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 Hematology / Oncology

50 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

Metabolic / Genetics

71 General Approach to Inborn Errors Of Metabolism……….. 410 72 Algorithm For The Sick Infant to Screen for Treatable

IEM……………………………………………………………… 416

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

Contributors 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 Consultant Paediatrician Selayang Hospital Dr. Chieng Chae Hee Paediatrician, Hospital Sibu Dr. Chin Choy Nyok Consultant Paediatric Neonatologist & Head Dept. of Pediatrics Hospital Kuantan Dr. Choy Yew Sing Consultant Paediatric Geneticist Hospital Kuala Lumpur Dr. Eni Juraida Consultant Paediatric Oncologist Hospital Kuala Lumpur Dr. Fong Siew Moy Consultant Paediatric Infectious Disease Specialist Hospital Queen Elizabeth Kota Kinabalu Dr. Fuziah Md. Zain Consultant Paediatric Endocrinologist & Head Dept. of Pediatrics Hospital Putrajaya

Dr. Hishamshah b. Mohd Ibrahim Consultant Paediatric Oncologist Hospital Kuala Lumpur Dr. Hung Liang Choo. Consultant Paediatric Cardiologist Hospital Kuala Lumpur Dr. Hussain Imam B. Hj Muhammad Ismail Consultant Paediatric Neurologist & Head Dept of Pediatrics Hospital Kuala Lumpur Dr. Irene Cheah Consultant Paediatrician Hospital Kuala Lumpur Datuk Dr. Jimmy Lee Kok Foo Consultant Paediatrician & Head Dept of Pediatrics Hospital Kuala Terengganu Dr. Kamarul Razali Consultant Paediatric Infectious Disease Specialist Hospital Kuala Lumpur Dr. Khoo Teik Beng Consultant Paediatric Neurologist Hospital Kuala Lumpur Dr. Kok Juan Loong Consultant Paediatrician Sarawak General Hospital Dr. Lee Ming Lee Consultant Paediatric Nephrologist Hospital Seremban Dr. Leow Poy Lee Consultant Paediatrician Hospital Malacca Dr. Liew Siaw Phin Private Paediatrician Kuching Dr. Lim Chooi Bee Consultant Paediatric Gastroenterologist Hospital Kuala Lumpur

Dato’ Dr. Lim Nyok Ling Consultant Paediatric Neonatologist & Head Dept of Pediatrics Selayang Hospital Dr. Lim Poi Giok Consultant Paediatrician Hospital Kuala Lumpur Dr. Lim Yam Ngo Consultant Paediatric Nephrologist Hospital Kuala Lumpur Dr. Lynster Liaw Consultant Paediatric Nephrologist Department of Paediatrics Hospital Pulau Pinang Dr. Mardziah bt Alias Consultant Paediatric Dermatologist Hospital Kuala Lumpur Dr. Mohd Hanifah bin Mohd Jamil Consultant Neonatologist & Head Dept. of Pediatrics Hospital Kota Baru Dr Neoh Siew Hong Consultant Neonatologist Hospital Taiping Dr. Ng Hoong Phak Consultant Paediatrician, Sarawak General Hospital Dr. Ngu Lock Hock Consultant Paediatrician, Hospital Kuala Lumpur Dr. Nik Khairulddin Consultant Paediatric Infectious Disease Specialist Hospital Kota Baru Dr. Norzila Bt. Mohd Zainudin Paediatric Respiratory Disease Specialist Hospital Kuala Lumpur Dr. Ong Gek Bee Consultant Paediatric Oncologist, Hospital Melaka Prof. Dr. Ong Lai Choo. Consultant Paediatric Neurologist Hospital University Kebangsaan Malaysia

Dr. Revathy Nallusamy Consultant Paediatric Infectious Disease 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 Consultant Paediatric Nephrologist Hospital Sultanah Aminah, Johor Bharu Dr. Tan Kah Kee Consultant Paediatric Infectious Disease 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 & Head Dept of Pediatrics Hospital Alor Setar Dr. Wan Jazilah Wan Ismail Consultant Paediatric Nephrologist Hospital Selayang Dr. Wilson Pau Paediatric Clinical Specialist Sarawak General Hospital Dr. Zuraidah Bt Abdul Latif Consultant Neonatologist 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

NORMAL VALUES IN PAEDIATRICSA. Vital Signs

Normal Respiratory RateInfant 30 - 40Toddler 24 - 40 School Age 18 - 30 Adolescent 12 - 16

Normal Heart Rate (from Gillette 1989)2 Awake

Mean Sleeping< 3 months 85 - 205 140 80 - 1603 mo to 2 yr. 100 - 190 130 75 - 1602 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:

Blood Pressure in HypertensionSignificant Hypertension Severe Hypertension

1 week Systolic 96 Systolic 1067d - 1 mo Systolic 104 Systolic 110

Infant Systolic 112 Systolic 118Diastolic 74 Diastolic 82

3 - 5 years Systolic 116 Systolic 124Diastolic 76 Diastolic 86

6 - 9 years Systolic 122 Systolic 130Diastolic 78 Diastolic 86

10 - 12 years Systolic 126 Systolic 134Diastolic 82 Diastolic 90

13 - 15 years Systolic 136 Systolic 144Diastolic 86 Diastolic 92

16 - 18 years Systolic 142 Systolic 150Diastolic 92 Diastolic 98

Normal Blood Pressure (from Hazinski MF 1992)1

Systolic DiastolicDay 1 (< 1000g)39 - 59 16 - 36Day 1 (> 3000g)50 - 70 25 - 45Neonate 60 - 90 20 - 60Infant 87 - 105 53 - 66Toddler 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 > 601 mo - 1 yr. > 70Older > 70 + (2 x age in years)

