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The PGI NICU

Handbook of Protocols
Fourth Edition

Newborr Unit
';(Department o · Pediatrics
Postgraduate Institute of Medical Education
and Research 1PGIMER)
Chandi 1arh
lndi.i

-
ii

©Copyright 2010 by The New Heart Trust

The Newborn Unit


Department of Pediatrics
Postgraduate Institute of Medical Education and Research (PGIMER)
Sector 12
Chandigarh 160012
India

All rights reserved. This book is protected by copyright under the


Copyright Act of India, 1957. No part of this book may be reproduced in
any form by any means, including photocopying, or utilized by any
information storage and retrieval system without written permission from
the copyright holders.

Previous editions
1971 edited by Omkar Nath Bhakoo
1995 edited by Praveen Kumar
2003 edited by Kanya Mukhopadhyay

Printed by
Chandika Press Pvt. Ltd., 240, HSIIDC Ind. Estate, Barwala (Hry.) India

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iii

rznis edition is aeaicaua


to <Professor OmJ.~r Natfi <B~
e1, <Professor;4.nifNarane-
mentors, teacliers antfrofe moae/S to 9eneration.s
ofneonatofogists in Intf'ta;

;4.ntfto a[[tlie 6aliie.s wlio Fi.aw 6een treatd


in tlie New6om Vnit of~I since its inception.-
for 1Jivi111J us tlie prnlikoe ofcari111Jfor tfiem.

( a. ,,II'~">I\ .
'\,") Cl (} ,. ~\ v..?-
~v., ~\'- Vi
c''{oV°' _7
iv

'
EDITORS

Sourabh Dutta
&
Praveen Kumar

CONTRIBUTORS
(in alphabetical order)

Anil Narang
Ashwini Kumar
Deepak Louis
Kanya \if ukhopadhyay
Neeraj Gupta
Praveer Kumar
S Giridhar
S Mangalabharti
S Venk1taseshan
Samir Sheikh
Shiv Sajan Saini
Sourabh Dutta
Sunil Aggarwal
Sunil SJi Kishore M
Swati C'hacham
Vandar. a Negi

Under the auspices of the ew Heart Trust, a registered


charitable trust associated with the Newborn Unit of PGI
Vi
vii

FORl:WORD

PG!MER has been in the forefro 1t of the neonatal care revolution in


India. The foundations of Nconatol<>gy at PG! were laid in 1968 when
Prof 0. N. Bhakoo started the neonatal unit. He soon undertook
advanced training at the best neonatal units of UK and Canada and very
ably adapted their best practices to Indian conditions. He was joined by
Prof Anil Narang in 1975, who had done his advanced neonatal training
in UK, and was a catalyst in starting modem neonatal intensive care. All
the current faculty members of the neonatal unit have had special training
in neonatology at the best institutions in India, Canada and Australia.
They have the experience of working exclusively with newborns for 6 to
20 years. Hence this handbook is a blend of the best of the developed
world with the best oflndian experience.
The country's first DM program in neonatology was started in PG! in
1989 under the stewardship of Prof Bhakoo and Prof Narang. The model
of this program has been replicated and adapted by other institutions
offering DM, DNB and fellowship programs. Till date, 49 students have
successfully completed this program. Of them, 70% are settled in India
and have taken leadership roles in establishing quality neonatal care
services and training programs in various parts of the country in
government, defense, institutional and private sectors. Many are
occupying excellent positions in North America, UK and Australia and
regularly contribute to the academic progress of their alma mater by
academic visits and collaborations.
The first protocol book of PGl-NlCU was compiled in 1971. Since
then it has been revised periodically. The revision process of each topic
involves critical appraisal of the literature, information gathering,
circulation and presentation of the draft write-up to the faculty, fellows
and residents; intense discussions, debates and feedbacks; followed by
revisions and re-revisions of the draft; and finally diligent editing and
formatting. With the exponential growth in knowledge and research, the
current format of the handbook should allow us to update it much more
frequently. The PGl-NICU handbooks were originally written for the
residents, fellows and nurses working locally. However, they have been
used extensively all over the country. The feedback of those users has
also been very useful in improving the handbook further. The current
'Blue Book' version is a culmination of this evolution and a
manifestation of the hard work of numerous contributors.

Praveen Kumar
August 2010
viii
ix

PREJ'ACE
This Handbook, informally called The Blue Book, is an extensively
revised, updated, formatted and r '-organized edition of the popular
manual of PGIMER (formerly calkd "Protocols in Neonatology") . .The
current edition incorporates separate sections on investigations, drugs,
nomograms and telephone numbers, apart from the chapters on
management protocols. The chapters have been divided into numbered
sections. A large number of management algorithms and tables have
been added. The Blue Book is comprehensively cross-referenced and
indexed. It is the culmination of an elaborate exercise of systematically
reviewing the literature, grading the evidence and adapting it to Indian
conditions.
A book of this scale would not have seen the light of day without
exceptional teamwork. The team comprised of the DM fellows, faculty
and staff of Neonatology at PGIMER. While the contributions of all the
contributors is gratefully acknowledged, there are some whose assistance
was extraordinary and I must make special mention of them. Foremost
among them are Dr S Giridhar and Dr Samir Sheikh, who corrected all
the raw manuscripts. Dr Sunil Sai Kishore and Dr Shiv Sajan Saini
helped out with collecting data. Dr Mangalabharti collated information
about investigations. Dr Vandana Negi updated the drugs and
nomograms.
The care of newborn babies demands a rare combination of
knowledge, art, skill, compassion, hard work and patience. Hence, it is
no surprise that an impending posting in the NICU evokes the entire
spectrum of responses from resident doctors- ranging from excitement
and expectation to doubt and despair. Every effort has been taken to
make this handbook user-friendly so that it decreases the stress levels of
residents and fellows working in the NICU. Although targeted at the
doctors of PGIMER, it would immensely benefit everybody who deals
with newborn infants.
Despite our best efforts, some mistakes may have crept in. To err is
human- and to point out other people's errors is even more human! If you
happen to spot any errors, kindly bring them to the notice of the editors,
so that they can be rectified in future reprints.
I hope the Blue Book will help to improve the short-term and long-
term outcomes of both neonates and resident doctors in the neonatal unit.

Sourabh Dutta
August 2010
x

DISCLAIMERS

Care has been taken to verify the accuracy of all the information in
this handbook. However, the contributors and editors are not responsible
for errors or omissions or for any consequences from the application of
information provided in this handbook and give no guarantee with
respect to the completeness or accuracy of the contents. Application of
the information in a situation outside the Newborn Unit of PGlMER
Chandigarh remains the professional responsibility of the concerned
physician.
The editors and contributors have made great effort to ensure that
information related to drug doses, storage conditions, reconstimtion and
administration are according to currently accepted recommendations.
However, given the rapidity with which such infomtation changes, the
reader is urged to check the package insert of each drug before use,
particularly so for infrequently used drugs.
In a few places, brand names of medicines or devices are mentioned,
simply because these are currently in use in the unit. This docs not
constitute an endorsement of any particular brand. The contributors,
editors and faculty of the newborn unit of PGIMER have no affiliation to
any of these companies,
Fees for certain services and prices of items mentioned in the
handbook are liable to change with time. The editors take no
responsibility for any discrepancy in these figures.
Personal landline numbers and personal mobile numbers of
employees of PG!MER have not been mentioned in the handbook. Only
internal numbers have been mentioned. Phone numbers of people outside
PGIMER have been mentioned only if they were already in the public
domain or where the individuals concerned had no objection to their
inclusion.
1
Several instructions related to patients files, administrative issues
and investigations might be altered once the hospital computerization
project is fully implemented,
In the interest of brevity, references have been quoted selectively.
American spellings have been used
xi

COl'TENTS

Sections Page
How to use this handbook I
Abbreviations used in the handbook 3

PROTOCOLS
No. Title Page
I Pregnant mothers from ncor:atal perspective 9
2 Neonatal resuscitation 17
3 Admission, transfer and discharge 19
4 Medical records and admini ,trative issues 25
5 Stable term and late preterm babies 30
6 Monitoring under various circumstances~ 42
7 Temperature maintenance a 1d hypothennia 46
8 Fluid and electrolyte management -;;< 54
9 Enteral nutrition ? 68
10 Acid base disorders 83
II Hypoglycemia and hypergl.)cemia ;;/' 92
12 Perinatal asphyxia .,it !OT
13 Apnea 109
14 Acute respiratory diseases ;>t. 115
15 Inhaled nitric oxide 149
16 Bronchopulmonary dysplasia 157
17 Anemia 163
18 Polycythemia 171
19 Bleeding neonate
qp Jaundice
Intra-cranial bleeds & pcrivt:ntricular lcukomalacia i7
22
23
Seizures
Asepsis routines
~
217
24 Sepsis @§)
25 Epidemic of septicemia 240
26 TORCH infections 244
27 Human immunodeficiency virus (HIV) mfection 257
28 Congenital heart diseases 268
29 Shock 287
30 Patent ductus arteriosus of prematurity 293
31 Necrotizing coterocolitis 298
32 Parenteral nutrition
,kf' 33
~ 34
35
Inborn errors of metabolisn
Genetic/ syndromic illncssb
Surgical problems
~
327
xii

36 Extremely low birth weight (ELBW) babies 339


37 Retinopathy of prematurity 347
38 Osteopenia of prematurity 350
39 Counseling in various situations 353
40 Withdrawal of support & procedure following death 356
41 Visual and auditory morbidities 362
42 Follow-up 365
43 Developmental delay and cerebral palsy 369
44 Pain 378
45 Fire and other emergencies 384
46 Equipments 389

INVESTIGATIONS
No. Title Page
1-1 Sampling methods 391
1-2 Practical issues regarding sending blood samples 392
1-3 Tests to be done at bedside/ NJCU lab 393
1-4 Biochemical investigations 396
1-5 Hematological investigations 404
1-6 Microbiological investigations 409
1-7 Endocrinological investigations 416
1-8 Genetic and pathological investigations 418
1-9 Radiological and miscellaneous investigations 419
1-10 Uncommon investigations available with private 421
laboratories in Chandigarh
1-11 Selected laboratories outside Chandigarh 427

DRUGS
No. Title Page
DI - Drug information organized alphabetically 429
DJ33
RF.I Dose modification of antimicrobials in renal failure 481
RF.2 Dose modification of non-antimicrobials in renal 488
failure

NOMOGRAMS
No. Title Page
NI PGIMER Intra-uterine Growth Chart 491
N2 Lubchenco's Intrauterine Growth Charts 492
N3 Fenton's Chart For Intrauterine Growth & Initial JO 493
Wks Of Postnatal Age
xiii

N4 Ebrenkranz's Postnatal Gro•vth Charts For VLBW 494


Neonates
N5 Kelly Wright's Postnatal Gnwth Charts For VLBW 497
Neonates
N6 WHO Growth Charts 498
N7 Growth Charts For Twins 502
NB Levene's Nomogram For Ventricular Width 503
N9 Body Surface Area 503
NIO Manroe's Chart For Leukocyte Indices Of Term 504
Neonates
NI 1 Mouzinho's Chart For ANC OfVLBW Neonates 505
Nl2 Christensen's Nomograms For Neutrophils In 506
Neonates (High Altitudes)
Nl3 Schelonka's Table OfNeutrophil Values In Term 507
Neonates At 4 H Age
N14 Zubrow's Charts For BP 507
Nl5 Age Specific BP Up To I Year 510
N16 Mean BP In Neonates With Gestational Age 23-43 511
Wks
Nl7 Hey's Charts For Thermoneutral Zone 512
NIB New Ballard Scoring For Gestational Age 513
Nl9 Bhutani's Prediction Nomograrn 514
N20 AAP Guidelines For Jaundice Management 515
N2l Acid-Base Nomog1am 516
N22 Umbilical Artery And Vein Catheter Length 517
N23 Weights Of Disposables 518

INDEX 519

TELEPHONE NUMBERS 533


xiv
1

HOW TO USE THIS HANDBOOK

• It must be appreciated that a handbook is not a substitute for a


textbook, and neither does th< Blue Book claim to be one. The
mandate of this handbook i> to provide handy and practical
information to doctors working in the Newborn Unit so that they can
discharge their duties in the most effective manner. It must be used
in conjunction with a standard textbook ofNeonatology.
• The Blue Book has four main parts- protocols, investigations, drugs
and nomograms.
• The protocols are in the form of chapters, which are divided into
sections and sub-sections with numbered headings and sub-headings
(e.g. l.l & I. I.I). Sections in the protocols do not have any
alphabetic prefix.
• The sections on investigations are prefixed with "I" (e.g. J-5); those
on drugs are prefixed with "D'' (e.g. 020) and on nomograms with
"N" (e.g. N2). There is extensive cross-reference between sections
and the reader is strongly encouraged to make use of the cross-
referencing.
• Tables and figures have independent numbering sequences (i.e.
independent of each other and of the sections in the text). Numbers
of all sections, figures and tables in a given chapter start with the
chapter number.
• Telephone numbers of all persons or areas referred to in the text are
listed in the section on telephone numbers.
• The steps of performance of various procedures have deliberate! y
not been discussed in detail. Cross-references to the PGIMER video
on procedures have been provided wherever appropriate.
• Since knowledge is not static, the faculty of the Newborn Unit will
issue updates or errata from time to time, which would supersede
what is given in the Blue Book. These will be referred to by the same
numbering system use in the Blue Book. The updates and errata will
be filed in binders placed in the NICU and NNN and placed on the
website of the unit: www.pginicu.org.
• It is expected of the doctors, nurses and para-medical staff in the
Newborn Unit of PGIMER that they would follow the Blue Book in
letter and spirit. Jt must be appreciated that a protocol is a general
guideline that is expected to work in the routine course of things and
bring in a measure of uniformity in management. However, each
patient is unique and circumstances may require one to deviate from
the protocol at times, provided the deviation is backed by sound
justification and documentatiot 1.
2
3

ABBREVIATIONS USE' > IN THE HANDBOOK


The following are abbreviated words or terms that have been used three
or more times in the text. Others are xpanded in the text 1tsel(
4' 3-TC Lamivudmc
5° • D 5 percent dextrose m water
10•,. D 10 percent dcxtr~ in wa er
a, A Arterial by alveolar
AJREDF Absent or reversed end di tolic flow
AA Aminoacid
A~ Al\colar-ancnal differcnl'C ofoxygen
AAP American Academy of PaJiatnc;
~ ABE Acute b11irubm enccphalcnalhy
ABG Anenal blood gas
ACF Angiotensin convening er zyrne
AED Anu-cpileptic drug
AFB Acid fast bacilli
AFI Amniotic fluid index
AFP Alpha fctoprO!ein
AFV Ammouc fluid volume
1 AGA ~ Appropriate for gcstauonil age
AIDS Acquired Lmmunodefic1ency syndrome
All"1S All India 1ns11tute ofmed1 al M:1enco
ALP Alkaline Phosphatase
'~ I Ab:.olutc ncutrophil COUOI
,,(:No Annual number
AOP Apnea of prematurity
APC Advanced Pediatric CentrF
APH Antepanum hemorrhage
APTT Acuvated panial throm, lastin time
ARF Acute renal failure
ART Anllrctroviral therapy
AS Aonic stenos~
ATT Anlltubcrcular therapy
AV Atrioventricular
~ Abdominal X-ray
CMLJ Z1dovudme
BIL Bilateral
BCG Bacillus calmeuc gucnn
BE Base excess
BERA Bramstem evoked re:.ponte audiometry
BID Twice m a day
~~A Behavioral observational udiomctry
Blood pressure
BPD Broncho pulmonary dyspl.\s1a
BPL Below poverty line
BPP Biophysical profile
BS Blood sugar (1.e. glucose)
BUN Blood urea nitrogen
BW Btnh weight
CAH Congenital adrenal hyperplasia
Cal K1localories ( JO()() calor es)
CBC Complete blood count
CD Cluster designation
CDC Centre for disease control
CDH Congerutal diaphragmauc cmia
CIT Capillary filling time
CHO Congenital hean disease
CHF Con esuvc bean failure
4

Cl Confidence interval
CLR Clean labor room
~ Comprehensive maintenance contract
' cMr Congenital malfonnation
CMV Cytomegalovirus
CNS Central nen oil!> system
CoA Coarctatmn of aona
CP Cerebral palsy
CPAP Conunuou:; pos1t1\'C airway pressure
CPDA Q!111~osphate-dextrosc-aoeninc
CPK-MB Crcatinc p-hospno1Ci1\ase - muscle, brain fraction
'"CR "lo. Central regtstratlon number
' CRD Central record departmeni
lCRP C-rcacti\c protcm
CRS Congenital rubella syndrome
csr Ccrcbro\pmal nu1d
CT Computenzed tomography
Card1othoracic and \ascular ::.urgery

@fCXR
\ dBllL
Ccntral venous catheter
Central venous pressure
Cardio vascular system
Chc>t X-ray
Decibel hearing Joss
DBP Diastolic blood pressure
OCT Direct Coomb's test
DIC Disscmmatcd mtravascular coagulat1on
D\,1SA Dimcrcaptosuccmic acid
DNA Dcoxynbonuclcic acid
DNS De>.trose 1'onnal Saline
DTPa Diphlhena. tetanus. pertussis (acellular)
DTPw Diphthena. tetanus. penussis (whole cell)
DVET Double volume exchange transfusion
EBM Expressed breast milk
EC Ex posurc code
ECF Extra-cellular tluid
ECG ElcctroeardJogram
Echo Echocardiogram
EDTA Ethylene diamim: tetra aceuc acid
EEG Electroencephalogram
ELBW fatremcly low binh weight
ELISA Enrymc linked immunosorbcnt assay
EMLA Eutectic mixture of local anesthetics
ENT Ear-nose-throat
EOS Early-<>nset ~cpsis
EPO Erythropo1etin
ET Endotrucheal
FcNa Fmcuonal excretion of sodium
FFP Fresh frozen plasma
FHR Fetal hcan rote
FlSll Fluorescent in-situ hybndi1.ahon
FiO: Fraction of inspired oxygen
G6PD Glucose 6 phosphate deh}drogenase
GA Gestational age
GALT Galact<>"e· l-pho,phatc undylyl traru.ferase
G-CSF Granulocytc colony stimulating factor
GER Ga·>tro e<;ophagcal renul(
GI! Growth hom1one
GIT Gastro mtcsunal traet
GM-CSF Grunulocyte macrophage colony sumuletmg factor
s
GYHD Graft versus host disease
H10 History of
Hb llcmoglobm
IIBig Hepauns-B 1mrnunoglob.:1lin
HBsAg Hepatitis-B surface antigen
HBV Hepautis-B virus
HCV Hepautis-C virus
llEV llepatttis-E virus
fHFOv High frequency cn.c11lato y ventilauo~
'11ib Hemophitus mfueniae t>re b
mE I lypoii:ic-ischemic enc~lopathy
HIV Human Lmmunodcfic1cn y virus
!ILi IS Hypoplasuc left bean S)' drom.iJ

~~?
Hyalinc membrane <tisca-.c
Human milk fortllier
'-f:PLC High performance hqu1d chromatography
WR I. Heart rate, 2. l~onia;ad + rifamp1cm
HRZ Ison111Zld • nfamp1cin nmtzmamide
HSV Herpes simpleJt virus
lit IIeight
IAP Indian academy of pcdrn rics
ICP lncracranial pressure
ICT Indirect Coomb's test
~~M Insulin dependent diabctt> mellnus
Infant ofd1abe11c mochcr
LllM Inborn errors ofmetabol m
IF lmmunofluorescence
~ lmmunoglobulm
l,!GDM Infant ofgestational diabetic mother
1\1 Intramuscular
l"lli lsoniazid

~
o Inhaled nitric oJtide
No In-born number
SURE lntubate-surfactant-eii:tufute
lntrapartum
IPPV Intermittent posmvc pre .sure vent1lat1011

~~
Injectable polio vaccine
Immature to total ratio
International unit
IUD lntra-utcnne death
IUGR Intrauterine growth retnJJ.ation
IUI lntrautcnnc infection(s)
IUT lntra-utenne tranSfusion
IV Intravenous
IVF Intravenous fluid(s)
lVH Intra-\ entrieular bC'lllO..i.age
JR Junior resident(s) .T
KUB Kidney ureter bladder
LAD Left axis deviation
LD'W Low bmh weight
LFT Liver function test(s)
l.GA Large for gestational ag
LL Lower limb(s)
LMWH
LOS
Low molecular weight
Late onset sepsis
'F°"
LP Lumbar puncture
LR Labor room
LSCS Lower segment cc:sllreall section
LV Left vcntnclc
6

_J.VH Left ventncular hypertrophy


mo
MAP
Left \entncular output
Mean airway pressure
MAS Meconium asp1ra11on syndrome
\1BP Mean blood p~urc
MCA Middle cerebral aneT)
MCT ~tedium cham triglyceride:.
MCU Mictunuing cy,tourethrogram
'vttN Mm1mal cnteral nuullion
mEq M1lliequivalent
MMR Mea~lcs mumps rubella
MR Mental retardation
MRI Magnetic resonance imaging
MRSA Methicillin =istant Staphylococcus aurcus
MSL Meconium stained liquor
MSSA 'vleth1cillm scns1uve Staphylococcus aureus
\'1TCT Mother to child transmission
mth(s) Monlh(s)
MU Million units

~
co Nauonal AIDS control organi1ation
c 1'ieubauer's chamber
PAP 1'asal continuous pos1uvc airv.ay pressure
NLC 1\ecrolizing enterocolitis
NFC 1\conatal follow up clinic
,J:iG !'\asogastric
LNJCHD National institute of child health and human development
NICU Nconatru 111tens1vc care unit
NIMHANS :Sational institute of mental health and neurosc1enctl.
rNIPPV Nasal intcrminent positt\C pressure \COt1lation
~NF Nauonal nconatology forum
1'N'\ Neonatal nursery
NPO Nil per oral
~PV Negati"c predicuve value
NRP Neonatal resuscitation program
NS Normal saline
NSR Neonatology seminar room

~
ST Non-stress test
TD Neural tube dcfect(s)
NTZ Neutral thermal zone
VP Nevi rapine
OD Oneca day
OFC Occ1p110-frontal circumference

~
Oroga>tric
Oxygen mdeic
Outbom number

~
Osteopema of prcmaturit)·
Out-patient department
OPV Oral polio \·acc111e
OR Odds ratio
OT Operation theatre

~
Partu1l pressure of carboo-dio1tidc in arterial blood
Pulmonary ar1enal hypcncns1on
PAO.• Panial pressure of o.'tygen m alveolar ga.
PoQ, Par11al pressure of oxygen 1n ancrial blood
PBF Pulmonary blood llo"
PC Platelet concentrate
(g, Pediatnc cardiology clinic
PCR Polymerase cham reaction
PCV Packed cell volume
7

Patent ductus aneriosus


Posiuve Old expiratory p Nurc
Post exposure prophylax1 .
Partial el\cbangc transfus Jn
Prostaglandtn EI
Postgraduate lnstirute of Medical Education & Rc:.carc:h
Post-hcmon'bag1c hy~phalus
PcrsislCTlt hyperinsulinen ic hypoglycemia of infancy
Pulsallhty mdex
Pcnpherally nm:ned cenrral venous catheter
Pulmonary interstitial emphysema
Pregnancy induced hype1'cns1on
Positive mspirotory pres'-Jre

cil
Cl'?!rN)
'-::ppm
Post menstrual age
Post natal age
per oral
Per..i~tent pulmonary hyp:nension of newborn
Parts per million
PPV I Po>1tive predictive val 1c: 2. Posi1ive prosure ventilation
PRBC Packed red blood cells
PRP Platelet nch plasma
PS Pulmonary stenos1s
P>i Pa..-.cals per square inch
~ Peak systolic velocity
PT I. Prolhrombin ume; 2 fhotolherap)
PTI Prothrombin index
P\L Penvcntncular leukomalac1a
PVR Pulmonlll} vascular res1Jotancc
PWD Pulse wave Doppler
QID Four times ma da)
RAD Right axis deviation
RBC Red blood cell
RCT Randomized controlled 1:'1al
RDS Re;p1ratory distress syndrome
Rf Renal fa1 lure
ff;!:1 Recommended flow ratC'
Renal function test
RJ Res1suve mdex
RL Ringer's Lac1ate
RNA Ribonucleic acid
ROP Rcunopathy of prematur ty
RR Respiratory rate
RSV Respiratory syncytial v1 11s
RV Right ventncle
RVH Right ventricular hypcruophy
SD Systolic'd1astolic \
SAii Suba.rachnoid hcmorrllage
sao, 0'<ygcn saturallon of aB:nal blood

~ Standard base excess


Systolic blood pressure
I. Subcutaneous; 2. Stams code

dru
SD
SERFT
Shop cum fla1
Shop cum office
Standard deviauon
Serum electrolytes and renal function test
SGA Smull for gestational ag.-
SGOT ~)·f Serurn glutarnic oxaloal ~lie transnminasc
SGPT !\'---.; Scrum glutamic pyruvic transaminase
SIADl l Syndrome ofinappropmtc ant1-diureuc hormone
8

SIMV Synchronized intermittent mandatory ventilation/


SLE Systemic lupus erythematosus
SLR Septic labor room
Sp02 Pulse oximeter saturation
SR Senior resident
SVT Supraventricular tachycardia
TAPVC Total anomalous pulmonary venous connection

~
Tuberculosis
Trans-cutaneous bilirubin
Tetanus, diphtheria, pertussis (acel\ular)
To Expiratory time
TEF T racheo-esophageal fistula
TG Triglyceride
TGA Transposition of great arteries
GD lnspiratory time
TID Thrice in a day
TLC Total leukocyte count
TMP/SMX Trimethoprim/ suphamethoxazo\e
TMS Tandem mass spectrometry
TOF Tetralogy ofFallot
TORCH Toxoplasma, others, rubella, CMV, herpes~
TPN Total parenteral nutrition
TR T ricuspid regurgitation
TSB Total serum bilirubin
TT Tetanus toxoid
TV Tidal volu1ne
U/L Unilateral
UA Umbilical artery
UAC Umbilical artery catheter
UL- Upper limb •
USG_ U\trasonogram
UT! Urinary tract infection
VDRL- Venereal disease research laboratory
VF Ventricular fibrillation
Vit Vitamin
VLBW Very low birth weight
VSD Ventricular septa! defect
VT Ventricular tachycardia
VUR Vcsico ureteric reflux:
VZIG Varicella zoster immunoglobulin
WBC White blood cell
wk(s) Week(s)
WFI Water for injection
WHO World health organization
Wt Weight
yr(s) Year(s)
µESR Micro erythrocyte sedimentation rate
System International (SI) units have been used for expressing
measurements. Standard abbreviations of SI units and acceptable
non-SI units are found in http://physics.nist.gov/cuu/Units/index.html.
Standard chemical abbreviations have been used.
9

!. PREGNANT MOTHERS FR0\1 NEONATAL PERSPECTIVE

1.1 MATERNAL RISK FACTORS AND THEIR IMPLICATIONS


FOR THE NEWBORN
The genesis of many neonatal problems starts during pregnancy. The
table below depicts common maternal conditions and the implications
thereof for the neonate (see Table I. I ).

