1- 

0.3 ml/kg. IV 

or ET 

40 ml 10 ml/kg 

IV 

20 ml or 

two 10mlprefilled 

syringes 

1 ml 

2 mEg/Kg 

IV only. 

(4 ml/kg) 

0.1 mg/kg 

(0.25 ml/kg) 

IV ET IM SC 

0.1 mg/kg 

(0.1 ml/kg) 

IV ET IM SC 

Rate/ 

Precautions 

Give rapidly. 

May dilute with 

normal saline to 

1-2 ml if giving 

via ET. 

Give over 5 – 10 

minutes. 

Give by syringe 

or IV drip. 

Give slowly, 

over at least 2 

minutes. 

Give only if 

infant is being 

effectively 

ventilated. 

Give rapidly. 

IV, ET 

preferred. IM, 

SC acceptable.

Summary: Use of medications during neonatal resuscitation: 

Prolonged arrest that does 

not respond to other 

therapy? 

Give sodium bicarbonate 

Post Resuscitation Care 

CXR 

ABG 

Correct metabolic acidosis 

BP monitoring 

Volume replacement if BP low 

Correct Hypocalcaemia & Hypoglycaemia 

Treat seizures 

Document the resuscitation. 

Begin: 

• HR zero OR 

• HR < 60/min after 30 secs. PPV and 

chest compressions. 

Give adrenaline 

HR above 

100? 

No 

Evidence of continuing depression? 

Yes 

Evidence or suspicion of acute 

blood loss with signs of 

hypovolaemia 

Give volume expander 

Yes 

1. Consider other causes, e.g. 

Pneumothorax 

Diaphragmatic hernia 

Persistent pulmonary hypertension (PPHN) 

2. Consider starting dopamine 

3. Obtain consultation. 

Severe respiratory depression and a history 

of maternal narcotics administered within the 

past 4 hours 

May be 

repeated every 

3-5 minutes if 

required 

Discontinue 

medications 

May be 

repeated if 

signs of 

hypovolaemia 

persist 

Give Naloxone hydrochloride.

Special Circumstances in Resuscitation of the Newly Born Infant 

Condition History/Clinical Signs Actions 

Meconium or mucus 

blockage 

Mechanical blockage of the airway 

Meconium-stained amniotic 

fluid. 

Poor chest wall movement. 

Choanal Atresia Pink when crying, cyanotic 

when quiet 

Pharyngeal airway 

Persistent retractions, poor 

malformation 

air entry 

Impaired lung function 

Pneumothorax Asymmetrical breath 

sounds. 

Persistent cyanosis / 

bradycardia 

Pleural effusion / ascites Diminished air movement. 


bradycardia 

Congenital diaphragmatic 

hernia 

Asymmetrical breath 

sounds. 

Persistent 

cyanosis/bradycardia. 

Scaphoid abdomen 

Pneumonia/sepsis Diminished air movement. 


bradycardia 

Impaired cardiac function 

Congenital heart disease Persistent cyanosis / 

Foetal / maternal 

haemorrhage 

bradycardia 

Pallor; poor response to 

resuscitation 

Intubation for suctioning / 

ventilation 

Oral airway. 

Endotracheal intubation 

Prone positioning, posterior 

nasopharyngeal tube 

Needle thoracentesis 

Immediate intubation. 

Needle thoracentesis, 

paracenteris. 

Possible volume expansion. 

Endotracheal intubation. 

Placement of orogastric 

catheter 

Endotracheal intubation. 

Possible volume expansion 

Diagnostic evaluation 

Volume expansion, possibly 

including red blood cells. 

Reference: 

1. Textbook of Neonatal Resuscitation from the American Academy of Paediatrics and AHA 2000. 

2. International Guideline for Neonatal Resuscitation Consensus (PEDIATRICS Vol. 106 No. 3 

September 2000).

Definition 

Premature infant: < 37 weeks gestation 

THE PREMATURE INFANT 

Low Birth Weight (LBW): < 2500 g 

Very Low Birth Weight (VLBW): < 1500 g 

Extremely Low Birth Weight (ELBW): < 1000 g 

Small for Gestational Age: < 10th centile of Birth Weight for age. 

Complications in premature infants 

a) Perinatal Asphyxia 

b) Hypothermia 

c) Respiratory (RDS and apnoea) 

d) CVS (Hypotension, PDA) 

e) Neurological: Intraventricular haemorrhage and Periventricular leukomalacia 

f) Gastrointestinal (Paralytic ileus, NEC) 

g) Hypoglycaemia and hyperglycaemia 

h) Neonatal Jaundice 

i) Hypoprothrombinaemia 

j) Fluid and Electrolyte imbalance (hyponatraemia, hyperkalemia, metabolic acidosis) 

k) Anaemia 

l) Neonatal Sepsis 

m) Rickets 

n) Oxygen therapy: ROP, CLD 

o) Neuro-developmental disabilities 

p) Psychosocial problems 

Management 

A. Before and During Labour 

Prewarmed incubator and appropriate equipment for neonatal intensive care 

should always be kept ready in NNU. 

B. Adequate Resuscitation 

C. Transfer from Labour Room (LR) to NNU (Neonatal Unit) 

a) Use prewarmed transport incubator if available. If not the baby must be wiped dry 

and wrapped in dry linen before transfer. 

b) If the infant's respiration is inadequate, keep the infant INTUBATED and 

AMBUBAGGED with oxygen during the transfer. 

D. Admission Routine 

- Ensure thermoneutral temperature for infant. An incubator or radiant warmer is 

necessary for more premature and ill babies. 

- Ventilation is often necessary if ventilated during transfer. 

- If oxygen saturation is < 90%, oxygen therapy should be given. 

- Head circumference (OFC), length measurements and bathing can be omitted. 

- Quickly and accurately examine and weigh the infant.

- Assess the gestational age with Dubowitz or Ballard score when stable (see end 

of chapter for score). 

- Monitor temp, HR, RR, BP and SaO2. 

E. Immediate Care for Symptomatic babies 

Investigations are necessary as indicated and include: 

Blood gases. 

Blood glucose (dextrostix). 

Full blood count with differential WBC and IT ratio (if possible) 

Blood culture. 

CXR (if respiratory signs and symptoms are present) 

a) Start on 10% dextrose drip. 

b) Correct anaemia. 

c) Correct hypotension (keep MAP > gestational age in weeks) 

Correct Hypovolaemia: Give 10 ml/kg over 20-30 minutes 

i) Normal saline 

ii) Albumin 5% (If a 25% solution, use 2 - 4 ml/kg diluted to 20 ml/kg 

with 0.9 % NaCl.) 

iii) Fresh blood if anaemic. 

d) Start inotrope infusion if hypotension persists after volume correction. 

e) Start antibiotics after taking cultures e.g. Penicillin and Gentamycin 

f) Start iv aminophylline in premature babies < 34 weeks if not mechanically 

ventilated 

g) Maintain SaO2 at 90-95% and PaO2 at 50 –80 mmHg 

F. General Measures for all Premature infant and SGA 

1. Monitor vitals signs (i.e. colour, temperature, apex beat and respiratory rate) for all 

babies. Observe for signs of respiratory distress (i.e. cyanosis, grunting, 

tachypnoea, nasal flaring, chest recession and apnoea). In VLBW and ill babies 

pulse oximetry and blood pressure monitoring are necessary. 

2. Check Dextrostix (see Hypoglycaemia protocol for schedule). 

3. Keep warm (Asymptomatic premature babies can be dressed up even while still in 

incubator) 

4. Feeding (See Chapter 8 and 9) 

5. Provide parental counselling and allow free parental access. 

6. Infection control : observe strict hand washing practices 

7. Immunisation: 

a. Hep B vaccine is given at birth if infant is stable and BW is >1.8 kg. 

Otherwise give when weight reaches 1.8 kg or just before discharge. 

b. BCG on discharge if infant has reached at least 1.8 kg and term gestation. 

Otherwise ensure that BCG is given at a later date. 

c. For long stayers other immunisation should generally follow the schedule 

according to chronological rather than corrected age. 

In the presence of acute illnesses immunisation is usually deferred.

8. Supplements: 

a. At birth : Vitamin K IM (0.5 mg for BW= 2.5 kg) 

b. Starting on Day 8 of life if enteral feed volume is more than 2mls/hr , and 

infant is not on parenteral nutrition with added vitamins: 

Multivitamin 0.5 mls OD ( to be continued for till fully established weaning 

diet) 

Folic acid 0.1 mg OD. 

c. Starting on Day 30 of life: 

Elemental Iron 2-3 mg/kg/day – to be continued for 3-4 months 

(Dose of ferrous fumerate needed 3 x 2 mg/kg/day.) 

G. ICU care and Criteria for Replacement Transfusion in Neonates 

See relevant chapter. 

H. Discharge 

Cranial Ultrasound for premature babies ≤ 30 weeks recommended at: 

a. within 72 hours 

b. around day 7 to look for IVH 

c. around day 28 to look for PVL 

d. as clinically indicated 

ROP screening at 34 - 36 weeks’ gestation or at 4-6 weeks of age is recommended for 

a. all babies < 32 weeks gestation at birth or birth weight

SCORE 

Neuromuscular: 

Physical: 

TOTAL: 

BALLARD MATURATIONAL ASSESSMENT OF GESTATIONAL AGE 

SCORE 

-1 0 1 2 3 4 5 

Score 

Neuromuscular Maturity Sign 

Posture 

MATURITY 

RATING 

Score Weeks 

Square Window 

(Wrist) 

Arm Recoil 

-10 20 

Popliteal Angle 

-5 22 

0 24 

Scarf Sign 

5 26 

Heel To Ear 

10 28 

TOTAL NEUROMUSCULAR MATURITY SCORE 

15 30 

Score 

20 32 

25 34 

30 36 

35 38 

40 40 

45 42 

50 44 

Physical Maturity Sign 

Skin sticky, friable, gelatinous, red, smooth pink, superficial cracking, pale parchment, deep leathery, 

transparent translucent visible veins peeling &/or areas, rare veins cracking, no cracked, 

rash, few veins 

vessels 

wrinkled 

Lanugo none sparse abundant thinning bald areas mostly bald 

Plantar Surface heel-toe >50 mm faint red marks anterior creases ant. 2/3 creases over entire 

40-50 mm: -1 no crease 

transverse 

sole 

Enteral Feeding in Neonates 

1. Introduction 

• The goal of nutrition is to achieve as near to normal weight gain and growth as 

possible. 

• Enteral feeding should be introduced as soon as possible. This means starting in 

the labor room itself for the well infant. 

• 

Breast milk is the milk of choice. All mothers should be encourage to give breast 

milk to their newborn babies. 

• The calorie requirement : Term infants 110 kcal/kg/day 

Preterm infants 120 – 140 kcal/kg/day. 

2. Type of milk for newborn feeding 

There are three choices: 

• Expressed breast milk 

• Normal infant formula 

• Preterm infant formula 

2.1 Breast Milk 

Breast milk is preferred as studies have shown that babies on breast milk had 

low risk for NEC and have better development quotient. 1 

However EBM might not be adequate for the nutritional needs of the very 

preterm infant as it:. 

• 

does not have enough calories to ensure optimal early growth at 20 

kcal/30mls. 1 

• does not have enough sodium to compensate for the high renal sodium 

losses of the preterm infant. 

• does not have enough calcium or phosphate which will predispose to 

osteopenia of prematurity. 2 

• deficient in vitamins and iron relative to the needs of a preterm infant. 

Human Milk Fortifier (HMF) 

• It is recommended to add HMF to EBM in babies < than 32 weeks or 

< 1500 grams. 

• HMF will give extra calories, vitamins, calcium and phosphate. 

• HMF should be added to EBM only when the baby is on feeding at > 

140 mls/kg/day. 

• 1 sachet (25g) added to 100 mls of EBM increases its strength to 81 

cal/100mls. 

2.2 Infant Formula 

Infant formula should only be given if there is no supply of EBM. There are 2 

types of infant formula: Preterm formula and Normal Term Formula. 

• Preterm formula : for babies born < 32 weeks or < 1500 grams. 

• Normal infant formula : for babies born > 31 weeks or > 1500 grams.

Composition of various milks 

Cow’s Standard Preterm Mature 

milk formula formula breastmilk 

Carbohydrate 

(g/100ml) 

4.6 7.5 8.6 7.4 

Fat 

(g/100ml) 

3.9 3.6 4.4 4.2 

Protein 

(g/100ml) 

3.4 1.5 2.0 1.1 

Casein/ 

4:1 2:3 2:3 2:3 

lactalbumin ratio 

Calories /100ml 67 67 80 70 

Na+ (mmol/L) 23 16 33 15 

K+ (mmol/L) 40 65 33 64 

Ca++ (mg%) 124 46 77 35 

PO4 (mg %) 98 33 41 15 

Fe++ (mg%) 0.05 0.8 0.67 0.08 

3. Strategies of administering enteral feeding 

3.1. Orogastric Route : Because neonates are obligate nose breathers 

nasogastric tube can obstruct the nasal passage and compromise the baby’s 

breathing. Thus orogastric route should be use for babies on tube feeding.. 

3.2. Continuous vs. intermittent bolus feeding: Studies have shown that bolus 

fed babies tolerated their feeds better and gain weight faster. 3 Babies on 

continuous feeding have been shown to take longer time to reach full feeding but 

there is no difference in days of discharge, somatic growth and incidence of 

NEC. 4 

3.3. Cup feeding : if baby is able to suckle and mother is not with the baby, cup 

feeding is preferable to bottle feeding to prevent nipple confusion (if breast 

feeding is intended as the final mode of feeding). 