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 cm4 - 6 mo. 1 cm per mo. Second yr. 2 cm6 - 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)Lowest

MCH (pg/cell). Lowest

TWBC(x1000)

Neu(Mean)

Lymp(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 40 633 mo 9.5–14.5 31-41 27 6-18 30 486 mo –6 yr

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

7-12 yr 11.0–16.0 34-401.0

76-80 26-32 4.5-13.5 55 38Adult Male

14.0–18.0 42-52 27-32

Adult Female

12.0–16.0 37-471.6 80

26-345-10 55 35

Eosinophils: 2-3%Monocytes: 6-9 %

Platelets are mildly decreased in 1st few months, by 6 months have reached 250 - 300 x 109.ESR should be < 16 in childhood provided PCV at least 35%.

b) Differential WBC

< 7 days - neutrophils > lymphocytes1 w - 4 yr. - lymphocytes > neutrophils4 - 7 yr. - neutrophils = lymphocytes> 7 yr. - neutrophils > lymphocytes

Hb electrophoresis – look under Thalassaemia protocol.

D. Others

Body Surface Area (BSA) (m2 ) = Ht (cm) x Wt (Kg)3600

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

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Immunisation

1. Immunisation schedule for Malaysia

Table 1: The current Immunisation Schedule Age (months) Age (Years)Immunisation0 1 2 3 5 6 12 18 6 12 15

BCG* 1 if no scarHep B 1 2 3DPT 1 2 3 4 DT TOPV* 1 2 3 4 5Hib 1 2 3Measles* SabahMMR* 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

3.5.1 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 3.4as 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 Weeks 3 Months

Live Vaccine HNIG Live Vaccine

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 OPVVaccine associated paralytic polio (VAPP) risk at 1 case/ 5.3 million doses highest risk after 1st 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 IPVNo serious side effects have been documented, apart from local reaction. Indicated for children with severe immunocompromised conditions e.g.immunodeficiency states (1o and 2o 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 1st 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

Age at first visitTime of ImmunisationBetween 6 weeks and 9 months

9 months and older

1st visit BCG, DPT-Hib1, OPV1 & HBV1

BCG, DPT1-Hib, OPV1 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 HBV32-8 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 Malaysia2. Immunization Precautions and Contraindications (2nd 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.(6th Edition). 2002.6. Cholera vaccines. WHO position paper ; Weekly Epidemiol Rec 2001;76:117-1247. 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 over8 mo Does not sit without support10 mo Does not stand while holding on18 mo Not walking unaided2 yr Not climbing up or down stairs2 ½ yr Not jumping with both feet3 yr Unable to stand on one foot momentarily4 yr Not hopping5 yr Unable to walk a straight line

back and forth or balance on onefoot

C. Fine Motor

5 mo Unable to hold rattle7 mo Unable to hold an object in each

hand12 mo Absence of pincer grasp15 mo Unable to put in or take out2 yr Not scribbling2 ½ yr Not turning a single page of a

book3 yr Unable to draw a straight line4 yr Unable to copy a circle5 yr Unable to copy a cross

D. Language

6 mo Not babbling9 mo Not saying “da” or “ba”11 mo Not saying “dada” or “baba”18 mo Has < 3 words with meaning2 yr No two-word phrases2 ½ yr Speech unintelligible to parents3 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 smile6-8 mo Not laughing in playful situation1 yr Hard to console, stiffens when

approached18 mo Not pointing to indicate wants2 yr Kicks, bites, and screams easily

and without provocationRocks 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 mother9 mo No interest in peek-a-boo12 mo Does not search for hidden object18 mo No interest in cause-and-effect

games2 yr Does not know categories3 yr Does not know own full name4 yr Cannot pick shorter or longer of

two lines4 ½ yr Cannot count sequentially5 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

Auditory Tests

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).

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.

Normal Hearing

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 level8 months Turns to sound source above ear level.12 months Looks up to sound above head

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 VisionWhen 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 < 90o, visual acuity 6/60 at this stage.

8 weeks Fixation, convergence, focusing.

12 weeks Hand regard. Dangling object 180o. 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

NB. If vision improves when child reads through pinhole, refer to optician for spectacles.Corneal reflection test for squintRefer funny looking eyes, abnormal eye movements/head posture.

At riskPrematurity.Small for Gestation.Family history of cataract, retinoblastoma, squint.

Global Developmental Delay

HistoryConsanguinityPregnancy: Drugs, Alcohol or Illnesses.Delivery: Premature or Birth AsphyxiaNeonatal: 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 boyso EEG if history suggestive of possible seizures

Isolated Speech Delay

HistoryCongenital RubellaPerinatal DrugsSevere Neonatal JaundiceFamily HistoryEar InfectionAsk for Quality and Quantity of speech

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

Consider1. Hypothyroidism2. Chromosomal anomaly e.g. Down or Fragile X3. Structural Brain Disorder4. Cerebral Palsy5. Congenital Infection6. Specific Syndromes including tuberous sclerosis or neurofibromatosis.7. Inborn error of metabolism8. Postnatal causes like head injury, intracranial bleed, CNS infections.9. Muscular Dystrophies10. Autism

Consider1. Hearing Impairment2. Familial or Genetic causes3. Social Cultural Deprivation4. IQ Low (Mental Retardation)5. Language Confusion6. Autism7. Hypothyroidism

Delayed Motor Development

Learning Difficulties In School

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;330:478-4834. Shevell M et al. Practice parameter: Evaluation of the child with global developmental delay.