Table 1.1: Maternal conditions ad implications for the newborn


infant
Maternal Condition Imolications for newborn
IUGR, birth asphyxia,
PIH
thrombocvtooenia
Use ofB- blocker Hvnoglycemia
Use of MgS0 4 (Mg has
cumulative effect and it
Neonatal respiratory depression
peaks after 6 h of
administration)
Diabetes mellitus (DM) l(G)DM and its complications
Hyperthyroidism, Prematurity, IUGR, Birth asphyxia.
hvnothvroidism IUD,
Severe anemia Prematuritv, IUGR, hemoglobinopathv
Anti-phospholipid
Thrombocytopenia
antibodies (APLA)
Thrombocytopenia, Heart block,
SLE
Hydrops fetalis, Birth asphyxia
Rheumatic heart disease
IUGR, prematurity, IUD
(especially with PAH)
CHO IUGR, recurrence risk
HELLP (Hemolysis,
Cautious interpretation of neonatal
elevated liver enzymes, low
RFT
platelets) svndrome
Poor antenatal supervision IUGR
Primi delivered by LSCS Hvoo~lvcemia
Mal presentation Instrumental delivery
Precipitate labor Birth trauma
Rh -ve; 0 blood group Isoirnmunization
Prematurity, !UGR, Birth asphyxia,
Malpresentation, Instrument delivery,
Multiple pregnancy
CMF, twin-to-twin transfusion
svndrome
Prematurity, CMF (atresia of GIT,
Polyhydramnios
NTDsl
10

Maternal Condition Imnlications for newborn


Birth asphyxia, CMF (Potter
Oligohydramnios
ohenotvoe, oulmonarv hvnoolasia)
Cho le stasis of nreonancv Intrauterine fetal death
Acute fatty liver Intrauterine fetal death
Phvsical Assessment
Advanced maternal aee Chromosomal anomalies
Malnutrition IUGR
Cephalo-pelvic disproportion leading
Short stature
to birth trauma, asohvxia
Abuse/exnosure in nrevnanc" -
Smoking or tobacco
IUGR, Prematurity, IUD
chewine
Alcohol intake during
Fetal alcohol syndrome, IUD
nren-nancv
Radiation exoosure CMF
Infectious diseases
Risk factors of EOS EOS
Chorioamnionitis EOS, nrematuritv, PVL
UT!, diarrhea, systemic
EOS, prematurity
infections
TORCH infection Coneenital/nerinatal TORCH infection
HIV Perinatal transmission
Perinatal transmission; need for HBIG,
Hepatitis B
vaccine
Miscellaneous
Previous baby affected by
significant Recurrence
h•merbilirubinemia

1.2 MATERNAL INVESTIGATIONS AND THEIR


IMPLICATIONS FOR THE NEWBORN
1.2.1 USG
The first USG is done to look for viability of pregnancy and confirm its
intrauterine position. After 1st USG, it is repeated in each trimester to
monitor growth, rule out CMF and determine AFV.
Level II scan ·
•For suspected CMF
•Positive triple test
Fetal echo
•If positive family h/o CHD
•Previously babies with CHD
•Syndromic association
• H ydrops fetalis
- - - 11

1.2.2 BPP _ l
• Fetal breathing movement: \.. ~ I ~pisode of ~O s of sustained
breathing movement during 30 rninlobservatio~ penOd
• Fetal movement: ~2 discretegrnss body/limb movements in 30 min
observatioo...p~rioa -
• Fetal tone\.~ 1 episodes of limb notion from JJ_cxiQn to extension and


rapid return back to flexion.
Fetal reactivity: reactive NST c1iteria
_L J
• AFV: ~ I pocket of fluidmeasuring ~2 ems in 2 perpendicylar pJanes
Placental matunty is also judged. f- l
Presence of each of the above get a score of 2 points and absence a
score of 0 points.
Interpretation ofscores :J
• 8-10 is nonnal, unless there isfciligohydramnios
• 4-6 is suspicious of chronic hypo~ -
• 0-2 is strongly suspicious oTChiomc hypoxia. In case of score 0-2,
BPP testing time is usually extended to 120 nun.,..... -
Action based on BPP1 ~
The action lines based on the BPP stores are shown in Table 1.2

Table I 2· Action based on BPP scores


Rlsl.. or fetal
Ri!!k or
BPP score dea h (per Recommendation
asphyxia<"'•)
IOOtl/'l\k)
8-10, nonnal AFV 0 0.6 Conservative
8-10, dccrea~ed Tenn: deliver
5 20
AFV Pretenn: rot twice wecklv
6, nonnal AFV 0 / 50
~ I

6, dccrea~ AFV 2::32 wh: deliver


> 10 >Sd
/ <32 wks: rpl 24 hourly
4, nonnal AFV 2::32 wks: deliver
36 115
<32 wks: rot 24 hourly
4, decreased AFV >36 >115 Deh\er 1mmed1ately
2 73 220 Deliver immediotelv
0 100 Alrr.ost ceTtain Deliver 1mmcdiatelv

Modified BPP
A modified BPP, consisting of a l\ST and AFI, is widely used. If either
the NST or AFI are abnormal, a c~e BPPls performed.
1.2:nnlniottc'fluid index (AFI) ---
• AFf is a measure of the amour t of amniotic fluid and is an index of
fetal wellbeing .
• AFI is the score given to the a noun! of amniotic fluid (by adding up
centimeters of depth of four pockets of fluid), seen on USG. An AFI
12

~ 5 1s considered as oligohydramnios and an AFI ~ 20 is considered


as polyhydramnios
1.2.4 Triple test
The triple test, also called triple screen. is an investigation perfonncd
during pregnancy m the secOria tnmesler:Jhe tnple test measures serum
levels of AFP. estnol. and beta-hCG, with a 70°/o sensitivity and 5°,o
false-positive rate for diagnosing all cases ofQown S)'.!ldrome (See Table
1.3). It is now replaced by the Quad test (81% sensitivity and 5°10 fats~
positiYc rate) for dia.rnosing all cases of Down syndrome1 by adding
inhibin A to the panel- ~ --
These tests also classify a patient as either higb.~!.!S~ or low-risk for
chromosomal abnormalities and~. An estimatedilSK TS-calculated
and adjusted for the expectant mother's age.

Table 1.3: Inter relation of tri le test


AFP UE hCG Associated conditions
Low Low
Low Low
NTD like ~bi~a (associated with increased
levels of AcetYfc:hOline esterase in amniotic
High NA N 'A
fluid), or omphalocele, or gastroschlsiS;or
multi le estation like twms or t · le

~
• Reactive NST: presence of 2 or more acceleration of 15 beats or
more lasting for 15 s or more In a 20 mm tracmg.
• Non-reactive NST: no accelcrat1ons seen with movements; and there
maybe decelerations with movement. Long-tcnn variability is absent
and short-term variability is reduced.
• Equivocal VST: No movements in lQ._min with no accelerations or
decelerations suggest an equivocal N~_T. In such a case. the NST can
be done for..4!LJ:nlns (extended NST) before labeling it as non-
reactive.
• U11satisfactory VST: if the quality of the tracing is )!1!.,dsuate. for
~t<;IJ)_retation,
Implications
Risk of fetal demise within I wk after reactive NST - 3 1000
False negative results - 3.2/ 1000 (for antenatal death after correction for
congenital anomalies and unrelated causes) 3
1.2.6 Fetal Doppler studies
Umbilical artery: For interpretation of doppler indices sec Table 1.4
13

Table 1.4: Interpretation of UA dor pier indices

Measurement Equation Normal Value

SD ratio SD*

RI )\)"\~../ (S-D)/S*

,,
Pl Pu.\)""'''
Mean of 23.3 at 18 wks
PSY ~~ V 1
emfs gestation; 64.4 at 40 wks
h estation
• dices d crease with advancing Gfl~
Any abnonnal u erine artery doppler findings is a significant predictor of
adverse neonatal outcome after controlling for occurrence of
preeclampsia (OR: 4.1, 95% CI, 2.2- '.5)4
MCA flow
The MCA is exammed close to its origin in the fi tfima] carotid arte~
(See Figure I. I). The risk of anem a is highest m etuses with a pre-
transfusion PSY :::: 1.5 times Multiple of median (MoMJ.

Figure I.I : Change in MCA peak _!!lloci!)'._ with GA teprinted from


Sermnan m Perinatology, volume 32, Mari G, lfanif F. Fetal DOppler: bilical anery.
middle cerebral anery and venous system, inges 253-7, copyright 2008, with pcnni~~ioa
from Elsevier)

r eo
I ~..._~~~~~~-=--..r

l 40 .,___,_-=--..--
~ )() .......,.::;;;....~~---,~~

MCA PSV velocity > 1.5 MoM diagnoses fetal anemia with -JOO
sensitivity, - 90% specificity with NPV and PPV - 100% and -55-56%
respective!/.
14

1.2.7 Amniocentesis
Amniotic fluid can be analyzed for various compound including AFP,
Acetylcholine esterase and bilirubin. Increased level of AFP along with
the presence of Acetylcholine esterase identifies NTD with 98%
sensitivity. Increased level of bilirubin in amniotic fluid reflects
erythrocyte destruction as in isoimmune hemolysis. The relation of
bilirubin level with degree of hemolysis is interpreted according to
Liley's chart. MCA PSV is a more accurate indicator ofhemolysis and in
modem-day, practice has replaced Liley's chart as a predictor of fetal
anemia and hemolysis.
1.2.8 Chromosomal analysis
Fetal cells can be extracted from the amniotic fluid and analyzed for
chromosomes.
• 73% of clinically significant karyotype abnormalities related to one
of these 5 chromosomes (13, 18, and 21, X or Y) can be detected by
FISH with 90% sensitivity.
• DNA analysis: can be done with direct or indirect methods. Allows
diagnosis of alpha-thalassemia, cystic fibrosis, Duchene and Becker
muscular dystrophy, Phenylketonuria (PKU) etc.
1.2.9 Cordocentesis
Cordocentesis can be done under ultrasonic guidance from 2nd trimester
until term. It has diagnostic and therapeutic implications. It provides
diagnostic samples for cytogenetic, hematologic, immunologic and DNA
studies. It provides access for treatment in utero like IUT for fetal
anemia.
Risk for fetal loss with the procedure: 1-2%
Risk for preterm delivery: 5%
1.2.10 Cardiotocography
Parameters measured are as follows:
Baseline HR: normal between 110 and 160 beats/min. Baseline fetal
bradycardia, defined as <110/min, may result from congenital heart
block. Baseline tachycardia, defined as FHR > 160/min, results from
fetal dysrhythmia, hyperthyroidism, maternal fever or chorioamnionitis.
Beat to beat variability: Healthy awake term fetus varies the HR from
beat to beat by approximately 5-25 beats/min. Reduced variability
results from depression of fetal CNS due to immaturity, hypoxia, fetal
sleep, or specific maternal medications such as sedatives, narcotics, P-
blockers and IV magnesium sulphate. Accelerations of the FHR are
reassuring.
Decelerations: These may be benign or indicative of fetal compromise
depending on their characteristic shape and timing in relation to uterine
contractions.
15

• Early (type 1) decelerations: symmetric in shape and closely mirror


uterine contractions in time of onset, duration and end. Benign in
nature. More commonly seen wit 1 head compression in active labor.
• Late (type 2) decelerations: visually apparent decrease of the FHR
with uterine contractions- the onset, nadir and recovery occur after
the beginning, peak and end of contractions respectively.
Decelerations are suggestive of uteroplacental insufficiency and
hypoxia. It serves as a surrogate marker of fetal hypoxia and its
repeated presence demands action.
• Variable (type 3) decelerations vary in shape and timing relative to
uterine contractions. Usually results from umbilical cord
compression. Generally resolves with shift in maternal or fetal
position. They are of concern if they decrease to 60 beats/min and
last for more than 60 s.

1.3 DRUGS IN PREGNANCY: For safety, categories of drugs in


pregnancy see Table l.5

Table 1.5: Safetv cateiwries of drul's in ore1mancv


Cate2ory Definition Examole
Controlled studies in women fail to
show a risk to the fetus in the l '' Prenatal vitamins
A trimester (and there is no risk in Thyroid medications
later trimester) and the possibility Mai,'Ilesium sulphate
of harm annears remote
Animal reproduction studies have
not shown a fetal risk but there are
no controlled studies in pregnant
Penicillin
women. Reproduction studies have
Cepha!osporins
B shown an adverse effect that was
Metronidazole
not confirmed in controlled studies
Ethambutol
in the first trimester (and there is
no evidence of risk in later
trimester)
Either studies in animals have
revealed adverse effects on the Aspirin
fetus and there are no controlled !NH
studies in pregnant women or Hydralazine
c animal studies are not available. Labetolol
Drugs should be given only if the Betamethasone
potential benefit justifies the Dexamethasone
ootential risk to the fetus.
There is positive evidence of Phenytoin
D
human fetal risk but the benefit for Valproic acid
16

Category Definition Example


use in pregnant women may be Lithium
acceptable despite risk.
Studies in animals or humans have
shown fetal abnormalities and/or
Isotretinoin
there is evidence of fetal risk based
Diethylstilbesterol
on human experience, and the risk
Methotrexate
x of the use of the drug in pregnant
Aminopterin
women clearly outweighs any
Thalidomide
possible benefit. The drug is
Radioactive markers
contraindicated in women who are
or may become oregnant.

REFERENCES
1. Vintzileos AM, et al. Am J Obstet Gynecol. 1987; 157: 627.
2. Wenstorm K D, et al. Am J Obst Gynecol 1999; 181: 887.
3. Freeman RK, et al. Am J Obstet Gynecol 1982; 143:778.
4. Mari G, et al. Semin Perinatal 2008; 32: 182.
5. Mari G, et al. Semin Perinatal 2008; 32: 253.
17

2. NEONATAL RESUSCITATION

2.1 ISSUES IN RESUSClT A TIO


For details of resuscitation, pleaser ·fer to the manual of NRP 1. Here we
arc restrictmg our discussion to certain unit poltc1es.
Anticipation: The SR's posted in he labor room, from Obstetrics and
Neonatology respcctwely, should communicate regularly about the
anticipated high-nsk deliveries based on known risk factors.
Personnel: The Pediatrics JR shou d attend all dclivenes. Following is
the list of conditions where the SR should also attend the delivery (the
list is not exhaustive).
I • GA < 32 wks and/or expected birth wt< 1500 a_:_
i..-. APH with mother in shock - -

.
'J .

"<·
Fetald~
Multiple birthi

.
.,' .
I lydrops fetalis
Antenatally diagnosed major £~
Whenever requested by the Ob tctricians •

2.2 USE OF DILUTED OXYGE. .


The CLR and CLR-OT resuscitaticp areas have air-oxygen blenders and
pulse oximeters. In keeping with the suggesttons made in the NRP1 , the
followmg recommendations may b followed:
• Blended air-oxygen mixtures can be used for the resuscitation of
preterm neonates <32 wks o GA. For more mature babies, use
100%02.
• Such neonates must be connected to a pulse oximetcr, but lack of a
satisfactory signal should not be a reason to delay resuscitation.
• Start with approximately 50% ~i0 2 •
• In the first few minutes, Sp02 of70-80% is acceptable.
• Thereafter, adjust the Fi02 to achieve Sp02 of85-95°'o.

2.3 NON-INITIATION A.~D Wif HDRAWAL


2.3.1 Ethics
Non-initiation and withdrawal of resuscitation are considered equal.
There 1s no role of delayed, grad~d, or partial resuscitation. In case of
doubt, always pro\ tde the best care possible
2.3.2 Non-initiation of resuscitation
These modified cnteria have been devised keeping in mind the local
circ~stances.
• Gestation age< 25 wks and/or BW <500 g :J
• cstation age betwcco,_25° 7 tc 266'7 and parents have given consent
for the non-mttiation of the re~ usc1tation

------
18

• _ MF known to be incompatible with life. If there is genuine


Major. .C
doubt about the nature of the mal~ is better to resuscitate,
perfonn investigations to ~stablish the diagnosis and then discuss
with the family about withdraw~
2.3.3 Discontinuation of resuscitation.
• There is no cardiac activity at I0 ~~f Ill])
• There are no spontaneous resptra ory efforts at 30 min of Jif~and
there is no ventilator available for providing mecnamcal ventilation
Discuss these cases with consultant before discontinuation of care.

REFERENCES
I. Neonatal Resuscitation, 51h edition, 2006. AM and AHA.
19

3. ADMISSION, TRANSFER AND DISCHARGE

3.1 ADMISSION POLICIES


3.1.1 Areas
The following are the areas where newborn infants are admitted:
• NICU
• NNN
• Maternity ward, Gynecology ward
• Private wards- 3A, 4A, SA, 40, SD
3.1.2 Criteria for admission in various areas
NICU
• Less than 32 wks and I or< I SOO g and asymptomatic
• Any sick neonate requiring intensive monitoring and therapy
• Neonates born out of high risk pregnancies requiring close
observation
• Neonates with major CMFs (SR must discuss with consultant)
• Neonates with suspected !EM (SR must discuss with consultant)
NNN
Admissions.from CLR:
• Sick neonates requiring intensive monitoring and therapy may be
admitted in the intensive care area of nursery, if beds arc not
available in NICU
• Gestation ~32 wks and/or >lSOO g and up to 34 wks and/or 1800 g
and asymptomatic may be admitted in the non-intensive area of
nursery
Transfers from NICU:
• Neonates who arc transferred for stepped down care
Transfers from post-natal ward:
• Neonates with significant hyperbilirubinemia for DVET
• Neonates who develop an acute illness (hypoglycemia,
polycythemia, apnea, sepsis, feeding difficulties, hypothermia)
Admissions from Emergency I OPD:
• Neonates with significant hyperbilirubinemia for DVET
• Neonates with significant illnesses requiring monitoring & therapy
(subject to availability of bed)
• Readmission of inborn infants due to various reasons
3.1.3 Activities before admission:
The following activities must be performed prior to admission, to ensure
that the process is smooth
For inborn neonates:
• Pre-transfer counseling of parents by the SR is essential. Take
written, infonned consent prior to transfer.
20

• Record the complete address (including temporary and permanent)


with telephone number (mobile and landline no) of the head of the
family in the file of the baby
• Hand over the list of disposables & articles required for the initial
management of the baby to the attendants well in advance. The JR
should ensure that these items reach in time to the NICU I NNN
• Poor free files can be made for families belonging to a low
socioeconomic status, especially who hold BPL cards. Discuss with
the consultant in case of ambiguity.
• Admission has to be prioritized based on the previous obstetric
history, booked status, and illness severity after discussion with the
consultant. Joint guidelines of the obstetrics and neonatology
departments have been laid down for prioritization of care. Kindly
refer to these guidelines.
For out born neonates:
• Before transfer from emergency, the SR on duty should assess the
status and fitness of the neonate for transport. The only exception to
this is an otherwise healthy neonate with hyperbilirubinemia who
has to be shifted for DVET. Decision of transfer must be taken in
consultation with the consultant on call.
• Neonates requiring DVET for jaundice should be given priority
without any delay (see section 20. l 0). Written, informed consent
should be taken. Blood products and disposables for DVET should
be arranged before transfer
• Out born neonates and neonates from pediatric emergency should be
preferably admitted in NNN. Admission of these neonates in NICU
can be considered if deemed non-infective.
3.1.4 Activities around the time of admission to an area:
• Adequate communication with the receiving area (NICU I NNN) is
1nandatory. This comprises of information regarding the maternal
illness, reason for delivery, estimated gestation and Wt of the fetus
(neonate after delivery) and the neonate's status before shifting. This
communication should preferably be between SR's of both the areas.
JR and staff nurse of the receiving area should also be informed
beforehand. JR and staff nurse should accompany all cases.
• The following parameters should be documented before transport:
Temperature, HR, RR, CFT, BS, oxygen saturation, peripheral
pulses. Transport should always be done in a transport incubator.
The transport incubator should be adequately pre-warmed at least 30
min prior to transfer. Oxygen cylinder and ventilator of the transport
incubator should be checked well in advance. Oxygen saturation
must be monitored during transport. Every day, the sister-in-charge
of NICU should check that the oxygen cylinder of the transport
incubator is full and the ventilator is working.
21

• The following activities must be performed in the receiving area:


o Clean the incubator and w.trm it at least 30 min before the
arrival of the baby. Spread sterile pre-warmed linen in the
incubator.
o An infusion pump with appropriate sized syringe loaded with
appropriate fluids should be kept ready
o Working status of the ventilator should be checked and
ventilator circuit set up in advance
• On arrival of the baby, the following steps must be followed:
o JR, SR and staff nurse in charge should receive the baby
o Check for identity, which includes name, CR No., sex, date and
time of birth & BW. Make sure the identification armband is in
place.
o Check the vitals at the time of receiving [HR, RR, temperature
(axillary), saturation, color, BP, CFT]
o Check BS level at the time ofreceiving
o Check for documentation of drugs & their doses, especially for
VitK
o Check for written, informed consent as well as address &
telephone number of the attendant
o Check which investigations have already been done. If the
reports are available, they must be in the file. If the reports are
not yet available, note must be made that these reports are to be
followed up. If a form has been sent for an investigation but the
investigation has not yet been done (e.g. radiological),
information must be sent to the concerned personnel that the
baby has been shifted so that their time is not wasted in
searching for the baby.

3.2 GUIDELINES FOR DISCHARGE


3.2.1 General guidelines (also see chapter 42):
• Anticipate discharge in high-risk neonates at least 7 d prior and plan
the discharge process. Prepare the discharge summary and provide
follow up advice accordingly.
• Inform the parents well in advance so that the family can make
adequate arrangements for discharge, transport and further care at
home.
• A well-prepared discharge summary, which explicitly states the
illnesses the baby had during the hospital stay including a detailed
hospital course, is vital for a successful follow up. Discharges of all
high-risk patients are made on computer using the NDM v2.0. All
discharge summaries must be countersigned by the SR.
• Assess the family environment and family support with the help of a
social worker/public health nurse.
22

• Involve the public health nurse in the care of the baby very early
during the hospital course to build a good rapport with the family,
which will later help in assessment of the family environment, and to
plan the discharge.
3.2.2 Prerequisites for discharge of a healthy, term neonate
• Antepartum, IP and postpartum course for both mother and baby are
uncomplicated.
• Baby's vital signs documented within 12 h prior to discharge are
normal. Vital signs include RR <60 /min, HR I 00-160/min, axillary
temperature of 36.5°C to 37.4°C in an open cot with appropriate
clothing.
• Baby has urinated and has passed at least one normal stool.
• Baby has completed at least two successful breast feedings with
documentation of coordinated sucking, swallowing and breathing
while feeding.
• Physical examination reveals no abnormality that requires continued
hospitalization.
• The clinical significance of jaundice, if present before discharge, has
been determined and appropriate plan and place for follow up visits
has been decided. (See section 20.5; N19).
• Mother's knowledge, confidence and ability to provide adequate
care for her baby are documented by the fact that they have received
instructions on: breast feeding- nursing position, latching on,
adequacy of swallowing, normal urine and stool frequency, cord,
skin and genital care, recognition of illness and common problems
particularly jaundice.
• Family member or other support person(s) are available to the
mother.
• Vaccinations at birth have been administered as per PGIMER policy
(BCG, OPV & Hepatitis B). (see section 5.2.6)
• A local physician who can provide medical care after discharge has
to be identified especially if discharged <48 h of life and in that case
parents must be advised to meet this physician for examination of
the newborn within the next 48 h.
• Family, environmental and social risk factors are assessed and
resolved.
• Maternal and infant blood test results are available and have been
reviewed, which should include: Maternal syphilis and hepatitis B
surface antigen status; Cord or infant blood type and Direct Coombs
test (if clinically indicated).
Note: Early discharge (discharge within 48 h of life) may be considered
if delivery is vaginal & baby is singleton at 38-42 completed wks of
gestation and BW is appropriate for that GA as per intrauterine growth
curves, provided all the above criteria are met.
23

3.2.3 Discharge planning of a high-1 isk neonate:


Discharge planning team: Parents, '.Jeonatologist, neonatal nurses, and
social worker/public health nurse.
When to initiate the discharge planning: Planning should begin as soon
as the recovery is evident
Goal: Successful transition to home care
Prerequisites (baby's)
• Preferably, postconceptional age >33 wks and Wt >1400 g. Note that
this is may not always be possible and an individual neonate may get
discharged at less than 1400 g in case of prolonged hospital stay, and
if the mother is confident about handling the baby at home.
• Recovered from all acute illnesses
• Apnea free for at least past 7 d
• Sustained Wt gain ofat least 15 gikg/d
• Able to maintain axillary temperature >36"C in an open cot fully
clothed in an ambient temperature of 25 - 26 ° C
• Able to accept breast feeds or spoon I paladay feeds with good
coordination of swallowing and breathing while feeding
Prerequisites (family's)
• Mothers should be confident about feeding technique (breast and
spoon) and preparation of formula feeds, if formula feeds are
medically indicated.
• The mother and other attendants should be well versed in basic
infant care including bathing, skin. cord and genital care,
temperature measurement, and comforting (see section 5.2.2)
• At least two family members should be provided basic information
about infant CPR and emergency intervention
• Parents should be taught about
o detection of general early signs of illness
o sleeping position (back to sleep)
o ongoing medications: right dose and reconstitution
Discharge screening:
The following activities must be performed before discharge:
• Cranial USG: Pre-discharge cranial USG should be done for all
babies with GA <:33 wks (see section 21.6). The goal is to pick up
v
PVL and sequel of 1 H. The images must be stored in the USG
machine of the unit and transferred to the attached computer. If there
is an abnormality detected. give a hard copy of the USG image to the
parents for future reference.
• ROP screen: Screening for ROP should be done at 4 wks,J;f
chronological age. This has to be checked at discharge (see section
37.4). If 1t 1s due within a day or two, it is preferable to screen before
discharge. Jfnot, mention must be made of the date, time and place
24

of the scheduled ROP screen in the discharge summary and the same

• - -
must be conveyed to the parents. Contact JR or SR Ophthalmology.
-
Metabolic screening: Premature neonates are prone for metabolic
bone disease, hypoalbuminemia and hyponatremia. Hence preterm
neonates who are > 3 wks old and sick neonates who had been on
IVFffPN should have their complete metabolic profile screened
before discharge.
Metabolic screening includes:
o Calcium, phosphorus and ALP
o Sodium
o Total proteins and albumin I globulin fraction
• PCV must be done to rule out anemia of prematurity (see section
17.4). -~~

3.3 IMMUNIZATIONS:
See section 5.2.6
25

4. MEDICAL RECORDS AND '\DMINISTRATIVE ISSUES

4.1 ADMINISTRATIVE ISSUES


4.1.I Getting the inpatient file mad•
• After the baby is born, information is sent to Emergency Reception
(located in main emergency, Nehru Hospital building) for making an
Emergency OPD card (payment of ~ 20) and an inpatient file
(payment of ~ 800). The card is made only in the main emergency
reception. Note that from 9 am to 4:45 pm the inpatient file is made
in window no. 16 (located in Main Reception ground floor) after
getting the card made in the emergency block. After 4:45 pm, the
file is made along with the card in the emergency reception itself.
Advise the attendants to preserve the receipt, which will be required
at the time of discharge for clearance of dues.
4.1.2 Patient numbers and file contents
• Annual No. (A-no) is allotted by neonatology office clerk
(Neonatology Computer Room) to all live born babies in the LR.
Details of live binhs are to be entered daily in live bitth register
(which is kept in LR) by JR on duty in each shift. This register must
be checked by the SR of the labor room periodically and the SR
must countersign at the bottom of each page to cettify that all live
bitths have been entered. Note that A-No., I-No. and 0-No. are
internal arrangements of the newborn unit; these numbers have
nothing to do with CR Number and Admission number, which
official numbers allotted by PGIMER.
• Inborn No. (I-No) is given to babies who have sickness requiring
therapy or monitoring or who are <34 wks or <1.8 kg. Outbom No
(0-No) is given to outbom babies. Information about these babies is
entered in the inborn/outbom register respectively by the concerned
SR. I No. and 0-No. are generated by the SR who has been assigned
the duty of record management and no other person is allowed to do
so.
• A. No. & I No. 10 No, mother's name, GA, BW, sex, CR No. and
date & time of birth are also to be entered on the cover page of the
file for ready reference.
• Sheets in file must be in the sequence recommended:-
o Mandatory sheets
• Admission Record Sheet depic.ting the CR No. &
Admission No. name, address and final diagnosis
• Problem Sheet
• Neonatal Proforma (To be filled by Labor Room Resident)
• New Ballard Score proforma for gestation assessment
• Investigation Charts
• Nutrition and growth summary
26

• Neurological Examination Sheet


• Master Sheet
o Sheets to be attached if required:
• Jaundice Flow Sheet
• Ventilation Sheet
• Monitoring Chart in Labor Room
• DVET proforma
• Complete address and phone No. (Including Mobile and Landline
No.) should be recorded on the back of admission record sheet.
Consent for intensive care or for any procedure as indicated must be
recorded in the file. Separate consent should be taken for each
procedure.
• An Investigation Folder should be appended to the main file for
preserving original laboratory reports. Results of the investigations
are to be simultaneously entered in the investigation sheet.
• Each X-Ray must have a label bearing the Serial number (S. No.).
date & time, level of respiratory support & whether any tube or line
position (be it endotracheal, chest or gastric tube; or central lines)
was changed after the X-ray was done and if so, by how many
centimeters. Jn long staying patients, a separate x-ray folder (distinct
from the Investigation Folder) may be required for filing all the x-
rays.
• Computer records must be updated for each baby weekly and before
transfer of the baby from one area of the newborn unit to another and
before transfer to another department. A printed transfer summary
should be provided to the receiving area filed in the inpatient file.
• Death notes: In case of death of the baby, detailed notes have to be
written in the file including various resuscitative measures done and
terminal events. The SR has to enter his/her notes depicting the
medical course of the baby, cause of death and various interventions
done.