4. When to start milk? 

As soon as possible for the well term babies 

However in the very preterm infant there is a concern of increase risk of NEC if feeding 

is started too early. Studies have suggested that rapid increment in feeding has a higher 

risk for NEC than the time at which feeding was started. 5 

In the very preterm infant MINIMAL ENTERAL FEEDING (MEN) has been 

recommended. The principle behind this is to commence very low volume enteral feeds 

on day 1 to 3 of life (i.e. at 5 to 25 mls/kg/day ) for both EBM and formula milk. MEN 

enhances DNA gut synthesis hence promotes gastrointestinal growth. This approach 

allows earlier establishment of full enteral feeds and shorter hospital stays, without any 

concomitant increase in NEC. 6

32 weeks Well babies Start milk immediately 

29 – 32 weeks Well babies IVD + slow increase enteral feed from 

day 1 

< 29 weeks Use MEN approach. Start feed on day 

2 or 3 at 1 mls 3 hourly with EBM 

> 28 weeks Sick babies Feed when clinically appropriate with 

EBM 

5. How much to increase? 

• Generally rate of increment of enteral feeding is about 20 to 30 mls/kg/day. 

• Well term babies should be given breast feed on demand. 

Milk requirements for babies on full enteral feed from birth: 

Day 1 60 mls/kg/day 

Day 2 – 3 90 mls/kg/day 

Day 4 – 6 120 mls/kg/day 

Day 7 onwards 150 mls/kg/day 

Add 15% if the babies is under phototherapy 

• In babies requiring IV fluids at birth: The rate of increment need to be 

individualized to that baby. Babies should be observed for feeding intolerance 

(vomit/large aspirate) and observe for any abdominal distention before 

increasing the feed. 

6. What is the maximum volume? 

• The target weight gain should be around 15g/kg/day (range 10-25g/kg/day). 

Less than this suggests calories need increasing. More than this should raise 

the possibility of fluid overload particularly in babies with chronic lung disease. 

Preterm infants • Increase feed accordingly to 180 to 200 mls/kg/day. 

• If on EBM, when at 150 mls/kg/day add HMF 

Term infant 

• Allow demand feeding 

o Study by Kuschel et al, a randomised trial in babies born before 30 

weeks comparing remaining at a final feed volume of 150 ml/kg/day (120 

cal/kg/day) to advancing to 200 mls/kg/day. About half the 200 group had 

to be cut back (to a mean of 180 mls/kg/day) due to feed intolerance or 

fluid overload. 7 

o Infants that require high calories due to increase energy expenditure e.g. 

chronic lung disease, should consider adding polycose and MCT.

7. When to stop HMF or Preterm Formula? 

Consider changing preterm to standard formula and stopping adding HMF to 

EBM when babies reach 1800 grams in weight. 

8. Vitamin and mineral supplementation. 

Vitamins: A premature infant’s daily breast milk/ breast milk substitute intake will 

not supply the daily vitamin requirement. Multivitamin can be commence after 

day 7 of life. Vitamin supplements at 0.5 mls daily to be continued for 3-4 months 

post discharge. 

Iron: Premature infants have been deprived of the intra uterine accumulation of 

iron and can become rapidly depleted of iron when active erythropoiesis 

resumes. Therefore babies born with a birth weight < 2000g should receive iron 

supplements. Iron is given at a dose of 3 mg/kg elemental iron per day. Ferric 

Ammonium Citrate (400mg/5mls) contains 86 mg/5 mls of elemental iron. Start 

on day 42. Continue until baby is 3-4 months post discharge or until review by 

doctor . 

Special Cases 

1. IUGR babies with reversed end-diastolic flows on antenatal Doppler: Studies 

have shown that these babies are at risk of NEC. Thus feeds should be introduced 

8, 9 

slowly and initially use only EBM. 

2. Pregestamil : contain glucose, MCT and protein as casein hydrolysate. Used in 

malabsorptive state in infants e.g. Post surgery, biliary obstruction and disaccharide 

deficiency 

References 

1. Lucas A, Gore SM, Cole TJ et al. Multicentre trial on feeding low birthweight infants: effects of diet 

on early growth. Arch Dis Child 1984; 59: 722-730. 

2. Lyon AJ. McIntosh N. Calcium and phosphorus balance in extremely low birthweight infants in the 

first six weeks of life. Arch Dis Child 1984; 59: 1145-50 

3. Schandler RJ, Shulman RJ, LauC, Smith EO, Heitkemper MM. Feeding strategies for premature 

infants: randomized trial of gastrointestinal priming and tube feeding method. Pediatrics 1999; 103: 

492-493. 

4. Premji S. & Chessel L. Continuous nasogastric milk feeding versus intermittent bolus milk feeding 

for premature infants less than 1500 grams. Cochrane Database of Systematic Reviews. Issue 1, 

2002 

5. Anderson DM, Kliegman RM. The relationship of neonatal alimentation practices to the occurrence 

of endemic necrotizing enterocolitis. Am J Perinatol 1991; 8: 62-7. 

6. Tyson JE, Kennedy KA. Minimal enteral nutrition to promote feeding tolerance and prevent 

morbidity in parenterally fed neonates (Cochrane Review). In: The Cochrane Library, Issue 1, 1999. 

Oxford: Update Software. 

7. Kuschel C, Evans N, Askie L, Bredermeyer S, Nash J, Polverino J. A Randomised trial of enteral 

feeding volumes in infants born before 30 weeks. Arch Dis Child 

8. McDonnell M, Serra-Serra V, Gaffney G, Redman CW, Hope PL. Neonatal outcome after 

pregnancy complicated by abnormal velocity waveforms in the umbilical artery. Arch Dis Child 

1994; 70: F84-9. 

9. Malcolm G, Ellwood D, Devonald K, Beilby R, Henderson-Smart D. Absent or reversed end 

diastolic flow velocity in the umbilical artery and necrotising enterocolitis. Arch Dis Child 1991; 66: 

805-7.

Total Parenteral Nutrition for Neonates 

1. Introduction 

Total parenteral nutrition (TPN) is the intravenous infusion of all nutrients 

necessary for metabolic requirements and growth 

The earlier introduction and more aggressive advancement of TPN was shown to 

be safe and effective, even in the smallest and most immature infants. 

Premature infants tolerate TPN from day 1 of post-natal life. 

The goal of TPN is to : 

provide sufficient nutrients to prevent negative energy and nitrogen balance and 

essential fatty acid deficiency 

support normal rates growth without increased significant morbidity. 

Indication for TPN: 

gastrointestinal tract abnormalities(omphalocele, gastroschisis, Tracheoesophageal 

fistula, malrotation with volvulus, etc). 

necrotizing enterocolitis (NEC), 

respiratory distress syndrome / BPD patients who are unable to tolerate feedings 

extreme prematurity, 

sepsis, 

malabsorption. 

2. Components of TPN 

The essential components of parenteral nutrition are: 

fluids; 

carbohydrate; 

electrolytes; 

protein; 

lipids; 

vitamins; and 

trace minerals. 

When a baby is on parenteral nutrition, our ultimate goal is to provide at least 100-110 

cal/kg/day. This will be achieved if we can deliver (for example) 150 cc/kg/day of 12.5% 

dextrose, 2.5 g/kg/day of synthetic amino acids, and 3.0 g/kg/day of intravenous lipids. 

2.1 Fluid 

Fluid is an essential component of parenteral nutrition. 

Fluids are usually started at 80-100 ml/kg/day (if newborn), or at whatever 

stable fluid intake the baby is already receiving. 

Volumes are increased over the first 7 days in line with the fluids and 

electrolytes protocol with the aim to deliver 150 ml/kg/day by day 7. 

2.2 Amino acids 

Amino acids prevents catabolism 

Prompt introduction of amino-acids via TPN achieves an early positive nitrogen 

balance for the infant

It also decreases the frequency and severity of neonatal hyperglycaemia by 

stimulating endogenous insulin secretion and stimulating growth by enhancing 

the secretion of insulin and insulin-like growth factors. 

Protein is usually started at 1g/kg/day of crystalline amino acids and 

subsequently advanced, by 3 rd to 4 th postnatal day, to 3.0 g/kg/day of protein in 

term and 3.7 to 4.0 g/kg/day in the extremely low birthweight (ELBW) infants. 

Reduction in dosage may be needed in critically ill, significant hypoxaemia, 

suspected or proven infection and high dose steroids. 

Adverse effects of excess protein include a rise in urea and ammonia and high 

levels of potentially toxic amino acids such as phenylalanine. 

2.3 Glucose 

There is a relatively high energy requirement in the ELBW because of relatively 

large body proportion of metabolically active organs i.e. head, liver kidney and 

brain and a large and continuous source of glucose is required for energy 

metabolism. 

In the ELBW minimum supply rate is 6 mg/kg/min to maintain adequate energy 

for the brain and an additional 25 cal/kg or 2-3 mg/kg/min of glucose per gram of 

protein intake is necessary to support protein deposition. The maximum rate is 

12 to 13 mg/kg/min (lower if lipid is administered concurrently) but in practice 

glucose administration is often limited by development of hyperglycaemia which 

is reported in 20-80% of ELBW infants. This is attributed to peripheral and 

hepatic insulin resistance presumably due to glucagon, catecholamine and 

cortisol release and decreased insulin secretion. 

Strategies for the management of hyperglycaemia in the ELBW include 

decreasing glucose administration, administering intravenous amino acids (which 

increases insulin secretion) and infusing exogenous insulin infusion. 

Glucose administration is usually initiated at 6 mg/kg/min advancing to 10 to 12 

mg/kg/min. If hyperglycaemia develops glucose infusion is decreased and if it still 

occurs at 3 to 4 mg/kg/min insulin is started. 

2.4 Lipid 

This is the most controversial of the major intravenous substrate. It is needed to 

prevent essential fatty acid deficiency, serve as energy substrate and 

improve delivery of fat soluble vitamins. 

LBW infants may have immature mechanisms for fat metabolism. A number of 

clinical conditions inhibit lipid clearance e.g. infection, stress and malnutrition. 

Lipid is usually started at 1g/kg/day and this is gradually increased to a limit of 3 

g/kg/day (sometimes up to 3.5g/kg/day in the ELBW) 

It is infused continuously over as much of the 24 hour period as practical and 

smaller doses are used in patients with infection, compromised pulmonary 

function or hyperbilirubinaemia. 

In the presence of jaundice requiring phototherapy the higher concentrations of 

lipid (>2g/kg/day) should be avoided. 

Preparation of 20% emulsion is better than 10% as higher phospholipid value in 

10% interferes with triglyceride (TG) clearance leading to higher TG and 

cholesterol values 

Enzymes responsible for lipid clearance are lipoprotein lipase, hepatic lipase and 

lecithin cholesterol acyltransferase. Activation of enzymes can be induced with 

the administration of low-dose heparin

Clearance is usually monitored by measuring plasma triglyceride levels. Maximal 

plasma triglyceride (TG) concentration ranges from 150 mg/dl to 200 mg/dl. 

It has been suggested that exogenous lipid interferes with respiratory function. 

Suggested mechanisms include impaired gas exchange from pulmonary 

intravascular accumulation or impaired lymph drainage resulting in oedema. 

There are reports of increased pulmonary vascular resistance of a dose and time 

dependent nature which suggest lipid may aggravate pulmonary hypertension in 

susceptible individuals . 

2.5 Electrolytes 

The usual sodium need of the newborn infant is 2-3 mEq /kg/day in the term and 

4-5 mEq/kg/day in the preterm. 

Potassium needs are 2-3 mEq/kg/day in both term and preterm infants. 

2.6 Minerals, Calcium (Ca), Phosphorus (P) And Magnesium 

Presently the premature infant is by no way able to maintain the intrauterine 

accretion rate of Ca and P when parenterally fed. 

Several methods to prevent precipitation of dibasic calcium phosphate in PN 

solutions have been proposed to circumvent this but until now the optimal 

retention of calcium and phosphate remains limited to half of the intrauterine 

accretion. 

Monitoring for osteopaenia of prematurity is important especially when PN is 

given for prolonged periods. 

A normal magnesium level is a prerequisite for a normal calcaemia. In well 

balanced formulations, however, magnesium does not give rise to major 

problems. 

2.7 Trace Elements 

Is indicated if PN is administered for more than 1 week or longer. Commercial 

preparations for paediatric use are available. 

2.8 Vitamins 

Both fat and water soluble vitamins are essential. It should be added to the to fat 

infusion instead of amino-acid glucose mixture to reduce loss during 

administration 

3. Administration 

TPN should be delivered where possible through central lines. 

Peripheral lines are only suitable for TPN of less than 3 days duration and 

dextrose concentration of less than 12.5%. 

Peripheral lines is also limited by the osmolality (not more than 600 mOsm/L) of 

solutions that can be used to prevent phlebitis. 

Usually a percutaneous central line is placed with the position of the tip of the 

catheter confirmed on x-ray prior to use. 

A strict aseptic technique in preparation and administration of the TPN is 

essential. 

Ideally, breakage of the central line through which the TPN is infused should be 

avoided, though compatible drugs can be administered if necessary.

Cautions 

Hyperkalaemia. Addition of potassium is rarely required in first three days of life 

unless the serum potassium is < 4.00 mmol/l. Also use caution when prescribing 

in renal impairment. A minimal amount is inevitable in TPN because of the type 

of amino acid formulation used. 

Hypocalcaemia. May result from inadvertent use of excess phosphate. Corrects 

with reduction of phosphate. 

NEVER add bicarbonate, it will precipitate calcium carbonate out. 

NEVER add extra calcium to the burette, it will precipitate out the phosphate. 

4. Complications 

4.1. Delivery 

The line delivering the TPN may be compromised by; 

Sepsis, minimized by maintaining strict sterility of the line during and 

after insertion. 

Malposition, x-ray mandatory before infusion commences. 

Thrombophlebitis, with peripheral lines, requiring close observation of 

infusion sites. 

Extravasation into the soft tissue, with resulting tissue necrosis. 

4.2. Metabolic complications 

Hyperglycaemia 

Hyperlipidaemia 

Cholestasis 

5. Monitoring 

TPN administration requires careful clinical and laboratory monitoring 

Before starting an infant on parenteral nutrition, investigation required: 

full blood count /haematocrit, 

renal profile 

liver function test 

random blood sugar/dextrostix 

serum bilirubin 

While on TPN, monitoring required : 

5.1. Laboratory 

Full blood count, renal profile. 