Neurology 2003;60:367-380

Consider1. Normal or Familial variation2. Previous Chronic Illness3. Cerebral Palsy4. Neuromuscular Diseases e.g.

Duchenne Muscular Dystrophy5. Orthopaedic Problems6. Emotional Neglect

Consider1. Previous developmental delay2. Medical Problems

Hypothyroidism Iron deficiency anaemia Chronic lead poisoning Epilepsy (eg Absence Seizures)

3. Specific Learning Difficulty (Dyslexia)

Developmental Milestones Table

AGE Gross Motor Vision & Fine Motor Speech & Language Personal Social6 weeks Pull to sit: Head lag and rounded back.

Ventral Suspension: Head momentarily in same plane as body.Prone: Pelvis high but knees no longer under abdomen. Chin raised occasionally.

Fixates and follows to 90 Vocalising by 8/52Quiets to sound. Startles to sound.

Smiles responsively.

3 months Pull to sit: Only slight head lag. Head occasionally bobs forward.Ventral Suspension: Head above plane of body.Prone: Pelvis flat. Lifts head up 45° - 90°.

Hand regard.Follows object from side to side (180°)Hands held loosely.Grasp object placed in hand. Not reaching out.

Squeals with delight.Turns head to sound.

Laughs.

5 months Pull to sit: NO head lag and sits with straight back.Lying supine : Feet to mouth.

Reaches for objects.Plays with toes.

Mouthing.

6 months Pulls to sit: Lifts head off couch in anticipation.Sits with support.Bears full weight on legs.Prone: Supports weight on hands with chest and upper abdomen off couch.Rolls prone to supine.

Palmar grasp of cube with ulnar approach.Moves head and eyes in all directions.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.

AGE Gross Motor Vision & Fine Motor Speech & Language Personal Social9 months Sits steadily. Leans forward but cannot

pivot.Stands holding on.Pulls self to stand.

Inferior pincer grasp. (Scissors grasp).

Localises sound at 3 feet, above and below the ear level.

Feeds with spoon occasionally.Looks for fallen toys.Understands “NO!”

10 months Crawls on abdomen.Pull self to sit.

Index approach. Uses index finger to poke at pea.Able to let go of cube in hand.

Waves “Bye bye”Plays “Pat-a-Cake”

11 months Creeping on all FOURSPivoting.Cruising.Walks with 2 hands held.

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

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.

Neat pincer grasp.Bangs 2 cubes.Sees and picks up hundreds and thousands.

Understands phases. (e.g. where is your shoes).2 - 3 words with meaning.Localising sound above head.

Casting (13 months)Less mouthing.Shy.

15 months Creeps upstairs.Stoops for toy and stands up without support. (best at 18 months)

Tower of 2 cubes.Scribbles spontaneously (15-18 months)

More words.Points to objects he wants.Continual jabber and jargon.

Takes off shoe.Feeds self with cup (able to pick up and put down) and spoon (but spills).Mouthing stops.

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.

Tower of 3 cubes.Scribbles spontaneously.Visual test: Picture charts.Handedness (18 - 14 months).

Points to 2 - 3 body parts.Picture Cards - identify one.

Imitates housework.Toilet trained.Uses spoon well.Casting stops.

AGE Gross Motor Vision & Fine Motor Speech & Language Personal Social2 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.

Tower of 6 cubesImitates cube of train with no chimney.

Imitates straight line.

Visual test: Snellen chart.

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.

Puts on shoes, socks, pants.Dry by day.Play near other children but not with them.

2 1/2 years

Jumps on both feet.Walks on tip toes.

Tower of 8.Imitates train with chimney.

Holds pencil well.

Imitates and .

Knows FULL name and sex.Names one colour.

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.

Tower of 9.Imitates bridge. with cubes:

Copies Imitates Draw a man test. (3 - 10y)

Can count to 10Names 2 colours.Nursery rhymes.Understands “on”, “in”, “under”.

Unbuttons.Dresses and undresses fully if helped with buttons and advised about correct shoe.Dry by night.Plays with others.

3 1/2 years

Copies bridge.

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

Imitates gate with cubes.Copies

Goodenough test 4.

Names 3 colours.Fluent conversation.Understands “in front of”, “between”, behind”.

Buttons clothes fully.Attends to own toilet needs.

4 1/2 years

Copies gate with cubes.Copies square.Draws recognisable man and house.

AGE Gross Motor Vision & Fine Motor Speech & Language Personal Social5 years Skips on both feet.

Runs on toes.Copies ‘X’ (5 years)

Copies (5½ years) triangle.Goodenough test 8.

Knows AGE.Names 4 colours.Triple order preposition.Tell time.

Ties shoelaces.Dresses and undresses alone.

6 years Walks heel to toeKicking, throwing, climbing.

Copies

Goodenough test 12.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

• 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

Supine abdominal X-ray showing free

intraperitoneal gas – loss of liver

shadow, falciform ligament seen and

Wrigler’s sign

Wrigler’s sign

Loss of Liver shadow

Falciform ligament seen

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 )

• 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 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

• 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

• 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

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

• 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

Apgar Score Apgar score

0 1 2

Colour (Appearance)

Blue or Pale

Pink centrally. Blue extremities

Completely Pink

Heart Rate Absent < 100/min > 100/min

Response to nasal stimuli (Grimace)

No Grimace Cough or sneeze

Tone (Activity) Limp Some flexion Active movement

Breathing (Respiration)

Absent Slow, irregular Cry

Vigorous cry

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 <7 at 5 minutes the Apgar Score is repeated every 5 minutes up to 20 minutes to note the progress. Apgar score at 20 minutes is a good prognostic index for neurological outcome.