4.2 DAILY NOTES


• Name & CR. No. must be written on the top right-hand corner of the
each Daily Progress Sheet.
• Date and actual time of writing notes must be entered in the file. It is
not enough to write "morning notes" or "'evening shift JR" etc.
• Notes should be signed by the JR followed by name of the JR in
Block Letters.
• Daily Notes should include vitals of the baby. findings on clinical
examination & current problems, their onset, present status, relevant
investigations & plan for further management.
• The SR should check daily notes, write notes in case of sick babies
and write weekly summaries.
27

• Notes should be entered in the file regarding all decisions made


during rounds or after discussio 1s with Consultant.
• Transfer notes should include 'itals of the baby and summary of the
illness of the baby until date.
• Specific events and interventions must be recorded in the file as soon
as the concerned JR becomes free, after stabilizing the patient. In the
notes, a reference must be made to the time at which the event or
intervention occurred.

4.3 FINANCIAL ASSISTANCE FOR POOR PATIENTS


• Making Poor Free File: In an emergency, the SR can get a poor free
file made by writing "Poor Free File" on the card, especially if the
parents possess a BPL card. In such situations, the card and the file
have to be countersigned later by the consultant. During routine
working hours, the consultant has to sign for making the file poor
free. If initially the file was not made poor free and later the parents
submit a BPL card and request for conversion to poor free file, then
the application must be sent to the Medical superintendent (MS)
through Head of the department (HOD) on the prescribed form
(available with store-keeper/ward aide). If the file was not made
poor free initially and the parents do not have BPL card, but the
treating team feels that the family is genuinely poor, then the
application to convert to poor free status has to be sent to director
through MS and HOD.
• Other forms of financial assistance are also available for poor
patients in PGIMER. These include the MS poor fund, Red Cross
society, Seva Bharti and The New Heart Trust. The procedures for
seeking assistance are shown in Table 4.1.

. t ance or ooor oa t'1ents


. I ass1s
Ta bl e 4 1 P roced ure or e:etti ne: fiananc1a
Application Contact Maximum
Source Remarks
procedure person assistance
BPL card &
Get form
doctor's
from
Mrs. ~ 20,000 recommendation
PGIMER
MS Surinder at a time; essential.
Main
poor Kaur, up to 3 Medicines
Emergency
fund MSW, MS times for a directly
or from
office patient provided. Not
contact
for chronic
person
disease.
28

Application Contact Maximum


Source Remarks
procedure person assistance
BPL card &
doctor's
Patient's Ashish
recommendation
relatives to Ahuja, 2"'
UT essential.
be sent to floor, Not
Red Medicines
contact Kamna specified
Cross directly
person for Sadan,
provided. Not
form. Sector 11-B
for chronic
disease.
Mon, Tue, Thu,
Patient's Mrs. Fri. BPL card &
relatives to Kapoor, doctor's
Punjab
be sent to Level 2, C Small recommendation
Red
contact block, amounts essential.
Cross
person for Nehru Medicines
form. Hospital provided on per
day basis.
Patient's R. No. 19,
relatives to Nehru
Seva Small Doctor's
be sent to Sarai,
Bharti amounts recommendation
office in Nehru
APC/PGJ hospital
On SR's
Fill list of recommendation.
New required Not for families
Dr Sourabh
Heart items on Flexible with 2 previous
Dutta
Trust NICU items living issues or
list antenatally sex-
determined baby

4.4 DISCHARGE PROCEDURE


• At the time of discharge, the Admission Record Sheet and the
Master Sheet have to be filled. Specifically, one must remember to
fill the provisional diagnosis at admission, the final diagnosis, the
date of discharge, surgical procedures & and outcome. Cause of
death and autopsy no. has to be entered in case of death of the
patient.
• Make sure that all the entries like date of admission, date of
discharge, diet, duration of stay in ICU and Non-ICU area is entered
in the Master sheet.
• The admission record sheet and the Master sheet are to be signed by
the SR with name in Block Letters. All x-rays, charts and monitoring
29

sheets should be sent to CRD a.ong with the file. After completing
the formalities of no dues, give t ie file to sister on duty to be handed
over to ward aide.
• The Hospital Attendant is sent with the patient's attendant for "no
dues" to window no. 16 in the Reception during 9 am to 9 pm. After
9 pm, "no dues" are done in the Emergency Reception. The "no
dues" receipt is attached with the file.
• Discharge summary must be provided to patient at the time of
discharge. In rare cases, if the discharge summary is not ready it
should be posted to the address of the patient with a covering letter
attached.

4.5 ACCOMODATION AND TRANSPORT FACILITIES FOR


FAMILIES
• Limited dormitory-type accommodation is available for mothers of
babies in the NICU and intensive care area ofNNN in the Mothers'
Room (located on corridor leading ftom NNN to Maternity ward). A
list of eligible mothers is provided everyday by the sisters-in-charge
of NICU and NNN to the security guard, who then ensures the
genuineness of the occupants of the Mothers' Room. These mothers
are those who have already been discharged ftom the Obstetric
Department of PGIMER and the personnel of the Newborn Unit are
not obliged to care of any medical problems that these mothers may
face. In case of any emergency, they may be advised to attend the
(adult) Emergency Department or Labor Room.
• Several Sarais and Dharamshalas are available on the PGIMER
campus. Forms and allotment are available ftom Main Reception.
o Nehru h ospiJal Old Sarai
o Rotary Sarai, Hari Sarai a11d Jania Sarai
o Hans Raj Dharamshala
• A van service for transporting attendants of patients is available
every 30 min from the Sarai near the Nehru Hospital reception.
Timings: 8 am to 4 pm and 5 pm to 10 pm.
30

S. STABLE TERM AND LATE PRETERM BABIES

S.t DEFINITIO!\S
Tenn: All babies~ 37 wks gestation
61
Late preterm (or near tcnn): 34 36 wks
Stable babies. Refers to well babies with no ad\erse health condition

S.2 CARE OF BABIES WHILE IN HOSPITAL


5.2. l In CLR
Neonatal Examination
After birth, the JR should examine the baby thoroughly as per the format
m the neonatal proforma
• Vital signs
• Gestational a.uessmenl: Use the New Ballard score (see section
N 18). The score 1s valid until day 7 of life.
• Anthropometry: Measure birth weight, OFC, length, ponderal index.
Read the values off the appropriate nomogrnms and c lassify
accordingly (See sections NI, N2. NJ, and N7). J\iote that the
PGlMER intra-utenne growth chart (Secuon N 1), though "t1me-
tested" and popular, is unconventional in that it 1s expressed in mean
and standard deviation (rather than percentiles, which 1s more
correct for skewed data); and is less reliable at ~33 wks gestation as
there were insufficient patients in each gestational week.
• Head and neck: Check for overriding sutures, the number of
fontanels and their size. Check for abnormal shape of head. Look for
swellings and bruises. Measure the OFC. Palpate all muscles over
the neck. Palpate c lavicles for possible fractures. Make a note of any
facial asymmetry and dysmorphic features (see section 34.5.2).
• Mouth and nose· A soft NG tube can be passed through each nostril
to confirm patency. Inspect the mouth for natal teeth and palate for
clefts. The patency of the esophagus should be checked by passing a
stiff rubber catheter into the stomach m the following situations (sec
section 35.2.2):

a
SGA baby (-2 SD)
Single UA
Pol yhydramnios
Excessive drooling of saliva
• Abdomen Kote the shape of the abdomen. A nat abdomen signifies
abdominal contents in the chest (see section 35.2. I), or abnormali ties
in abdominal musculature. Note abdominal distension. Examine the
umbilical cord and count the vessels. Note color of the cord. Palpate
the liver and spleen. It may be normal for the liver to be about 2 cm
below the nght costal margin. The spleen 1s not usually palpable; if
the spleen is felt, be alert for congenital infection or cxtramedullary
31

hematopoiesis. After locating these organs (checking for situs


inversus), palpate for any abn>rmal masses. Examine for hernias -
umbilical or inguinal. Inspect anal area for patency.
• Male genitalia: Term normal renis is 3.6-± 0. 7 cm stretched length.
Inspect glans, urethral opening, prepuce and shaft. Observe for
hypospadias, epispadias. Tenm and near term infant should have
brownish pigmentation and rugated scrotum. Palpate the testes.
• Female genitalia: Inspect the labia, clitoris, urethral opening and
external vaginal vault. Often a whitish discharge is present; this is
normal, as is a small amount of bleeding, which usually occurs a few
days after birth and is secondary to maternal hormone withdrawal.
Hymenal tags may be present normally.
• Spine: Check for scoliosis, kyphosis, lordosis, spinal defects, and
meningomyeloceles.
• Extremities: Inspect creases and fingers. Do Barlow and Ortolani
maneuver to check for developmental dysplasia of hip. The Ortolani
test elicits the sensation of the dislocated hip reducing, and the
Barlow detects the unstable hip dislocating from the acetabulum. The
Orto/ani test is performed with the newborn supine and the
examiner's index and middle fingers placed along the greater
trochanter with the thumb placed along the inner thigh. The hip is
flexed to 90° but not more, and the leg is held in neutral rotation. The
hip is gently abducted while lifting the leg anteriorly. With this
maneuver, a "clunk" is felt as the dislocated femoral head reduces
into the acetabulum. This is a positive Ortolani sign. The Barlow
provocative test is performed with the newborn positioned supine
and the hips flexed to 90°. The leg is then gently adducted while
posteriorly directed pressure is placed on the knee. A palpable clunk
or sensation of movement is felt as the femoral head exits the
acetabulum posteriorly. This is a positive Barlow sign. The Ortolani
and Barlow maneuvers are performed I hip at a time. A dislocatable
hip has a rather distinctive clunk, whereas a subluxable hip is
characterized by a feeling of looseness, a sliding movement, but
without the true Ortolani and Barlow clunks.
• Thorax: look for cardiac apical impulse, murmurs and B/L air entry.
Abnormal location of apical impulse can be a clue to pneumothorax,
diaphragmatic hernia, situs inven;us, or other thoracic problems.
• Pulse: Check pulses. Note any decrease in femoral pulses as a sign
of possible CoA. Note character of pulses (bounding or thready).
• Skin: Look for bluing, mottling and common skin lesions like
Mongolian blue spots
Instructions for the CLR JR
32

• All babies should be administered vit K prophylaxis in CLR as a


single dose ofVit Kl I mg IM into the anterolateral aspect of thigh.
(see section Dl31)
• Babies born by vaginal delivery (including forceps, ventouse and
breech) should be given to the mother immediately after birth.
• The JR should ensure that all babies are initiated on breast feeds at
the earliest after birth, ideally within one hour
• Separation of the mother and her baby within the first hour of the
birth for routine postnatal procedures such as needle-sticks should be
delayed until after the first feeding is completed, unless monitoring is
necessary for the immediate care of the baby.
• Avoid procedures that may interfere with breastfeeding or that may
traumatize the infant, including unnecessary, excessivei and over-
vigorous suctioning of the ora1 cavity; and to avoid oro-pharyngeal
mucosa! injury that may lead to aversive feeding behavior
5.2.2 In The Post Natal Ward
Thermal regulation
Mothers should be encouraged to have skin-to-skin contact with their
babies as soon as possible after the birth. 1 Babies should be clothed as
soon as possible. Two layers of clothing are preferred during the summer
months and 4 layers during the winter months. Diapers and a cotton knit
undershirt are important as the first layer of clothing. Woolens, mittens
and flannels are used as additional layers. Head and feet should be
covered with caps and socks.
Neonatal examination:
A thorough neonatal examination should be done in the postnatal wards.
Special attention should be paid to the cardiovascular examination for
new onset murmurs and femoral pulsation, jaundice and hip examination.
Wt and OFC must be done at least once prior to discharge. Note the time
of passage of urine and meconium as babies generally pass meconium
within first 24 h and urine in the first 48 h.
Breastfeeding (see sections 9.3 and 9.6)
• Exclusive breastfeeding should be the rule. For detailed breast-
feeding policy, see the unit's breastfeeding policy document.
Exclusive breastfeeding is defined as an infant's consumption of
human milk with no supplementation of any type (no water, no juice,
no non-human milk, and no foods) except for vitamins, minerals, and
medications.
• From the first feed, women should be offered breastfeeding support
(from doctor, nurse or lactation counselor) to enable comfortable
positioning and attachment and prevent concerns such as sore nipples.
• Additional support should be offered to women who have had:
o a narcotic or a general anesthetic, as the baby may not initially
be responsive· 2
33

o a caesarean section, par :icularly to assist with handling and


positioning the baby to pr Jtect the woman's abdominal wound
o initial contact with their b iby delayed for any reason.
• Mothers should be encouraged to give 8 to 12 feedings at the breast
every 24 h, offering the breast whenever the infant shows early signs
of hunger such as increased alertness, physical activity, mouthing, or
rooting. 3 Crying is a late sign of hunger.
• Non-demanding infants should be aroused to feed if 4 h have elapsed
since the beginning of the last teeding. 4
• The infants should be fed 10 to 15 min on each breast. 5 The baby
should be fed one breast completely and then put to the second
breast, so that both breasts get equal stimulation for milk production.
Breasts should be alternated with each feed. 6
• Breast feeding counseling should also involve the father.
• The drugs taken by the mother should be reviewed with the
obstetrician so that medications that have the potential for altering
the infant's alertness and feeding behavior are best avoided. 2
Comprehensive web references providing information on drug
effects when used during lactation are available,
o LactMed:www.toxnet.nlm.nih.gov/cgi-in!sis/htmlgen,LACT
o Drugs in breast milk:
www. ukmicentral. nhs. uk!drugpreg/qrg_p I .him
o Drugsafetysite.com
Breast feeding positioning and technique
• The mother can feed the baby in any comfortable position such as
lying (sideways) or sitting. Poor positioning often results in poor
attachment. The mother should hold the baby with the head at the
mother's elbow, such that the baby faces the breast with nose
opposite to mother's nipple, supporting the baby's whole body and
not just the neck and shoulder. The nipple should touch the infant's
mouth. The mother must wait until the baby's mouth opens wide,
and offer the breast to the baby to get as much as he/she can into
his/her mouth.
Indicators ofsuccessful breastfeeding 7
Indicators of good attachment
• mouth wide open
• less areola visible underneath the chin than above the nipple
• chin touching the breast, lower lip rolled down, and nose free
• no pain.
Successful feeding (indicators in babies):
• audible and visible swallowing
• sustained rhythmic suck
• relaxed arms and hands
• moist mouth
34

• regular soaked/heavy nappies.


Successful breastfeeding (indicators in women):
• breast softening
• no compression of the nipple at the end of the feed
• woman feels relaxed and sleepy.
Problems related to breast-feeding
The mother should be counseled regarding breastfeeding problems. For
the management of common problems related to breast-feeding see Table
5.1

T able 5 IM anae:ement o f common b reast i ee d'1ne: pro bl ems


Problem Comment Solution
The length of the
Flat nipple resting nipple is not
Don't worry
important for
breastfeedini::
Hoffman Technigue - breaks
adhesions at the base of the
nipple. The mother must
place the thumbs of both
hands opposite each other at
the base of the nipple and
gently but firmly pull the
Nipple that does not thumbs- up and down and
come out erect and on sideways. Repeat over the
Inverted
trying to pull out rather day
nipple
it goes deeper into the Kesaree method: Cut a
breast is an inverted disposable syringe one
nipple centimeter from the nozzle.
The piston is then inserted
into the cut end and the
smooth end is placed over the
areola. The user then pulls out
the piston to maintain a steady
pressure and ever! the nipple.
Repeat before each feed.
35

Problem Comment Solution


Counsel regarding positioning
and attachment. Breastfeeding
should be continued on the
affected breast
Cracked nipples: washing the
Sore nipples
Occurs due to incorrect nipple once daily only with
cracked
position/attachment of water and exposure of nipple
nipples
the baby at the breast to air and sun as much as
possible and application of a
drop of hind milk on the
nipple after each feed and
continued breastfeeding.
Avoid medicated creams
The engorged breast is
tight, shiny and very Correct attachment and
painful. If breast is positioning. Avoid other
engorged, the baby will feeds. When engorgement
Breast not be able to take feed occurs, expression of breast
engorgement properly due to poor milk should be done to relieve
attachment, inadequate breast engorgement, reduce
emptying which further pain and make the mother
leads to decreased comfortable.
production.
If the baby does not
suckle well on a Improve suckling I
particular segment of positioning. Massage the
Blocked
the breast, the thick lump towards the nipple to
duct
milk blocks the milk promote emptying of the
duct leading to a painful breast.
hard swelling.
Express the milk frequently
and continue breastfeeding.
If the blockage of the
Wann water fomentation may
duct or engorgement
also help alleviate pain.
continues, infection
Mastitis Incision to drain the abscess
may supervene. The
may be necessary sometimes.
breast becomes red, hot,
Restart breastfeeding from the
tender and swollen
affected breast as soon as
possible.
Result of an active
Leakage of
ejection reflex during
milk from Reassurance
first few wks of
the breast
lactation
36

Problem Comment Solution


Some mothers notice a
Blood in the
little blood in the milk,
milk Reassurance
even in the absence of a
ninole fissure

Bathing
As a hospital policy, bathing of babies must not be done in PGlMER.
The only exception is a baby born to an HIV+ve mother. Daily sponging
of the baby must be done in the morning by the mother using clean
lukewarm water taking care to clean the flexural areas.
Care of diaper area
The mother should be counseled that the diaper area should be cleaned
gently with warm water and soaked cotton to remove stuck feces. The
bottom should be wiped from front to back to avoid fecal matter from
reaching the genitals. The area should then be dried by patting with a
towel to avoid any undue friction. Skin should then be exposed to air for
a few minutes. 8 Nappy rash can be prevented by reducing moisture by
the frequent changing of nappies or by using diapers using absorbent
gelling material. 9 Barrier pastes like Zinc oxide/petrolatum should be
applied on the area after each change for nappy rash.
10
Umbilical cord care
Keep the umbilical cord clean and dry. Antiseptics should not be used
routinely. The cord clamp should be removed once the cord becomes dry
and shriveled. Air exposure helps the cord stay dry and eventually fall
off, so keep diapers folded down below the cord.
Immunization
See section 5.2.6.
Jaundice:
Before discharge (especially so if discharged at <72 h) every newborn
should be assessed for the risk of developing severe hyperbilirubinemia
(see section 20.5). Measure the TSB and plot the results on the Bhutani
nomogram (sec section N 19). Infants in the high risk and high
intermediate risk zone should not be discharged early as they are prone
for hyperbilirubinemia. Others can be discharged if adequate follow up
can be ensured.
5.2.3 Problems with Near Term Infants
• The care of the healthy near-terrn infant deserves special
consideration because these babies often appear robust but may have
physiologic vulnerabilities and are prone to hypothermia.
hypoglycemia, jaundice, dehydration and breastfeeding problems.
• Such infants born must be monitored for 1-2 h in the CLR until their
vital signs are stable and then transferred to the mother. Needle
sticks may be avoided unless clinically indicated. They must be seen
37

by the SR prior to transfer to t'le mother. The CLR JR must inform


the maternity and gynecology ward JR before transfer.
• Since these babies may not fetd well, the area JR must ensure that
these babies take timed breast feeds. Mothers should be advised to
express their milk and spoon/cup feed the baby every 3 h if baby is
not feeding well.
• Lactation assistance should be provided to the mother by involving
the lactation consultant and public health nurses of the unit. These
infants must not be discharged until they are feeding well and
gaining Wt. 11
5.2.4 General Discharge Advice
• Exclusive breast feeds must be given for the first 6 mths of life.
Nothing else should be given unless medically indicated. The breast-
feeding advice given at the postnatal wards is also applicable at
discharge.
• Parents should be informed about hygiene and to wash the hands
before handlings, feeding and after each nappy change.
• Parents should be informed to keep the baby warm with extra layers
of clothes. Hands and feet should be pink and warm to touch.
• Cord care should be advised in the form of ensuring a dry cord with
no external application.
• In case of early discharge, the mother should be informed that for the
first 1-2 d the baby only has 1-3 wet nappies per 24 h but should
pass meconium several times.
• All infants should be examined by a pediatrician in the first few days
after discharge to assess infant well-being and the presence or
absence of jaundice (See Table 5.2). 12

T able 5.2: Review after earlv discharee


Infant Discharoed Should Be Seen bv Age
Before age 24 h 72 h
Between 24 and 47.9 h 96 h
Between 48 and 72 h 120 h

• Parents should be given information about Sudden infant death


syndrome (SIDS) even though the entity is rarely reported in lndia. 13
o Always have baby sleep on the back (supine)
o Place the baby on a firm mattress
o Avoid loose bedding, pillows, and blanket rolls
o Avoid overheating
o Encourage breastfeeding
• Advise the mother to return to PGIMER Emergency (APC, 28) or
report to the nearest pediatrician immediately if the child develops
any of the following danger signs:
38

o not able to drink or breastfeed


o looks yellow or the urine color becomes yellow
o has difficult and fast breathing or blue lips
o pale in color or bleeding from any site
o too hot or cold to touch
o has abnormal limb movements
0 has pus discharge from the umbilicus
0 diarrhea or blood in stools
5.2.5 General advice regarding care at home
Bathing"
• The infant may be bathed 2 or 3 times a wk; frequent bathing is not
necessary. Instead sponging may be done. Frequent bathing may
lead to drying of the skin and/or irritation. The acid mantle is also
affected by bathing.
• The bath water level should be kept below the navel or sponge baths
advised until a few days after the navel cord has fallen off as
submerging the cord could cause infection or interfere with its
drying out and falling off.
• The room should be warm, without drafts. The water temperature
should be around l 00.4 degrees F or 38 degrees C. (neither too hot
or too cold to touch)
• Soap is too drying for the skin and is usually not necessary. The acid
mantle may be removed entirely by soaps with an alkaline pH. If at
all soap is used, it should be mild with neutral pH (some soap brands
with neutral pH are: Dove, Johnsons, Oilatum, and Dermadue).
Antimicrobial soap is not recommended due to the harshness of the
soap as well as the adverse effects on skin colonization.
• Duration of bath should not be for more than 5 min as a longer bath
duration might soften the skin and reduce the threshold of friction"
• Advise washing the face and neck; otherwise, chemicals from
dribbled milk and food can build up and cause a rash. Also, rinse off
the eyelids with water.
• Advise washing the genital area. Never use soap to wash the inside
of the female genital area. Rinse the area with plain water and wipe
from front to back to prevent irritation. At the end of the bath, rinse
the baby well as soap residue can be irritating.
Oil Massage
• Complete head to toe massage can be a daily routine.
• The benefits to the newborn include tactile kinesthetic stimulation,
improved skin barrier function, thcrmoregulation and growth. 15
• Coconut oil is safe and may be preferred over proprietary oils.
Others oils that may be used are sunflower, saftlower or olive oil.
Do not use mustard oil, ghee and milk.
39

Nails
Nail should be regularly cut and kert short and clean. Special nail cutters
for newborn babies or small scissor; may be used.
Ears
Routine cleaning of the inside of the ear canal is not advised. If done,
cotton swab soaked in warm water can be used to avoid injury to the
auditory canal. Oil must not be instilled into the ear.
Napkin changes and diaper care
• In general, nappies should be made of cotton cloth and should be
home laundered with mild detergents. If affording, parents may use
diapers and super-disposable diapers as they keep the skin relatively
dry, maintain pH and reduce the risk of rash. There are concerns that
the materials used in diapers are non-biodegradable and hence
environmentally unfriendly.
• Parents should forego tight-fitting diapers and consider a diaper
slightly larger than the infant to minimize the contact between skin
and urine or feces
• Wash hands well after each diaper change to prevent germs from
spreading.
5.2.6 lmrnunization:
• Term, healthy neonate: Recommendations of !AP have to be
followed. (see Table 5.3)
o OPV - soon after birth
o BCG intraderrnal - at birth but not later than 30 d of age
o Hepatitis B vaccine at birth or before discharge. Babies born to
HBSAg +ve mothers should receive hepatitis B vaccine at birth
irrespective of GA or BW along with HBIG.
• Pretenn neonate: Vaccines should be administered as per the
schedule for term infants. This should be according to chronological
age of the infant and not postconceptional age.
As far as possible, babies must be administered BCG, Hepatitis B and
OPV at least 1d prior to discharge to monitor for any adverse effects due
to immunization. Contact vaccinators for inborn babies in case of
emergency discharges. Babies discharged within 24 h should be advised
immunization at the earliest either at PGIMER (Room No. 2422, APC-
2D) or with a local practitioner, whichever is convenient.