Required daily for 1 week then 3 times a week 

Plasma calcium, magnesium, and phosphate. 

Twice a week until stable then weekly 

Lipid levels. 

Twice a week first week then weekly unless complication arises 

(sepsis etc) 

Long term TPN (> 2 weeks duration) requires, liver function tests. 

5.2 Clinical 

Blood sugar / dextrostix, 4-6 hrly first 3 days, twice a day once stable.

Daily weight 

Meticulous care of the catheter site and monitoring of infection. 

This protocol is adapted from : 

1 .Feeding in the Neonatal Unit 

Dato Dr.Lim Nyok Ling, Consultant Neonatologist, Hospital Selayang. 

2. Total Parenteral Nutrition for Neonates. 

Department of Neonatal Medicine Protocol Book 

Royal Prince Alfred Hospital. 

3. Total Parenteral Nutrition for Premature Infants 

Elizabeth Brine, MMSc, RD; Judith A. Ernst, DMSc, RD 

4. Neonatology on the Web 

Teaching Files: Parenteral Nutrition (PN) for Neonate 

Ray Duncan, MD, Staff Neonatologist, Cedars-Sinai Medical Center, Los Angeles, California.

ICU/NICU: Guidelines. General Pointers for Care and Review of 

Infants in NICU 

A. Checklist for Review of infant in Intensive Care 

i) Age of infant, if 72 hours : 150 ml/kg/day 

Generally a 10% dextrose is started on the 1 st day and sodium and potassium is 

added on the second day. Empirically a 

Preterm baby needs 4-5 mmol/kg/day of sodium and 2-3 mmol/kg/day of 

potassium and a 

Term infant 2-3 mmol/kg/day of both sodium and potassium 

Fluid and electrolyte therapy will be influenced by the child’s underlying illness 

and complications and adjustments will have to be made based these conditions, 

the child’s intake output, his weight, and blood urea and electrolytes.

Monitor BUSE and correct any imbalances after considering the underlying 

cause. 

Ensure the urine output is > 1 ml/kg/hr. 

vi) Infection 

Is there a possibility of infection? Is the child on antibiotics. Fungal infection 

should be considered if the infant has been given multiple courses of antibiotics, 

is very premature or on central venous catheters and parenteral nutrition 

vii) Feeding 

Parenteral nutrition should be started in VLBW infants who are unwell as soon as 

possible. Bigger babies may be started on parenteral nutrition if not able to be fed 

enterally for 3-4 days. Enteral feeds can be given via oro or nasogastric tube. 

Encourage expressed breast milk. 

viii) Temperature Control 

Ensure thermoneutral environment. Covering the open area of open hoods 

with cling wrap and increasing water content with a humidifier will help in 

temperature control and fluid regulation of the ELBW infant. 

ix) Skin care 

This is a vital component of care especially for the premature infants. 

Avoid direct plastering onto skin and excessive punctures for blood 

taking and setting up of infusion lines. Meticulous attention must be 

given to avoid extravasation of infusion fluid and medication which can is 

to lead to phlebitis, ulceration and septicaemia. 

x) CNS 

Check for fontanel tension and size, condition of sutures i.e. overriding or 

separated, OFC (when indicated e.g. in a case of subaponeurotic 

haemorrhage) 

Sensorium, tone, movement, responses to procedures e.g. suctioning of 

pharynx, and presence or absence of seizure should be assessed. 

xi) Ventilation 

Check if the ventilation adequate. Is the child maintaining the optimum blood 

gases? Can we start weaning the child off the ventilator?

Criteria for Replacement Transfusion in Neonates 

B. ETT Care 

Clinical Status of the neonate Consider transfusion of 15-20 ml/kg 

of packed cells if 

Ventilated Hb < 14 g% or vHct < 40% 

Symptomatic 

(apnoeic spells, poor weight 

gain, poor feeding, tachypnoea 

tachycardia or oxygen 

dependent) 

At 1 -2 weeks of life 

Hb < 12 g% or vHct < 36% 

At 3 - 5 weeks of life 

Hb < 10 g% or vHct < 30% 

Asymptomatic Hb < 8 g or vHct < 25% 

ETT size 3000g size 3.5-4.0 

One month - 1 year size 4 

1- 2 years size 5 

> 2 years size = Age + 4 

4 

ETT position 

a) Oral ETT the "tip-to-lip" distance 

1 kg = 7 cm 

2 kg = 8 cm 

3 kg = 9 cm 

or weight in kg + 6 

b) Nasal ETT: add 2 cm respectively. 

c) Check X-ray after intubation. 

Ensure the tip of the ETT is at T2 

d) ETT should be shortened if more than 4 cm extends from the lips 

Suction of ETT 

- Should be done on a prn basis, as it is associated with desaturation and 

bradycardia. During suction the FiO2 may need to be increased as guided 

by the SaO2 monitor during suctioning. Remember to reduce to the level 

needed to keep SaO2 89-95%.

C. UAC and UVC care 

UAC position 

Length to be inserted measured from the abdominal wall is 3 X BW(kg) + 9 

cm. This usually put the tip above the diaphragm. Confirm with X-ray to 

ensure that the tip of the UAC is above T12 or below L4. 

Wash hands before taking blood from the UAC. Ensure sterile procedure 

when handling the hub or 3 way tap of the line. 

The UAC is kept patent with a heparin infusion (1U/ml) at 1 ml/hr and can 

be attached to the intra-arterial blood pressure monitor. 

UVC position 

½ UAC +1 cm 

D. Ventilation 

a) Initial Ventilator Setting (in most situations): 

Total Flow: 8 - 10 litres/min 

Peak Inspiratory Pressure (PIP): 20-25 mmHg (lower in ELBW infants) 

Positive End Expiratory Pressure (PEEP): 4 - 5 mmHg 

Inspiration Time:0.4- 0.5 sec 

Ventilation rate:40- 60 / min 

FiO2: 60 to 70% 

The ventilator setting is then adjusted according to the clinical picture, pulse 

oximetry reading and ABG which is usually done within the 1st hour. 

Note: 

1. The inspiration time is usually kept at 1) unless ordered specifically by a 

specialist. 

3. Tailor the ventilation settings to the baby’s ABG. 

Keep: pH 7.35 - 7.45. 

PaO2 50 - 80 for premature babies 

60 - 100 for term babies 

PaCO2 40 - 60 (NB. the trend is not to ‘chase’ the PaCO2 

by increasing ventilator settings unless there is 

respiratory acidosis). 

SaO2 89 - 95%

) Changing of Ventilator settings: 

1. To produce an increase in pO2 either: - 

a) Increase FiO2 concentration. 

b) Increase PEEP. 

c) Increase PIP (increases minute volume). 

d) RARELY Increase I/E ratio (prolong inspiration) 

2. To produce a decrease in pCO2 either: - 

a) Increase Rate (increases minute volume) 

b) Decrease I/E ratio (prolong expiration) 

c) Increase PEEP in worsening lung disease. Decrease PEEP in 

recovery phase. 

3. Do the opposite to decrease paO2 or to increase paCO2. 

Minute volume = tidal volume (volume per breath) x rate per minute 

With volume-limited ventilators minute volume can be calculated (use tidal volume = 4-6 

ml/kg) 

With pressure-limited respirators - increasing peak inspiratory pressure results in increased 

minute volume. 

e) Sedation and Ventilation 

Avoid paralysing the child (e.g. with pancuronium) as far as possible. Paralysing 

has been shown to result in poorer lung function and other complications. 

Use morphine infusion or intermittent bolus as an analgesia and sedative. 

d) Complications of ventilation 

Consider the following if the child deteriorates on ventilation: 

ETT Dislodged; 

Obstructed. 

Pneumothorax 

Esophagus position 

Ventilator tubes disconnected. 

Ventilator malfunction 

Intraventricular Haemorrhage 

Worsening of the primary condition.

HIGH FREQUENCY OSCILLATORY VENTILATION 

Indications 

• When conventional ventilation fails HFOV should be considered. This is to be 

discussed with the specialist. 

Practical management 

Switching from conventional ventilation to HFOV : 

A. Initial setting 

1. Leave FiO2 at that on CMV 

2.MAP - start at 2 cm H2O above the MAP of conventional ventilation 

3.Amplitude - 50-100%; watch thorax vibration 

4.Frequency - 10Hz 

5.Tidal volume - about 2 to 2.5ml/kg 

B. Continuation of HFOV 

1. CXR after 30-60 minutes . aim at 8-9 rib level 

2. Hypoxia - increase MAP 

3. Hyperoxia - reduce FiO2 or decrease MAP 

4. Hypercapnia 

- increase amplitude 

- decrease frequency 

- increase MAP 

5. Hypocapnia 

- decrease amplitude 

- increase frequency 

- decrease MAP 

6. Overinflation 

1. reduce MAP 

2. decrease frequency 

3. discontinue HFOV 

C. Weaning 

1. Reduce FiO2 to 0.3-0.5 

2. Reduce MAP by 1 to 2 mbar per hour until 8 to 9 mbar 

3. Reduce amplitude 

4. Extubate to head box/CPAP or change to PTV/ SIMV

Guidelines for the Use of Surfactant 

Surfactant is expensive, however evidence for its effectiveness is very strong. A systemic 

review of 35 randomised controlled trials on surfactant administration over 6000 infants 

showed there was a reduction in mortality of 30-40% and there was a reduction in 

pulmonary air leak 1,2 . Therefore it is important that a guideline be made available allowing 

for optimum usage at minimal expense. 

1. All Infants who are require mechanical ventilation for respiratory distress 

syndrome (RDS), which is due to surfactant deficiency, should ideally be given 

surfactant. However because of the high cost of the drug it is often only given 

readily to these infants if they are preterm of 32 weeks and below or birth weight 

of 1.5 kg and below. More mature or larger infants should also be given surfactant 

if the RDS is severe i.e. arterial alveolar (a/A) PO2 ratio of 0.5 

Calculation for a/A PO2 ratio : PaO2 (mmHg) 

_________________________ 

(760-47)FiO2 –PaCO2 (mmHg) 

2. Timing of therapy 

First dose should be given as early as possible to all preterm infants on 

mechanical ventilation for RDS. There is no benefit in administering surfactant 

after 24 hours of age. It has been shown that infants who received surfactant 

before 2 hours of age had reduced mortality and decreased long term oxygen 

dependence and there was no benefit in using more that 2 doses 3 . 

3. Types of surfactant and dosage 

Survanta, a natural surfactant is the only available surfactant in Malaysia currently. 

Dose : 4 ml/kg per dose. Give the 1st dose as soon as possible preferably within 

first 2 hours. Repeat at 6 hours later if needed. 

Onset of action within minutes. 

4. Method of administration 

Surfactant is delivered as a bolus directly through an ETT over 15 minutes period, 

either via 

i) a catheter inserted into the ETT in 2 aliquots via a side port in the ventilator 

circuit adjacent to ETT or on the ETT adaptor without the need of removing the 

infant from ventilator or 

ii) into the side port on ETT adaptor 

Rapid installation over 5 minutes is not recommended as it results in an increase in CBFV 

(Cerebral Blood Flow Velocity) and PCO2 compared to slower 15-minute bolus 5,6 

Infant who remained connected to ventilator during surfactant installation has been shown 

to experience less oxygen desaturation compared to those who were disconnected. This 

also result in more homogenous distribution of surfactant within the lung

6. Infants must be monitored closely with a pulse oximeter and regular blood gas 

measurements. An indwelling intra-arterial line will be useful. Ventilator settings 

must be promptly wound down to reduce the risk of pneumothorax. 

7. A single dose may be sufficient if after dosing , the oxygen requirement falls 

below 30%. 

8. Cost effectiveness 

Studies on the cost-effectiveness of surfactant therapy show that in spite of the 

high cost of drug, its use reduces cost per survivor 7,8 . 