Preparing for Resuscitation A staff should be assigned to check resuscitation equipment at every shift and replenish after every resuscitation.

Equipment for Resuscitation

1. Resuscitation trolley 2. Stop clock (with second hand). In working order. 3. Overhead heater and light. Turn heater on well before delivery.

Resuscitation area should not receive draughts from air conditioner or fan.

4. Resuscitation area which is padded shelf and covered with a clean dry cloth

5. 2 laryngoscopes with spare bulbs and batteries (size 0 and 1,straight blade laryngoscope and check lights)

6. Masks for preterm and term infants 7. 250ml Self-inflating Bags with oxygen reservoir. Blow off valve working. 8. Wall or Oxygen cylinder with flow meter and connecting tubes. Ensure

tank is full or nearly full. 9. Suction apparatus (Set at not > 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.

1. Evaluate Respiration **

Spontaneous None or gasping

2. Evaluate Heart Rate (Count for 6 seconds,X10)

Can attempt tactile stimulation once only and briefly. Slap foot, flick heel, or rub back.

> 100/min

3. Evaluate Colour

Blue Pink or peripheral cyanosis

Observe and monitor

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.

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

< 100/min

Evaluate Heart Rate

After 30 secs of PPV with 100 % O2

Below 60

• Continue ventilation

• Chest Compressions

60-100

⇒ Discontinue chest compressions

⇒ Continue ventilation

Above 100

• Watch for spontaneous respiration (and do appropriate bagging if nil)

• Once spontaneous respiration is established discontinue ventilation.

Reevaluate every 30 secs

Initiate medications if HR below 60 after 30 secs of PPV with 100% oxygen and chest compressions.

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:

� Tracheal suctioning can be done by

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.

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.

Infant vigorous? - Good respiration

-- HR > 100/min

-- Good muscle tone

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 YES

NO

Medications used in Neonatal Resuscitation: Type Indications Concentration

to Administer Prepara-tion

Dosage/ Route

Rate/ Precautions

Adrenaline 1) HR < 60/min despite a minimum of 30 seconds of adequate ventilation with 100 % O2 and chest compressions.

2) Heart rate is zero.

1:10 000

(The only preparation available is 1:1000. Dilute 1ml of Adrenaline 1:1000 with distilled water to 10ml)

1 ml 0.01-0.03 mg/kg. 0.1-0.3 ml/kg. IV or ET

Give rapidly. May dilute with normal saline to 1-2 ml if giving via ET.

Volume Expanders

1) Prolonged arrest not responding to resuscitation 2)Evidence or suspicion of acute blood loss with signs of hypovolaemia

Normal Saline Ringer's lactate

40 ml 10 ml/kg IV

Give over 5 – 10 minutes. Give by syringe or IV drip.

Sodium Bicarb.

1)Severe metabolic acidosis is suspected or proven by blood analysis; 2)Prolonged arrest not responding to resuscitation

0.5 mEq/ml (4.2% solution)

20 ml or two 10-ml pre-filled syringes

2 mEg/Kg IV only. (4 ml/kg)

Give slowly, over at least 2 minutes. Give only if infant is being effectively ventilated.

0.4 mg/ml (dilution that is usually available)

0.1 mg/kg (0.25 ml/kg) IV ET IM SC

Naloxone HCl

Severe respiratory depression and a history of maternal narcotics administered within the past 4 hours.

1.0 mg/ml

1 ml

0.1 mg/kg (0.1 ml/kg) IV ET IM SC

Give rapidly. IV, ET preferred. IM, SC acceptable.

Summary: Use of medications during neonatal resuscitation:

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

May be repeated every 3-5 minutes if required

HR above 100?

Discontinue medications

Prolonged arrest that does not respond to other therapy? Give sodium bicarbonate

Evidence or suspicion of acute blood loss with signs of hypovolaemia Give volume expander

May be repeated if signs of hypovolaemia persist

Yes

No

Evidence of continuing depression?

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

Give Naloxone hydrochloride.

Special Circumstances in Resuscitation of the Newly Born Infant

Condition History/Clinical Signs Actions

Mechanical blockage of the airway

Meconium or mucus blockage

Meconium-stained amniotic fluid. Poor chest wall movement.

Intubation for suctioning / ventilation

Choanal Atresia Pink when crying, cyanotic when quiet

Oral airway. Endotracheal intubation

Pharyngeal airway malformation

Persistent retractions, poor air entry

Prone positioning, posterior nasopharyngeal tube

Impaired lung function

Pneumothorax Asymmetrical breath sounds. Persistent cyanosis / bradycardia

Needle thoracentesis

Pleural effusion / ascites Diminished air movement. Persistent cyanosis / bradycardia

Immediate intubation. Needle thoracentesis, paracenteris. Possible volume expansion.

Congenital diaphragmatic hernia

Asymmetrical breath sounds. Persistent cyanosis/bradycardia. Scaphoid abdomen

Endotracheal intubation. Placement of orogastric catheter

Pneumonia/sepsis Diminished air movement. Persistent cyanosis / bradycardia

Endotracheal intubation. Possible volume expansion

Impaired cardiac function

Congenital heart disease Persistent cyanosis / bradycardia

Diagnostic evaluation

Foetal / maternal haemorrhage

Pallor; poor response to resuscitation

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).