Table 5.3: Revised !AP immunization time table, 2009 16


Age Vaccines Note
Birth BCG
OPV-0
Heoatitis-8 - I
6wks OPV-1 + IPV-1 I OPV alone if IPV cannot be given.
OPV-1 DTPa has fewer side effects than DTPw,
40

DTPw-l I DTPa but the two have equal efficacy and the
-l cost of DTPa is inordinately high.
Hepatitis-B -2
Hib - I
IOwks OPV-2 + IPV-2 I
OPV -2
DTPw-2 I DTPa
-2
Hib-2
14 wks OPV-3 + IPV-3 I
OPV -3
DTPw-3 I DTPa
-3
Hepatitis-B -3
Hib - 3
9 mths Measles
15 - 18 OPV-4 + IPV-Bl OPV alone if IPV cannot be given
mths I OPV -4
DTPw-Booster l
I DTPa -Booster
l
MMR-l
Hib - Booster
2 yrs Tvohoid Revaccinate every 3-4 vrs
5 yrs OPV-5 Second dose of MMR vaccine can be
DTPw-Booster 2 given at any time 8 wks after the first dose
I DTPa -Booster
2
MMR-2
Vaccines that can be given a~er discussion with oarents
More than Pneumococcal 3 primary doses at 6, I 0, and 14 wks,
6 wks conjugate followed bv a booster at l 5-l 8 mths
More than Rotavirus vaccine 2 or 3 doses (depending on brand) at
6 wks 4-8 wks interval
After 15 Varicella Age less than l 3 yrs: one dose
mths Age more than l 3 yrs: 2 doses at 4-8
wks interval
After 18 Hepatitis A 2 doses at 6- l 2 mths interval
mths
This list is not exhaustive. Newer vaccines are constantly being
introduced.
41

REFERENCES:
I. Righard Let al. Lancet.1990;3:6:1105
2. Ransjii-Arvidson AB et al. Birt:1. 200 I ;28:5.
3. Gunther Met al. Lancet 1955;2\8:575.
4. Klaus MH et al. Obstet Gynecol Clin North Am. 1987;14:623.
5. De Carvalho Met al. Pediatrics 1983;72:307.
6. Breastfeeding Promotion Network of India.
http://www.bpni.org/breastfeed1ng.html
7. Baumer J H et al. Arch. Dis. Child. Ed. Pract. 2007;92:61.
8. Dhar S et al. Indian J Dermatol 2007;52: I.
9. Lane AT et al. AmJDisChild. 1990;144:315.
I 0. Zupan Jet al. Cochrane Database Syst Rev. 2004.
11. Stellwagen Let al. Pediatr Rev. 2006;27:89.
12. AAP, Subcommittee on Hyperbilirobinemia. Pediatrics
2004;114:297.
13. Mitchell EA et al. Arch Dis Child. 2007;92:155.
14. Association of Women's Health, Obstetric and Neonatal Nurses.
www .awhonn.org
15. Darmstadt GL ct al. Acta Paediatr.2002;91 :546.
16. !AP guide book on immunization, 2009.
42

6. MONITORING UNDER VARIOUS CIRCUMSTANCES

6.1 MONITORING IN LR
6.1.1 Normal term neonates without risk factors:
HR, respiration, temperature, color, and CFT should be monitored once
after stabilization. Monitor these parameters once per nursing shift if the
baby remains stable.
6. 1.2 Late preterm babies:
They should be monitored 2 hourly for 6 h and then 12 hourly until
transfer.
6.1.3 High risk asymptomatic babies (except near term babies):
This group predominantly includes (but not limited to) preterm, SGA,
IDM, babies born through MSL, perinatal asphyxia (see Table 6.1)

Table 6.1: Monitorin<> hi<>h-risk neonates in LR


Parameters Frequency
Vital signs Every 2 h
(Temperature, HR, RR, CFT, (for 24 h or till transfer -
saturation) whichever is earlier)
Other parameters
See sections 11.3.3 and 18.3
(BS, PCV)

Adequacy of feeding Every 2 h

All babies are evaluated for jaundice at transfer and at least 12 hourly.

6.1.4 Symptomatic babies:


These groups of babies are hemodynamically unstable and/or awaiting
shifting. Monitoring of sick babies in the LR nursery should be done and
mentioned in the file.
• Babies with respiratory distress should be monitored as per the
monitoring scores mentioned in section 14.5 along with Sp0 2 and
blood gases. Frequency of monitoring should be individualized for
each baby by the SR on duty but should not be more than 6 h.
• Babies who are premature or SGA should be monitored for
metabolic problems like hypoglycemia, polycythemia,
hyperbilirubinemia according to the schedule mentioned in sections
11.3.3, 18.3, 20.3.1

6.2 MONITORING IN THE NICU


6.2.t General principles
• Vital parameters are monitored continuously and recorded hourly in
the Nurses' Observation Chart.
43

• Blood gases should be done 1s and when clinically indicated and


have to be entered in the ventilation flow sheet and nursing
observation chart immediately
• All significant events like seiwres, apnea, and bradycardia must be
entered in the remarks column of the nursing chart as well as in the
file. This should include time of the event, number of events, extent
of resuscitation required, and time taken to recover. All procedures
should be noted in the files as well as nurses' observation chart
mentioning the names of JR and SR and nurse assisting the
procedure.
• Events that took place during procedures must be duly monitored
and recorded in the monitoring sheet
• Check the following daily:
o Alann settings of various vital parameters that are set on the
monitor
o Appropriateness of NTZ (see section 7.2.1)
o Incubator mode
• Fluid input and output status should be calculated once in every 6 h
as well as for the whole of last 24 h to help in modifying fluid
management.
• Calculate the daily Calories & protein intake in the nursing chart
(to be done by night shift JR)
• Venous cannula site and patency, arterial line patency & evidence
of vascular compromise, probe site (temperature, saturation,
transcutaneous) are to be evaluated 2 hourly by the staff nurse.
• The following has to be duly recorded in the nursing chart
o Amount of blood letting
o Frequency of suctioning (ET & oral), nature of secretions
o Physiotherapy (chest) timing and tolerance
o ET Tube position
6.2.2 Parameters to be monitored: For frequency of monitoring,
various parameters see Table 6.2

6.3 MONITORING IN STEP DOWN CARE AREA OF NNN:


• Vital signs (temperature, HR, RR, color): Every 12 hourly
• Monitor for feed tolerance: abdominal girth and bowel sounds
(daily) and pre-feed aspirate.
• Anthropometric parameters: Wt - twice weekly, Length & OFC -
weekly (by the JR).
• Neurological examination: weekly. The neurological examination
chart (by the JR, supervised by the SR) and the growth & nutrition
chart (by the JR) must be updated every Monday afternoon.
44

Table 6.2: Frenuencv of monitorin" various narameters in NICU


Parameter
Parameter Frequency
descrintion
Temperature, HR,
Vital signs Hourly
RR, CFT, saturation
Daily.
Babies who are ELBW or
Wt record --
have over/underhydration:
monitor 12 hourlv.
Retractions, grunt,
nasal flaring (use
Hourly - during initial acute
Respiratory Silverman-Anderson
illness & during ventilation
system score & Downe
Later - as clinically indicated
score) (see sections
14.5.1 and 14.5.2)
Circulatory system
Pulse volume, BP,
PDA pulse pressure, 6 hourly (or as clinically
precordial activity, indicated)
liver size
HR, pulse volume, Hourly, after each dose
Shock
CFT, MBP, urine modification I each new drug
outnut added
All parameters of
CHF shock+ liver size, Hourly
CVP
Special circumstances
Abdominal girth,
Feed bowel sounds, Every 2 hourly (prefeed)
intolerance I prefeed aspirates.
suspect NEC Radiology (AXR) Refer to NEC protocol
Stool - occult blood
Urine output (24 h,
each quadrant), BUN
6 hourly - acute phase, 12
Renal failure & creatinine, edema,
hourly - improving phase
other evidence of
fluid retention

• Calculate the daily Calories, protein & mineral intake in the


treatment chart (by the night shift JR)
• Metabolic profile and PCV: weekly. Must be done every Tuesday
morning (by the night shift JR).
45

• Routine neurosonograms (by !lie SR) as per the schedule: Mondays


and Thursdays
• Screening for ROP (by Ophthalmologists): Saturday afternoon.

6.4 MONITORING IN POSTNATAL WARDS:


• The LBW babies must be moni1ored like the step down care ofNNN
(see section 6 .3)
• Normal term babies:
o Vital signs - HR, RR, temp, color- 24 hourly (should be tailored
according to the need of the baby)
o BS and PCV as and when indicated
o Visual assessment of jaundice - At least twice daily
o Feeding adequacy of breast-fed neonates and any feeding
problems.
o TSB, adequacy of feeding and pattern of Wt loss in babies under
PT.
46

7. TEMPERATURE MAINTENANCE AND HYPOTHERMIA

7.1 TEMPERATURE RANGES (WHO 1997) 1: For definitions of


euthermia and hypothermia see Tables 7. I and 7.2.

Table 7. I: Definition of euthermia


Axilla 36.5-37.5 °C (97.7-99.5 °F)
36-36.5 C (96.8-97.7 F)

Table 7.2: Definition of hvnothermia


Mild hypothermia or Axillary temperature 36 - 36.4°C (96.8-97.5 °F)
cold stress or Skin temnerature of35.5 - 35.9°C
Moderate Axillary temperature 32 - 35.9°C (89.6-96.6°F);
hvnothermia or Skin temncrature of 31.5 - 35.4 °C
Severe hypothermia Axillary temperature of< 32°C (89.6°F) or Skin
temoerature < 3 I .SOC

Hyperthermia is defined as: Axillary temperature >37.5°C

7.2 BACKGROUND INFORMATION


7.2.1 NTZ
NTZ is the range of environmental te1nperatures wherein the body
temperature is maintained in a normal range with minimal basal
metabolic rate (sec section N 17). The provision of a NTZ allows
diversion of Calories to growth and differentiation rather than to
thennoregulatory needs. An environment in which the temperature of the
baby is n1aintaincd in the NTZ is the thcrmoncutral environment
7.2.2 Heat production
• Generated by voluntary muscle activity
• Generated by involuntary tonic muscle activity such as non-
shivcring thermogenesis. contributed in large part by brown fat
metabolism
7.2.3 Heat loss
• Conduction (minimal)
• Convection,
• Radiation, and
• Evaporation (exceeds all other sources in YLBW babies in first few
days oflifc)

7.3 ASSESSMENT (See PGIMER video on neonatal procedures, for


temperature measurement)
7.3.1 Touch method:
The warm feet and hands of the baby indicate that the baby is in thermal
comfort. When feet arc cold and abdomen is wann, it indicates that the
47

baby is in cold stress. In hypothermia, both feet and abdomen are cold to
touch.
7.3.2 Thermometer
Mercury-in-glass thermometers o,. digital thermometers: Preferably,
use a low reading thermometer that can record temperature as low as
30°C. Disadvantage is single point determination.
Rectal temperature
Infants must be placed on their stomach and held securely in place. It is
recorded by inserting the greased bulb of the thermometer into the
rectum to a depth of3 cm in a term baby or 2 cm in a preterm baby. Keep
thermometer in place at least for 3 min. It is the best guide for core
temperature in cold (hypothermic) sick neonates.
Axillary temperature
It is recorded by placing the bulb of the thermometer against the roof of a
dry axilla perpendicular to the arm. Baby's arm is held close to the body
to keep thermometer in place. The temperature is read after 5 min (WHO
recommendation) 1. The recommendations are similar for term and
preterm babies. There is a wide variation across studies regarding the
agreement between axillary and rectal temperature although most studies
agree that the variation is less in pretcrrn infants.
7.3.3 Thermistor
Skin temperature is recorded by a thermistor. Site of attachment: supine -
right upper abdomen; prone position - flank. When possible
simultaneously measure temperatures over the abdomen and sole. Attach
probe to skin using a reflective thermal pad.
False high temperature recordings are due to:
o Probe over interscapular area (area of brown fat)
o Probe sandwiched between the mattress and the skin.
o Probe covered with a tight fitting cloth.
False low temperature record
o Low environmental relative humidity
o Probe over bony prominences

7.4 SIGNS AND SYMPTOMS OF HYPOTHERMIA


• Initial signs: pallor, cold extremities, acrocyanosis, irritability, and
respiratory distress.
• Later signs: apnea, bradycardia, central cyanosis, lethargy,
hypotonia, weak cry, weak suck, increased gastric residuals,
abdominal distention, or emesis.
• Extended periods of cold stress can lead hypoglycemia, respiratory
distress, hypoxia, metabolic acidosis, coagulation defects, and
delayed adjustment from fetal to newborn circulation, ARF, NEC,
failure to increase Wt or Wt loss and in extreme cases death.
Metabolism of brown adipose tissue releases nonesterified fatty
48

acids that compete with bilirubin for albumin binding sites,


increasing the risk posed by hyperbilirubinemia

7.5 TEMPERATURE MAINTENANCE IN DELIVERY ROOM


• After birth, core and skin temperature of the term newborn can drop
at a rate of approximately 0.1°C and 0.3°C per min respectively
unless immediate action is taken. Preterm babies <1000 g can have
temperature drop of up to l°C per min.
• Maintain warm labor room temperature (28 - 30° C). Labor rooms
must have a room thermometer. Room temperature must be checked
in each shift by the labor room nurse.
• The infant must be resuscitated under a radiant warmer. Follow the
standard NRP guidelines for prevention of hypothermia. A few
salient features are enumerated here:
o Dry the skin especially the head. Remove wet linen.
o Wrap the infant in prewarmed blankets or, alternatively, place
the dried infant skin-to skin on the mother's chest to use her
body as a heat source.
• Eliminate draughts in labor room
• Clothe the baby as soon as possible. Put on caps and socks.
• Transfer normal term babies to mother as soon as possible after
appropriate clothing.
• Postpone routine procedures until temperature stabilizes, unless
absolutely essential.
• Polythene occlusive wraps; This intervention consists of placing the
premature infant in a polyethylene bag or sheet that is applied from
the neck down immediately after birth, even before the baby is dried.
The baby should be under a radiant warmer. Food-standard
polyethylene (e.g. WRAP it™) should be used. This approach
reduces evaporative heat loss while permirting radiative heat
transfer. This option may be considered for preterm babies <28 wks
gestation, after discussion with the consultant.
A Cochrane review (2008l' has confirmed the efficacy of plastic
bags in addition to the customary radiant heat in significantly
improving the admission temperature of premature babies <28 wks'
gestation.
• Monitor temperature in labor room: record temperature hourly until
stable. Then monitor 4 hourly in sick, LBW and preterm babies.

7.6 WARM TRANSPORTATION


• Stable preterm and LBW babies should be transported to the
maternity/Gynecology wards well wrapped and in skin-to-skin
contact with the mother if possible.
49

• Babies admitted to NICU/Nur;ory must be transported in a transport


incubator. The CLR resident snould anticipate transfer of babies to
NICUINNN and keep the tramfer incubator pre-warmed. The CLR
JR must inform the NJCU/NN~>J JR in advance so that the incubator
or radiant warmer is pre-warmed (see section 3.1.4).
• Record the temperarure before transport and document it in the
neonatal pro forma.
• The transport incubator must be used to transport babies for
investigations (e.g. CT scan, nuclear scan) or to the OT. Inform
personnel doing the investigation before transport of the baby and
ensure an appropriate environmental temperature in that area (switch
off local air conditioners, iffeai;ible). Record temperature before and
after transport and frequently during procedure.
• Transfers to and from the Pediatric Emergency by a transport
incubator should only be done if the incubator can be mounted onto
an ambulance. If such an ambulance is not available, the transport
incubator must not be used for road transportation to/from the
Emergency. Instead, the baby should be adequately wrapped and
taken in the ambulance. Skin-to-skin care can be utilized during
transport ifthe mother, father or grandparents are accompanying.

7.7 PREVENTION OF HYPOTHERMIA IN NICU OR NURSERY


• The temperature of NICU1NNN must be maintained between 28 ±
20C.
• The SR in charge of the N ICU/Nursery should ensure that the
temperahire of his/her area is checked regularly.
• Maintain an inspired air temperature at 37°C for ventilated infants.

7.8 CLOSED CONVECTIVE INCUBATORS:


• Incubators are preferred over radiant warmers for the care of preterm
babies in PGIMER. Incubators decrease insensible water losses.
• Skin servo mode is preferable when caring for sick babies. It helps to
assess the temperature requirement of the baby. Set skin temperature
to 36.5°C. In skin mode, fluctuations in air temperature are greater
especially when the baby is handled and there is a risk of
overheating ifthe probe is dislodged.
• Switch to air mode when the baby becomes stable. The neonate
should have been thermally stable for several days in air mode
before weaning the baby to an open cot. When switching over to air
mode, set the air temperature to equal the average incubator air
temperature during the previous 24 h of skin mode or use the
guidelines below (See Table 7.3). Air mode is preferred while doing
procedures.

/
so

Table 7.3: Average incubator air temperatures needed to provide a


suitable thermal environment for naked healthy infants.' (see section
NI 7)

BW Environmental temoerature
(kg) 35°C 34 °C 33 °C 32 °C
1.0 - Forl"IOd After 10 d After 3 wks After 5 wks
1.5
1.5 - Forl"IOd After 10 d After4 wks
2.0
2.0 - For1"2d After 2 d After 3 wks
2.5
> 2.5 For1"2d After 2 d

In a single walled incubator, add 1°C to the above mentioned set


incubator temperature when the room temperature is less than 27°C;
and subtract 1°C from the above mentioned set incubator air
temperature for every 7°C by which room temperature exceeds
27°C.
• Working through the portholes should be the preferred method in
order to reduce convective heat loss, unless increased access to the
infant is essential. Only for emergency interventions, should one
open the front panel of the incubator. In this case, additional heat
sources should be used to compensate for the rapid fall in air
temperature and air mode must be used in preference to skin mode.
• A cap must be used in all babies and most babies nursed in an
incubator can be clothed, even if they have a mild or moderate
illness.
• Use a double walled incubator whenever possible to reduce radiant
heat loss. Plexiglas heat shields may be used in single walled
incubators.
• Humidification:
Humidity should be commenced in all infants :S31 wks gestation at
85% humidity (>85% results in rainout and temperature instability).
o Infants of28-30 wks gestation: If temperature remains stable for
24 h, start to reduce humidity by 5% daily.
o Infants of <28 wks gestation: Maintain humidity of 85% for first
7 d and then decrease by 5% daily as temperature allows.
Humidification is achieved by filling the humidification chamber
with the appropriate volume of distilled water. The water must be
changed daily and should never be topped up - a complete exchange
of water is necessary if refilling. The chamber should be washed (tap
51
water) and dried thoroughly with hand towels whenever the water is
being changed (this reduces the ·isk ofa bacterial biofilm build up).
• Weaning from incubator to 'pen cot can be accomplished by
manually lowering the incub.Hor's ambient temperature. The
following should be satisfied
o 5 d of consistent Wt gain
o Euthermic at ambient temperature of :S30°C while clothed.
o Free of major medical complications.
• Check the axillary temperature after 30 mins and then hourly for 4 h
after weaning to open cot.

7.9 RADIANT WARMER


• Radiant warmer is more convenient for the management of sick term
newborns and babies with Wt .• 1800 g and babies in whom open
access for doing procedures is required (e.g. DVET). It affords ease
of handling and visualizing the infant compared to closed convective
incubators. But insensible water loss and oxygen consumption is
more in babies nursed under radiant wanners.
• Skin servo control mode is preferable. The set skin temperature
should be 36.5 °C.
• Insensible water loss under radiant warmers can be minimized
through the use of polyethylene sheets (e.g. Clingwrap). Using a
polyethylene sheet stretched across the infant from wall to wall
across the plastic side panels of the radiant warmer bed allows
radiant heat from the warmer to be transmitted to the infant.
• Cover the infant's head with a cap. Also cover the arms and legs of
sick babies. Clothing of baby under warmer should be done only
when the baby is stable.
• Manual control mode should not be used routinely except for very
short periods of time (e.g. while initiating resuscitation) because the
manual control lacks feedback information about body temperature
and increases the risk of overheating or underheating. The infant's
condition and temperature should be checked at least every 15 min
on manual mode.
• Due to the higher insensible water loss (depending on both the
gestational and post-natal age of the infant), increase the fluid intake
by 20 ml/kg. unless contraindicated (see section 8.5).

7.10 PREVENTION OF HYPOTHERMIA WHEN BABY IS WITH


THE MOTHER
• Babies should be kept with their mothers 24 h a day in a warm room
(at least 25°C/77°F). This is known as "rooming-in".
• Ensure kangaroo mother care and breastfeeding
52

• Extra layers of clothing are advisable during winter months and in


preterm and LBW infants (see section 5.2.2). The baby should be
uncovered as little as possible during assessment of its condition.
Clothing and bedding should not be too tight so as to allow air
spaces between the layers, as trapped air is a very efficient insulator.
Swaddling - the custom of wrapping bands around the baby - should
not be done tightly. Swaddling aids temperature maintenance; but it
done too tightly it excludes air, restricts movement and may increase
the risk of respiratory infections.
• In winter, ambient environmental temperature can be made wanner
by advising mothers to use extra heating devices.
• Always teach the mother how to assess temperature by touch
method.

7.11 MANAGEMENT OF HYPOTHERMIA


7. I I.I Investigations
• Monitor SpO, - all babies. ABG must be done for babies with
moderate and severe hypothermia (to assess for hypoxemia and
metabolic acidosis) (see section 10.9)
• Sepsis screen must be done in case of unexplained hypothermia
and/or other evidence of sepsis. (See section 24.4)
• BS level - all babies (to assess for hypoglycemia) (see section
11.2.2)
• Serum electrolytes, renal functions and urine specific gravity - in
moderate and severe hypothermia (to assess hydration status and
hyperkalemia)
• Thyroid studies (if hypothyroid state is suspected)
7. 11.2 Treatment
• In cases of mild hypothermia, the baby can be rewarmed by skin-to-
skin contact, in a warm room4 • This is only useful for term and near
term appropriate for date babies who arc stable and otherwise active
and whose mothers are ready. Record axillary temperature every 30
min until baby is euthermic. In case of progressive fall in
temperature while rewarming by skin-to-skin contact and in case of
moderate or severe hypothermia or hypothermia in sick babies the
principles stated below apply (See Figure 7. I).
• Use radiant warmer or incubator
• The appropriate rate of re-warming is controversial. Rapidly re-
warming till cuthermic is recommended by many authors. 5
• Do not cover the body with cotton or clothes during re-warming as
this will interfere with re-warming. After re-warming baby can be
clothed.
• Diminish heat loss through convection, radiation, evaporation, and
conduction (double walled incubators, plastic wraps, heat shields, oil
53

application and warming mattTesses may be used to diminish heat


loss.)
• Determine cause and treat appropriately. Refer to appropriate section
for specific management.
• Watch out for complications related to rewarming.

Figure 7.1: Management of hypotllermia

Moderate to severe hypothermic neonate,


failure of rewarming by skin to skin contact,
hypothermia in sick babies
Ensure no further
temperature loss. Remove
cold, wet clothing. Do not
cover baby

Rapid rewarming- preferred.


Set temperatures:
Radiant warmer manual mode-heater output 100%
Radiant warmer skin mode - set at 36.5"C
Incubator- air mode temperature - set at 38-39"C

l
Monitor skin temperature continuously. Record
axillary temperature Yi hourly till euthcrmic

Apneic - slow the rate of rewarming.


Oxygen & ventilation - maintain Sp02
Hypoglycemia - IV glucose
Hypotension - slow the rate of rewarming, give
volume expansion or pressors.
Monitor BP & Urine output to evaluate hydration and
renal function.
Monitor bilirubin and initiate phototherapy at low
threshold levels.

REFERENCES
l. World Health Organization. Thermal protection of the newborn: a
practical guide. 1997.
2. McCall EM et al. Cochrane Database Syst Rev. 2008.
3. Hey E. Br Med Bull. 1975;3 I :69.
4. Christensson Ket al. Lancet. 1998;352:1115.
5. Kaplan Met al. J Pediatr. I 984; 105:470.
54

8. FLUID AND EL ECTROLYTE M ANAGEMENT

8. I GENE RAL PRINC IP LES


At birth, there is an excess of ECF. and this decreases over the first few
days after birth. Furthermore, ECF at birth and insensible water loss
decrease as BW and GA mcrease. Appropnate management of l1u1ds and
electrolytes in prctcnn infants must take into consideration the BW, GA
and postnatal age.

8.2 I NDICATIO NS FOR START ING IV FLUIDS


• GA < 30 wks or BW < 1200 g
• Sick neonates (the list includes, but is not limited to the following)
Respiratory distress
Severe Birth asphyxia
Recurrent apnea
Se17urcs
Intestinal obstrucuon
lieus /NFC
Metabolic abnormalities- hypoglycemia. dyselectrolytem1as
Shock
Dehydration

8.3 CALCULATING FLU ID REQ UI REMENTS


8.3.1 Basic principles
• Total l1u1d and electrolyte reqmrement = Maintenance + Dcticat ..t:
Ongoing losses. Maintenance fluid requirement Insensible water
loss (skin lungs) + Sensible water loss (urine + stool) + Water
required for tissue growth.
• The principal determinant of water balance in very immature infants
is the extent to which water is lost through the skrn. Urine output is
variable. Stool water loss is small and usually less than 5 mUkg d in
the first few days afier birth, but losses from the respiratory tract
may be high if inspired gases are not adequately humidified.
8.3.2 G uid eline~ for maintenance flu id require ments
The fluid requirements in mUkgtd are approximately as given m the table
below (see Table 8.1 ). Note that these arc general guidelines for starting
maintenance fluids on the day of admission. Ideally. advances m fluids
are to be made based on assessment of fluid status.

T a ble 8. I : Maintena nce fluid re uire meo ts

< 1000 80-100 Advance 11uids strict! as er h dration status


1-1.5 k 80 100 120 140 150
> 1.5 k 60 80 100 120 140
55

8.3.3 Maintenance Electrolyte requirement


Sodium:
Do not add on day I. Start when ct.mulative Wt loss from birth reaches
2:6% 1 after ensuring initial diuresi; (urine output of 2:1 mL/kg/hour)
unless serum sodium falls to <: 130 mEq/L
Term 2 mEq/kg/d
Preterm 2-3 mEq/kg/d to hegin with & 3-5 mEq/kg/d after l"
wk
Potassium
Add from day 3 (make sure baby has urine output of2'.1 mL/kg/hour and
K < 5.5 mEq/L). Caution must be exercised for ELBW babies, who may
develop severe hyperkalemia in the initial days of life.
Both term & preterm: 2 mEq/kg/d
Calcium
Given to all sick babies and babies <1500 g
Add from day I
36-72 mg/kg/d of elemental calcium i.e. 4-8 mL/kg/d of 10% calcium
gluconate

8.4 ASSESSMENT OF HYDRATION STATUS AND PLANNING


FURTHER INCREMENTS: For assessment of hydration status see
Table 8.2.

8.5 ADDITIONAL ALLOWANCES


Additional allowances may be required under certain circumstances.
Note that these are applicable more for very preterm babies rather than
moderately preterm or term babies.
Increased insensible water loss
Radiant warmer 20 mL/kg/d
PT* 20 mL/kg/d
Increased body temperature 10-20 mL/kg/d
*It is unnecessary to increase fluid intake routinely on starting PT if baby
is nursed in an incubator with humidification 3 .