References 

1. Soll RF and McQueen MC. Respiratory distress syndrome. In: Effective Care of Newborn 

Infant. Sinclair JC, Bracken MB(eds). Oxford University Press. 1992 pp 325-355 

2. Jobe AH. Pulmonary surfactant therapy. New Eng Journal Med 1993; 328(12):861-68 

3. OSIRIS Collaborative Group. Early versus delayed administration of a synthetic surfactant: 

the judgement of OSIRIS. Lancet 1992;340: 1363-1369 

4. Broadbent R, Fok TF, Dolovich M, et al. Chest position and pulmonary deposition of 

surfactant in surfactant depleted rabbits. Arch Dis Child 1995; 72: F84-9 

5. Saliba EW, Nashashibi M. Vaillant M-C,et al. Instillation rate effects.Exosurf on cerebral 

and cardiovascular haemodynamics in preterm neonates. Arch Dis Child 1994;71: F174-8 

6. Skinner J. The effects of surfactant on haemodynamics in hyaline membrabe disease. Arch 

Dis Child 1997;76:F67-9 

7. Mugford M, Piercy J, Chalmers I. Cost implications of different approaches to prevent 

respiratory distress syndrome. Arch Dis Child 1991; 66; 757-64 

8. Mauskopf JA, Backhouse ME, Jones D, Wold DE, Mammel MC, Mullet M, Guthries R Long 

WA. Synthetic surfactant for rescue treatment of RDS in preterm infants weighing from 

700-1350g: Impact of hospital resource use and charges. J Paedtr 1995;126:94-101 

9. Clinical Practice Guidelines in Perinatology, first edition; 1998:pg 21-28.

Newborn and Acid Base Balance 

Rate of metabolism in infants is 2 times as great in relation to body mass as in adult, 

which means 2 times as much acid is normally formed which leads to a tendency toward 

acidosis. Functional development of kidneys is not complete until the end of the first 

month and hence renal regulation of acid base may not be optimum 

A. Causes of Acidosis 

1. Respiratory Acidosis 

i) Asphyxia : Damage to respiratory 

centre 

ii) Obstruction to respiratory tract e.g. 

secretions, blocked endotracheal 

tube 

iii) Respiratory conditions : 

Respiratory distress syndrome 

(RDS) 

Pneumonia 

Pulmonary oedema 

Apnoea 

2. Metabolic Acidosis 

i) Renal failure 

ii) Septicaemia 

iii) Hypoxia 

iv) Hypothermia 

v) Hypotension 

vi) Cardiac failure 

vii) Dehydration 

viii) Hyperkalaemia 

C. Effects of acidosis and alkalosis in the body 

ix) Hyperglycaemia 

x) Anaemia 

xi) Intraventricular haemorrhage 

xii) Drugs (e.g. acetazolamide which is 

a carbonic anhydrase inhibitor) 

xiii) Metabolic disorders (often 

associated with hypoglycaemia) 

B. Causes of Alkalosis 

1. Respiratory alkalosis 

i) Asphyxia –over stimulation of 

respiratory centre 

ii) Over ventilation while on mechanical 

ventilation 

2. Metabolic alkalosis 

i) Administration of sodium 

bicarbonate 

ii) Pyloric stenosis 

iii) Hypokalaemia 

iv) Use of diuretics like thiazides and 

frusemide 

1. Acidosis 

i) Depression of central nervous system (CNS) 

ii) Disorientation and coma 

iii) Increased depth and rate of respiration in metabolic acidosis and depressed 

respiration in respiratory acidosis 

iv) High PaCO2 in respiratory acidosis increases cerebral blood flow and risk of 

intraventricular haemorrhage 

2. Alkalosis 

i) Over excitability of the CNS 

ii) Decreased cerebral blood flow cerebral ischaemia convulsions 

D. Measurement of Acid Base Status 

Done by analyzing following parameters in an arterial blood gas sample:

pH , PaCO2, PaO2, HCO3 - , Bases Excess 

Normal values are: 

pH 7.34-7.45 

PaCO2 

4.7-6.0 kpa (35-45 mmHg) 

HCO3 - 

20-25 mmol/L 

PaO2 

8-10 kpa (60-75 mmHg) 

BE ± 5 mmol/L 

E. Interpretation of Blood Gases 

1. pH 7.45 alkalosis 

If PaCO2 is low respiratory alkalosis 

If HCO3 - and base excess are high metabolic alkalosis 

Acidosis and alkalosis may sometimes be compensated partially or fully by the 

opposite mechanism for example a metabolic acidosis compensated by respiratory 

alkalosis will be associated with a low bicarbonate and PaCO2 but pH will be almost 

(partially compensated) or completely (fully compensated) normal 

3. Low paCO2 hypocarbia 

High PaCO2 hypercarbia 

4. Low PaO2 Hypoxaemia 

High PaO2 Hyperoxaemia 

F. Management of Metabolic Acidosis and Alkalosis 

1. Prevention of risk factors for acidosis is important 

2. A base deficit of > 5 mmol/L (BE of > -5 mmol/l) in a very sick and premature ( 10 mmol/L usually would need correction in most infants 

4. Sodium Bicarbonate (NaHCO3) is the alkali normally used. To prevent the corrosive 

effects of hypertonic solutions, Na HCO3 must be diluted with equal parts of distilled 

sterile water (i.e. use 4.2% solution) 

5. To prevent the toxic effects from large changes in osmolality, smaller dose of 

NaHCO3 is used. Since the acid base status is in a dynamic situation the specific 

amount of bicarbonate cannot be calculated from any formula but has to be 

determined by serial blood gas studies. As a start however the amount to be given 

can be based on the following calculation. (8.4% NaHCO3 contains 1 mmol of 

bicarbonate per ml)

Dose in mmol of NaHCO3 = Base deficit (mmol/L) x Body weight (kg) x 0.4 

6. The underlying cause of acidosis must be sought and treated. For e.g. if the cause is 

hypotension the primary treatment is to correct the basic problem and alkali is the 

adjunct 

7. For metabolic alkalosis treatment is that of the underlying condition 

G. Treatment of respiratory acidosis and alkalosis 

1. A steadily rising PCO2 at any stage in the disease is an indication that ventilatory 

assistance is likely to be needed 

2. A sudden rise may be an indication of acute changes in the infant’s condition e.g. 

pneumothorax, collapsed lobes, misplaced endotracheal tube 

3. A swift rise in PaCO2 often accompanied by hypoxia following weaning is often an 

indication that the infant is not ready. 

4. A gradual rise in PaCO2 at the end of the first week in a LBW infant on ventilator may 

be an indicator of the presence of a patent ductus arteriosus 

5. In a child on ventilator, low PaCO2 means the child is likely to be overventilated, 

hence treatment is to wean down the ventilation. However in some conditions like 

persistent hypertension or cerebral oedema a slightly low PaCO2 may be necessary 

in the treatment. 

H. Examples of Arterial Blood Gas (ABG) Interpretation 

1. A 20 weeks’ gestation and 1.1 kg BW infant has RDS. He is 20 hours old and is being 

nursed on nasal CPAP. His ABG shows: 

pH 7.21 

PaCO2 6.6 kpa 

PaO2 7.5 kpa 

HCO3 - 

20 mmol/L 

BE -4 mmol/L 

Question (Q) : What does the ABG show? 

Answer (A) : Mild respiratory acidosis due to worsening RDS 

Q: What is the next appropriate mode of therapy? 

A : Mechanical ventilation 

2. Below is the ABG of a 10 hour old 28 weeks’ gestation infant 

pH 7.22 

PaCO2 7 kpa 

PaO2 10 kpa 

HCO3 - 

17 mmol/L 

BE -8 mmol/L 

Q. What does the ABG show 

A. Mixed respiratory and metabolic acidosis

Q. Name a likely diagnosis 

A. RDS 

3. The following is the ABG of a 40 day old 26 weeks’ gestation baby 

pH 7.38 

PaCO2 8 kpa 

PaO2 8 kpa 

HCO3 - 

35 mmol/L 

BE +10 mmol/L 

Q. What does the ABG show? 

A. Fully compensated respiratory acidosis by metabolic alkalosis 

Q, What is a likely diagnosis? 

A. Chronic lung disease 

4. An infant of 30 weeks’ gestation and BW 1.3 kg is being ventilated . ABG shows: 

pH 7.35 

PaCO2 3 kpa 

PaO2 15 kpa 

HCO3 - 

12 mmol/L 

BE -12 mmol/L 

Q. Interpret the ABG 

A. Fully compensated metabolic acidosis by respiratory alkalosis and hyperoxaemia 

Q What is your next course of action? 

A. Reduce FiO2, administer a small dose of NaHCO3, treat any other contributory 

cause of acidosis and wean down ventilation setting 

5. A term infant is being ventilated for meconium aspiration. His ABG is as follows : 

pH 7.16 

PaCO2 10 kpa 

PaO2 6 kpa 

HCO3 - 

16 mmol/L 

BE -10 mmol/L 

Q. What is likely to have happened? 

A. Pneumothorax 

Q. What is your interpretation of the ABG 

A. Mixed respiratory and metabolic acidosis with hypoxaemia

6. A 6 day old infant is being ventilated for a cyanotic heart disease. ABG shows : 

pH 6.8 

PaCO2 4.5 kpa 

PaO2 3.0 kpa 

HCO3 - 

8 mmol/L 

BE -24 mmol/L 

Q. What does the ABG show? 

A. Severe metabolic acidosis with severe hypoxaemia 

Q. What is your next course of action ? 

A. Administer sodium bicarbonate, consider prostaglandin infusion, confirm heart defect 

and consider surgery

A. Definition 

Birth Asphyxia 

There is no accepted definition. It is a result of a combination of hypoxia and 

hypoperfusion and affects many organ systems of which the cerebral complication is the 

most devastating. 

B. Incidence of Birth Asphyxia 

C. Diagnosis 

Depends on definition used and ranges from 3.7 to 9/1000 livebirths (average of 

6/1000 LBs) 

Depression of Apgar score of 5 in 5 min. is 4/1000 (Levene 1986) 

Hypoxic ischaemic Encephalopathy (HIE) 5-6/1000 term infants and 

1 per 1000 dies or survives with neurological damage. 1 

1. Meconium staining of amniotic fluid may be an indicator of foetal distress or 

intrapartum hypoxia. 

2. Abnormal CTG tracing is sometimes present. 

3. Acidosis. A low umbilical cord pH is a better indicator of perinatal asphyxia than the 

Apgar score 2-4 A pH of

Staging of Neonatal /Hypoxic Ischaemic Encephalopathy (HIE) 

MILD (Stage I) 

subtle abnormality 

days 

Irritable with exaggerated 

and frequent Moro’s. 

Hyperalert (look of 

hunger, wide eye gaze, 

failure to fixate. 

Normal tone 

Weak suck ( NG) 

Sympathetic dominance 

with tachycardia and 

mydriasis. 

No seizure clinically 

No Impairment 

Important to note: 

Only constant in term infants or > 35 weeks. Not consistent in Prems. 

MODERATE 

ENCEPHALOPATHY 

(Stage II) 

Lethargy with 

spontaneous movement 

Moro’s and other 

primitive reflexes lost in 

early stages, tendon jerks 

exaggerated. 

Differential tone with 

LL>UL and neck 

extensors>flexors 

Seizures ++ (lip 

smacking, sucking, tonic 

or clonic seizures.) 

Poor suck (NG required) 

Parasympathetic 

dominance with 

bradycardia and 

constricted pupils. 

25% Impaired 

SEVERE 

ENCEPHALOPATHY 

(Stage III) 

Comatose with little 

spontaneous movement 

Seizures prolonged and 

frequent. In very severely 

asphyxiated babies no 

seizures clinically or EEG 

due to completely 

exhausted brain energy) 

Severely hypotonic 

initially with lost of 

reflexes 

Death 

If recovers there is 

excessive hypertonia. 

Persistent abnormal 

neurological signs beyond 

6 weeks means CP. 

92% Impaired . 

i) Absence of encephalopathy does not mean infant has not suffered significant intrapartum 

asphyxia (kidney and heart may be affected). 

ii) Encephalopathy can be caused by hypoglycaemia or cerebral haemorrhage and therefore have 

to be excluded before diagnosing HIE. 

D. Complications of Birth Asphyxia 

Brain: Periventricular haemorrhage and periventricular leukomalacia. Intracranial 

haemorrhage (subdural (5%), subarachnoid (some), choroid plexus, cerebellum 

and thalamus). Cerebral oedema occurs after 24-28 hours. 

Kidney: Acute tubular necrosis; oliguria; usually recovers with supportive Rx. Rule 

out acute urinary retention. 

Heart: Hypoxic ischaemic damage (cardiogenic shock, hypotension, heart failure 

with atrioventricular valve regurgitation, arrhythmia). 

Lungs: Meconium aspiration common 

GIT:stress gastric ulcer, feed intolerance and NEC 

Metabolic: SIADH (secondary to head injury) , hypoglycaemia, hypocalcaemia, 

hypomagnesaemia 

Haematological : DIVC

E. Management 

I. Good intrapartum care 

II. Adequate and effective resuscitation 

III. ICU monitoring for complications. Regular BP, respiratory, urine output, acidosis etc. 

IV. General measures: 

a) Nurse in thermoneutral environment. Avoid high environmental temperature as 

fever is associated with adverse outcome 

b) Avoid hypo or hyperglycaemia 

c) Adequate ventilation and avoid hypoxaemia and hypercarbia or hypocarbia 

d) Review infection risk and Rx with antibiotics 

e) Maintain adequate hydration but do not dehydrate or overhydrate 

f) Treat jaundice as necessary 

V. CVS Rx hypotension with plasma expanders and inotrope support. 

Renal Careful assessment of fluid status; if output < 1ml/kg/hr start renal 

failure regime; peritoneal dialysis if needed. 

Lungs IPPV 

Metabolic In SIADH, restrict fluids. Rx hypoglycaemia. 

DIVC No specific Rx. Replace with fresh frozen plasma., cryoprecipitate, 

platelet or packed cell as indicated 

Nutrition Enteral feeding is preferable to parenteral but avoid rapid increase in 

feeding to decrease risk of NEC 

VI. Brain Orientated Management. 

a) Cerebral perfusion: Maintain BP (Mean Arterial Pressure > 40 mmHg) 

b) Seizure (Also see chapter on Neonatal Seizures) 

o frequent convulsion ( over 3 per hour) or prolonged convulsion ( lasting 3 

or more minutes) should be treated 4,5 

o Phenobarbitone (loading dose 20 mg/kg with another 20mg/kg for 

persistent seizures , and 5 mg/kg OD maintenance dose) 

o Clonazepam, lignocaine or phenytoin for persistent seizure. Phenytoin best 

avoided for maintenance. 

o Prophylactic barbiturate therapy did not show any benefit 

c) Intracranial Hypertension 

o Fluid restriction and give enough fluid to keep infant on dry side of normal. 

(usually less 20 % of daily fluid requirement). 

o If full fontanel and seizures give 20% mannitol at 1 g/kg over 20 min. 

Mannitol contraindicated in oliguria. Can repeat 6 hourly for maximum 

2 - 3 doses. 

o Ventilate and keep PaCO2 at 35-45 mmHg. Keeping the PaCO2 less 

than this as it can cause cerebral ischaemia. Maintain for 24 - 48 hours 

only. 

o Steroids are of no use. 6

F. Prognosis 

a) Apgar score and mortality. 

Mortality in the first year of life for premature babies. 

Babies < 2500g : mortality > 80% if Apgar is 0 - 3 at 15 min. 

mortality > 95% if Apgar is 0 - 3 at 20 min. 

Babies > 2500 g: mortality is 50% if Apgar is 0 - 3 at 15 min. 

mortality is 60% if Apgar 0 - 3 at 20 min. 

Mortality very high in infants who do not breathe spontaneously at 30 min. 