THE PREMATURE INFANT

Definition Premature infant: < 37 weeks gestation 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 and 1 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 <1250 g. (some centers < 1500 g)

b. all preterms <36 weeks who received oxygen therapy depending on individual risk as assessed by the clinician The infants are discharged once they are well, thriving and achieved a weight of 1.8 kg and/or gestational age of at least 34 weeks. Vitamins on discharge home a. Multivitamin (volume depending on preparation)OD c. Elemental Iron 2mg/kg OD (maximum of 15mg/day)

Prognosis Mortality and morbidity are inversely related to gestation and birth weight. Complications include Retinopathy of Prematurity, Chronic Lung Disease, Neurodevelopmental delay, Growth Failure, Cerebral palsy, Mental retardation, Epilepsy, Blindness and Deafness. References

1.Perinatal society of Malaysia. Clinical practice guideline in perinatology. First edition 1998; 11-15.

2. Department of Neonatal Medicine Protocol Book, Royal Prince Alfred Hospital

3. Roberton NRC, Rennie. Textbook of Neonatalogy (3rd edition )1999

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3-4 m

m bud

full areola

5-10 m

m bud

Eye/E

ar

lids fused

loosely: -1

tightly: -2

lids open

pinna flat

stays folded

sl. curved pinna;

soft; slow recoil

well-curved

pinna; soft but

ready recoil

form

ed &

firm

instant recoil

thick cartilage

ear stiff

Genit

als

(m

ale

) scrotum flat,

smooth

scrotum empty,

faint rugae

testes in upper

canal,

rare rugae

testes

descending,

few rugae

testes down,

good rugae

testes pendulous,

deep rugae

Genit

als

(fe

male

) clitoris

prominent &

labia flat

prominent

clitoris & small

labia m

inora

prominent clitoris

& enlarging

minora

majora &

minora equally

prominent

majora large,

minora small

majora cover

clitoris & m

inora

TO

TA

L P

HY

SIC

AL

MA

TU

RIT

Y S

CO

RE

MA

TU

RIT

Y

RA

TIN

G

Score

Weeks

-10

20

-5

22

0

24

5

26

10

28

15

30

20

32

25

34

30

36

35

38

40

40

45

42

50

44

References : Ballard JL, Khoury JC, Wedig K, et al: New

Ballard Score, expanded to include extrem

ely premature infants. J Pediatrics 1991; 119:417-423.

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 milk

Standard formula

Preterm formula

Mature 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/ lactalbumin ratio

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

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 slowly and initially use only EBM.8, 9

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, Tracheo-

esophageal 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 3rd to 4th 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 ElementsIs indicated if PN is administered for more than 1 week or longer. Commercial preparations for paediatric use are available.

2.8 VitaminsBoth 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. DeliveryThe 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 monitoringBefore 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 InfantsElizabeth Brine, MMSc, RD; Judith A. Ernst, DMSc, RD

4. Neonatology on the Web Teaching Files: Parenteral Nutrition (PN) for NeonateRay 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 state in exact hours of age. Beyond this state in

completed days.

ii) Weight : Note birth weight and current weight. An initial drop in weight is to be expected for newborn babies, term up to 10% BW in the first 3-5 days and preterm up to 15% in first 1-2 weeks. Abnormal weight gain or losses in the first few days often implicate suboptimal fluid therapy

iii) General condition e.g. ill, unstable, handles poorly e.g. desaturates on handling, stable, active, responsive to handling, improving, or good is to be noted

iv) Cardiopulmonary system. Check for:

a) Signs of poor perfusion (with poor peripheral pulses,

rapid pulse, poor capillary refilling and cold peripheries).

b) Adequacy of the blood pressure c) Examine for presence of a PDA in preterm infants

a) If perfusion is poor infuse a fluid bolus of 10 ml/kg of normal saline. This may

be repeated if there is no improvement. After the 2nd dose of normal saline 5%

albumin can be considered for volume expansion.

b) Inotropic agents like adrenaline, dobutamine or dopamine or amrinone may be needed.

V) Fluids and Electrolytes. Is the volume and type of fluid given to the child appropriate? Empiric fluid therapy for newborns

0-24 hours : 60 ml/kg/day 24-48 hours : 90ml/kg/day 48-72 hours : 120ml/kg/day > 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

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%

B. ETT Care ETT size <1000g size 2.5

1000g-2000g size 3 2000g-3000g size 3.5 >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 <0.5 sec for rates < 60 / min. Shortest inspiration time is 0.3 sec. Occasionally the time may be increased to 0.7 sec. for term babies.

2. The I:E ratio should not inverted (i.e. > 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%

b) 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 weightof 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 <0.22 or Fraction of inspired (FiO2) >0.5

Calculation for a/A PO2 ratio : PaO2 (mmHg) _________________________ (760-47)FiO2 –PaCO2 (mmHg)

2. Timing of therapyFirst 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 doses3.

3. Types of surfactant and dosageSurvanta, 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 administrationSurfactant 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 orii) 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 effectivenessStudies on the cost-effectiveness of surfactant therapy show that in spite of the high cost of drug, its use reduces cost per survivor7,8.