8.6 PATHOLOGIC LOSSES AND DEFICIT REPLACEMENT


8.6.I Estimating losses
• Volume by volume replacement is needed (in addition to
maintenance requirements) in situations like diarrhea with
dehydration, chest tube drdinage, excess gastric aspirates, surgical
wound drainage, and excessive urine losses from osmotic diuresis.
56

T abl e 8 2 : P aramet ers or assessment ofhIVId ration st at us


Normal
Parameter Frequency of monitoring Fluid deficit Fluid overload
limits
Absence of signs listed Loss of skin turgor Puffiness of eyes
Clinical signs 8 hourly under deficit & Dry mucosa Edema
overhvdration Depressed fontanels Sudden increase in liver size
Wt Term OD 1-2% per day >2 °/o per day Wt gain/ no loss/less than
Preterm 121b hourly 2-3o/o per day >3 o/o per day expected loss in sick infants
Q 8-12 h x 3-4 d,
<750g
then dailv
Serum sodium* 750-1500g Q 12hx 3-4d, 135-145 mEq/L >145 mEqlL <135 mEq/L
then daily
>1500 g daily
Urine volume# 8 hourly 1-3 mUkglh <lmUkglh -
Urine specific
Test each sample voided 1005-1015 >1015 <1005
gravity
Initially and at least every other day until
Urea & Increase in urea
stable, then weekly until feedings are well Normal values -
creatinine"' disproportionate to creatinine
established.
Glucose 6 hourly*
*jor babies receiving 2: 50 % of their fluid requirements as !VF
#Babies <32 wks of gestation may continue to pass large amounts of· urine despite dehydration because of renal immaturity.
Hence urine output may be an unreliable indicator in this group of babies.
57

• Estimate losses over past 6-12 11. Replace urinary losses only if total
loss > 4 mL/kg/h in 6 h period. Replace the volume that is in excess
of 4 mL/kg/h- volume by volume- over next 6-12 h. Other losses are
replaced volume for volume every 6 h. In all VLBW babies, the
calculation oflosses and replacement should be done every 6 hourly.
• Type of fluid used for replacement:
o Vomiting, NG aspirations and excess urine output in polyuria
(>4 ml/kg/hour): replace "ith N/2 saline with+ 10 mEq/L KC!
(0.5 mL KCI added per eve1y I 00 mL offluid)
o Chest tube drainage and third space losses (approximate clinical
assessment) with NS
o Diarrheal losses (10-20 ml per stool) with 0.2 NS in D5 + 20
mEq/L KCI (I ml KC! added per every 100 ml offluid)

8.7 GENERAL INSTRUCTIONS


• Try to reduce insensible water losses to a minimum (see section
36. 7) rather than increasing the amount of fluids.
o Nurse babies in incubators as far as possible. Use double walled
incubators or plexiglass heat shield for ElBW babies (sec
section 36.3)
o Keep babies clothed with a cap
o Maintain thermoneutral environmental temperature (see section
7.2.1, Nl7)
• Fluid recharting needs to be done every 6 hourly based on
assessment of hydration status. Chart fluid requirement as hourly
rates of fluid administration.
• Always use infusion pumps. If not available, use pediatric microdrip
infusion set ( 60 microdrops give I mL in these sets and hence
number of drops per min ~ ml/hour of fluid). Never load more than
4 h fluid in a pediatric micro drip set (especially during transport).
• While calculating the fluid volume, deduct the volume of blood
products (unless one is replacing direct losses) and drugs from the
total fluids. Calcium gluconate can amount to a substantial volume
especially in small babies.

8.8 FLUID AND ELECTROLYTE DISORDERS


8.8.1 lsonatremic disorders
Dehydration
Predisposing factors: frequently involve equivalent losses of sodium and
water (via thoracostomy, NG, or ventriculostomy tubes) or third space
losses that accompany peritonitis, gastroschisis or omphalocele. Renal
sodium and water losses in ELBW infants can lead to hypovolemia
58

8.6.2 Composition of available electrolyte solutions: Shown in Table 8.3


T a ble 8.3 : C ompos1"fion o f e Iect ro I1yt c soIu f ions
Solution Na K Cl Ca Lactate mosm/L
5% Dextrose - - - - - 278
I 0% Dextrose 5 10
lsolyte - P 25 20 25 350
RL 130 4 109 4 28 272
NS (0.9% NaCl) 154 154 308
NS in 5% dextrose 154 - 154 - -
Yz NS (0.45% NaCl) 77 77 154
Yi NS with 05 77 77 432 ,,,.,,.
Y. NS (0.2% NaCl) 34 34 77
Y. NS with 05 34 34 355 1
3%NaCI ·~ 513 5 13 1026
~~
1'.
59

despite normal tonicity.


The most precise method of assessing amount of fluid deficit is based on
pre-illness Wt:
Fluid deficit (L) = Preillness Wt (kgl -Illness Wt (kg)
% Dehydration= {(Preillness Wt - Illness Wt) I Preillness Wt} x 100
If wt is not available, clinical observation may be used,
Mild dehydration (<5%): normal or increased pulse; decreased urine
output, normal physical findings
Moderate dehydration (5-10%): tachycardia; little or no urine output;
irritable/lethargic; sunken eyes and fontanel; decreased tears; dry mucous
membranes; mild delay in elasticity (skin turgor); delayed capillary refill
(> 1.5 s); cool and pale
Severe dehydration(> 10%): rapid and weak or absent peripheral pulses;
decreased BP; no urine output; very sunken eyes and fontanel; no tears;
parched mucous membranes; delayed elasticity (poor skin turgor); very
delayed capillary refill (>3 s); cold and mottled; limp, depressed
consciousness.
The degree of dehydration is underestimated in hypernatremic
dehydration because the movement of water from the intracellular space
to the extracellular space helps to preserve the intravascular volume.
Fluid Management of isonatremic dehydration
• Restore intravascular volume (in shock) NS: 20 mL/kg over 20 min.
Repeat as needed.
• Rapid volume repletion: 20 mL/kg NS or RL over 2 h.
• Calculate 24-h fluid needs: maintenance + deficit volume. Subtract
isotonic fluid already administered from 24 h fluid needs.
Administer remaining volume over 24 h using D5 Y, NS + 20 mEq/L
KC!.
• Replace ongoing losses as they occur.
8.8.2 Hyponatremia
Definition- Serum [Na+] < 130 mEq/L.
For approach to identify the cause of hyponatremia, see figure 8.1. It can
be either due to true deficit of total body sodium or can reflect fluid
overload (dilutional hyponatremia). In general in the first few days after
birth, hyponatremia usually indicates fluid overload. After the l" wk, it
may be either dilutional or indicate a true deficit of total body Na+.
Hyponatremia may cause hypotonia, apnea, and, if acute and severe,
seizures.
Management
• Dilutional hyponatremia should be treated primarily by fluid
restriction. However, if serum [Na+] is < 120 mEq/L, the baby may
require additional Na+ as well.
60

• Hyponatremia due to deficit of total body Na - and water should be


treated by replacement of deficit along with daily maintenance
requirement and ongoing losses if any. Underlying cause of sodium
loss should be treated.
Na deficit (mEq) =(desired [Na] - current [Na]) x 0.7 x body Wt (kg)
Symptomatic hyponatremia: (e.g., seizures) or [Na+] <120 mEq/L).
Calculate Na deficit to raise [Na] to 125 mEq/L and give as 3% NaCl
(0.5 mEq/mL) over 3-6 h. Correct remaining deficit over next 24 h.
Asymptomatic hyponatremia: Calculate total deficit of Na-. Add the
deficit to maintenance sodium requirement and ongoing Na' losses, if
any. Similarly, calculate fluid deficit, maintenance requirement and
ongoing losses. Identify the appropriate fluid that meets both Na and
fluid requirement. Correct over 24-48 h.
Monitor sodium I 2'h hourly.
SIADH
Diagnostic features
• Wt gain without edema
• Hypotonic hyponatrcmia
• Decreased urine output
• Increased urine sodium excretion and specific gravity
• Urine osmolality >plasma osmolality
• Normal renal, adrenal and thyroid function
Common causes
• Pain
• Drugs - Opiates, Barbiturates, Diuretics, Indomethacin, Oxytocin
• Asphyxia, IVH, Meningitis
• Pneumothorax, Pneumonia, PPV
• Post operative states
Management
• Water restriction. Restrict initially to 2/3 maintenance for 24 h.
Further restriction would be based on clinical and lab assessment.
• Hypertonic sodium may be administered only if serum sodium <120
mEq/L or if neurological signs and symptoms are present. Use 3%
NaCl with IV frusemide to get rid of water (see section D55).
• Increase urinary free water excretion with frusemide
61

Figure 8.1: Approach for identifying underlying cause of


hyponatremia

Hyponatrrmia
(Serum Na <13(1 mEq!L)

Rule out factitious hyponatremia*


Recheck with another sample immediately

Loss of Wt Absence of expected Wt loss


I Wt gain

Sodium Deficiency Dilutional


Hyponatremia

+
Inadequate Intake Excessive Loss

I
+
Decreased urine
output

Normal/ Increased urine
output

FENa # >2.5 FENa <I i


Urine specific
!
Excessive IVF
gravity

(Renal losses)
Diuretics
Prematurity
Renal tubular
(Extra renal losses)
GI losses
Third space Joss >1015 •
<1005

acidosis
CAH i
CCF Renal failure
Sepsis
SIADH
Muscle relaxants

*Factitious hyponatremia
Hyperlipidemia: Na~ decreases by 0.2 for every 100 mg/dL rise in total
lipids.
Hyperproteinemia: Na+ decreases by 0.25 for every g/dL rise in total
protein beyond a value of 8 g/dL.
Hyperglycemia: Na decreases by 1.6 mEq/L for each 100 mg/dL rise in
glucose
# FENa values may not be useful in <32 wks gestation
62

8.8.3 Hypernatremia
Definition: serum [Na+] >150 mEq/L
Causes: Hypcmatremia is secondary to negative water balance or excess
Na+ intake.
Hypernatremia with normal or deficient ECF volume
• Increased IWL- Hypematremia is often a problem in the l" wk of
life in summer months, particularly if the mother has poor milk
output.
• Skin sloughing- e.g. SSSS, epidermolysis
• ADH deficiency - IVH, meningitis, birth asphyxia. Note that
SJADH is more common in these conditions than ADH deficiency.
• Acute gastroenteritis
Hypernatremia with excess ECF volume
• Excessive administration of isotonic or hypertonic fluids
• Administration ofNaHC0 3 , other Na containing medications
• High solute formula feeding
Hypematremia may cause hyperexcitability and hyperreflexia. Severe
hypematremia (serum [Na+] >160 mEq/L) may cause permanent CNS
damage.
Management of hypernatremic dehydration
There are complex ways of calculating the exact fluid composition that
meets Na+ requirements, but the following guidelines are appropriate for
most circumstances.
Restore infravascular volume
NS: 20 mL/kg over 20 min (Repeat until intravascular volume restored)
Determine time.for correction based on initial sodium concentration
[Na]:J45-157 mEq/L: 24 h
[Na]: 158-170 mEq/L: 48 h
[Na]:\71-183 mEq/L: 72 h
[Na]:184-196 mEq/L: 84 h
Administer fluid at constant rate over time for correction
Typical fluid: D5 Y, NS (with 20 mEq/L KCI unless contraindicated)
Typical rate: 1.25-1.5 times maintenance
Follow serum sodium concentration to adjust fluid based on clinical
status and serum sodium concentration
Signs of volume depletion: administer NS (20 mL/kg)
Sodium decreases too rapidly- Increase sodium concentration of IVF, or
decrease rate of JVF
Sodium decreases too slowly- Decrease sodium concentration of IVF, or
increase rate of IVF
Replace ongoing losses as they occur
If hypernatremia is corrected too rapidly, brain edema, seizures, and
death can occur. Scrum Na should not drop by> 10 mEq/L/d. If seizures
63

occur during correction, they are us ially due to water intoxication. Treat
by giving 5 mL/kg of NS.
Peritoneal dialysis - If serum Na·: 180 mEq/L, rapid correction may be
done by putting 45 mL/kg of a dialysis solution containing 4.25%
glucose intra·peritoneally and withdrawing it one hour later. After a few
cycles as the serum sodium falls, subsequent dialysis may be carried out
using the normal PD solution with I .5% glucose.

8.8.4 Hypokalemia
Definition: Serum K' <3.5mmol/L
Common causes
• Inadequate intake
• Alkalosis (bicarbonate treatment or loss of acid from gastric
secretions). Metabolic alkalosis is more often associated with
hypokalemia than respiratory alkalosis.
• Renal losses · tubular defects
• GIT losses · Diarrhea, NG or ileostomy drainage
• Medications (diuretic therapy, sodium bicarbonate infusions,
salbutamol, amphotericin B and insulin)
ECG changes · Prolonged QT interval, U waves, ST depression,
depressed T waves
Treatment:
Treatment will depend on the underlying cause and the severity of the
hypokalemia. Caution: Consider delayed treatment or monitor carefully
if urine output is low or renal function is abnormal
• Reduce gastro-intestinal or renal losses & replace fluid losses
• Increase oral or parenteral potassium intake as needed.
• Oral potassium supplements· molar KC! supplements (I mL ~ 2
mmol KC!). Usually start at 2 mmol/kg/d KC! supplement.
• IV potassium supplementation-
o Maximum permissible is 40 mEq/L, i.e. 2 mL of 15% KCl/100
mL fluids, without ECG monitoring.
o With ECG monitoring, one can go up to 60-80 mEq/L, i.e. 3-4
mL KCI/ I 00 mL fluid.
• Monitor the serum K" carefully and adjust dose accordingly.

8.8.5 Hyperkalemia
Definition: serum potassium >6 mEqiL.
Causes (Shown in Table 8.4):
The most important cause to investigate is oliguric renal failure.
However, extremely premature babies may develop hyperkalemia
without significant renal impairment in the initial days of Ii fe. This is due
to relative aldosterone resistance and low glomerular filtration rate
(GFR).
64

Table 8.4: Causes of hyperkalemia

Asphyxia, birth trauma


IVH, Bleeding, cephalhematoma
Increased potassium release lntravascular or extra vascular
hemolysis
Hvnothermia
Renal failure
Oliguria
Decreased potassium clearance
H yponatremia
CAH
Dehydration, acidosis
VLBW
Blood transfusion
Miscellaneous
Inadvertent excess KC!
administration
DVET

ECG changes: Tall T waves, prolonged PR interval, short QT interval,


prolonged QRS, absent P waves, sine wave and VT/fibrillation (see
section 28.9)
Complications: In general, elevated potassium levels, even above
7 mmol/L, are tolerated well by neonates. The main complication is
arrhythmia, with the most common arrhythmias being VT and sinus
bradycardia.
Management: For approach and treatment see Figure 8.2
65

Figure 8.2 Approach and management


Serum K+ >6 mEq/L
• Continuous ECG monitoring
• Obtain ECG strip
• Immediately send non hemolyzed arterial J
venous sample to lab to recheck potassium
• Send SERFf, urine electrolytes, pH
• Discontinue potassium in IVF (even if lab error
is suspected, until repeat values arc available)

Serum K' > 7 mEq/L or ECG changes present


• Assess cardiovascular status. If needed, support
with inotropes
• 10~0 calcium gluconate 1-2 mL/kg IV over 2-4
min
• Ncbulized salbutamol (400 µgin 2 mL NS q 2 h
until K_,_ <5; or maximum 12 doses reached)
• I mEq!kg of sodium bicarbonate IV
• Start insulin dextrose infusion*
• Frui.emide 1 mg/kg if renal function is
adetiuate
• Kayexalate (potassium exchange resin) 0.5 -
LO g/kg dissolved in NS at 0.5 g/mL given
rectally (through feeding tube inserted 2·3 cm)
If serum K+ is not controlled by above measures

+
Peritoneal dialysis
DVET with fresh whole blood I fresh PRBCs with FFP in dire
emergency if peritoneal dialysis is not possible, especially if
sepsis co-existent

*insulin dextrose infusion: Begin with a bolus of regular insulin 0.05 units/kg and 2 mUkg
of 10% dextrose. Follow it up with 10°/o dextrose infusion at the rate of2·4 mUkg/h along
with regular insulin 0.1 units/kg/h (10 units of insulin in 100 rnL of 10% dextrose@ l
mlJkg/h) (see section 070)
66
1 Itt
8.8.6 Hypocalcemia
Defined as total scrum calcium concentration of <7 mgidL or an ionized
calcium concentration of <4 mg. dL (i.e. 1 mEq L). Postnatal changes in
serum calcium: at birth, umbilical calcium level is 10-11 mg dL, which
decrease in healthy term newborns to reach a nadir of 7.5-8.5 mgldL for /7
the first 24-48 h. Thereafter. level rises to adult value. /
Classification: early onset (<3 d) and late onset(>3 d) / D..-//.,,7 1-~ "~
Causes: - _.J ]
Early onset: Prematurity, IDM. perinatal asphyxia, maternal. intake of
anticonvulsants, lUOR. If hypocalcemia docs not resolve within 72 h of
~hera~y investigate for causes of late onset hypocalcem1a.
Late onset:
• Increased phosphate load - Cow's milk, advanced repal insufficiency J
• rlypomagnesemia
• Vit D deficiency- Maternal vit D deficiency, Malagsorption, Renal
insuffic1eacy, Hepatobiliary disease
• Parathyroid hormone resistance- Transient neonatal
pseudohypoparathyroid1sm
• Hypoparathyroid1sm
• Metabolic Syndromes- Kenny-CafTey syndrome, Long-chain fatty
acyl coenzymc A (CoA) dehydrogenasc deficiency, Keams-Sayre
syndrome
• Iatrogenic - C1tmted blood products. Lipid infusions. Bicarbonate
therapy, Diuretics (loop diuretics), Glucocomco1ds, Phosphate
therapy, Alkalos1s, PT
C/i11ical manifestations: generally non-specific like apnca, irritability, ~
J
I
jittcrincss, increased extensor tone, seizures, clonus, hypcrreflex1a, and
stridor (due to layngospasm).
Monitor: VLBW babies or gestation :532 wks~h asphyxia (moderate
to severe), IDM, lUGR (<2SD), shock, sepsis with multi-organ
dysfunction syndrome (MODS), D1Georgc sequence, DVET - 24 hourly
for 48 h.
Diag110.\is: laboratory serum and ionized calcium values. ECG - Q0 Tc
>0.2 or QTc >0.45. A diagnosis of hypocalcemia based only on ECG
criteria 1s likely to yield a high false pos1t1vc rate. A simple formula to
evaluate hypocalcemia 1s: ·•if (number of small squares in Q0 T) squared >
(number of small squares m RR). that means Q0 Tc 1s prolonged.
lllvestigatio11s: Send serum calcium, magnesium, phosphate, pH, ionized
calcium fraction. Get Chest X-ray for thymic shadow if Di George's
syndrome suspected
Treatment
Maintenance: 4-6 mL kgld of Ca gluconatc IV (added in last 2 h of 6
hourly IVF) {~ec section D20)
67

Preparation: Ca-gluconate I 0% (IV) - 9 mg/mL (preferred), Ca-chloride


(IV) - 27 mg/mL - . - -
Therapeutic:
Asymptomatic: increase maintenance to 8-12 mL/kg/d of Ca-gluconate
Symptomatic: 2 mL/kg of Ca-gluconate diluted in I: I dilution with NS
or 5% DIV over 10-15 min under strict cardiac monitoring (stop infusion
if HR drops for >20 beats/min than baseline or any other arrhythmia
appears on ECG). Start maintenance calcium after bolus dose.
8.8. 7 Hypercalcemia
Defined as total serum calcium > 11 mg/dL or ionized calcium > 1.5
mmol/L. Serum values> 14 mg/dL can be life-threatening.
Causes: Iatrogenic, hypophosphatemia, TPN without adding phosphate,
hyperparathyroidism, hyperthyroidism, hypervitaminosis D, decreased
renal calcium clearance, maternal hypocalcemia, William's syndrome,
SC fat necrosis.
Clinical manifestations: hypotonia, encephalopathy, poor feeding,
vomiting, constipation, polyuria, hepatosplenomegaly, anemia, extra
skeletal calcification (e.g. nephrocalcinosis)
Diagnosis: by lab estimation.
Investigations: serum calcium, magnesium, phosphate, x-ray wrist (for
demineralization, subperiosteal resorption, metaphyseal rarefaction and
calcification), X-ray KUB if chronic. Urinary Ca/Cr for hypocalciuric
hypercalcemia
Treatment:
Emergency treatment: If calcium >15 mg/dL - give NS bolus 10-20
mL/kg over 30 min. Frusemide 1-2 mg/kg/dose to induce calciuria (see
section D55). Omit calcium intake. Glucocorticoids are helpful in
hypervitaminosis and SC fat necrosis (to be given after discussion with
consultant). Calcitonin is potent inhibitor of bone resorption (transient
effect).

REFERENCES
I. MacDonald M G. Avery's Neonatology. Pathophysiology and
management of newborn. Lippincott Williams & Wilkins 6th edition
2005; Chapter 21.
2. Dutta S. Acta Paediatr 2009; 98: 970.
3. Gaylord MS. J Perinatol 2001; 21: 438.
68
9. ENTERAL NUTRITION

9.1 INTRODUCTION
Nutrition is one of the most important aspects in the management of
neonates. especially for LBW babies. The objective of this chapter is
primarily to address the issues involved in the optimal feeding of the
LBW infant. For feeding of term & near term infants refer to section
5.2.2. The use of feeding bottles, pacifiers and pre-lacteal feeds is
prohibited in PGIMER.

9.2 NUTRIENT AND FLUID REQUIREMENT:


For fluid requirement. see section 8.3.
9.2.1 Recommended nutritional requirements of preterm and term
infants (see Table 9.1)

Table 9.1: AAP-CON* Enteral intake recommendations for preterm


& term infants
Nutrient Preterm infants Term infants
Calories (lkg/d) 105-130 100-110
Protein ( o/lrn/d) 3.5-4.0 1.5 - 2.5
Fat ( •lk•/d) 5-7 5-6
Carbohydrate (g/h/d) 10-14 10-14
Calcium (mnilrnid) 210 40-60
Phosphorous ( mg/kgJd) 110 20-30
Iron (mg/kg/d) 2-3 1-2
Vit A (IU/kg/d) 90-270 700 - 1500
Vit D (IU/d) 400 400
Vit E (IU/kg/d) >1.3 6-12
Vit K (uo/kgJd) 4.8 1-2
Vit C (moilrn/d) 42
Vit Bl2 (uo/kg/d) > 0.18
Folatc (u•fknid) 39.6
Sodium (mEq/kg/d) 2-3 1-3
Potassium (mEo/kg/dl l.7-2.5 1-2
Zinc (µgJkg/d) >600 1000
Copper (uo/ko/d) 108
Iodine (u•/kg/d) 6
(* - AAP-CON: AAP, Commltlee On Nutrition)

9.3 BENEFITS OF HUMAN MILK (IN SUMMARY) (also see


breastfeeding in section 5.2.2)
• For full term AGA infants, breast milk is the recommended
nutritional source, exclusively for the first 6 mths of postnatal life
69

and in combination with com ilementary foods until the infant


reaches 2 yrs of age.
• Preterm-mother's milk, for the initial 3 wks after the delivery is
denser in nutrients compared to term-mature milk.
• Apart from the nutritional advantages, breast milk has the benefits of
its anti-infective constituents, growth factors, exocrine/endocrine
factors etc. Feeding human milk protects against NEC, sepsis, atopy
etc. It improves the neurodevelopmental outcome and has beneficial
effects on BP and lipid profile.

9.4 COMPOSITION OF TERM HUMAN MILK AND OTHER


TYPES OF MILK (See Table 9.2)
The composition of term human milk in comparison to other sources is
presented in the table below. Yerka milk plant supplies packet milk in
Chandigarh and Punjab. "Standardized Yerka milk" (green packet) is
closer to human milk in its fat content and hence should be used
undiluted, if human milk has to be substituted by animal milk.
Fat content in Standardized Yerka milk (green packet) - 4.5%
Fat content in double toned Yerka milk (yellow packet) - 1.5%
Fat content in skimmed Yerka milk (violet packet) - 0.5%

Table 9.2: Composition of milk


Per 100 mL Term Formula Cow's Buffalo's
human milk milk* milk milk
Cal 67 67 67 117
Protein (g) 1.1 1.7 3.2 4.3
Fat I u) 4.5 3.3 4.1 6.5
Carbohydrate (g) 7.1 7.5 4.4 5.1
Calcium lmu1 33 62 120 210
Phosphorus (mg) 15 47 90 --
Iron (mg) 0.03 0.8 0.2 0.2
Yit A IIU) 250 200 -- --
Yit D (JU) 2.2 40 -- --
Sodium (mEa) 0.8 1.3 -- --
*Lactogen-1 was used here for the sake of companson. Other formulas
may vary slightly.

9.5 CONTRA-INDICATIONS TO MILK FEEDING:


• Major GIT malformations (TEF, suspected duodenal, jejuna! atresia
etc.) (see section 35.3)
• NEC (see section 31.2)
• Suspected IEM involving protein or carbohydrate metabolism (see
section 33.2)
70

• Relative contra-tndtcauon-
o Significant respiratory distress (Downe's score >4)
o Severe bemodynamic instability (requmng inotropes > 15
µg/kg/min)

9.6 FEEDING REGIMEN (see breastfeeding in section 5.2.2)


9.6.1 Initiation & Method of feeding of stable neonates:
• Wt < 1250 g <30 wks of gestation:
o Start with 10 ml.Jkg/d feeds by gavage
o Advance by 20 mL kg/d
• Wt 1250-1500 g/ 30-31 wks of gestation
o Start with 40 mL kg/d by gavage
o Advance every 4 hourly by 2 mL/kg to make to 80 mL/kg/d by
1
the end of l ' d.
• Wt 1500-2000 g/ 32-34 wks of gestation
o Start total enteral feeds 60 mL kg d by cup and spoon.
o Breast feeding can be started 1f suck, swallow and breathing co-
ordination are good.
• Wt '>2 kg/ 34-36 wks of gestat10n:
o Start breast feeds from birth.
The above guidelines should be individuali?cd according to the baby's
chmcal status and seventy of illness. Use clinical cues and amount of
gastnc aspirates to decide on progression of feeds. feeds could be
increased up to 180-200 mL/kg, d depending on the tolerance.
9.6.2 Feeding interval
Start 2 hourly feeds for infants <750 g 1• A study in PGIMER has shown
that for practical convenience, a 3 hourly feeding schedule may be
preferred over 2 hourly schedule in neonates weighing $ 1750 g as it
results in less nursing time but did not increase the incidence of feed
intolerance, hypoglycemia and apnoea. 2 Feeding interval can be modified
on an individual basis depending on feed tolerance, gastric aspirates and
physiological stability.
9.6.3 Advancement of feeds- Rapid vs. Slow
Rapid advancement of feeding (increase of 35 mL kg'd) may shorten the
time to reach full enteral feeds and may decrease the time to regain BW 3,
but may increase the risk of NEC in infants of <32 wks gestation.
9.6.4 Feeding tubes (Sec PGIMER video on neonatal procedures, for
feeding tube placement)
There 1s no difference m Wt gain, apnea or bradycardia between
mdwelhng NG and intermittent OG feeding. Thus, indwelling tubes are
preferable because they reduce costs and trauma. The best method for
Judging the length of the feeding tube to be inserted is from the comer of
the mouth (or nose in case of NG) to the car lobe and then to the mid-
point between the end of the xiphoid process and the umbilicus. The UK
·x-- 71

National Patient Safety Agency recommends that only demonstration oJ


low pH by litmus paper or X-ray ca1 ascertain correct position of the tip
[ of the tube, and not mere auscultattm .