Risk of CP. is 60% for BW > 2500 g if Apgar is 0 - 3 at 20 min. 

93% of babies with Apgar 0 at 1 min. and 0-3 at 5 min. were entirely normal 

on follow-up. Therefore 15 min and 20 min score is important. 

b) Severity of HIE and outcome (most accurate predictor) 

No infant with mild HIE alone developed impairment. Mild encephalopathy 

carries an excellent prognosis irrespective of Apgar score and parents 

should be strongly reassured of excellent outcome. 

The median risk for impairment is 25% in moderate NE and 92% in severe 

NE. 

c) CT scans done after 1st week of life. 

Extensive areas of low attenuation with apparent brightness of basal ganglia 

are associated with very poor prognosis. 

d) Doppler U/S appears to be an accurate predictor for full term babies done after 24 

hours of life. 

Decrease Pourcelot’s resistivity index (PRI 3 SD of the 

normal mean has a +ve predictive value for adverse outcome of 94%. 

e) U/S of head can be done at discharge and at 2 - 3 weeks of life to look for 

periventricular haemorrhage or periventricular leukomalacia. 

f) EEG: 

severe abnormalities include burst suppression, low voltage or isoelectric EEG. 

moderate abnormalities include slow activity 

The overall risks for death or disability were 95% for severely abnormal EEG, 

64% for moderately abnormal EEG and 3 % for normal or mildly abnormal EEG 7,8 

Continuous EEG monitoring in the first 6-12 hours after birth has been shown to 

identify infants at risk of subsequent brain damage 9 

Long term : 

a. Phenobarbitone will be taken off on discharge if the child is neurologically normal 

and feeds normally (by day 7-10). 

b. If CNS is abnormal - the duration of phenobarbitone use is controversial. 

Probably 3-6 mths. (Longer if EEG abnormal)

c. All doctors managing such infants should never reassure the parents the child is 

"Normal" unless on prolonged follow up (at least up to 2yrs) - the milestones are 

within normal limits (including normal speech - suspect deafness/mental 

retardation if speech delayed). 

References 

1.Levene ML, Sands C, Grindulis H, Moore JR. Comparison of 2 methods of predicting outcome in perinatal 

asphyxia. Lancet 1986;1:67-71 

2. Silverman F, Suidan J, Wasserman J, Antoine C, Young BK. The Apgar score: Is it enough? Obstet Gynae 

1985;66:331-6 

3. Low JA, Panagiotopoulos C, Derick EJ. Newborn complications afterintrapartumasphyxia with metabolic 

acidosis in term fetus. Am J Obstet Gynecol 1994;170:1081-7 

4.LeveneML. Management of asphyxiated full term infant. Arch Dis Child 1993;68:612-6 

5. Evan D, Levene M. Neonatal seizures. Arch Dis Child 1998;78:F70-5 

6. Levene MI, Evan DH Medical management of raised intracranial pressure after severe asphyxia. Arch Dis 

Child 1985; 60:12-6 

7Holme G ,Rowe J, Hafford J, Schmidt R. Prognostic value of EEG in neonatal asphyxia. Electroenceph Clin 

Neurophysiol 1982;53: 60-72 

8. Thornberg E. Ekstrom-Jodal B. Cerebral function monitoring: a method of predicting outcome in term 

neonates after severe perinatal asphyxia .Acta paediatr 1994;83:596-601 

9.Helllstorm-Westas L, Rosen I, Svenningsen NW. Predictive value of early continuous amplitude integrated 

EEG recording on outcome after severe birth asphyxia in full term infants. Arch Dis Child 1995; 72: F34-8

NEONATAL SEIZURES 

Seizures are the most frequent manifestation of neonatal neurological diseases. 

It is important to recognize seizures, determine their etiology and treat them because: 

1. the seizures may be related to significant diseases and may require specific 

treatment 

2. the seizures may interfere with supportive measures e.g. feeding and assisted 

respiration for associated disorders 

3. the seizures per se may be a cause of brain injury. 

Clinical 

A seizure is defined as a paroxysmal alteration in neurologic function that is behavioral, 

motor or autonomic function. This includes clinical phenomena that are associated with 

or without surface recorded EEG seizure activity. 

Epileptic phenomena can be generated at subcortical (deep limbic, diencephalic, brain 

stem) levels in the absence of surface recorded EEG discharges. 

Classification of Neonatal Seizures 

Clinical seizure EEG seizures Manifestation 

Subtle 

Clonic 

Common Ocular phenomena 

- tonic horizontal deviation of eyes common in term infants 

- sustained eye opening with fixation common in preterm infants 

- blinking 

Oral-buccal-lingual movements 

- chewing common in preterm infants 

- lip smacking, cry-grimace 

Limb movements 

- pedaling, stepping, rotary arm movements 

Apneic spells common in term infants 

Focal 

Common Well localized clonic jerking, infant usually not unconscious 

Multifocal 

Tonic 

Focal 

Generalized 

Myoclonic 

Focal , 

Multifocal 

Generalized 

Common 

Common 

Uncommon 

Uncommon 

Common 

Multifocal clonic movements; simultaneous or in sequence 

or non-ordered ( non-Jacksonian) migration 

Sustained posturing of a limb, asymmetrical posturing of trunk or 

neck 

Tonic extension of upper and lower limbs (mimic decerebrate 

posturing) 

Tonic flexion of upper limbs and extension of lower limbs( mimic 

decorticate posturing) 

Those with EEG correlates; autonomic phenomena e.g. 

increased blood pressure are prominent features. 

Well localized, single or multiple, migrating jerks usually of limbs 

Single or several bilateral synchronous jerks or flexion 

movement occurring more in upper than lower limbs.

Etiology 

Determination of etiology is critical because it gives the opportunity to treat specifically 

and also to make a meaningful prognosis. 

The most important etiology, their usual time of onset and relative frequency in preterm 

and term infants are shown in the table below. 

Major Etiologies of Neonatal Seizures in Relation to Time of Seizure Onset 

and Relative Frequency 

Time of onset * Relative frequency # 

Etiology 0-3 days > 3days Premature Full term 

Hypoxic –ischemic encephalopathy + +++ +++ 

Intracranial hemorrhage + + ++ + 

Intracranial infections + + ++ ++ 

Developmental defects + + ++ ++ 

Hypoglycaemia + + + 

Hypocalcaemia + + + + 

Other metabolic disturbances & IEM + + 

Epileptic Syndromes + + + 

* postnatal age 

# relative frequency of seizures among all etiologies: +++ most common, ++ less common, +least common 

( From JJ Volpe: Neurology of the Newborn 4 th edition. Page 190) 

Notes: 

Hypoxic –ischemic encephalopathy (HIE) 

Usually 2º to perinatal asphyxia. Most common cause of neonatal seizures in both preterm and term 

infant 

Characteristically seizures occur in the first 24 hours of life 

Present with subtle seizures; multifocal clonic or focal clonic seizures. If focal clonic seizures may 

indicate associated focal cerebral infarction. 

Intracranial hemorrhage 

Hemorrhages are principally germinal matrix-intraventricular (GM-IVH), often with periventricular 

hemorrhagic (PVH) infarction in the premature infant. 

- Premature infants with severe GM-IVH; onset of seizures in first 3 days, usually generalized tonic type 

with subtle seizures. 

- Those with associated PVH usually develop seizures after 3 days of life. 

In term infants intracranial hemorrhages are principally subarachnoid and subdural hemorrhage. 

Subarachnoid hemorrhages may occur in association with HIE. Subdural hemorrhage is often 

associated with a traumatic event and present with focal seizures usually in the first 2 days of life. 

Intracranial Infection 

Intracranial bacterial infections commonly 2º group B streptococci and E. coli. 

Nonbacterial infections include toxoplasmosis, herpes simplex, coxsackie B, rubella and 

cytomegalovirus. 

Developmental Defects 

Commonly due to a disturbance in neuronal migration resulting in cerebral cortical dysgenesis e.g. 

lissencephaly, pachygyria and polymicrogyria. 

Metabolic Disturbances 

Hypoglycemia common in SGA infants and infants of diabetic mothers 

- occurrence of neurological symptoms is determined by the duration of hypoglycemia. This is more 

common in SGA infants compared to IDM 

- neurological symptoms include jitteriness, stupor, hypotonia, apnea and seizures. 

- often to establish that hypoglycemia is the cause of seizures because of frequently associated 

perinatal asphyxia, hypocalcaemia, hemorrhage.

Hypocalcaemia has 2 major peaks of incidences. 

1st peak in first 2 to 3 days of life, usually in low birth weight infants, IDM and infants with HIE of 

perinatal asphyxia. A therapeutic response to intravenous calcium is helpful in determining low 

serum calcium as a cause of the seizures. It is much more common for early hypocalcaemia to be 

an association of early seizures rather than a cause. 

Later -onset of hypocalcaemia are associated with endocrinopathy ( maternal hypoparathyroidism, 

neonatal hypoparathyroidism) and heart disease ( with or without Di George Syndrome), rarely with 

nutritional type ( cow’s milk, high phosphorus synthetic milk). Hypomagnesemia is a frequent 

accompaniment. 

Other metabolic disturbances include neonatal intoxication with lidocaine, hyponatraemia, 

hypernatraemia, amino acidopathy ( nonketotic hyperglycinemia), organic acidopathy, 

hyperammonemia, mitochondrial disturbance, perioxisomal disorders, pyridoxine dependency 

(recalcitrant seizures ceased with intravenous pyridoxine ) and disorder of glucose transport ( low 

glucose in CSF but normal blood glucose, treatment with ketogenic diet) 

Seizures versus Jitteriness and Other Non-epileptic Movements 

Some movements e.g. jitteriness and other normal movement during sleep 

(Myoclonic jerks or generalized myoclonic jerks as infant wakes from sleep) or when 

awake/ drowsy (roving sometimes dysconjugate eye movements, sucking not 

accompanied by ocular fixation or deviation) in newborn may be mistaken for seizures. 

Jitteriness versus Seizure 

Clinical Features Jitteriness Seizure 

Abnormality of gaze or eye movement 0 + 

Movements exquisitely stimulus sensitive + 0 

Predominant movement tremors* clonic, jerking# 

Movements cease with passive flexion of affected limb + 0 

Autonomic changes ( tachycardia, ↑ BP, apnea, 

0 + 

salivation, cutaneous vasomotor phenomena) 

* tremors – alternating movements are rhythmical and of equal rate and amplitude 

# clonic, jerking – movements with a fast and slow component 

( Adapted from JJ Volpe: Neurology in the Newborn 4 th Edition. Page 188) 

Management. 

Selection of the infant to treat with anticonvulsant depends on identification of the 

infant with epileptic seizure. Consensus is lacking on necessity for treatment of 

minimal or absent clinical phenomena. 

Treatment with anticonvulsant is to prevent potential adverse effects on ventilatory 

function, circulation and cerebral metabolism ( threat of brain injury) 

Controversy regarding identification of adequacy of treatment, elimination of clinical 

seizures or electrophysiology seizures. Generally majority attempt to eliminate all or 

nearly all clinical seizures.

FLOW CHART: MANAGEMENT OF NEONATAL SEIZURRES 

Infant with clinical 

seizure 

Ensure ventilation and perfusion 

adequate (ABC’s) 

Dextrostix stat 

No Hypoglycemia 

Actively convulsing 

Hypoglycemia 

Phenobarbitone: 20mg/kg IV over 10 -15 minutes 

A repeat loading dose of 20mg/kg may be 

necessary 

Phenytoin: 10mg/kg IV as loading dose 

(repeat a 2 nd loading dose if fits recur) via 

infusion at 1mg/kg/min – cardiac rate and 

rhythm should be monitored during infusion 

Actively convulsing 

Benzodiazepine: 

*Diazepam: 0.3 mg/kg/h IV infusion 

*Midazolam:1-4 mcg/kg/min IV infusion 

*- limited small study 

OTHERS: 

Calcium Gluconate, 10% solution: 2 ml/kg, IV 

Magnesium sulfate, 50% solution: 0.2 ml/kg, IV 

Pyridoxine: 50-100mg IV 

Investigations to consider: 

Blood sugar, Se Ca, Mg, electrolytes 

Septic screen - FBC, Bld C&S, LP, TORCHES 

Metabolic screen - blood gas, Se. Ammonia 

amino acids, organic acids, other metabolites 

Neuroimaging: US,CT Scan brain 

EEG 

IV 10% Dextrose at 

2 ml/kg (200mg/kg) 

Then IV glucose infusion 

at 8 mg/kg/min infusion 

Maintenance therapy: 

3-4mg/kg/d q12h, IV or PO 

Given 12-24 h after loading 

AE: respiratory depression 

hypotension 

Maintenance therapy: 

3-4mg/kg/d q12h, IV 

Given 12-24 h after loading 

AE: Heart block 

hypotension 

Maintenance therapy 

Midazolam: 

AE: respiratory depression, seizure 

hypotension, urinary retention

Duration of Anticonvulsant Therapy- Guidelines 

(JJ Volpe: Neurology of the Newborn: pg 207) 

Optimal duration of therapy relates to the probability of recurrence of seizures if the 

drugs are discontinue and the risk of subsequent epilepsy. This can be determined by 

considering the neonatal neurological examination, cause of the seizure and the EEG. 

Neonatal Period 

If neonatal neurological examination becomes normal, 

discontinue therapy 

If neonatal neurological examination is persistently abnormal 

consider etiology and obtain electroencephalogram(EEG) 

In most cases – continue phenobarbitone 

discontinue phenytoin 

reevaluate in a month 

One Month after Discharge 

If neurological examination has become normal, 

discontinue phenobarbitone over 2 weeks 

If neurological examination is persistently abnormal, obtain EEG 

If no seizure activity or not overtly paroxysmal on EEG, discontinue phenobarbitone 

over 2 weeks 

If seizure activity is overtly paroxysmal continue phenobarbitone until 3 months of 

age and reassess in the same manner. 