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):861-683. OSIRIS Collaborative Group. Early versus delayed administration of a synthetic surfactant:

the judgement of OSIRIS. Lancet 1992;340: 1363-13694. Broadbent R, Fok TF, Dolovich M, et al. Chest position and pulmonary deposition of

surfactant in surfactant depleted rabbits. Arch Dis Child 1995; 72: F84-95. 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: F174-86. Skinner J. The effects of surfactant on haemodynamics in hyaline membrabe disease. Arch

Dis Child 1997;76:F67-97. Mugford M, Piercy J, Chalmers I. Cost implications of different approaches to prevent

respiratory distress syndrome. Arch Dis Child 1991; 66; 757-648. 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 Acidosis1. 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 Acidosisi) Renal failureii) Septicaemiaiii) Hypoxiaiv) Hypothermiav) Hypotensionvi) Cardiac failurevii) Dehydrationviii) Hyperkalaemia

ix) Hyperglycaemiax) Anaemiaxi) Intraventricular haemorrhagexii) Drugs (e.g. acetazolamide which is

a carbonic anhydrase inhibitor)xiii) Metabolic disorders (often

associated with hypoglycaemia)

B. Causes of Alkalosis1. Respiratory alkalosisi) Asphyxia –over stimulation of

respiratory centreii) Over ventilation while on mechanical

ventilation

2. Metabolic alkalosisi) Administration of sodium

bicarbonateii) Pyloric stenosisiii) Hypokalaemiaiv) Use of diuretics like thiazides and

frusemide

C. Effects of acidosis and alkalosis in the body

1. Acidosisi) Depression of central nervous system (CNS)ii) Disorientation and comaiii) Increased depth and rate of respiration in metabolic acidosis and depressed

respiration in respiratory acidosisiv) High PaCO2 in respiratory acidosis increases cerebral blood flow and risk of

intraventricular haemorrhage

2. Alkalosisi) Over excitability of the CNSii) 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 7.34-7.45PaCO2 4.7-6.0 kpa (35-45 mmHg)HCO3

- 20-25 mmol/LPaO2 8-10 kpa (60-75 mmHg)BE ± 5 mmol/L

E. Interpretation of Blood Gases

1. pH <7.34 acidosisIf PaCO2 and HCO3

- are low and base deficit is high metabolic acidosisIf PaCO2 and HCO3

- are high and base excess is high respiratory acidosisIf both PaCO2 and base deficit are high mixed acidosis

2. pH > 7.45 alkalosisIf PaCO2 is low respiratory alkalosisIf 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 hypocarbiaHigh PaCO2 hypercarbia

4. Low PaO2 Hypoxaemia High PaO2 Hyperoxaemia

F. Management of Metabolic Acidosis and Alkalosis1. Prevention of risk factors for acidosis is important2. A base deficit of > 5 mmol/L (BE of > -5 mmol/l) in a very sick and premature (<32

weeks) infant usually needs some alkali therapy unless there is a readily corrected cause

3. A base deficit of > 10 mmol/L usually would need correction in most infants4. 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 alkalosis1. A steadily rising PCO2 at any stage in the disease is an indication that ventilatory

assistance is likely to be needed2. A sudden rise may be an indication of acute changes in the infant’s condition e.g.

pneumothorax, collapsed lobes, misplaced endotracheal tube3. 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 arteriosus5. 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 7.21PaCO2 6.6 kpaPaO2 7.5 kpaHCO3

- 20 mmol/LBE -4 mmol/L

Question (Q) : What does the ABG show? Answer (A) : Mild respiratory acidosis due to worsening RDSQ: 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 7.22PaCO2 7 kpaPaO2 10 kpaHCO3

- 17 mmol/LBE -8 mmol/L

Q. What does the ABG showA. Mixed respiratory and metabolic acidosis

Q. Name a likely diagnosisA. RDS

3. The following is the ABG of a 40 day old 26 weeks’ gestation baby

pH 7.38PaCO2 8 kpaPaO2 8 kpaHCO3

- 35 mmol/LBE +10 mmol/L

Q. What does the ABG show?A. Fully compensated respiratory acidosis by metabolic alkalosisQ, 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 7.35PaCO2 3 kpaPaO2 15 kpaHCO3

- 12 mmol/LBE -12 mmol/L

Q. Interpret the ABGA. Fully compensated metabolic acidosis by respiratory alkalosis and hyperoxaemiaQ 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 7.16PaCO2 10 kpaPaO2 6 kpaHCO3

- 16 mmol/LBE -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 6.8PaCO2 4.5 kpaPaO2 3.0 kpaHCO3

- 8 mmol/LBE -24 mmol/L

Q. What does the ABG show?A. Severe metabolic acidosis with severe hypoxaemiaQ. What is your next course of action ? A. Administer sodium bicarbonate, consider prostaglandin infusion, confirm heart defect and consider surgery

Birth Asphyxia

A. Definition

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

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 and1 per 1000 dies or survives with neurological damage.1

C. Diagnosis

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 <7.0 is present if cerebral palsy results from birth asphyxia

4. Apgar Score. Poorly predictive of adverse outcome and not a useful method of defining significant asphyxia. 50% of children with CP. evident at 7 years of age had an optimal A/S of 7-10 at 1 min.

Use of the Apgar Score5 min : Measures effectiveness of resuscitation.20 min : All babies with Apgar < 6 at 5 min. should have a 20 min. score.Apgar < 5 at 20 min.: an important prognostic indicator of poor CNS outcome

(most will be quadriplegic).

5. Delay in Establishing Respiration. . If there is no spontaneous respiration by 20 minutes despite adequate resuscitation - the neurological outcome of such survivors is invariably bad.

6. Severity of Neonatal Encephalopathy (NE) is the best clinical method currently available to predict subsequent outcome following asphyxia.

Staging of Neonatal /Hypoxic Ischaemic Encephalopathy (HIE)

Only constant in term infants or > 35 weeks. Not consistent in Prems.

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

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 .

Important to note:

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 outcomeb) Avoid hypo or hyperglycaemia c) Adequate ventilation and avoid hypoxaemia and hypercarbia or hypocarbiad) Review infection risk and Rx with antibioticse) Maintain adequate hydration but do not dehydrate or overhydratef) 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 IPPVMetabolic In SIADH, restrict fluids. Rx hypoglycaemia.DIVC No specific Rx. Replace with fresh frozen plasma., cryoprecipitate,

platelet or packed cell as indicatedNutrition 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 benefitc) 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. Prognosisa) 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 <0.55) i.e. relative increase in the end diastolic blood flow velocity compared to peak systolic blood flow velocity or high mean flow velocity (or anterior cerebral artery) > 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).