9.7 MINIMAL ENTERAL NUTRI rION


• MEN (also called '1rophic feed ng,") refers to feeds tn the first few
d!)'!> ~ in sub-nutritional 1uantities i.e. approximately I0-15
mUkg/d.
• Start MEN tn all sick neonate who arc unlikely to tolerate full
feeds, unless there is an absolut.! contraindication for feeding. The
term "trophic feedmg" is not used for those mfants, for whom we are
planning to hike up feeds dail> Note that ventilation, respiratory
distress and hemodynamic instability are not contra-indications to
trophic feeding.
• Though EBM 1s preferred, term brmula can be used in the absence
of EBM. Non-availability of F.,BM is not a sufficient reason to
withhold trophic feeds.
• Trophic feeding in infants of <32 wks of gestation is associated with
a shorter time to reach full ent·ral feeds and shorter duration of
hosp1tahzatton 4 There is no sign ficant increase in the risk of NEC.

9.8 DECISION FOR W ITH-HOLDING T HE FEED A.l\ffi


DEFINING FEED INTOLERANCl:
9.8.1 With-holding the feed until next feed- Withhold if there are
'excessive gastric residuals' and thuc are no other clinical findings.
Excess ~astnc residual IS defined as r•refeed aspirate > 50% of the feed
volume.· If the gastric residual is <50°0 & milky, re-feed the aspirate and
if the gastric residual is >50%, discard the aspirate.
9.8.2 Indications for with-holding feeds for longer periods- include
two or more of the following: 6
• Excess gastnc residual
• Minimal blood-tinged or coffee-g1ound aspirates
• Increase in abdominal girth meas..ired at the umbilicus by 2 cm or
more from baseline in 6 b interval
• Visible dilated loops of bowel
• Apnea or bradycardta occurring more than 3 times m an 8-h period
• Bilious aspirate or frankly blood- tained aspirates b> themselves are
indications for withholding feeds. lowever, make sure that the tip of
the feeding tube is not in the duodenum or beyond, when faced with
bilious aspirates.
The decision to withhold feeds should be taken by the SR. Any tnfant
whose feeds are withheld for more th;tn 12 h is considered to have an
episode of 'feed intolerance·.
72

9.9 SHIFTING FROM GAV AGE FEEDS TO SPOON AND


BREAST FEEDS
• The desired goal is to achieve direct breast feeds. Transition should
be slow from one form of feeding to another one.
• Start non-nutritive sucking once you are planning to shift to spoon/
breast feeds (usually after 31 wks of gestation). Encouraging the
infant to suck on the emptied breast, after expression of breast milk,
results in improved breast feeding rates at discharge and follow-up.
• Attempt cup and spoon feeds from 32 wks post-conceptional age.
While shifting to spoon feeds, first a single supervised spoon feed is
given, if the baby accepts well, then the number of feeds given PO
can be gradually increased on a daily basis as in the example given
below:
o One spoon feed every 6 gavage feeds
o One spoon feed per 2 gavage feeds
o Alternate spoon and gavage feeds
o 2 spoon feeds per gavage feed
o After that shift to full spoon feeds.
• Assess for the suck and swallow co-ordination and start direct breast
feeds as early as possible.

9.10 PRETERM HUMAN MILK


The milk of mothers delivering preterm has higher protein, sodium and
Calorie content for the first 3 wks postnatally.
LBW neonates if they are fed preterm human milk alone will have
significant deficit of vitamins and minerals even with maximum
permissible volume. A preterm neonate on 200 mL/kg/d of human milk
will have a daily deficit of calcium up to 150 mg/kg/d, phosphate up to
75 mg/kg/d and vit A up to 200 U/kg/d. Preterm human milk contains
very little amount of Vit D and Iron as compared to the daily
recommended need.

9.11 SUPPLEMENTS:
9.11.1 Iron: The store of iron is low in preterm infants. Start iron at 2
wks of life. Babies <1000 g must be given 3-4 mg/kg/d and babies >1000
g 2-3 mg/kg/d of iron. Continue until 1 yr of age. For composition and
dosage of commonly used iron supplements in our unit see Table 9.3.

..
T a bl e 9 3 C omoos1"ti on & dosae:e of some iron sunn ements:
Commercially available Elemental Vit 812 Folic acid
brands iron m!!lmL) luP/mL) luPimL)
Tonoferon (lmL~20 droos) 25 5 200
Provive Fe drops 15 4 200
Hemsi drops 30 5 200
73

9. 11.2 Vit A: Various organizations ~ecommend a dally supplementation


of 700-1500 lU.kg/d. This can be achieved with the multivitanun
preparations like 'A to Z drops' (se ·Table 9.4 for compos1t1on). Other
preparations include Visyneral-Zn cir Jps or Dex~drops etc The policy
m PGIMER is to give these until the >aby attl!}ns a Wt ~

T a bl e 9.4 : C onstituents of A to Z droos


Constituent Content/mL
Thiamine hvdrochloride I 0.3
Vit 82 II 0.4
Pvridoxine hydrochloride l 0.4 mg
Yit A r 1150 IU
Cholecalci ferol Ii 200 TU
Biotin II 5 UI!
Yit E ~ 2IU
Ascorbic acid i 20m2
Zinc ~! 40 UI!
Elemental iron II 0.4 ml?
Ener2v I 2.27 Cal
r
9. 11.3 Calcium a nd Phosphate
Preterm infants <34 wks require botl Calcium and Phosphate in a 2: I
ratio until they reach 40 wks of post-menstrual age. The minimum
requirements are 150 mg/kg/d anl 75 mg/kg/d of Calcium and
Phosphorus respectively. Very few cc mmercially available preparations
have both Calcium and Phosphorus- one of them is Syrup Ostoealeium. 5
mL of Ostocalcium provides 82 mg as elemental Ca, 41 mg as elemental
phosphorus, 200 IU of Yit D and 2.5 µg of vit B 12 . Preparations
containing only Calcium must not be used. Failure to supplement
Phosphorus can result in hypercalcemta. Vit D must not be used without
adequate su lementation of both Cale um and Phosphorus.
9. 11.4 Unit policy
The vitamin-mineral preparations used in the PGIMER umt are·
Tonoferon drops: 3 dropslkg/G in 2 d1v1ded doses
Syrup Ostocalcium: I 0-15 mLi g;d divided in multiple doses,
mixed with ceds
A-Z drops: 0.5 mL twic · a day

9. 12 Hl\fF:
As preterm mother's milk is inadequ 1te as the sole source of all the
nutrients, the use of multicomponent fortifier allows the infant to receive
a nutrient intake that meets the estim~ed needs. In infants <32 wks of
gestation, mu lticomponent fortifier leads to short-term increases in Wt
gain, linear growth, head growth and minerali1.:ation7. There appears to be
74
no efTect on growth beyond I yr of age. A study done in our unit had also
shown that HMF addition resulted in increased Wt, length and head
growth in pretcrm VLBW SGA rather than AGA infants, when compared
to no HMF supplcmentation. 8
9. 12.1 Using multicomponent fortifier:
Consider using HMF in babies with <32 wks of gestation who arc not on
direct breast feeds and are not gaining adequate Wt in spite of receiving
full feeds. Unfortunately, an optimum HMF is still not available in the
Indian market. The available one (Lactodex-HMF) does not have the
desired protcm content {sec Table 9.S below).
• If a decision to use HMF is taken, fortification must start once full
feeds are reached ( 180-200 mUkg/d.
• The manufacturer's recommendation is to add I sachet of HMF to
SO mL of milk under aseptic precautions, refrigerate the unused
human milk and use 1t within 8 h of preparation.
• If a mother expresses less than SO mL milk it poses certam practical
problems. One option is to press the HMF sachet such that the
contents arc layered uniformly inside. The sachet can be cut with a
sterile blade into 4 parts. These parts can be stored m a sterile
container The HMF powder does not generally spill out because it is
sticky. The contents of each cut part can be added to 12 mL of EBM.
• Dividing the HMF powder in the pharmacy into smaller sachets
contaimng the exact Wt of HMF required per feed sounds ideal.
However, multiple handlers may mcrease the risk of contamination;
the paper (1f absorbent) may deplete the fat; and it would be difficult
to constantly juggle wi th HMF quantities when the volume of EBM
feeds is rapidly graded up.
• Do not mix fortifier in fonnula mHk
• lrthe baby gets partly preterm formula and partly EBM, IIMF must
be added to the EBM feeds, unless the EBM constitutes <I/3rd of the
total volume or the absolute volume of each EBM feed is <12 ml.
This holds true for Lactodex-LBW as well as Dexolac Special Care.
• Continue fortifier until the baby reaches 2 kg or goes on to full
breast feed.
• When the fortifier is stopped. start supplements with calcium and
mult1v1tamms. Do not mtroduce these supplements as long as HMF
is given.
• HMF docs not contain iron. Hence iron supplementation must stan
as scheduled at 2 wks age.
• For those who can't afford HMF, addition of LBW formula 4 gt I 00
mL feed is an alternative option. This amounts to I g of powder
added to 2S mL EBM (an average feed volume). This option has
been found safe only in terms of osmolarity (390 mOsm/L), but not
been evaluated for clinical outcomes. Once the tin of pretem1
75

fonnula is opened, it cannot ~e kept for more than 3 wks. This


method should never be recommended for domestic use because of
the practical problems of weighing -1 g of powder and the hazards
of using an opened tin for beyoad 3 wks. It also leaves very limited
scope for its use in the hospital. It may be used only after discussing
with the consultant.
• In view of the various practical problems and limited benefits
associated with HMF and preterm fonnula, and risks associated with
non-human milk usage, they should not be used as a routine. It is
worthwhile to try more physiological options such as hind-milk.

Table 9.5: Composition of Lactodex- HMF (2 g/ sachet)


Protein (g) - 0.2 Sodium (mg) - 1.75
Fat (g) - 0.1 Vit A (JU)- 730
Carbohydrate (g) - 1.2 Vit D (JU)- 250
Calcium (mg) - 50 Energy (Cal)- 7. 5
Phosphate (mg) - 25 No iron
9.13 PRETERM FORMULA:
If the breast milk output is inadequate, then preterm fonnulas can be used
for preterm infants. These are Calorie-enriched and variably protein-
enriched to support intra-uterine nutrient accretion rates. However, as the
fonnulas do not contain any of the biologically active immune
substances, honnones or growth factors, they are inferior to breast milk.
9.3.1 Using pre-term formula:
• While initiating feeding, if the pretenn mother's milk is not
available, use term formula. This is because in this phase of feeding
the objective is to assess for the feed tolerance, for which less
osmolar term formula is better.
• During the stable-growing period, if the preterm mother's milk is
unavailable, use preterm formula to meet the recommended
nutritional intake. For composition of preterm-human milk and
commercially available pretenn formulas see table 9.6.
• Pretenn fonnula is to be given until the infant has attained a Wt of
2500 g. After that, switch to term formula.
• When preparing milk from the formula powder, all hygienic
precautions should be observed to ensure asepsis.
• VLBW infants, especially those who have illnesses causing
nutritional deprivation, may benefit from feeding with formulas
having a higher nutrient concentration. (Supplementation with
medium chain triglycerides ( MCT)- 0.25 mL/ 30 mL of fonnula
increases the energy content by about 2 Cal/30 mL)
76

Table 9.6: Composition of prcterm-human milk and commercially available preterm formulas

PT Lactodex- Dexolac- PT EBM +


PT EBM+
Prctcm1 milk Preterm EBM EBM•+ LBW special care
LBW fonnula
HMF + MCT
(per 100 mL) (per 100 mL) !IMF (per (per 100 (per 100 (0.8
4 (4g/ 100 mL)
100 mL) mL) mL) mL/ lOOmL)
Cal 69 82 88 76 89 88
Protein (g) 1.6 1.99 2 2.2 1.9 2. 1 2
Fat(g) 3.6 4.9 3.8 4.4 3.9 4.6
Carbohydr (g) 6.7 6 9.1 9.7 8.4 8.9 9.1
Calcium (mg) 28 26 128 140 124 61 128
Phosph (mg) 14 13 64 70 62 31 64
Iron (mg) 0.09 0.09 0.9 1.3 0.45 0.09
Vit A (IU) 50 1510 264 647 222 1510
Vit D (IU) 4 504 79 77 24 504
Sodium
(mEq)
0.9 1.2 1.05 2.3 1.28 1.25 l.05
Osmolality
290-300 392 390 394
(mOsm/kg)
*PT EBM - refers to EBM in the !'1 three wks of l!fe from mothers who deliver before 37 wks
77

9.14 GROWTH MONITORING:


It is believed that in the pretem infant who is receiving adequate
nutrition, the postnatal growth should mimic intrauterine growth. Though
it is the desired goal, it is often dif!icult to achieve. The desired average
gain in the various growth parameters is presented in the table 9.7.

Table 9. 7 Desired 2ains in anthrooometric oarameters


Preterm Term (0-3 mths)
> 15 g/kg/d in <2 kg
Wt 20-30 g/d
>20 g/d in >2 kl!.
Length 0.7-1 cm/ wk 2 cm/ mth
OFC 0.7-1 cm/wk 0.5 cm/wk

Wt should be measured twice weekly. Length & OFC should be


measured once weekly. Growth parameters should be plotted on
reference postnatal growth curves (see sections N4, NS). Postnatal
growth after a premature infant has reached term should be assessed
using the WHO growth reference curves for term infants (see section
N6).

9.15 MONITORING OF LAB PARAMETERS:


• PCV: weekly
• Sodium, calcium, phosphorous, ALP (see sections 38.3.1, 38.4, 38.5)
and serum albumin: fortnightly till discharge and monthly until
postmenstrual age of 40 wks.
• Those who are receiving HMF, monitor: Serum calcium,
phosphorous, ALP and sodium weekly until discharge and monthly
until postmenstrual age of 40 wks.

9.16 SUPPORT FOR FEEDING OF THE LBW INFANT:


• Involve mother in care and feeding from the beginning.
• Institute Kangaroo Mother Care (KMC) (see section 9.16.1 ). Regular
KMC classes for mothers are conducted by the lactation consultants
and public health nurses in PGIMER NICU- Mrs. Rama Mahajan,
Mrs. Uma Arora and Mrs. Santosh (Room No 16, NICU corridor,
contact I 0.30- 11.30 am)
• Drug therapy for enhancing lactation: Use metoclopramide or
domperidome I0 mg/dose TDS for 7 d (see section D82). It is
indicated if there is decrease in the total daily volume of milk
despite:
o Adequate counseling and reassurance
o Correct milk expression technique
o Normal maternal diet
78

o Inability to increase volume despite increasing the number of


times of expression.
A recent RCT has shown that metoclopramide is ineffective in
augmenting breast milk production in mothers of preterm infants, 9
but domperidome has been found to be effective. 10 Medications are
not a substitute for adequate lactation counseling.
9.16.1 KMC policy
• The 2 components of KMC are skin-to-skin contact and exclusive
breast-feeding. It involves support to the mother in hospital and at
home. KMC must be continued after discharge.
• KMC should be started after the baby is hemodynamically stable. IV
fluids, tube feeding and 0 2 administration are not contra-indications
for KMC.
o If BW is> I 800 g, KMC can be initiated soon after birth
o lf BW is 1200- 1799 g, it might take a few days before KMC
can be started, as the baby may have neonatal problems
o If BW is <1200 g, it may take days to weeks before KMC can
be started.
• When the baby is ready for KMC, the mother must be counseled and
the KMC procedure demonstrated in a caring, gentle manner and
with patience. Encourage the mother to bring her mother/mother-in-
law, husband etc and allow her to interact with other mothers who
are already practicing KMC.
• KMC can be provided using any front-open customized dress or
with blouse and sari, gown or shawl. The mother's privacy should be
maintained so that she does not get de-motivated. The baby can be
dressed with cap, socks, nappy and a front-open sleeveless shirt.
• The baby should be placed between the mother's breasts in an
upright position. The head should be turned to one side and kept
slightly extended. The hips should be flexed and abducted in a
"frog" position. The arms should also be flexed. The baby's
abdomen should be at the level of the mother's epigastrium. The
mother's breathing movements stimulate the baby, thus preventing
apnea. Support the baby's bottom with a sling.
• Babies receiving KMC should be carefully monitored during the
initial stages. The neck should not be too flexed or extended,
breathing should be normal and peripheries warm. The mother
should be involved in monitoring.
• The mother should be explained how to breastfeed while the baby is
in KMC position.
• KMC sessions must start even while the baby is in the NICU or
NNN. Sessions should not be less than 1 h. Gradually, the length of
the sessions should be increased up to 24 h a day, interrupted only
79

for diaper changes. The mother can sleep with the baby in kangaroo
position in a semi-recumbent position, at an angle of 15-30 degrees.
• When the mother is not free, '·ther family members, including the
father or grandmothers can also provide KMC.
• The baby can be weaned from KMC when the corrected GA is about
40 wks, weight about 2500 g, when the baby wriggles, pulls her
limbs out, or cries whenever the mother tries to resume KMC. While
weaning the mother can provide occasional KMC, e.g. after giving
the baby a bath or on cold nights.

9.17 FEEDING IN SPECIAL SITUATIONS:


9.17.1 A/REDF:
The incidence of NEC is increased in infants who exhibit fetal NREDF
in the UA (OR 2.13)-"
Initiate feeding with trophic feeds on day 1, only if
• There are no abnormal abdominal signs (abdominal distension,
visible loops)
• Bowel sounds are well heard and
• There are no other contraindications for feeding.
Passage of meconium is a reassuring sign, but failure to pass meconium
is not necessarily a bad sign because the more premature the infant the
longer it may take to pass meconium.
Trophic feeds should be started with either EBM or formula milk (see
section 9. 7). If trophic feeds arc tolerated for a day, the feeds should be
graded up cautiously. There are no guidelines in literature about the onset
or the rate of advancement of feeds. One can advance it at half the usual
rate for normal infants. If this is well tolerated, the advancement can be
faster. Feed advancement should preferably be done with EBM.
Do not initiate feeding on day 1 if
• There are abnormal abdominal signs
• Bowel sounds are absent/sluggish
• There are other contra-indications to feeding
Initiate feeds cautiously, once the above signs remit.
9.17.2 BPD: (see chapter l 6)
• Metabolic rate and energy expenditure are elevated in BPD, while
caloric intake is poor. Providing more Calories by administration of
lipids instead of carbohydrates lowers the respiratory quotient, thus
minimizing the C0 2 production.
• The caloric requirement for these infants ranges from 120-150
Cal/kg/d and protein of 4 g/kg/d. Some of the severely affected
infants require more than 150 Cal/kg/d to achieve sustained growth.
Fluids need to be restricted to 140-150 mL/kg/d and severe cases
may be up to 120-130 mL/kgid. Giving 150 mL/kg/d of PT EBM+
HMF+ MCT oil will provide 132 Cal/kg/d and 3 g/kg/d of protein.
80

• Additional protein supplementation remains a problem in India,


because oral protein supplements designed for neonates are not
available currently.
• Vitamin and trace elements: Vit A may promote epithelial repair
and minimize fibrosis. A dose of 5000 JU/dose given IM 3 times per
wk for the first 4 wks has been recommended as a measure to
prevent BPD but it is not practicable as it necessitates frequent
painful injections. 12 A recent RCT done in our unit has shown that a
combined IM and oral vit A supplementation regimen (5,000 JU IM
alternate days till establishment of adequate enteral feeds followed
by oral dosing of 10,000 JU daily till 28 d) in infants <1250 g
significantly reduced the risk of vit A deficiency. All babies with
BW <1250 g in whom >50% of the total fluid intake comes from
enteral feeds, must receive the above regime. IM vit A is available as
Aquasol-A. Oral vit A is available as 50,000 JU Vitamin A tablets
(manufactured by Nicolas Piramal) which can be crushed and
reconstituted into sachets of 10,000 JU each by pharmacy; or oral
water soluble Aquasol-A (capsules of 25,000 JU) whose contents
can be aspirated by a syringe and needle and diluted with milk or
sterile water to make 2.5 mL (thus, 1 mL= 10,000 JU). Oral vit A is
also available as drops through the national program (0.1 mL =
10,000; manufactured by Hindustan Antibiotics Ltd).
9.17.3 Gastro esophageal reflux:
IfGER is suspected, conservative measures should be adopted-
• Burp orally fed babies immediately after feeds (do not burp gavagc
fed babies)
• Place the baby in the left lateral position or prone position with head
end elevated by 30°. Babies placed in prone position must be under
continuous cardio-respiratory monitoring because of the risk of
SIDS.
• Decrease the feeding interval to one hour. The volume per feed will
automatically decrease.
• If the above measures fail, try thickening the feeds if it is a term
neonate. Thickening has been shown to reduce GER episodes in
term infants. Potential for bezoar formation precludes usage in
preterrn infants. The thickening agents reported in literature (bean
gum, smectite) are not easily available in India. Starch (available
from main kitchen) may be used as an alternative.
• Continuous NG or trans-pyloric feeding may be helpful in some
neonates with severe reflux, although evidence in literature is weak.
The following precautions must be taken whenever continuous feeds
are given:
o A syringe infusion pump should be used.
81

o Neonates must be continm·usly monitored for abdominal girth


and vital parameters. An unmonitored neonate may land up with
massive aspiration because the infusion pump will continue to
pump irrespective of gastril emptying.
o If the nozzle of the syringe is eccentrically oriented, the syringe
infusion pump must be kept horizontally with the nozzle of the
syringe above. If the nozzle is centrally placed, the syringe
infusion pump must be kept vertically with the nozzle of the
syringe pointing upwards (like a rocket). These positions
decrease the loss of fat.
o The tubings must be as short as possible to decrease fat loss.
o If formula milk is used, the volume required for a 2-h period
must be drawn up at a time, to prevent spoilage. If EBM is used,
the volume required for a 4-h period must be drawn up at a time.
• Pharmacological measures are highly unsatisfactory in the
management of GER. They may be tried only if the symptoms of
proven GER are associated with episodes of aspiration pneumonia,
choking with milk in the trachea or growth restriction. Note that
GER is not a cause of apnea.
o High dose erythromycin (> 12 mg/kg/d) may be used in neonates
> 32 wks. 13 Some improvement has been reported, although the
evidence is not robust. (see section D48)
o Cisapride is contra-indicated because of its cardio-toxicity.
Domperidome or metoclopramide have not been consistently
shown to be effective. (see sections D44, D82)
o Proton-pump inhibitors have a role in acid reflux, but are still
under investigation. Use only after discussing with consultant.
• Cow milk protein allergy is a close (but under-recognized)
differential diagnosis of GER, because it can also present with
recurrent vomiting, irritability, hematemesis, failure to thrive,
wheezing. Infants fed cow's milk or cow milk-based formula milk
who presents with features of GER must be investigated for cow
milk protein allergy.
9.17.4 Feeding ofSGA babies:
The energy requirements of SGA babies are more as compared to AGA
babies due to higher turnover and catch-up growth. They usually have
higher fluid intake. The method of feeding should be decided according
to the GA & neurological maturity. Initiate the feeds as early as possible
soon after birth.
Term & Near-term SGA: These babies should be with the mother. Give
20 mL/kg/d supplemental spoon feeds to these babies.
Preterm SGA: Shift these babies to nursery. Chart 20 mL/kg/d extra
feeds to that mentioned in the table in section 9.2.1. The BS should be
monitored for all SGA babies. (See section 11.2.2)
82

9.18 STERILIZING FEEDING BOTTLES


The use of feeding bottles and pacifiers is strictly prohibited in the
PGIMER neonatal unit. Mothers should be actively discouraged from
using feeding bottles at home. Nevertheless- regardless of strong advice
to the contrary- some mothers may insist on using a feeding bottle after
going home. In such a situation it is important for the doctor to know the
correct steps of bottle sterilization and instruct accordingly. There is no
credit in being ignorant about these steps.
• Wash all parts of the bottle soon after the last feed, with hot soapy
water. Use a feeding bottle brush to scrub the inside of the bottle,
paying special attention to the threading of the bottle and the rim.
Use a small brush to scrub the inside of the nipple, and squirt hot
water through the hole of the nipple.
• Immerse all parts (bottle, rim, nipple, and cap) along with a pair of
metal tongs under water in a large utensil, ensuring that all parts are
completely submerged in the water.
• Boil the water, taking care that it is boiled for at least 10 min- by the
clock- from the point of onset of roll boiling. ~-
• Allow the water to cool. After washing hands thoroughly, pick out
the metal tongs and using it remove the bottle and the cap and place
them on a clean plate. Pick the rim with the tongs, hold it only from
the outside and without touching the nipple, and maneuver it with
the tongs into its place in the rim. Screw the rim on to the bottle and
fix the cap.

REFERENCES
1. Optimal feeding of low-birth-weight infants. WHO technical review,
2006.
2. Dhingra A. J Matern Fetal Neonatal Med. 2009;22: 198.
3. Kennedy KA. Cochrane Database Syst Rev.1998.
4. Tyson JE et al. Cochrane Database Syst Rev.2005.
5. Schanler RJ. Pediatrics 1999;103:1150.
6. Akintorin SM. Pediatrics 1997;100: e4.
7. Kuschel CA. Cochrane Database Syst Rev.2004.
8. Mukhopadhyay K. Indian Pediatr. 2007;44:286.
9. Hansen WF. Obstet Gynecol. 2005; 105:383.
10. daSilvaOPCMAJ.2001;164:17.
11. Darling J. Arch Dis Child Fetal Neonatal Ed. 2005;90:f359.
12. Tyson JE. N Engl J Med. 1999;340:1962.
13. Ng E. Cochrane Database Syst Rev. 2008.
83

10. ACID BASE DISORDERS

JO.I INTRODUCTION
Maintenance of plasma pH within the range 7.35- 7.45 is an essential
requirement for life, because many metabolic processes (e.g. enzymatic
reactions) are exquisitely sensitive to changes in H+ concentration.
Buffers are the substances that attenuate changes in pH. Bicarbonate
buffers are the most effective buffers in the body. Non bicarbonate
buffers include proteins (albumin & Hb ). phosphate and bo11e.
~

10.2 TERMS USED IN ABG ANALYSIS


To know the acid base status we perform a blood gas analysis in the
blood gas machine. Terms used in the ABG analysis are:
• pH-The negative of the log ofH" ions in the body
• PaO,- Partial pressure of oxygen in the blood
• PaC0 2 - Partial pressure of carbon dioxide in the blood
• HC03 - Concentration of bicarbonate in the blood. The actual
bicarbonate level has 2 components: respiratory and metabolic. It
cannot, therefore, be an ideal measure of either. Bicarbonate is not
directly measured; it is calculated from the PaC0 2 and pH.
• Standard bicarbonate concentration (SBC) - It is defined as the
bicarbonate concentration that would have existed under standard
conditions: i.e. PaCO, of 40 mm Hg, and temperature 37"C. It is an
excellent measurement of the metabolic component.
• BE: It represents the amount of acid or base that would have to be
added to neutralize the metabolic disturbance. It takes into account
the buffering capacity of the body, including bicarbonate, Hb and
other buffers.
• SBE - It is the BE value calculated for the extracellular fluid
compartment, assuming the intravascular compartment and
interstitial compartment to be a single entity. Since Hb is present
only in the intravascular compartment, the Hb value is divided by
three to compensate for the interstitial compartment. SBE gives the
most accurate method of deciding on the amount of alkali or acid
required to return the blood pH to normal.
• Sa02 - % saturation of Hb in the blood sample. This is derived from
the Pa0 2 using the oxygen Hb dissociation curve.