PROGNOSIS OF NEONATAL SEIZURES 

Most important determinant of neurological prognosis is the underlying nature of the 

neuropathological process. 

Neurological Disease Normal 

Development (%)^ 

Hypoxic Ischemic Encephalopathy 50 

Severe Intraventricular Hemorrhage with PVH infarction 10 

Primary Subarachnoid Hemorrhage 

Hypocalcaemia 

Early onset (depends on the prognosis of complicating illness, if no 

50 

neurological illness present prognosis approaches later onset ) 

Later onset ( nutritional type) 

Hypoglycemia 50 

Bacterial Meningitis 50 

Developmental defect 0 

^ - Prognosis is based on those cases with the stated neurological disease when seizures are a 

manifestation. This will differ from overall prognosis of the disease. 

(based on JJ Volpe: Neurology in the Newborn:4 th edition. Page 202) 

References: 

1. JJ Volpe: Neurology in the Newborn: Fourth Edition 

100

2. Klauss & Fanaroff: Care of The High Risk Neonate: Fifth Edition 

3. McDermott CA, Kowalczyk AL, Schnitzler ER et al: Pharmacokinetics of 

lorazepam in critically ill neonates with seizures. J Pediar 120: 479- 483,1992 

4. Deshmukh a, Wittert W, Schnitzler ER et al: Lorazepam in the treatment of 

refractory neonatal seizures: a pilot study.Am J Dis Child140:1042-1044. 1986. 

5. MaytalJ, Novak GP, King KC: Lorazepam in the treatment of 

refractory neonatal seizures:J Child Neuro6;319-323,1991 

6. Hu KC, Chiu NC, Ho CS, Lee ST, Shen EY Continuous midazolam infusion in 

the treatment of uncontrollable neonatal seizures. Acta Paediatr Taiwan. 2003 

Sep-Oct;44(5):279-81. 

7. Ng E, Klinger G, Shah V, Taddio A.Safety of benzodiazepines in Newborns. 

Ann Pharmacother. 2002 Jul-Aug;36(7-8):1150-5. 

8. Gamstorp I, SedinG; Neonatal convulsions treated with continuous 

intravenous infusion of diazepam:Ups J Med Sci87: 143-149, 1982.

NEONATAL HYPOGLYCAEMIA 

A. Definition: 

Blood sugar < 2.6 mmol/L (approximately 45 mg/dl) in a term or premature infant. 

B. Prevention and Early Detection 

Anticipation & prevention, when possible, are keys to the management of 

hypoglycaemia. Hypoglycaemia may produce long term neurological injury and 

the level at which it occurs is controversial. 

(i) Identify all high-risk neonates 

Prematurity Small for gestational age 

Hypothermia Birth Asphyxia / Perinatal Stress 

Sepsis Infant of Diabetic Mother 

Infant > 4 kg. Polycythaemia 

Rhesus disease 

(ii) Check glucometer/dextrostix on admission 

(iii) Immediate feeding for all well babies who are at risk. 

If hypoglycaemic on admission, repeat glucometer 1 hour later after feeding. 

Continue monitoring at 2 hours and 4 hours later. (i.e. O,1,2, 4 hours) 

If normoglycaemic on admission feed and monitor 6-8 hourly till past stage of 

hypoglycaemic risk 

(iv) Unwell babies (e.g. birth asphyxia or premature): set up a 10% dextrose drip. 

Monitor blood sugar Hourly X 2 

Then 2 hourly X 2 

Then 4 → 6 → 8 hourly until stable 

(v) Clinical features are: 

Symptoms are non-specific. For example: apathy, hypotonia, apnoea, poor 

sucking, cyanosis, abnormal cry, jitteriness, seizure, lethargy and temperature 

instability. 

C. If Hypoglycaemia is detected 

1. Repeat the glucometer test. Send RBS stat for confirmation. 

(Note: monitoring using reagent strip measurement is quick, cheap and easy 

but not a precise method) 

Check expiry date of test stick! 

2. Is the infant symptomatic? 

3. When was the last feed given? Is the intravenous drip adequate and running 

well? (i.e. not disconnected or extravasated)

D. Asymptomatic Hypoglycaemia 

Feed early or bring forward next feed due. 

Feed 3 hourly. 

Recheck glucometer after 1 hour. 

If glucometer still < 2.6 mmol/L and child asymptomatic, can increase 

feeds if child can tolerate. Otherwise, 

Set up IV D 10% and give at least 72 ml/kg/day 

(5 mg/kg/min of glucose) 

Continue enteral feeds as tolerated. 

Recheck glucometer hourly until stable and then 4-6 hourly. 

E. Symptomatic Hypoglycaemia (Glucometer level immaterial) 

Give a bolus of 2 ml/kg of IV Dextrose 10% slowly . 

Follow-up by an infusion of glucose at 4-6 mg/kg/min (72ml/kg/day 

D10%) 

Keep nil by mouth 

Repeat glucometer after 1/2 to 1 hour and increase the infusion as necessary 

to 6-8 mg/kg/min (90 ml/kg/day D10%) 

If infection is suspected or there is no alternative explanation for 

hypoglycaemia take Blood C&S and treat as sepsis. 

Once the blood glucose normalised, feeds can be reintroduced gradually and 

infusion tailed off 

F. If Hypoglycaemia persists 

Take Blood C&S and treat as sepsis if not done yet. 

Increase the rate of dextrose infusion if possible (i.e. do not increase beyond 

daily requirement). 

Increase the concentration of dextrose. Concentrations of 12.5% to 15% may 

be needed. If concentration of 12.5% is used, a central line is required 

If glucose infusion rates of more than 12mg/kg/min are required, 

hyperinsulinism should be seriously considered and investigated accordingly. 

Refer specialist 

Consider 

1. Glucagon 0.2 mg/kg IV (IM) bolus 

2. Hydrocortisone 2.5 -5 mg/kg/dose bd IV 

3. Diazoxide 5 mg bd orally 

4. Adrenaline 500 ng/kg/min IV infusion 

5. Somatostatin 1 - 4 microgram SC. 

Also need to consider metabolic (See Approach to Hypoglycaemia under 

Metabolic section) and endocrine workup.

Key points: 

A. Serial blood glucose should be routinely monitored in infants who have risk factors for 

hypoglycaemia 

B Bolus injections of large volumes of hypertonic glucose solutions should be 

avoided - dangerous to neurological function and may be followed by a rebound 

hypoglycaemia, cerebral oedema and is caustic to neonatal veins. 

C Milk formula provide more energy/ml than 10% dextrose and supply important nonglucose 

fuels, which have a glucose sparing role in neurological function. 

(Energy content of formula milk is 2750 kJ/l while that of 10% D is 1600 kJ/l). It 

promotes ketogenesis and gut maturation. 

Breast-feeding should be encouraged as it is more ketogenic. 

D. Milk feeds must not be discontinued or reduced when intravenous fluids are given 

unless the child develops NEC or other causes of feeding intolerance. The 

recommended practice is to feed the baby with as much milk as is tolerated and 

to infuse glucose at a rate sufficient to prevent hypoglycaemia. The IV glucose is 

then reduced slowly while milk feeds is maintained or increased. May need to 

continue over a few days. 

E. Ensure volume of intravenous fluid is appropriate for patient, taking into consideration 

concomitant problems like cardiac failure, cerebral oedema and renal failure. If unable 

to increase volume further, concentration of dextrose to be increased. 

Glucose requirement (mg/kg/min) = % of dextrose x rate (ml/hr) x 0.167 

------------------------------------------------------wt 

(kg) 

F. Plasma glucose is 13-18% higher than whole blood glucose. Arterial blood has higher 

glucose concentration than venous blood. Capillary sampling can be unreliable in the 

presence of poor peripheral circulation. 

G. Requirement of >9mg/kg/min suggests hyperinsulinism. Truly hyperinsulinaemic babies 

may require 15-20 mg/kg/min 

References 

Koh G Aynsley-Green A 1988a Neonatal hypoglycaemia- the controversy definition. Arch Dis 

Childhood;63:1386-1398 

Koh G Aynsley-Green A Tarbit A Etre J 1988b Neural dysfunction during hypoglycaemia. Arch Dis 

Childhood;63:1353-1358 

DK Pal et al 2000 Neonatal hypoglycaemia in Nepal. Prevalence and risk factors Arch Dis 

Childhood;82:F46-52 

AA M Moris et al 1996 Evaluation of fast for investigating hypoglycaemia or suspected metabolic disease 

Arch Dis Childhood;75:115-119 

Gomella, Cunningham ,Eyal and Zenk: Neonatalogy 4 th edition Lange

NEONATAL JAUNDICE 

What is jaundice? 

Jaundice is apparent clinically when the level of bilirubin in the serum rises above 

85µmol/l (5mg/dl). Physiological jaundice is a reflection of the bilirubin load to the liver, 

rate of hepatic excretion (liver maturity) and ability of the serum binding protein to retain 

the bilirubin within the plasma. 

What can go wrong in jaundice? 

Elevated serum bilirubin can result in kernicterus, when unconjugated bilirubin is 

deposited in the cell wall of neurons in basal ganglia, brain stem and cerebellum 

resulting in cell death. Kernicterus is associated with a high mortality, and survivors 

usually suffer sequelae like athetoid cerebral palsy, high frequency hearing loss, 

paralysis of upward gaze and dental dysplasia. The factors influencing bilirubin toxicity 

in the brain cells of the neonate are complex and incompletely understood. There is no 

specific level of total serum bilirubin above which kernicterus can be predicted to 

happen. 

Causes of neonatal jaundice (NNJ) 

The following are the recognised causes of NNJ: 

• Haemolysis due to ABO or Rh isoimmunisation, G6PD deficiency, 

microspherocytosis, drugs 

• Physiological jaundice & idiopathic jaundice 

• Polycythaemia 

• Sepsis e.g. septicaemia, meningitis, urinary tract infection and intra-uterine 

infection 

• Breastfeeding and breastmilk jaundice 

Factors affecting severity of NNJ 

The following factors are said to affect the severity of jaundice 

• Dehydration 

• Large weight loss after birth 

• Extravasation of blood, cephalohaematoma, contusion 

• Swallowed maternal blood 

• Infant of diabetic mother 

• Acidosis 

• Asphyxia 

• Gastrointestinal tract obstruction: increase in enterohepatic circulation 

G6PD deficiency 

G6PD deficiency is an inherited disorder of the red blood cell, inherited in an x-linked 

recessive manner – males are affected while the females are carriers. G6PD is an 

enzyme essential in keeping glutathione in the reduced state that in turn is vital to 

maintain the integrity of the red cell membrane. In G6PD deficiency the red blood cells 

are prone to haemolysis when exposed to oxidants or when certain foods or herbs are 

ingested. A list of drugs and herbs that can precipitate haemolysis is provided in Table 1 

.

Table 1 

Agents to be avoided in G6PD Deficiency Patients 

1) Foods and Herbs to be avoided 

Fava Beans (Kacang Parang) 

Documented Chinese herbs/medicine 

Chuen Lin 

San Chi 

13 herbs 

12 herbs 

Other traditional herbs/medications are also not 

to be taken unless with medical advice 

2) Other chemicals to be avoided 

Naphthalene (moth balls) 

Mosquito coils and insect repellants which 

contains pyrethium 

3) Drugs to be avoided or contraindicated 

Acetanilide 

Doxorubicin 

Furazolidone 

Methylene Blue 

Nalidixic acid 

Niridazole 

Nitrofurantoin 

Phenazopyridine 

Primaquine 

Sulfamethoxazole 

Bactrim 

MANAGEMENT OF NNJ 

4) Drugs that can be safely given in 

therapeutic doses 

Paracetamol 

Ascorbic Acid 

Aspirin 

Chloramphenicol 

Chloroquine 

Colchicine 

Diphenhydramine 

Isoniazid 

Phenacetin 

Phenylbutazone 

Phenytoin 

Probenecid 

Procainamide 

Pyrimethamine 

Quinidine 

Streptomycin 

Sulfisoxazole 

Trimethoprim 

Tripelennamine 

Vitamin K 

Mefloquine 

History: 

The following information needs to be obtained: 

• Age of onset and rate of progress (both clinically and also if serial serum bilirubin 

(SB) results are available) 

• Previous infants with NNJ, kernicterus, neonatal death, G6PD deficiency 

• Mother’s blood group (from antenatal history) 

• Gestation: although term gestation is taken as 37 completed weeks, infants born 

at 37- 38 weeks of gestation are more prone to hyperbilirubinaemia, the 

incidence of hyperbilirubinaemia increasing with decreasing gestational age. 

• Presence of abnormal symptoms such as apnoea, difficulty in feeding, feed 

intolerance and temperature instability.

Physical examination 

• General condition: ill-looking if jaundice is severe or if there is presence of some 

other illnesses e.g. infection. Neurological signs are present if kernicterus 

develops. 

• Pallor, presence of cephalohaematoma/subaponeurotic haematoma, petechiae, 

purpura, ecchymosis , and hepatosplenomegaly implicate a pathological cause 

of jaundice 

• Cephalo-caudal progression of severity of jaundice may be seen in some infants, 

but correlating with levels of bilirubin is often inaccurate 

• Intensity of yellow discoloration in skin and mucosa helps with assessment of the 

severity of jaundice 

When should a neonate be referred for hospital management? (When to worry?) 

The following are indications for referral. 

1. Jaundice below umbilicus, corresponding to serum bilirubin of 12-15 mg/dl (200- 

250 µmol/L). 

2. Jaundice up to level of the sole of the feet - likely to need exchange transfusion. 

3. Jaundice within 24 hours of life. 

4. Rapid rise of serum bilirubin of more than 8.5 µmol/L/hour (>0.5 mg/dl/hour). 

5. Prolonged jaundice of more than 14 days - other causes/conditions need to be 

excluded e.g. neonatal hepatitis, biliary atresia. 