References1.Levene ML, Sands C, Grindulis H, Moore JR. Comparison of 2 methods of predicting outcome in perinatal asphyxia. Lancet 1986;1:67-712. Silverman F, Suidan J, Wasserman J, Antoine C, Young BK. The Apgar score: Is it enough? Obstet Gynae 1985;66:331-63. Low JA, Panagiotopoulos C, Derick EJ. Newborn complications afterintrapartumasphyxia with metabolic acidosis in term fetus. Am J Obstet Gynecol 1994;170:1081-74.LeveneML. Management of asphyxiated full term infant. Arch Dis Child 1993;68:612-65. Evan D, Levene M. Neonatal seizures. Arch Dis Child 1998;78:F70-56. Levene MI, Evan DH Medical management of raised intracranial pressure after severe asphyxia. Arch Dis Child 1985; 60:12-67Holme G ,Rowe J, Hafford J, Schmidt R. Prognostic value of EEG in neonatal asphyxia. Electroenceph Clin Neurophysiol 1982;53: 60-728. Thornberg E. Ekstrom-Jodal B. Cerebral function monitoring: a method of predicting outcome in term neonates after severe perinatal asphyxia .Acta paediatr 1994;83:596-6019.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 Common Ocular phenomena- tonic horizontal deviation of eyes common in term infants- sustained eye opening with fixation common in preterm infants- blinkingOral-buccal-lingual movements- chewing common in preterm infants- lip smacking, cry-grimaceLimb movements- pedaling, stepping, rotary arm movementsApneic spells common in term infants

Clonic Focal Multifocal

Common

Common

Well localized clonic jerking, infant usually not unconscious

Multifocal clonic movements; simultaneous or in sequenceor non-ordered ( non-Jacksonian) migration

Tonic Focal

Generalized

Common

Uncommon

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.

Myoclonic Focal , Multifocal

Generalized

Uncommon

Common

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.

EtiologyDetermination 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 termHypoxic –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 4th 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 MovementsSome 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 SeizureAbnormality of gaze or eye movement 0 +Movements exquisitely stimulus sensitive + 0Predominant movement tremors* clonic, jerking#Movements cease with passive flexion of affected limb + 0Autonomic changes ( tachycardia, ↑ BP, apnea, salivation, cutaneous vasomotor phenomena)

0 +

* 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 4th 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

Hypoglycemia

No Hypoglycemia

Phenytoin: 10mg/kg IV as loading dose (repeat a 2nd loading dose if fits recur) via infusion at 1mg/kg/min – cardiac rate and rhythm should be monitored during infusion

Maintenance therapy: 3-4mg/kg/d q12h, IVGiven 12-24 h after loadingAE: Heart block hypotension

Benzodiazepine:*Diazepam: 0.3 mg/kg/h IV infusion*Midazolam:1-4 mcg/kg/min IV infusion*- limited small study

Actively convulsing

Actively convulsing

Infant with clinical seizure

Ensure ventilation and perfusion adequate (ABC’s)

Dextrostix stat

IV 10% Dextrose at 2 ml/kg (200mg/kg)Then IV glucose infusion at 8 mg/kg/min infusion

OTHERS:Calcium Gluconate, 10% solution: 2 ml/kg, IVMagnesium sulfate, 50% solution: 0.2 ml/kg, IVPyridoxine: 50-100mg IV

Phenobarbitone: 20mg/kg IV over 10 -15 minutesA repeat loading dose of 20mg/kg may be necessary

Maintenance therapy: 3-4mg/kg/d q12h, IV or POGiven 12-24 h after loadingAE: respiratory depression hypotension

Maintenance therapyMidazolam: AE: respiratory depression, seizure hypotension, urinary retention

Investigations to consider:Blood sugar, Se Ca, Mg, electrolytesSeptic screen - FBC, Bld C&S, LP, TORCHESMetabolic screen - blood gas, Se. Ammoniaamino acids, organic acids, other metabolites Neuroimaging: US,CT Scan brainEEG

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 weeksIf seizure activity is overtly paroxysmal continue phenobarbitone until 3 months of age and reassess in the same manner.

PROGNOSIS OF NEONATAL SEIZURESMost important determinant of neurological prognosis is the underlying nature of the neuropathological process.

Neurological Disease NormalDevelopment (%)^

Hypoxic Ischemic Encephalopathy 50Severe Intraventricular Hemorrhage with PVH infarction 10Primary Subarachnoid HemorrhageHypocalcaemia Early onset (depends on the prognosis of complicating illness, if no neurological illness present prognosis approaches later onset ) Later onset ( nutritional type)

50

100Hypoglycemia 50Bacterial Meningitis 50Developmental 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:4th edition. Page 202)

References:

1. JJ Volpe: Neurology in the Newborn: Fourth Edition

2. Klauss & Fanaroff: Care of The High Risk Neonate: Fifth Edition3. McDermott CA, Kowalczyk AL, Schnitzler ER et al: Pharmacokinetics of lorazepam in critically ill neonates with seizures. J Pediar 120: 479- 483,19924. 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;319-323,19916. 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 DetectionAnticipation & 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 ageHypothermia Birth Asphyxia / Perinatal StressSepsis Infant of Diabetic MotherInfant > 4 kg. PolycythaemiaRhesus 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 2Then 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 easybut 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 mouthRepeat glucometer after 1/2 to 1 hour and increase the infusion as necessaryto 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

Also need to consider metabolic (See Approach to Hypoglycaemia under Metabolic section) and endocrine workup.