10.3 PROCEDURE OF OBTAINING AND PROCESSING A


SAMPLE
• Arterial blood is taken from any easily accessible artery (typically
either radial, posterior tibial) or out of an arterial line (See PGIMER
video on neonatal procedures, for peripheral arterial line insertion).
84

• The syringe needs to be heparinized, by drawing up a small amount


of heparin ( 1000 U/mL) and squirting it out again.
o Use l mL or 2 mL syringe as they have lowest dead space
volume ( l mL syringe with non-detachable needle not to be
used)
o Remove the excess heparin by repeatedly squirting out until no
visible heparin is seen except in hub (dead space). Generally
0.3-0.4 mL of blood is enough.
o Once the sample is obtained, care should be taken to eliminate
visible gas bubbles, as these bubbles can dissolve into the
sample and cause inaccurate results.
o When a sample is obtained, date, time, patient's body
temperature, RR, sample site, results of Allen test, inspired
oxygen concentration or supplemental oxygen flow, and mode
of supported ventilation should be documented in the patient's
medical record with the results of blood gas analysis.
o If the sample cannot be immediately analyzed it should be
chilled in crushed ice to slow metabolic processes that may also
cause inaccuracy. The sample has to be warmed back to body
temperature before processing.
o The sample at room temperature must be analyzed within 15
min.
o The machine measures the pH and the partial pressures of
oxygen and carbon dioxide. The bicarbonate concentration, BE
and saturation are calculated. For calculation of derived
parameters, it is essential to provide accurate information about
Fi0 2, Hb and temperature to the machine.

10.4 MODIFIED ALLEN'S TEST


This must be done to test the collateral circulation to the hand by
evaluating the patency of the radial and ulnar arteries.
• The hand is elevated and blanched by applying pressure
• Pressure is applied over the ulnar and the radial arteries so as to
occlude both of them.
• Still elevated, the hand is then opened. It should appear blanched.
(pallor can be observed at the finger nails).
• Ulnar pressure is released and the color should return in 15 s.
Inference: Ulnar artery supply to the hand is sufficient and it is safe to
cannulate/prick the radial. lf color docs not return or returns after 15 s,
then the ulnar artery supply to the hand is not sufficient and the radial
artery therefore cannot be safely pricked/ cannulated.
85

10.S REFERENCE RANGES AND INTERPRETATION: Shown in


Table 10.I

Table 10.1: ABG oarameters


Normal Meas ired/
Parameter Abnormality
range Calculated
7.35 - Acidemia < 7.35;
pH Measured
7.45 Alkalemia > 7.45
Hypoxia <60;
Pa02 (mmHg) 60 - 80 Measured
llyperox1a >80
PaC02 Hypocapnea <35;
35 - 45 Measured
(mmHg) Hypercapnea >45
HC03 22 - 26 Calculated Metabolic acidosis
Standard <22;
22 - 26 Calculated Alkalosis >26
HC03
BE -4to~ Calculated Metabolic acidosis <-4;
SBE -4 to +4 Calculated Alkalos1s >+4

Hypoxia <87
Sp02 87 - 95 Calculated
Hyperoxia >95

10.6 EFFECTS OF CONTAMINAT' ON OF ABG SAMPLE


• With room air
o Decreased PaC02, as air has I w C02
o Increased Pa01 and Sa02 as a r has high 0 2 content.
o No change m pH.
• With excess heparin
o Decreased C02, as heparin is equilibrated with air, which has
lowC02
o Increased Pa02 as heparin i equilibrated with air, wluch has
high 0 2 content.
o pH is lowered as the pH of heparin is acidic.

10.7 EFFECT OF DELAY IN A~ALYSIS


If analysis is delayed (without chilling), it results in inaccurately low
oxygen and high carbon dioxide lev Is as a result of ongoing cellular
respiration (see Table 10.2).
86

Table 10.2: Change in the hlood gas parameters over time stored at
Room temperatureI Ice:
Blood gas Room temperature Iced sample
parameter 15 min 30 min 15 min 30 min
Pa0 2 ! 5 mmHg ! 8 mmHg j 1 mmHg j 1 mmHg
Paco, j 0.8 mmHg i 1.3 mmHg j 0.6mmHg j 0.5 mmHg
pH ! 0.007 ! 0.016 ! 0.005 ! 0.004

10.8 ABG, venous blood gas or capillary blood gas:


• Venous blood gas can be done only to follow pH values in babies
who have difficult arterial cannulation or sampling. There is a mean
difference of 0.4 in the pH values between ABG and venous blood
gas (95% limits of agreement: -0.11 to +0.04 units)'.
• Arterialized capillary blood gas samples may be used in place of
ABG to estimate pH and PaC0 2 but not Pa0 2• A puncture or small
incision is made with a lancet or similar device into the skin of the
lateral aspect of the heel after preparing it ("arterialization") by
wrapping the area in warm sponges (at 40 'C for 5 min)2 .

10.9 METABOLIC ACIDOSIS


Metabolic acidosis is characterized by a decrease in serum pH that results
from either a primary decrease in plasma bicarbonate concentration
([HC0 3-]) or an increase in hydrogen ion concentration ([H+]). The body
compensates by increasing RR and washing out C0 2. Metabolic acidosis
can be partially or fully compensated. See section N2 l for an accurate
assessment of compensation.
The rule of thumb is "'Expected PaC02 ~ (1.5 X [HC0 3 ']) + 8 ± 2"

10.9.1 Interpretation of measured versus expected PaC0 2 : Shown in


Table 10.3

Tab e 10.3 : Interpretation measured vs. expected Pa 2 co


Metabolic acidosis with
Measured PaC0 2 ~ expected
aooropriate compensation
Measured PaC0 2> expected, Metabolic acidosis with partial
but less than normal range compensation
Metabolic acidosis with
Measured PaC0 2 <expected
respiratory alkalosis (mixed disorder)
Measured PaC0 2 ~normal Metabolic acidosis with
range respiratory acidosis (mixed disorder)
87

I 0.9.2 Anion gap


• For a neutral electrochemical st<te, the number of anions should
equal the number of cations in the ECF. Routinely measured serum
anions are chloride and bicarbonate, and the (so called) unmeasured
anions include phosphates, sullates, proteins etc. The primary
measured serum cation is sodium, and (so-called) unmeasured
cations include calcium, potassiwn, magnesium etc. Under typical
conditions, unmeasured anions exceed unmeasured cations; this is
referred to as the anion gap.
Anion Gap~ (Sodium) - (Chloride+ Bicarbonate)
• Metabolic acidosis is of 2 kinds: that associated with a normal anion
gap (8-16 mEq/L) or an elevated anion gap (>16 mEq/L). A normal
anion gap metabolic acidosis involves no gain of unmeasured
anions; however, because of the need for electrical neutrality, serum
chloride replaces the depleted bicarbonate, and hyperchloremia
develops. In contrast, an elevated anion gap metabolic acidosis is
caused when extra unmeasured anions are added to the blood.
• Increased anion gap is seen in A.RF, lactic acidosis (e.g. asphyxia,
shock, hypothermia, anemia, sepsis, increased work of breathing),
!EM, late metabolic acidosis, toxins (e.g. benzyl alcohol).
• Anion gap is normal in renal bicarbonate losses, increased
bicarbonate losses, (e.g. diarrhea. fistula, ileostomy), renal tubular
acidosis (RTA), hyperalimenation acidosis, aldosterone deficiency.
10.9.3 Management of metabolic acidosis
• Actively hunt for the underlying cause and treat it.
• Volume expansion (i.e., bolus 10 mL/kg of0.9% NaCl, over 30 min)
should be used to treat acidosis if there are signs indicative of
hypovolemia. In the absence of any clues regarding etiology and
absence of any signs of overhydration, a I 0 ml/kg volume bolus
may still be given.
• Alkali treatment should be used only if significant metabolic
acidosis is present (e.g., pH <7 .2) 3 along with myocardial
dysfunction, after ventilation and volume expansion have been
achieved. Without adequate ventilation, NaHC0 3 will worsen
acidosis because of the liberation of C0 2.
o The dose is mmol ofNaHC0 3 ~Standard base deficit (mmol/L)
x Body Wt (kg) x 0.4; at a rate not exceeding I mEq/kg/min.
o Undiluted NaHC0 3 (7.5% w/v) has a concentration of
approximately I mEq/mL. Always dilute l: I in distilled water
before administration.
10.9.4 Adverse effects ofNaHC0 3
It is hyperosmolar (1790 mOsm/L). Acute hyperosmolality causes rapid
shift of water from intracellular to extracellular space, increasing the risk
of intracranial hemorrhage in preterms. It decreases ionized Ca'· and
88

causes hypokalemia. It shifts the 0 2-Hb dissociation curve to left. For


each 0.1 increase in pH, oxygen availability may decrease by 10%. It
results in paradoxical CNS acidosis because CO, diffuses through the
blood-brain barrier, whereas bicarbonate does not. It increases total body
sodium load.

10.10 METABOLIC ALKALOSIS


Metabolic alkalosis is an acid-base disturbance caused by an elevation in
plasma bicarbonate (HC0 1) concentration. Metabolic alkalosis can result
from either:
• Loss of H+ ions: from GIT, kidney e.g. continuous NG aspiration,
vomiting, diuretics. Less common causes include congenital
chloridorrhea, certain forms of CAH, hyperaldosteronism, post-
hypercapnea, Barrter syndrome.
• Gain of HCO,· Alkali therapy; citrate or acetate in IV and blood
products.
• Loss of ECF containing disproportionately more Cl than HC0 3 -
contraction alkalosis following dehydration or diuresis.
10.10.1 Approach to etiology of metabolic alkalosis
• The etiologies of metabolic alkalosis are divided into two categories
based on the urinary chloride. The alkalosis in patients with a low
urinary chloride is due to volume depletion, and, thus, volume
repletion is necessary for correction of the alkalosis. They are called
"chloride responsive." In contrast, the patients with an elevated
urinary chloride do not respond to volume repletion; they are called
"chloride resistant."
• Low urinary chloride is seen in conditions like NG suction,
vomiting, secretory diarrhea, post hypercapnic, diuretic therapy
(late). These conditions are chloride responsive.
• Normal urinary chloride is seen in conditions like Bartter Syndrome,
alkali therapy, massive blood transfusion, hypokalemia, diuretic
therapy (early). These conditions are chloride resistant.
10.10.2 Management of metabolic alkalosis
ln children with a mild metabolic alkalosis ([HC0 3] < 32) intervention is
often unnecessary, although this depends on the specific circumstances,
e.g. in a child with CHD receiving a stable dose ofa loop diuretic, a mild
alkalosis does not require treatment; whereas intervention may be
required in a child with a worsening metabolic alkalosis due to NG
suction. Intervention is usually necessary if HC0 3 ?:32. The most
effective approach is always to address the underlying etiology.
Treatment based on etiology
• Compensation for respiratory acidosis: correct ventilation
• Diuretic Rx (especially frusemide): Decrease diuretic dose, add
spironolactone, replace K+ and er deficit
89

• Loss of gastric fluid: Replace def cit with saline


• Excessive administration of alkal : Give KCI
• Bartter syndrome (rare): Replace electrolyte losses
In children with the chloride resistant causes of a metabolic alkalosis that
are associated with hypertension, volume repletion is contraindicated
because it exacerbates the hypertension and does not repair the metabolic
alkalosis. Ideally, treatment focuses on eliminating the excess
aldosterone effect.

10.11 RESPIRATORY ACIDOSIS


Respiratory acidosis is secondary to either severe pulmonary diseases or
hypoventilation.
The acute metabolic response to respiratory acidosis occurs within
minutes: Plasma bicarbonate is expected to increase by 1 for each 10 mm
Hg increase in the PaC0 2 (acute compensation). With a chronic
respiratory acidosis, the kidneys increase acid excretion. This response
occurs over 3-4 d: Plasma bicarbonate is expected to increase by 3.5 for
each 10 mm Hg increase in the PaC02 (chronic compensation).
10.11.1 Interpretation of measured versus expected bicarbonate:
Shown in Table I 0.4

..
T a ble 10 4 I nterpretation of meas•red vs. expect ed b'1carb onate
Respiratory acidosis with
Measured HC0 3 ~expected
appropriate compensation
Measured HC0 3 <expected, but Respiratory acidosis with
higher than normal range partial compensation
Respiratory acidosis with metabolic
Measured HC0 3 > expected
alkalosis (mixed disorder)
Respiratory and metabolic acidosis
Measured HC0 3 $normal range
(mixed disorder)

10.11.2 Etiology
Respiratory acidosis is seen in conditions like _CNS depression (e.g.
infection, birth trauma, hypoxic brain damage, drugs overdose, apnea,
anesthesia, raised ICP), neuromuscular disorders (e.g. diaphragmatic
paralysis, muscular dystrophies, spinal cord injury, medications like
paralytic agents and aminoglycosides), i:Y.eakness of respiratory muscles
(e.g. hypothyroidism, hypokalemia, hypophosphatemia), pulmonary
s!isease and upper airway obstruction.
10.11.3 Treatment --
The history and physical often point to a clear etiology.
In ventilated babies one should proceed in following fashion- (also see
section 14.12)
90

• Rule out 'DOPE' (Displacement, Obstruction, Pneumothorax,


Equipment failure)
• Look at the chest movements and efforts
o If retractions are present, efforts adequate
• Predominantly upper intercostal: perform ET suction and, if
needed, re-intubate (See PGIMER video on neonatal
procedures, for ET suction).
• Lower intercostals: Hike ventilator settings (after ruling out
pneumothorax) (See PGIMER video on neonatal
procedures, for inter-costal drain insertion)
o Efforts inadequate
• Respiratory muscle fatigue: Hike ventilator settings
• Drug overdose: If opiate, Naloxone (0.1 mg/kg/dose).
• CNS disease: USG head
• Muscle disease
• Hypokalcmia
o Stridor is a clue to upper airway disease.

10.12 RESPIRATORY ALKALOSIS


Respiratory alkalosis is an inappropriate reduction in the blood carbon
dioxide concentration. In neonates this is usually secondary to
hyperventilation, causing removal of carbon dioxide to surpass
production. Hyperventilation could be spontaneous as a result of the
beginning of parenchymal disease or secondary to inappropriately high
ventilator settings.
A metabolic response to an acute respiratory alkalosis occurs within
minutes, mediated by hydrogen ion release from non-bicarbonate buffers.
Plasma bicarbonate is expected to fall by 2 for each 10 mm Hg decrease
in the PaC0 2 (acute compensation). Chronic respiratory alkalosis leads to
renal metabolic compensation. Acid secretion decreases producing a
decrease in the serum bicarbonate concentration. Plasma bicarbonate is
expected to fall by 4 for each 10 mm Hg decrease in the PaC0 2 (chronic
compensation).
10.12.1 Interpretation of measured versus expected bicarbonate:
shown in Table 10.5
10.12.2 Etiology
Respiratory alkalosis is seen in conditions causing hypoxia (e.g. early
stages of pulmonary diseases, MAS, cyanotic CHD, hypotension, severe
anemia), stimulation of CNS (SAH, trauma, encephalitis, theophylline,
pain) and iatrogenically during mechanical ventilation.
10.12.3 Treatment
There is seldom a need for specific therapy of respiratory alkalosis.
Rather, treatment focuses on the underlying disease. Mechanical
ventilator settings are adjusted to correct iatrogenic respiratory alkalosis.
91

Table 10.5: Interpretation of measured vs. expected bicarbonate in


th e cont ext of .
resp1ratorv aUral"
OSI~

Respiratory alkalosis with


Measured HC0 3 = expected
aooropriate compensation
Measured H C03 >expected, but Respiratory alkalosis with partial
lower than normal range compensation
Respiratory alkalosis and metabolic
Measured HC0 3 <expected acidosis
(mixed disorder)
Respiratory alkalosis and metabolic
Measured HC0 3 ;:>:normal alkalosis
(mixed disorder)

REFERENCES
I. Kelly AM. Emerg Med J 2001; 18: 340.
2. McLain BI. Arch Dis Child 1988; 63: 743.
3. Forsythe SM. Chest 2000; 117: 260.
92

11. HYPOGLYCEMIA AND HYPERGLYCEMIA

HYPOGLYCEMIA

11.1 DEFINITION OF HYPOGLYCEMIA:


Plasma glucose < 45 mg/dL by laboratory estimation. Treatment should
not be delayed pending the laboratory report. Initiate treatment if whole
BS measured by glucometer is < 40 mg/dL. In certain situations, the
operational threshold is BS >65 mg/dL- hyperinsulinism, infants on TPN,
1
ELBW & extremely premature babies

11.2 INFANTS AT RISK OF HYPOGLYCEMIA:


The blood glucose of the following neonates must be monitored.
11.2.1 Maternal conditions: Diabetes (pregestational and gestational),
drug treatment CB-blocker, oral hypoglycemic drugs), any mother who
has received JP glucose administration
11.2.2 Neonatal conditions: Pretcrm, SGA (both <l & <2 SD) & LGA
(only >2 SD), perinatal hypoxia-ischemia, hypothermia, hydrops fetalis,
hypothermia, infection & hemodynamically unstable infants,
polycythemia, TPN, DVET with citrate-phosphate-dextrose (CPD)
blood, all the babies on !VF, babies of primigravida mother delivered by
LSCS, syndromes (Beckwith Weidemann, midline defects etc - consult
SR)

11.3 MEASUREMENT OF BLOOD GLUCOSE


11.3.1 Practical points for glucose estimation by glucometer:
• In PGIMER, we are currently using OPTIUM Xceed, Abbott
laboratory (Representative's cell 9915342773, 9356407742)
• Prewarm the heel before puncture.
• Take the reagent strip out of the foil and insert in the glucometer
port.
• The sign for application of blood will appear on glucometer screen
as it starts automatically with insertion of strip.
• Give a bold prick and wipe the first ooze of blood.
• Let the futther drop of blood fall from top in sample area/fill the area
from side.
• If sample is inadequate, fill it with another drop within 30 s. Don't
squeeze the heel with excess pressure. Don't rub the strip against the
skin as it may damage the electrode.
• Sample required - 2.5 µI/test.
• Test time - 20 s.
• Reliable for BS in the range of 50-500 mg/dL.
93

11.3.2 Practical points for laboratc ry estimation of glucose


• With normal PCV, whole BS 1 12-15°'0 lower than plasma glucose
because the Water content Of rlasma IS approximately 126/o higher
than whole blood.
• Fluonde inhibits glycolysis and keeps glucose stable for 3 d at room
temperature.
• Don' t send blood in oxalate vi 1ls for any other investigations esp.
RFT.
• If you are sure that the measurement of BS will be done within one
hour of sampling, any vial is SLitable for sending sample (except in
cases of leukocytosis)
• Don't send hcmolyzed samples for laboratory estimation of glucose
(>0.5 g/dL of free Hb interfcrCll with measurement of glucose with
hcxokinase method).
• Remove the visible reagent fro111the vial before taking sample as the
reagent provided is as per the ample quantity of 5 mL. Excess of
reagent bemolyzes the sample "'hich means waste of a valuable
sample and more bloodletting.
1 I .3.3 Frequency of monitoring: Slown in Table 11 . I J(; ~

Tablel 1.1 Fre uencv of monitorin1) of BS


Condition Fre uenc' of monitorin
Hyperinsulinemie states• [JDM, O. I, 2. 3, 6 & 6 hourly for 48
LGA(+2SD), Hydrops fetalis & h
mother received IP glucose
administration > 20 g/h or matem I
BS level > 120 m dL2
I, 2, 3, 6 & 6 houri for 72 h
6 houri
Primigrav1 a mother delivered by 6 hourly for 24 h
LSCS
Received DVET with CPD blood At 2 h after the DVET
*glucose monitoring to be done only till 24 h of life

11.3.4 Time of monitoring: prefeed (if neonate 1s being fed)

11.4 \.fANAGEMENT: Shown in figure t I.I


Neonates receiving IV dextrose infusions for the management of
hypoglycemia must have 2 working cannulas m situ at all times. This is
to ensure that no time is wasted it insertmg a new cannula when the
existmg cannula malfunctions.
94

Figure I I.I: Management protocol of hypoglycemia

'
1
Hypoglycemia I
'
Ful! term AGA infant who is not at risk
but incidentally detected to have
hypoglycemia
_____, Take sample for
laboratory estimation
of plasma glucose

Blood glucosel
l
Blood Glucose
2 ml/kg of I 0% IV dextrose over 1 min
~ (don't treat with intennittent boluses, don't
>25 mg;dL I <25 mg/dL
give bolus with either 25% or SQl'/o dextrose)

Give one full measured feed,


H Ensure 2 IV
lines in situ I
preferably EBM. IfEBM is
not available, give fonnula
milk.
Start gloco'< ;nfimon
at a rate of6
I
I mg/kg/mm

Check blood glucose


l hour after feeding Moniwr BS e'very 11.,_min after_ staning
infusion twice. lfnonnal, momtor·
hourly for 4 h' and every·;, h
subsequentlf' Jf not. .monitor q 15 min.

H Drops or doesn't rise


to euglycemic range
I
r Send laboratory value if
possible before increasing
--t
the glucose rate
I Normal blood glucose

If BS found to be in hypoglycemic range anytime


Continue monitoring during monitoring. increase the glucose rate by 2
6 hourly for 24 h mg/kg/min. (Give a bolus of 10% dextrose only if
symptomatic)
--------- - -

Don't infuse >12.5% of


dex:trose through
peripheral IV route

If glucose rate is >12 mg/kg/min I


Arrange for glucagon if
hypoglycemia persists for >7days
(Persistent or Refractory glucose rate reaches to 10
mg!kglmin (not available in
hypoglycemia)
Chandigarh)

Send first line investigations Start tapering down g]U<;osc rate by 2 mg/kg/min every 6
and start medications hour if BS.rate remain~ in euglycemic range for >6 h or
bl d glucose remains >I 00 mg/dL for 2 h.
95

11 .4.1 Medications (see sections I .7.3 and 11. 7.4 and figure 11 .2)

Figure J 1.2. Medications for proltnged hypoglycemia


II ydrocortisone I0 mg/kg/day
rIV in 2 divided doses
l
Start
D1 zoxide Octreoude.'Nifedipine
Afer discussion with consultant
11

Glucagon 0.3 mg/kg/dose


(max I mg) CM, IV, SC

Send 2nd line inv~tigations base. on


the suspicion if diagnosis could nc t be
establ!!hed by I ,. line investigation .

11.S CALCULATION OF GLUCOSE RATE ANO PRESCRIBlNG


DEXTROSE INFUSION:
11.S.1 Manually worked out exam ple
For example, if we are preparing de. trose infusion for a 2 kg baby who is
receiving I 00 mL kg/d of fluids wilh glucose rate of 6 mg/kg/min. It is
solved using s imultaneous equations
• I 00 mUkg;d ~ 6 mg/kg.Imm for a 2 kg baby works out to be 50 mL
IYF and 4320 mg of glucose evt ry 6 hourly.
• Presume that we are trying to [Iepare a dextrose infusion with help
of 10% ( l mL= 100 mg of g,ucose) and 5% (!ml 50 mg of
glucose) dextrose and x mL o I 0% and y mL of 5% dextrose is
required to prepare this stock so ution.
• Hence, x + J' - 50 mL (equation I) as well as lOOx + 50y = 4320 mg
(equation 2)
• Now mu luply equation l with l ~O.
• I00 x + 100 y 5000 (equation 3)
• Now subtract equation 2 from e 1uation 3 i.e. 50y = 680, i.e. y = 13.6
ml.
Hence, our infusion will comprise cf 13.6 mL of 5°'o dextrose and 36.4
mL of I 0% dextrose to be infused over 6 h.
l 1.5.2 Read} reckoners for deciding the glucose infusion rate and
fluid r econstitution
The following tab les (see Tables 11.2 and 11.3) have been designed as
ready reckoners:
96

Table 11.2: Estimation of concentration of dextrose infusion: Read


the fluid requirement from the rows and infusion rate from the colunms;
the cell at which the row and colunm intersect shows the required
e: ucose 1n the sou
concentration orfl Ifton
Fluid Glucose infusion rate lme/k~lminl
requirement 16
6 8 10 12 14
(mL/ko/d)
40 22 29 36 43 50 58
50 17 23 29 35 40 46
60 14 19 24 29 34 38
70 12 16 21 25 29 33
80 11 14 18 22 25 29
90 IO 13 16 19 22 26
100 10 12 14 17 20 23
110 10 10 13 16 18 21
120 10 10 12 14 17 19
130 10 10 11 13 16 18
140 10 10 10 12 14 16
150 10 10 10 12 13 15
160 10 10 IO II 13 14
170 10 10 10 10 12 14
180 IO 10 IO 10 11 13

Table 11.3: Preparation of 100 mL dextrose infusion: After


determining the desired concentration from Table 11.2, determine the
volume of 25% and I 0% dextrose or 25% and 50% dextrose to make a
100 mL solution of the desired concentration
Concentration of 25% dextrose 10% dextrose
dextrose infusion lmLl (mL)
10 0 100
11 7 93
12 13 87
13 20 80
14 27 73
15 33 67
16 40 60
17 47 53
18 53 47
19 60 40
20 67 33
21 73 27
22 80 20
23 87 13
97

Concentration of 25% dextrose 10% dextrose


dextrose infusion (mL) (mL)
24 93 7
25 100 0
25% dutrose 50% dextrose
lmL) (mL)
I
30 80 20
35 60 40
40 40 I 60
45 20 ii 80
fl
11.5.3 Computer program
Open NDM v2.0. C lick on the button "Dextrose" located in the toolbar at
the top. A window will open up. Enter the required \Blues to get the
volumes of dextrose solutions tr be mixed to get the desired
concentration and infusion rate.

1 J .6 FEEDING WHEN TREATI G HYPOGLYCEMIA: shown in


(' [Figure 11 J
/:ur=eeding is not contra-indicated wh le treating hypoglycemia with IV
//; infusions. In fact, feeding helps in be1ter glycemic control.
/~ 11.6.1 Example of enteraJ feeding
For example, if a 3 kg baby who rci·eives glucose @,, 6 mg/kg/min and
fluids ~1 I 00 mUkg/d is fit to recei te enteral feeds, start feeds with 20
mL/kg/d i.e. 5 mL 2 hourly. Obser\e for 3 feeds. If the baby toter~
feeds, increase the feeds to 40 mL gtd: reduce the fluids and glucose
rate lo 60 mUkg/d and 4 mg/kg/mi1 respectively. Observe for 6 more
hours. lf the BS remains in the euglycemic range and the baby tolerates
feeds; increaSefeeds. rcduceJYf1iiicJgT"uco~ ta!& -
Ifthe baby deVciops hypoglycemia again on increasing feeds to 40
mL,'kg/d and decreasing glucose ra e to 4 mgkg mm. keep the total

0
fl uids cg I 00 mL kg,d and increas the concentration of IV dextrose
infusion to provide glucose rate )f 6 mg/kg/min and IVF @ 60
mUkg/ min. Insert central line if lextrose concentration is > 12.5°10
through peripheral line.
If the baby is already on full eeds and develops symptomatic
hypoglycemia, reduce the feedSto 50% of the requirement and give rest
of the fluids rv @, 6 mglkg/nlin to bt]!n with. Continue monitoring and
if BS remains 10 euglycemtc range, tirrate fluids as well as feeds m above
mentioned manner
If a baby on TPN develops hypoglycc.mia, increase the daily fluids by 20
mL/kg/d. Prepare extra fluids in a way that the glucose rate increases by
2 mg/kg/min and continue monitoring.
98

Figure 11.3 Feeding while treating hypoglycemia

Hypoglycemic infant who is on dextrose infusion 11.ith


blood glucose in euglycemic range

l
I Hemod:rnamically uru;table
1
-
I Hemodynamically !>table I
If NPO, introduce feeds by increasing total intake
by .];O mUlc_fd O\er marntenance requirementJ>.