6. Family history of significant haemolytic disease or kernicterus 

7. Clinical symptoms/signs suggestive of other diseases e.g. sepsis. 

Laboratory diagnosis 

Investigations for NNJ include: 

• Total serum bilirubin – sufficient in most cases 

• Unconjugated & conjugated fractions in specific conditions e.g. prolonged NNJ 

• Infant’s blood group, maternal blood group (if not already known) 

• Direct Coomb’s test (if blood group incompatibility is suspected) 

• G6PD status (if not known yet) 

• Full blood count 

• Reticulocyte count 

• Peripheral blood film 

• Blood culture, urine microscopy and culture ( if infection is suspected) 

Treatment 

PHOTOTHERAPY 

The aim of phototherapy is to prevent potentially dangerous indirect bilirubin levels and 

to decrease the need for exchange transfusion, since phototherapy changes bilirubin 

into more soluble forms to be excreted in the bile or urine. The effectiveness of 

phototherapy is affected by the intensity, or irradiance, of the phototherapy light, 

increased irradiance producing increased effectiveness, until the saturation dose of 40 

µW/cm 2 /nm of appropriate light is reached. The minimum irradiance is 6-12 µW/cm 2 /nm. 

Other factors affecting the effectiveness are the spectrum of light delivered by the 

phototherapy unit, the surface area of the infant exposed to phototherapy, and the

distance of the light source from the baby, the optimum distance being 35 - 50 cm in 

conventional lights. 

Types of photolights 

Conventional phototherapy 

Fibre optic phototherapy (Biliblanket) 

Intensified phototherapy 

In cases of mild to moderate jaundice conventional and fibre optic phototherapy usually 

suffice but where jaundice is significantly high (e.g. >300 umol/L in a 5 day old or 250 

umol/L in a 24 hour old infant ) intensified phototherapy should be used. 

The methods of providing intensified phototherapy are as follows: 

i. high intensity blue lights ( F20 T12 / BB ) with 7 overhead lamps, and 4 lamps 

placed below the infant. 

ii. combined fibreoptic blanket with standard phototherapy system above, thus 

increasing the surface area of the infant exposed to light. 

iii. several phototherapy lamps placed around the infant, if a fibreoptic unit is not 

available. 

iv. placing a white reflecting surface (e.g. sheet) around the bassinet, so that light is 

reflected onto the baby's skin when using a single phototherapy unit so as to 

increase the area of exposure. 

Phototherapy : Practical considerations. 

Position light source 35-50 cm from top surface of the infant (when conventional 

fluorescent photolights are used.) 

Expose infant appropriately 

Cover infant's eyes 

Turn infant every 2 hours 

Monitor serum bilirubin levels as indicated 

Monitor infant's temperature 4 hourly to avoid chilling or overheating 

Allow parental-infant interaction 

Discontinue phototherapy when bilirubin is less than threshold levels and has been 

falling for 24 hours. In infants without haemolytic disease, the average bilirubin 

rebound after phototherapy is less than 1 mg/dl (17 µmol/dl). Discharge from hospital 

need not be delayed in order to observe the infant for rebound, and in most cases, 

no further measurement of bilirubin is necessary. However, if phototherapy is 

initiated early and discontinued before the infant is 3 to 4 days old, additional 

ambulatory follow-up may be necessary 

Measure intensity of phototherapy light periodically using irradiance meters 

Turn off light during feeding and blood taking 

Hydration- there is no evidence to support any influence of excess fluid 

administration on serum bilirubin concentration. Some infants admitted with high 

bilirubin levels may also be mildly dehydrated, and may need fluid supplementation. 

More frequent breastfeeding is recommended because it inhibits the enterohepatic 

circulation of bilirubin and thus lowers the serum bilirubin level. Other routine 

supplementation e.g. with dextrose water is not indicated

Once the baby is on phototherapy, visual observation as a means of monitoring is 

unreliable. Serum bilirubin levels must guide the management. 

EXCHANGE TRANSFUSION (ET) 

Bilirubin levels beyond which kernicterus may occur if an ET is not carried out have not 

been established. The modality of treatment should be based on the clinical history, risk 

factors and physical examination of the infants. The table below illustrates the 

recommended levels for various modalities of treatment adapted from the American 

Academy Pediatrics for infants of 35 or more weeks of gestation based on different 

levels of risk. (Pediatrics 2004, 114: 297-316). 

Table 2. Guidelines for Phototherapy and ET in Hospitalised Infants of 35 or More 

Weeks’ Gestation 

Hours 

of life 

Infants at lower risk (≥ 38 

wk and well) 

Intensive 

Phototherapy 

Total Serum Bilirubin levels mg/dL (umol/L) 

Infants at medium risk (≥ 

38 wk + risk factors OR 35- 

37 6/7 wk and well) 

ET Intensive 

Phototherapy 

Infants at higher risk (35- 

37 6/7 wk + risk factors) 

ET Intensive 

Phototherapy 

< 24* 

24 12 (200) 19 (325) 10 (170) 17 (290) 8 (135) 15 (255) 

48 15 (255) 22 (375) 13 (220) 19 (325) 11 (185) 17 (290) 

72 18 (305) 24 (410) 15 (255) 21 (360) 13 (220) 18.5 (315) 

96 20 (340) 25 (425) 17 (290) 22.5 (380) 14 (240) 19 (325) 

> 96 21 (360) 25 (425) 18 (305) 22.5 (380) 15 (255) 19 (325) 

Note: 

1. Immediate exchange transfusion is recommended if infants show signs of acute bilirubin 

encephalopathy (hypertonia, arching, retrocollis, opisthotonus, fever, high pitch cry) or if 

TSB is ≥ 5 mg/dL (85 umol/L) above the exchange levels stated above. 

2. Start conventional phototheraphy at TSB 3 mg/dL (50 umol/L) below the levels for 

intensive phototherapy. 

3. Risk factors – isoimmune hemolytic disease; G6PD deficiency, asphyxia, significant 

lethargy, temperature instability, sepsis, acidosis or albumin < 3.0 g/dL 

4. Use total bilirubin. Do not subtract direct reacting or conjugated bilirubin. 

5. During birth hospitalisation, ET is recommended if the TSB rises to these levels despite 

intensive phototherapy 

6. For readmitted infants, if the TSB level is above the ET level repeat the TSB 

measurement every 2 to 3 hours and consider ET if the TSB levels remain above the ET 

level for 6 hours under intensive phototherapy 

7. *Infants jaundiced at < 24 hours of life are not considered healthy and require further 

evaluation. 

Infants who are of lower gestation will require phototherapy and ET at lower levels, 

(please check with your specialist) 

ET

Breastfeeding and Breastmilk Jaundice 

Two types of NNJ are associated with breastfeeding, the first known as breastfeeding 

jaundice is related to inadequate nursing on the breast resulting in dehydration and 

otherwise physiological jaundice becoming more intense; and the second is breastmilk 

jaundice which is associated with prolonged jaundice extending beyond the first two 

weeks of life. One or more substances in breastmilk e.g. beta glucuronidase may be 

responsible for breastmilk jaundice. 

PREVENTIVE MEASURES for SEVERE NNJ 

Evaluation 

1. Maternal prenatal testing should include ABO and Rh(D) typing. When the mother is 

Rh-negative, a direct Coombs’ test, ABO blood type, and an Rh(D) type on the 

infant’s (cord) blood are recommended 

2. All infants must have a glucose-6-phosphate dehydrogenase (G6PD) screening done 

on cord blood. The results of G6PD screening must be known before discharge. 

Babies with G6PD deficiency must be observed in hospital for at least 5 days, the 

period of highest risk for severe jaundice. During this period parents should be 

educated on the disorder (e.g. avoidance of certain oxidising drugs and foods) and 

monitoring of jaundice can be closely observed and monitored. Breastfeeding must 

be encouraged and supported but mothers must avoid taking herbs that have not 

been found to be safe and certain foods (e.g. fava beans) 

3. Infants whose mothers are of O blood group and infants with a strong family history 

of severe neonatal jaundice should be observed for at least 24 hours in the ward. If 

earlier discharge is necessary, arrangements must be made for these infants to be 

reviewed the next day. 

4. Mothers must be assisted and provided support to manage breastfeeding 

successfully before discharge. 

5. Parents must be alerted to the significance of early onset (within 24 hours) and 

severe jaundice and advised that in these situations medical attention is necessary. 

6. Follow-up should be provided to all neonates discharged less than 48 hours after 

birth by a health care professional in an ambulatory setting, or at home within 2-3 

days of discharge 

7. Approximately one third of healthy breast-fed infants have persistent jaundice after 2 

weeks of age. A measurement of total and direct serum bilirubin should be obtained 

and a history of dark urine or light stools should be sought. If the history, physical 

examination and direct bilirubin results are normal, continued observation is 

appropriate. 

Treatment of Jaundice Associated with Breast-feeding in the Healthy Term 

Newborn 

1. Interruption of breastfeeding in healthy term newborns is discouraged and frequent 

breast-feeding (at least 8-10 times every 24 hours) should be continued. 

2. Supplementation of breast-feeding with formula with or without phototherapy can be 

considered. Supplementing with water or dextrose water does not lower bilirubin 

level in jaundiced, healthy, breast-feeding infants.

Reference: extracted from MOH publications 

1. CPG on Management of Jaundice in Healthy Term Newborns 

2. Guideline on Screening and Management of NNJ with Special Emphasis on G6PD Deficiency

Exchange Transfusion (ET) for Neonatal Jaundice 

Purpose 

1. To lower the serum bilirubin level and reduce the risk of brain damage and kernicterus. 

2. To remove the infants’ sensitised red blood cells and the circulating antibodies and reduce 

the degree of red cell destruction. 

3. To control the blood volume and relieve potential heart failure.. 

Preparation of infant 

a. Ensure pulse, temperature and respiration are stabilised and maintained. 

b. Continue feeding the child and omit only the LAST feed before ET. If needed, empty gastric 

content by doing NG aspiration before ET. 

c. Proper restraint. 

d. Check resuscitation equipment. 

e. Set a peripheral IV line. 

f. Get a signed informed consent from parent (mortality from ET is 1%). 

Grouping of Blood to be used 

Rh isoimmunisation- ABO compatible, Rh negative 

Other conditions - X match with baby and mother's blood 

Emergency - 'O' Rh negative 

Fresh whole blood collected in citrate phosphate dextrose ( CPD) 

Fresh blood not more than 24 hours old for sick or hydropic infants 

Not more than 48 hours (definitely not > 5 days) for other neonates. 

Procedure 

1. Nurse to assist. 

2. Connect baby to cardiac monitor if available. 

3. Nurse checks the baseline observations (either via monitor or manually) and record down 

on the neonatal exchange blood transfusion sheet. The following observations are recorded 

every 15 minutes; apex beat, respirations, colour, tone and behaviour. Dextrostix is to be 

done hourly, 

4. Doctor performs the ET (See Protocol). At the same time the Nurse keeps a record of apex 

beat, condition of baby and the amount of blood given or withdrawn. The whole process 

takes at least 90 minutes. 

5. Doctor to scrub, gown and mask. 

6. Drape the umbilical area. 

7. Cannulate the umbilical vein to depth NOT > 5-7cm. 

8. Aliquot for removal and replacement : < 2kg - 5 mls 

2 to 3 kg - 10 mls 

> 3kg - 20 mls 

Alternatively blood can be replaced as a continuous infusion into a large vein while removing 

blood from an arterial catheter. In smaller infant pumps delivering 120mls an hour allowing 10 

ml of blood to be removed every 5 mins can be used. Higher rates will be necessary for bigger 

infants. . 

Points to note 

a. Volume of blood to exchange 160mls/kg body weight. Pre-warm blood if possible.

- 1ml of 4.2% NaHCO3 given for every 100mls of blood * 

- 1ml of 10% Calcium gluconate for every 160mls of blood exchanged * 

* Agitate Blood bag frequently to prevent settling. NEVER give the two solutions 

together. Give via peripheral vein and NOT UVC. 

b. Rate of exchange 3 minutes/cycle (1 min in, 1 min pause and 1 min out) and total 

exchange should be about 90 minutes. 

c. Exchange should start with removal of blood, so that there is always a deficit to avoid 

cardiac overload. 

d. If child anaemic (Hb < 15) give an extra aliquot volume of blood at the end, leaving a 

positive balance). 

e. Always discard the serum and the last portion of blood remaining in the tubing to avoid 

electrolyte imbalance. 

f. If initial SB is > 25mg%, DO NOT remove the UVC as ET may need to be repeated. 

g. Place back under phototherapy lights after the procedure 

h. Feed after 3 hours. 

Investigations 

a. Pre-exchange (1st volume of blood removed) 

i) Serum Bilirubin 

ii) FBC 

iii) Blood glucose 

iv) Serum electrolytes 

v) Serum calcium 

vi) Blood gases 

vii) Others e.g. Blood C&S as indicated 

b. Post-exchange (Last volume of blood 

removed) 

i) Serum Bilirubin 

ii) FBC 

iii) Blood Sugar 

iv) Serum electrolytes 

v) Serum Calcium 

vi) Blood gases 

c. 6 hour post-exchange 

i) SB 

Complications of ET 

1. Catheter related 

a. Infection 

b. Haemorrhage 

c. NEC 

d. Portal and splenic vein thrombosis 

e. Air embolism 

2. Haemodynamic problems 

a. Overload cardiac failure 

b. Hypovolaemic shock 

c. Arrhythmia (Catheter tip near sinus 

node in R Atria) 

3. Electrolyte imbalance 

a. K+ 

b. Ca 

c. or Blood glucose 

d. Acidosis (sometimes late alkalosis due 

to breakdown of citrate) 

Tissue hypoxia (old blood) 

Follow-up 

1. Review SB at Polyclinic 2 days after discharge. 

2. For infant who had exchange transfusion, follow-up for 2 years and discharge if normal. 

Look for signs of deafness, cerebral palsy and mental retardation.