Consider 1. Glucagon 0.2 mg/kg IV (IM) bolus

2. Hydrocortisone 2.5 -5 mg/kg/dose bd IV3. Diazoxide 5 mg bd orally4. Adrenaline 500 ng/kg/min IV infusion5. Somatostatin 1 - 4 microgram SC.

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 non-glucose 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;63:1386-1398Koh G Aynsley-Green A Tarbit A Etre J 1988b Neural dysfunction during hypoglycaemia. Arch Dis

Childhood;63:1353-1358DK Pal et al 2000 Neonatal hypoglycaemia in Nepal. Prevalence and risk factors Arch Dis

Childhood;82:F46-52AA M Moris et al 1996 Evaluation of fast for investigating hypoglycaemia or suspected metabolic disease

Arch Dis Childhood;75:115-119Gomella, Cunningham ,Eyal and Zenk: Neonatalogy 4th 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

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

MANAGEMENT OF NNJ 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/cm2/nm of appropriate light is reached. The minimum irradiance is 6-12 µW/cm2/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

Total Serum Bilirubin levels mg/dL (umol/L) Hours of life

Infants at lower risk (≥ 38 wk and well)

Infants at medium risk (≥ 38 wk + risk factors OR 35-37 6/7 wk and well)

Infants at higher risk (35-37 6/7 wk + risk factors)

Intensive Phototherapy

ET Intensive Phototherapy

ET Intensive Phototherapy

ET

< 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)

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

Purpose1. 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 infanta. 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 usedRh isoimmunisation- ABO compatible, Rh negativeOther conditions - X match with baby and mother's bloodEmergency - 'O' Rh negative

Fresh whole blood collected in citrate phosphate dextrose ( CPD)Fresh blood not more than 24 hours old for sick or hydropic infantsNot more than 48 hours (definitely not > 5 days) for other neonates.

Procedure1. 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 Bilirubinii) FBCiii) Blood glucoseiv) Serum electrolytesv) Serum calciumvi) Blood gasesvii) Others e.g. Blood C&S as indicated

b. Post-exchange (Last volume of blood removed)

i) Serum Bilirubin ii) FBCiii) Blood Sugariv) Serum electrolytesv) Serum Calciumvi) Blood gases

c. 6 hour post-exchangei) SB

Follow-up1. 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.

Complications of ET

1. Catheter relateda. Infectionb. Haemorrhagec. NECd. Portal and splenic vein thrombosise. Air embolism

2. Haemodynamic problemsa. Overload cardiac failureb. Hypovolaemic shockc. Arrhythmia (Catheter tip near sinus

node in R Atria)

3. Electrolyte imbalancea. K+b. Cac. or Blood glucosed. Acidosis (sometimes late alkalosis due

to breakdown of citrate)Tissue hypoxia (old blood)

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 JaundiceConjugated Hyperbilirubinaemia Unconjugated HyperbilirubinaemiaNeonatal Hepatitis Syndrome Septicaemia or UTIBiliary Atresia HaemolysisCholedochal Cyst Breast milk JaundiceSepticaemia or UTI HypothyroidismCongenital Infection (TORCHES) GalactosaemiaMetabolic Disorders (e.g. galactosaemia or -1 antitrypsin deficiency).Post Total Parenteral Nutrition

Initial Management

Child unwell or Child well pale stool

If it is obstructive (conjugated) jaundice admit

Initial InvestigationsTotal 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

Further Ix depends on whether it is unconjugated or

conjugated hyperbilirubinaemia

Admit for investigations and treatment

Investigate at OPD

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 BMfor 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 liverPreferably 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 SyndromeFollow 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.

AetiologySymptomatic of underlying problems commoner ones of which are:1. Respiratory conditions – RDS, pulmonary haemorrhage, pneumothorax, Upper airway obstruction, respiratory depression 2 drugs2. Sepsis 3. Hypoxaemia 4. Hypothermia5. CNS abnormality e.g. IVH, asphyxia, increased ICP, seizures6. Metabolic disturbances – hypoglycaemia, hyponatraemia, hypocalcaemia7. Cardiac failure, congenital heart disease, anaemia8. Aspiration/ Gastro-oesophageal reflux9. NEC/ Abdomen distension10. 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.

Management1. 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 therapye.g. Septic workup if sepsis suspected and commence antibioticsRemember to check blood glucose via glucometer.

3. Management to prevent recurrence.

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 monitorProblem 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)

Ref

1. N.R.C. Roberton. Textbook of Neonatology. Churchill Livingstone2. Gomella, Cunningham, Eyal and Zenk. Neonatology. 4th edition Lange3. Halliday, McClure and Reid. Neonatal Intensive Care. 4th edition. Saunders4. Rennie and Roberton. Manual of Neonatal Intensive Care 4th edition Arnold

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

E. Coli Cefotaxime ± Gentamycin

70 - 80% of early onset-neonatal infection

Pseudomonas Ceftazidime ± Gentamycin

Other Gram negative bacilli Cefotaxime ± Gentamycin

Staphylococcus Cloxacillin

Listeria Monocytogenes Ampicillin + Gentamycin

Anaerobes Metronidazole

Candida Fluconazole / Amphotericin

History 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

• <36oC or >37.5oC 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 109/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.

77.. 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: NN..RR..CC.. RRoobbeerrttoonn.. TTeexxttbbooookk ooff NNeeoonnaattoollooggyy.. CChhuurrcchhiillll LLiivviinnggssttoonnee