PROLONGED NEONATAL JAUNDICE 

Definition: Visible jaundice (or serum bilirubin (SB) >100 umol/L) that persists beyond 

14 days of life in a term infant or 21 days in a preterm infant 

Importance: The early diagnosis of biliary atresia and hypothyroidism is very important 

for favourable long-term outcome of the patient. 

An investigation as to the underlying cause is a matter of great urgency! 

Causes of Prolonged Neonatal Jaundice 

Conjugated Hyperbilirubinaemia Unconjugated Hyperbilirubinaemia 

Neonatal Hepatitis Syndrome Septicaemia or UTI 

Biliary Atresia Haemolysis 

Choledochal Cyst Breast milk Jaundice 

Septicaemia or UTI Hypothyroidism 

Congenital Infection (TORCHES) Galactosaemia 

Metabolic Disorders (e.g. galactosaemia 

or -1 antitrypsin deficiency). 

Post Total Parenteral Nutrition 

Initial Management 

Child well 

Child unwell or 

pale stool 

Investigate at OPD 

Initial Investigations 

Total and fractionated SB 

Serum T4,TSH. 

Urine FEME and C&S. 

Urine reducing sugar & 

G6PD Status if screening 

results not available. 

FBC, Retic count and Film 

Admit for 

investigations 

and treatment 

Further Ix depends on 

whether it is unconjugated or 

conjugated 

hyperbilirubinaemia 

If it is obstructive (conjugated) jaundice admit 

For Further 

Investigations 

as below

a. If unconjugated hyperbilirubinaemia, 

Admit if SB is >300umol/L or child unwell. Otherwise follow-up with weekly SB. 

Important investigations are; Thyroid Function Tests, Urine FEME, C&S and reducing 

sugar, and FBC, Retic count & Film 

Exclude UTI and Hypothyroidism. 

Congenital Hypothyroidism is a neonatal emergency. (Check Screening TSH 

result if done at birth). See protocol on Congenital Hypothyroidism. 

FBC to be done for AB0, G6PD deficiency and Rh incompatibility at 6 weeks to look 

for anaemia. KIV Haematinics. 

Breast milk Jaundice is a diagnosis of exclusion. Child must be well, gaining 

weight appropriately, breast-feeds well and stool is yellow. Management is to 

continue breast-feeding. There is a need to tell the parents that the jaundice is likely 

due to BM but it is usually of no harm and conversely may confer benefit as bilirubin is 

a strong anti-oxidant. Rarely, if the SB is too high (i.e. 25 mg%) then withdrawal of BM 

for 48 hours may be appropriate after which breast-feeding should continue. In the 

meantime the mother should express her milk to ensure her supply does not diminish. 

b. If conjugated hyperbilirubinaemia (conjugated bilirubin > 2mg%) 

Admit and observe colour of stool for 3 consecutive days. Further investigations 

should include LFT, Hep B and C status, TORCHES and VDRL tests 

Start phenobarbitone on admission at 5 mg/kg OD for 5 days to prime the liver for 

HIDA scan if eventually required. 

If the stool is pale over 3 consecutive days, suspect biliary atresia, and refer to 

paediatric surgery. Plans should be made for : 

a) Ultrasound of liver 

Preferably done after 4 hours of fasting, dilated intrahepatic bile ducts and absent 

gall bladder is highly suspicious of extra hepatic biliary atresia. 

b) HIDA Scan (if available) after 5 days of phenobarbitone. 

Slow uptake with normal excretion: Neonatal Hepatitis syndrome. 

Normal uptake with absent excretion: EH Biliary Atresia 

c) Liver biopsy (hardly ever done now) 

With a good pathologist biliary atresia can be confirmed in 85% by biopsy. 

Ensure PT and aPTT normal. If not give Vit K 1 mg IV. 

Platelet count at least 40 000 

d) Operative Cholangiogram followed by definitive surgery if necessary. 

This is now the investigation of choice in most centres.

Biliary Atresia 

The importance of distinguishing biliary atresia from neonatal hepatitis is that surgery for 

the former (Kasai Procedure) may be successful if carried out within the first 2 months of 

life. 

With early diagnosis and biliary drainage through a Kasai Procedure before 60 days of 

age, successful long-term biliary drainage is achieved in >80% of children. In later 

surgery good bile flow is achieved only in 20-30%. Liver transplantation is indicated if 

there is failure to achieve or maintain bile drainage. 

Neonatal Hepatitis Syndrome 

Follow up with LFT fortnightly. Watch out for liver failure and bleeding tendency (Vit K 

deficiency). 

Repeat Hepatitis B & C screening at 6 weeks. 

Most infants with neonatal hepatitis make a complete recovery. 

Reference: 

1. Lactation Management Course. 

2. Nelson’s Textbook Of Pediatrics. 

3. Arneil and Forfar’s Paediatrics.

APNOEA IN THE NEWBORN 

Definition : Pause in breathing lasting > 15 sec (term) or >20sec (preterm) during 

which the infant may develop cyanosis (SpO2 < 80%) and bradycardia (heart rate < 

100 per min). In very immature infants, shorter duration of apnoea may produce 

bradycardia and cyanosis. 

Types: Central – absence of respiratory effort with no gas flow 

Obstructive – continued ineffective respiratory effort with no gas flow 

Mixed central and obstructive 

Periodic breathing – Regular sequence of respiratory pauses of 10-20 sec 

interspersed with periods of hyperventilation (4-15 sec) and occurring at least 3x/ 

minute, not associated with cyanosis or bradycardia. 

Aetiology 

Symptomatic of underlying problems commoner ones of which are: 

1. Respiratory conditions – RDS, pulmonary haemorrhage, pneumothorax, 

Upper airway obstruction, respiratory depression 2 drugs 

2. Sepsis 

3. Hypoxaemia 

4. Hypothermia 

5. CNS abnormality e.g. IVH, asphyxia, increased ICP, seizures 

6. Metabolic disturbances – hypoglycaemia, hyponatraemia, hypocalcaemia 

7. Cardiac failure, congenital heart disease, anaemia 

8. Aspiration/ Gastro-oesophageal reflux 

9. NEC/ Abdomen distension 

10. Vagal reflex: Nasogastric tube insertion, suctioning, feeding 

Recurrent apnoea of prematurity 

- usually occur after 3 days of life with no other pathological conditions. Most 

disappear by 34- 36 weeks, but some may persist even after 40 weeks ‘corrected’ 

gestation. 

Management 

1. Immediate resuscitation. 

Surface stimulation 

(Flick soles, touch baby) 

Gentle nasopharyngeal suction 

(Be careful: may prolong apnoea) 

Ventilate with bag and mask on previous FiO2. 

Be careful not to use supplementary oxygen if the infant has been in air as the child's 

lungs are usually normal and a high PaO2 may result in ROP. 

Intubate and IPPV if child cyanosed or apnoea recurrent/persistent

2. Review possible causes (as above) and institute specific therapy 

e.g. Septic workup if sepsis suspected and commence antibiotics 

Remember to check blood glucose via glucometer. 

3. Management to prevent recurrence. 

Ref 

a. Keep at thermoneutral range. Nursing prone may reduce episodes of 

apnoea. 

b. Titrate the FiO2 to keep the PaO2 between 50 - 80 mmHg 

c. Monitoring: 

Apnoea monitor 

Problem with movement sensitive devices:- 

- Very small infants have imperceptible shallow breathing that 

causes frequent false alarms. 

- Some apnoeic infant will struggle for some time becoming 

progressively hypoxic before lying still and triggering the 

monitor alarm. 

Pulse Oximeter 

d. Drug therapy: 

IV Aminophylline 

Oral Theophylline 

e. If repeated attacks. 

Regular prophylactic tactile/surface stimulation 

Nasal CPAP (3 - 4 cm of H2O) 

IPPV (usually low settings) 

1. N.R.C. Roberton. Textbook of Neonatology. Churchill Livingstone 

2. Gomella, Cunningham, Eyal and Zenk. Neonatology. 4 th edition Lange 

3. Halliday, McClure and Reid. Neonatal Intensive Care. 4 th edition. Saunders 

4. Rennie and Roberton. Manual of Neonatal Intensive Care 4 th edition Arnold

History 

NEONATAL SEPSIS 

Septic Neonates deteriorate very rapidly within hours, therefore: 

1) Early diagnosis essential 

- even very trivial clinical findings suggesting infection demands full laboratory 

evaluation. 

2) Initial therapy must be started on clinical suspicion. 

Common Bacterial Infection in New-borns and the Antibiotic of Choice 

Bacteria Antibiotic of Choice Comments 

Group B Streptococcus Penicillin / Cefotaxime 70 - 80% 

E. Coli Cefotaxime ± Gentamycin of early 

onsetneonatal 

infection 

Pseudomonas Ceftazidime ± Gentamycin 

Other Gram negative bacilli Cefotaxime ± Gentamycin 

Staphylococcus Cloxacillin 

Listeria Monocytogenes Ampicillin + Gentamycin 

Anaerobes Metronidazole 

Candida Fluconazole / Amphotericin 

1. Is the infant compromised? (e.g. prematurity, indwelling catheter, endotracheal tube) 

2. Perinatal history (prolong rupture of membrane, maternal fever, positive HVS) 

3. Risk of nosocomial infection from staff, relatives or other sick infants. 

Early signs & symptoms 

1. Temperature instability: Hypo & Hyperthermia 

• 37.5 o C for >1hr or 2hrs in an appropriate environmental 

temperature is due to infection until proven otherwise. 

2. Refusal to feed in a previously healthy baby. 

3. Poor weight gain. 

4. Listlessness, lethargy, hypotonia, pallor, mottled skin 

• Baby just doesn't seem right 

• When a nurse tells you this, please take serious note 

5. Irritable; will not stop crying or whimpering even after feeding. 

6. Rapidly increasing neonatal jaundice in the absence of haemolytic disease. 

7. Vomiting and Diarrhoea (NB ‘Acute Gastroenteritis’ in a neonate is septicaemia 

until proven otherwise) 

8. Ileus/intestinal obstruction - vomiting, abdominal distension and constipation 

9. Pseudoparalysis - arthritis/osteomyelitis 

10. Apnoea - common early sign in Prems. 

11. Tachypnoea 

Investigations

Always: 

1. FBC: Hb, TWBC with differential count, Platelet. 

There is normally a leucocytosis up to 30 x10 9 /L at birth. 

Indicators of infection: 

1st day - Neutropenia; immature cells & toxic granulation 

Beyond 3 days- Polymorph > 7.5-8.0x10 9 /L or < 2x10 9 /L 

Monocytes > 0.8 x 10 9 /L 

Both thrombocytopenia and thrombocytosis may implicate infection 

2.. Blood C&S 

When available: 

1. C reactive protein (CRP) : A raised CRP is presumptive of infection and will help in 

deciding on the start of antibiotics if clinical picture is uncertain till the result of culture and 

sensitivity is available. It may also help in deciding on the duration of antibiotic therapy. 

When indicated : 

1. Lumbar Puncture (CSF biochemistry, microscopy, latex agglutination for bacterial 

antigen and culture and sensitivity) 

2. CXR 

3. AXR 

4. Maternal HVS C&S (Ring up postnatal ward to see if it has been done) 

5. Culture of ETT aspirate 

6. Culture of tip of IV cannula / umbilical catheters. 

7. Urine FEME and C&S / SPA urine C&S 

8. ABG 

Treatment 

1. Antibiotics 

- Start immediately when diagnosis is suspected and after all appropriate specimens 

taken. Do not wait for C&S result! 

Recommended Empiric Therapy: 

For early-onset infection: 

IV Penicillin and IV Gentamycin to cover for GBS and Pneumococci. / Gram negative 

organisms (Use high dose Penicillin 100,000U/kg) 

For late-onset community acquired infection: 

IV Cloxacillin and Gentamycin to cover for Staphylococci / Gram negative organisms in 

non-CNS sepsis, cefotaxime and penicillin for CNS infection 

For nosocomial (hospital acquired) infections:

Antibiotic choice will depend on prevailing infecting organisms and their sensitivities. A 

carbapenem and vancomycin are often used in units where ESBL and MRSA/MRSE are 

common 

- Add metronidazole if intra-abdominal sepsis or NEC present. 

- Consider fungal septicaemia if child does not respond especially preterm with or without 

long lines and usage of TPN. 

Adjust final antibiotics according to C&S results. 

Duration of therapy: 

- If cultures are negative and infection is clinically unlikely after further review, off 

antibiotics by 48-72 hours. 

- If proven infection: 10 days for septicaemia, 7-14 days for pneumonia and 14 to 21 

days for meningitis and septicaemia 

2. Supportive Measures 

i) Monitoring: Temp, fluid balance, weight, hydration state, ABG 

ii) Temperature control 

- servo - controlled incubator is contraindicated as it will affect temperature 

recording. 

- maintain environment temp at top end or above the normal thermoneutral range. 

iii) Treatment of Shock - hypotension esp. in Gram-neg. septicaemia. 

- Keep MAP to around Gestation + 5 mmHg 

- May need to transfuse albumin or FFP (Albumin 25% give 4 ml/kg made up with 

NaCl to 20 ml/kg) 

- Start inotropes ( dopamine / dobutamine/adrenaline or noradrenalin) as indicated 

iv) Removal of central lines - Remove UAC or UVC in NEC or other abdominal sepsis. 

Also consider removal of UAC, UVC and peripherally –inserted central venous catheter if 

sepsis is not readily cleared 

v) If DIVC occurs 

- Check APTT, PT, Platelet count 

- treat with FFP/cryoprecipitate/platelet or blood transfusion as indicated 

Prevention 

The prevention of cross infections in the NNU is of utmost importance. The most 

effective preventive measure is hand washing. Other infection control measures e.g. 

aseptic techniques in patient procedures must also be strictly adhered to. 

References: 

N.R.C. Roberton. Textbook of Neonatology. Churchill Livingstone

Contents Chapter Topic Page Neonatology Respiratory Cardiology

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