I
Minimal F.ntcral
Nutrition (MEN) ] -
Maximum limitJ> of increasing total intake before
abandoning this policy and reducing the t~
MEN are:
<I kg 20 mL /kg/day
-

1-2 kg- 40 mllkg/day,


>2 kg- 60 mUlcg/day _...
Continue deMrose infusion
and manage a!> per the
algonthm given above
J ~
+,
I Obscne foqJ fec<b'
l \... I
Blood glucose in euglycemic range with 20
mL'kg'd feeds ... maintenance tlu1ds as dextr'()';
infusion )
-
l
Increase feeds to:W ml..ikg'd and rcduceJY-tluids

I Euglycemia ~
by 2 mg/kg/min
- l
Observe for 3 feeds
-
to maintenance 40 mukg'd and rt.'duce glucol>C rate

l +
Increase feeds nnd reduce IV I Hypoglycemia I
fluid!> as well as Glucose rate
every 6 hourly +
Keep feeds @, 40 mllkg/d and increase glucose rate
lo pre"fous level by mcrcasmg dextrose
+
I Continue monitoring I concentration

+
I If glucose rate exceeds > 12 mg 'kg.'min I
!
Reduce feeds to ML:-! and give rest of the
I maintenance fluids as dex~e infu,ion I
99

11.7 INVESTIGATION FOR REFRACTORY OR PROLONGED


HYPOGLYCEMIA:
11.7.1 Refractory hypoglycemia:
Hypoglycemia is said to be refractory fthe infant remains hypoglycemic
despite receiving glucose> 12 mg/kg/n~
11.7.2 Prolonged hypoglycemia
Hypoglycemia is said to be prolon~ed if need for glucose infusion
persists for > 7 d
11.7.3 First hne Investigations
• If hypoglycemia is prolonged, evaluation for rare causes of
hypoglycemia should be considered. In case of refractory
hypoglycemia, investigations may be considered if the high glucose
requirement persists for >24 h.
• The first line investigations done are insulin, cortisol, thyroid profile
d urine for ketone and reducing u6"stances.
• yperinsullnem1Us a cause of hypoglycemia in SGA babies is
ng increasingly recognized. Have a low threshold for sending
insulin levels in SGA babies w!-ose hypoglycemia is difficult to
control beyond 96 h.
11.7.4 Second linlilIVestigations
Other investigations may be done if a specific underlying etiology is
suspected or if first line investigations are normal or equivocal.
• CAH..Jambiguos genitalia, hyperp gmcntation, hyperkalemia) - 17-
0H-P
• Suspected IEM - Blood gas, ammonia, lactate, GALT, TMS and
urine for M""RSCfeenlna (see sections 33.6 2· 33 7)..
• H ypopituitarism (Mid line defects, conjugated jaundice, micropenis)
- GH, adfeno corticotrop1c hormo1 e (ACTH) (thyroid to be done as
§!_st line inve!!i_g~ionJ.
Note: Glucagon levels may be done if all other causes are ruled out to
-
diagnose congenital glucagon deficienc ~. '

t 1.8 DIAGNOSIS OF PHHe f


• Hyperinsulinemia (plasma insul n >2 µU/mL, depending on
sensitivity of insulin assay), in presence of documented laboratory
hypoglycemia (<50 mg/dL)
• and/or evidence of excessive insuli 1effect
I. Increased glucose consumptior rate (>8 mg/kg/min)
2. Hypofattyacidemia (plasma free fatty acids < l.5 mmol/L) (not
done in PGIMER)
3. Hypoketonernia (plasma P-hydroxybutyrate <2.0 mmol/L) (not
done in PGIMER)
4. Glycemic response to 1 mg TV glucagon 50 µg/kg (max 1mg)
(6 glucose >30 mg/dL) (see se ~tion D60)
100
Insulin level is to be obtained only during presence of hypoglycemia.
Simultaneous measurement of BS level may be done to find out the
insulin-glucose ratio. Elevated insulin-glucose ratios are found in
hypennsulinem1c states (normal - up to 0.2; elevated - >0.4). A 'normal'
level of insulin is abnonnal if it occurs in the face of hypoglycemia,
especially in the context of high glucose requirement to maintain
normoglycem1a.3
HYPERGLYCEMIA
11. 9 DEFINlTION:
Whole BS > 125 mg/dL or plasma glucose> 145 mg/dL.

11.10 EXPECT IN:


• ELBW
• Sepsis
• Hypothermia
• Infants on TPN
• All those who are receiving treatment for hypoglycemia
• Neonatal diabetes

11.11 MA1'AGEMENT:
• Decrease glucose rate to 4 mg/kg/min with monitoring of BS every I
hourly. Don't give less than 5% concentration of dextrose. Minimal
permissible glucose rate for term AGA babies is 3 mg/kg, min
• Initiate insulin therapy (see section D70) when osmotic diuresis
(urine output >4 mUkg/h) occurs (expect osmotic diuresis with BS
>215 mg/dL). Start insulin infusion: 10 units of regular insulin in
100 mL of maintenance fluid @ 0.01 to 0.2 unit/kg/hour if BS
remains >215 mg/dl for >6 h after decreasing glucose rate to
maintenance. Flush IV tubing with SO mL of insulin stock solution.
Monitor whole BS every 15 min for I" hour and then hourly.
Monitor serum potassium every 6 hourly.
• Taper insulin infusion if BS remains <200 mg/dL and omit insulin
infusion if BS < 150 mg/dL.
• If a neonate on TPN develops hyperglycemia, increase the
maintenance fluid by 20 mLJkg/d and use that fluid to prepare
insulin infusion to be gi\'en @ 0.10 to 0.2 unit of 1nsulin/kg/hour.
• Monitor BS every 15 min for 2 readings and then hourly for 6 h and
then every 6 hourly.

REFERENCES
l. Williams AF. Semin Fetal Neonatal Med. 2005; I0:363.
2. Mendiola J. Anesth Analg.1982;61 :32.

--
3. Stanley CA. Pediatr Cl in North Am l 997;44:363.
4. Aynslcy-Grcen A. Arch Dis Child Fetal Neonatal Ed. 2000;82:F98.
101

12. PERINATJ\L ASPHYXIA

12.1 BACKGROUND
Perinatal asphyxia is an insult to the fi·tus or the newborn due to lack of
oxygen (hypoxia) and/or a lack o perfusion (1schemia). Perinatal
asphyxia is classified into moderate ~vxia (slow gasping breathing or
I min Apgar score of 4-6) and severe asph ia (no breathing or 1 min
Apgar score o - . v1dence of eta distress ts de me as e a
m>riormalit1es ± cord blood pH < 7 0. Immediate management
neonate with asphyxia is shown in Figl.re 12. I

Figure 12.J: Immediate management

I mm Apgar < 7
and/or e/o fetal distress

Monu°' ( 15 min, I hr,2 hr) Normal


>---- •Cardictc:.piratory status 1----..
•Featum of II IE
<7 •Rouunc care
•Shift to mother
(SR to decide)
•Monuor for HIE
•Ruic out other causes of at 6hr.24hr & 48hr
neonatal depression
•Monitor
-Cardiorcspiratory status
-features of IUE
•Check BS. PCV (pale1shock)
•IV dextrose ifhypoglyecmie
•Shift to NICU/NNN

12.2 MONITORING A MODERATE TO SEVERELY


ASPHYXIATED INFANT
12.2.1 Clinical monitoring: Shown in ,.able 12. I
12.2.2 Laboratory monitoring: Shown in table 12.2
12.3 HIE
Recognition of HIE requires careful observation and examination as the
spectrum of signs varies with the severity of the insult.
12.3.l Early clinical course (HIE): Shown in table 12.3
102

Table 12.1 Clinical monitorin" of an asnhvxiated neonate

Parameter Frequency

HR
RR
Continuously
Sao,
Temperature
BP
Capillary-filling time
Every hourly
Color
Peripheral pulses
Neurological examination for signs of
6 hourly
HIE
Wt
Urine output 12 hourly
Abdominal girth
anterior fontanel tenseness
Daily
OFC
Other systemic examination As clinically indicated

Table 12.2 Lab monitorinl! of an asohvxiated neonate


Parameter Frequency
BS At admission and then 6 hourly
Blood gas At admission and then as required
CPK-MB
At admission
Urine routine microscopy
PCV At 2 h. 12 h and then as required
Serum Na
Serum K Daily or more ftequently if
BUN clinically required
Creatinine
Urine osmolality/ specific gravity 6 hourly
To look for myocardial ischemia
ECG
and electrolyte disturbances
103

Parameter Frequency
Serum calcium As clinically required
Sepsis screen and blood culture
and sensitivity In unexplained cases of asphyxia

LP, coagulogram, platelet count,


As clinically required
CXR, Echo, and AXR

Table 12.3 Clinical course of HIE


Mild insults u~uall roducc a hypervi ilant
appearance with excessive irrita 1 1 Mod rate to
First 12 h sev s e to e associated with seizures.
Severe msults have markedly depressed
sensorium tonia from first ho~
Infants with mtl msults may have normal
sensorium, but W1tfi failure to fix and follow.
12-24 h
SevereTy encephalopathtc persistent seizures and
a dechrun level f consciousness
Infants with mild insults recover normal levels of
alertness and beg n feeding.
Severely encepl alopathic infants continue to
24-72 h deteriorate and, begin to develop prominent
brainstem abnormalities, such as ataxic
respiration, impaired eye movement, facial
weakness, and ilia d sfunction.
A gradual improvement in mental status and
neurologic exam nation is usually evident; the
72 h 7 d
extent and rate o recovery depend on the imtial
severi of the insult.

12.3.2 Staging of HIE


Clinical features that distinguish bet ·een different grades of severity
include level of consciousness, seizure , brainstem dysfunction including
swallowing and feeding, and muscle to 1c. (See Table 12.4 & 12.5)

12.3.3 Specific patterns of motor c ysfuoction and topograph) of


brain lesions: Shown in Table 12.6
104
Table 12.4 Classification of HIE (Levene) (both term and preterm
babies) I
Feature Mild Moderate Severe

Consciousness Irritable Lethargy Comatose


Marked
Tone Hypotonia Severe hypotonia
hvnotonia
Seizures No Yes Prolonged
Unable to sustain
Unable to
Sucking/respiration Poor suck spontaneous
suck
respiration
2
Table 12.5: Sarnat and Sarnat Sta >es of HIE (>36 wks)
State 1 Stage 2 Stage 3
Level of Hyperalert; Lethargic or Stuporous,
Consciousness irritable obtunded comatose
Neuromuscular Control
Muscle tone Normal Mild hypotonia Flaccid
Mild distal Strong distal Intermittent
Posture
flexion flexion decerebration
Overactive, Decreased or
Stretch reflexes Overactive
disinhibited absent
Segmental Present or
Present Absent
mvoclonus absent
Complex Reflexes
Suck Weak Weak or absent Absent
Weak,
Strong; low
Moro incomplete, high Absent
threshold
threshold
Oculovestibular Normal Overactive Weak or absent
Tonic neck Slight Strong Absent
Autonomic Generalized Generalized Both systems
Function sympathetic parasympathetic depressed
Midposition,
often unequal;
Pupils Mydriasis Miosis
poor light
reflex
Spontaneous,
Respirations Spontaneous Periodic, apnea
occasional apnea
105

State 1 Stage 2 Stage 3


HR Tachycardia Bradycardia Variable
Bronchial and
Salivary Sparse Profuse Variable
Secretions
Normal or Increased;
GIT Motility Variable
decreased diarrhea
Common; focal Uncommon
Seizures None or multi focal (6 (excluding
to24 hour of age) decerebration)
Early:
generalized low-
voltage slowing
Early: periodic
(continuous delta
pattern with
and theta)
Normal Isopotential
EEG Findings Later: periodic
(awake) phases
pattern (awake)
Later: totally
Seizures: focal
isopotential
or multifocal, 1-
to 1.5 Hz spike-
and-wave
Duration <24 h 2-14 d Hours to weeks
80%normal,
About 50% die,
About 100% abnormal if
Outcome remainder with
normal symptoms > 5-7
severe sequelae
d

Table 12.6 ToDO!!raohv of brain lesions and motor dvsfnnction


Hypotonia & weakness
Parasagittal watershed injury predominantly involving shoulder
girdle
Apneas, facial diplegia,
Brainstem/basal ganglia gaze abnormalities,
impaired sucking, swallowing

Focal infarct (MCA territory) U/L weakness (UL> LL)

PVL LL weakness only


Peri-ventricular hemorrhagic
Hemiparesis (LL> UL)
infarction
106

12.3.4 Management of HIE


The management consists of supportive care to maintain temperature,
perfusion, ventilation and a normal metabolic state including glucose,
calcium and acid-base balance.
• Maintenance of adequate oxygenation and ventilation: PaO, should
be maintained between 60-80 mm Hg and PaCO, between 35-45
mm Hg. Both hypo and hypercarbia should be avoided.
• Maintain of adequate cerebral perfusion and MBP. Keep MBP
between 45 to 50 mm Hg in term, 35 to 40 mm Hg in infants
weighing I 000-2000 g, and 30 to 35 mm Hg in infants weighing <
1000 g.
• Give volume slowly and minimize boluses of colloid or NaHCO,
• Maintain normal BS, serum calcium and acid-base status
• Maintain temperature in NTZ (see section NI 7).
• Control seizures. Phenobarbitone is the drug of choice (see section
D99). Concomitant evaluation and correction for treatable causes
like hypoglycemia, hypocalcaemia, hypomagnesaemia, hypo and
hypcrnatremia, and pyridoxine deficiency is required.
• Cerebral edema is usually a consequence rather than the cause of
cerebral injury. Therapy involves maintenance of adequate cerebral
perfusion pressure only.
• SIADH: Manifests as oliguria and abnormal Wt gain without edema.
Investigations show hyponatremia, normal BUN and serum
creatinine and elevated urine sodium, specific gravity and
osmolality. Therapy includes restriction of fluids and correction of
hyponatremia. (see section 8.8.2)
• All babies with HIE who are transferred to NICU must be connected
to EEG monitors, with continuous monitoring.
• Neuroprotective strategies. Although several interventions currently
under investigation show encouraging results in animal models
(calcium channel blocker, allopurinol, oxypurinol), brain cooling 3
strategies seem to be the most promising approach as of now. But all
modalities are still in experimental / investigational stage and hence
should not be used in routine clinical practice.
4
• Prophylactic phenobarbitone does not have any benefit .
12.3.5 Other organ specific management
Oligoanuria: Therapy involves correction of hypovolemia and
hypotension (see section 8.8.1 ). Fluid management is best decided based
on CVP measurement, which in a term spontaneously breathing baby is
5-8 cm of water. Fluid restriction is required only in cases of acute
tubular necrosis and SIADH.
Shock: Myocardial dysfunction should be considered early in the course.
For management of myocardial dysfunction dobutamine should be
preferred (see section 29.6).
107
Acidosis: NaHCO, has many adver;e effects (see section 10.9.4). Before
giving bicarbonate correction, alwa:'s discuss with consultant.
Sepsis: Asphyxiated babies are more prone to develop infection and
intrauterine sepsis per se could be . he cause of asphyxia. Hence, a high
index of suspicion should be maint.1ined, appropriate work up done and
antibiotics initiated whenever indicated.
Fluid therapy: Give normal maintenance fluid unless there is intrinsic
renal failure or SIADH.
Nutrition: Feeds may be intrcxluced as soon as the baby is
hemodynamically stable; shock has remitred; bowel sounds have
normalized; and the baby has passed meconium.
12.3.6 Role of EEG
No changes are absolutely diagnostic of HIE, however it helps in
• Differentiating seizures from non-epileptic behaviors
• Providing background patterns that provide an insight into the
severity of the asphyxia! insult
• Detection of clinically occult electrographic seizures. Electrographic
status epilepticus (<: 30 min) or frequent prolonged electrographic
seizures (no clear definition) are indications for treatment even in the
absence of clinical seizures. Brief, sporadic electrographic seizures
need not be treated.
• Prognostication oflong-term outcome
12.3.7 Neuroimaging to be done in HIE
• In preterms (<34 wks)
o USG: within first 7 d, at 14 d and then at 40 wks corrected age
or discharge (see section 21.6)
• In term and near-term ~4 wb)
o USG: if JVH/intraparenchymal bleed is suspected and baby is
too unstable to be shifted for a CT scan. USG may be able to
pick up cerebral edema and chinked ventricles but the
interpretation is subjective and requires expertise. Measurement
of cerebral flow velocities should be done in these babies as per
the unit's cranial USG form.
o CT scan: can detect all forms of intracranial bleed & cerebral
edema
o MRI: can accurately define the site and extent of damage.
Should be considered in all HIE stage 2 & 3 when stable or at
discharge
12.3.8 Discharge planning and long-term follows up
At discharge detailed neurological assessment should be done and
recorded in the discharge summary. Periodic follow-up is mandatory for
early detection and management of sequelae (see section 42.3 and
chapter 43).
108

REFERENCES
I. Levene ML. Early Hum Dev 1985; II: 21.
2. Samat HB. Arch Neural 1976; 33: 696.
3. Lantos ID. NeoReviews 2009; 10: e65.
4. Cochrane review, 2007
(}J.. ~fit.,. I ,., •JI 6 . [,.,
?rye,.'C!P'{E. '-" j; >~ ~
109

13.1 D&:NlTION: l3 APNEA - (h'\,Cr •


Cessation of breathing for 20 s; o less, if associated with cyanosis (or
desaturation) and/or bradycardia (HR < I 00/min)

13.2 TYPES OF APNEA:


13.2.1 Obstr uctive: Respiratory efforts are present initially, but nasal
airflow is absent. This can be because of neck flex.ion, secretions, nose
block or collapsed pharyngeal mu culature. It is difficult to clinically
label obstructive apnea. Electronic RR monitoring using ECG leads or
transducers enable this diagnosis lo be made.
13.2.2 Central: Respiratory efforts ire absent
13.2.3 M ixed : Both central and obstructive components are present.

0
Often central component precedes Obstructive component.
Frequency according to the type: Mixed> Central> Obstructive.

13.3 MONITORING AND PREVE NTION:


All neonates < 34 wks of gestation hould be on HR & Sp02 monitor for
the first2J!..!s far as possible (see ections 6.1.3 and 6.2.2). There is no
evidence to support the use of met 1ylxanthines or any other agents for
the prevention of apnea.

13.4 IMMEDIATE MANAGEME~T OF APNEA:


Initial resuscitation is similar irresrective of the etiology and type (see
Figure 13.1).

13.5 MANAGEMENT AFTER CESSATION OF ACUTE


EPISODE:

• The baby's HR, Sp02 should be monitored.


• Maintain proper posture with neck slightly extended.
• Maintain ambient temperature a the lower end ofNTZ
• Maintain Sp02 at 87-93% by su· plemental oxygen if necessary
• Treat the underlying cause.

13.6 EVALUATION BASED ON CLINICAL CLUES:

Evaluatton must be directed ba ed on the possible cause. AJI


investigations need not be done in al patients (Sec Table 13. l ).
110

Table 13. l: Investigations guided by clinical signs

Associated Possible cause(s) Relevant


Symotoms/Si!ms investieation(s)
Lethargy, feed Sepsis Septic screen, blood
intolerance/ poor culture
feeding, temp.
instability
Jitteriness Hypoglycemia, BS, S. Ca'
hvnocalcemia
T emperaturc Environmental, sepsis, Assess temp of baby
instability poor perfusion and look for the cause
(Hypothermia,
hvnerthermia)
Respiratory distress, Hypoxia Sp0 2 , ABG, CXR
cvanosis
Seizures, hypotonia or lntracranial bleed USG head
other neurological
findings
lntennittent dips in PDA Look for other signs,
Sp02 , systolic Echo
murmur
Abdominal NEC, Sepsis Investigate NEC &
distension, prefeed sepsis
aspirates
Blood loss, pallor Anemia PCV
Plethoric, IUGR, IDM Polycythemia PCV
PGE 1 infusion, Drug induced Mg levels ifrelevant
maternal h/o MgS0 4
Pretenn, otherwise AOP Rule out secondary
well causes
Choking episodes Massive GER* Nuclear scan
with milk in the
trachea
*- Apnea and GER occur m same group of babies. The common garden
variety of GER has not been shown to be a cause of apnea. However,
occasionally a massive aspiration may physically obstruct the trachea to
cause apnea.
(Note: The list above mentioned is not exclusive, but refers to the
common causes. Jn some cases, more than one cause may co-exist)
111

Figure 13.J: Algorithm of manag •ment of apnea

eek
, Breathing effons pre~nt or not
Airway obstruction (11eck position. secretions)
Tactile stimulalton twice
l Gentle oropharyngca sucuon

E\Sluate llR, Resp, color


only ~yunosis

Apne1c or
HR<60 Con11nuc
mon1111nng&
evaluate
Provide effective PPV x 30 s cause

HR < 60 l t HR > 60

PPV - Chot compressions" 30 s•

HR< 60

I Administer Epinephrine•
S- Response - nonnal respiration, HR> 100. pink
•.Consider intubation

J3.7 APPROACH TO DETERMINING THE CAUSE OF APNEA


• WeU neonate- Possible etiologies are AOP, metabolic causes. PDA,
anemia, drugs. Calltion: Apnc11 can be the initial sign for other
illnesses like sepsis and NEC in an apparently well looking neonate.
One should actively look for the signs of these illnesses.
• Sick neonate- Possible etiologies arc c sis NEC, IC bleed.
• According to day of onset: The.re ca be overlap m e age of onset
among the etiologies mentioned below. but the usual presentation ts
given below.
Day I: !:!i'J>othermi~ pennatal asphyxia, hypoglycemia,

8 !!!,atemal a~s. lVH -


Day 2-7: AOP, PDA, sepsis, lVH, NEC, hypoglycemia,
~YJ>OC~ ~----~~~~~~~~~~~-
--

p is a diagMsis of exclusion and should be


considered only after reaso1ably ruling out other causes. Even
in a labeled case of AOP. f apneas recur frequently, look for
112

secondary causes. Episodes of AOP usually begin towards the l


end of day I or 2 and usually present within first 7 d. )
o Beyond Day 7: Sepsis, NEC, anemia ·
• Term or near term infants- Apnea is always abnormal and nearlyJ
associated with serious i?entifiable caus~s like birth. asphyxia.
mtracranial hemorrhage, seizures or depression from med1ca11on.

13.8 CONDIT IONS T HAT CAN MIM IC APNEA I


Period ic breathing: This benign pattern of breathing is seen in 30-50%
of preterm infants. The infants exhibit regular respiration for a period of
15-20 s, followed by cessation of breathing for 5-10 s. There is no
cyanosis or bradycardia.
Seizures: Apnea can be a manifestation of seizure and prolonged apnea
can lead to seizure (see section 22.2). The sequence of events will help in
j
differentiating the two. J
'Epileptic Apnea' will have initial tachycardia, other manifestations of
subtle seizures and it rarely lasts longer than 20 s. Apnea due to seizures
may have bradycardia following hypoxia.

13.9 RECURR ENT A PNEAS:


• Recurrent apnea is defined as ~ apneas/h or ~ in 2 consecutive
hours. Management 1s shown in Figure 13.2. Note: In case of
recurrent apnea, each apneic episode doesn' t warrant repeated work
up unless a ne"" etiology is suspected.
• Stop caffeine/aminophylline once baby is on SIMV, and restart prior
to extubation to CPAP. Downgrade the ventilatory support if the
baby is apnea free for 24-48 h.

13.10 PHARMAC OTHE RAPY: 1


13.10.1 Caffeine (see section 018): ;]
• Loading dose is 20 mg/kg of caffeine citrate o. ver 30 min, followed by
5-12 mg/kg OD beginning 24 b after the loading dose. Caffeine has
longer t1 2. wider therapeutic index (less side effects) and smal
interpatient variability compared to theophylline. 2
• If financial issues are not a constraint, caffeine must be preferred over
aminophylline. The use of caffeine has also been shown to reduce
BPD and improve survival without disability at 18 mths of a~.
DOXaj)i1iffi should not be used because of its side effects.
13.10.2 Aminophy lline (see section D7):
• Give loading dose of 3 mg leg as infusion over 30 min. followed by
maintenance of 2 mg/kg/dose q 12 hourly as infusion. This can be
di luted with NS or 5% dextrose.
• In SFD babies, loading dose is 2 mg/kg followed by 1.5 mg/kg/dose
q 12 hourly.
113

• One should attempt to get the drug levels if feasible (not routinely
done in PG!). The therapeutic It vels: 7-15 µg/mL.
• Once the baby is eligible for <·ral drug administration, shift to oral
theophylline (see section Dl23)
• Toxic effects- Tachycardia, jitteriness, irritability, seizures,
abdominal distension, feed intolerance, vomiting, GER,
hyperglycemia.

Figure 13.2: Algorithm of management of recurrent apneas

Recurrent apnea (2:2 apneas/h or


:::_3 in 2 consecutive h)
Are apneas occurring very frequently
mandating immediate support

Load with Caffeine/ Load with Cafeine/Aminophylline


Aminophylline + start CP AP* Continued apneas

CPAP*

-r - I

Continued ;neas

~ ~C:~~~~~;~: ~'.~~ ~~~:r!1;!:~; lungs


Continued apneas i
SJMVwith (Guidelines: PIP: 12-13, PEEP: 3-4,
minimal settings Rate: 25-30, Fi0 2 21 % for normal lungs

(• Start with CPAP of 5 cm H20. One can consider increasing CPAP up to 6, if apneas
continue on 5 cm H 20, as optimal PEEP for splinting chest wall & airway can vary with
the babies).

13.10.3 Duration of therapy:


• If a cause for apnea has been found, stop caffeine/arninophylline
once the primary disease is under control and apnea has remitted.
• For AOP, stop caffeine/aminophylline once the baby attains 34 wks
of PMA and is apnea free for a 7-d period.
• After stopping, keep the baby under observation for at least 3 d prior
to discharge if on theophylline (elimination ty, 24-36 h) and 5 d if on
caffeine (elimination tv, 103 h).
• Persistent apnea: Some infants, especially those <28 wks of
gestation, apneic spells may persist up to 43 wks of post-menstrual
114

age. In these infants discharge on theophylline and reassess every


month. Prior to discharge the parents should be educated about the
basic steps of resuscitation.

REFERENCES:
I. Henderson-Smart DJ. Cochrane Database Syst Rev. 2001.
2. Comer AM. Paediatr Drugs. 200 l ;3 :61.
115

14. ACUTE RESPIRffORY DISEASES

14.1 DEFINITIONS

of the 3 features is essential





Tachypnea (RR > 60 per min)
Retractions (mtercostal and or sut costal)
Expiratory grunt
J
14.1.1 Definition of respiratory distress (NNF) 1: Presence of at least 2

14.1.2 Normal oxygenation: Pre-ductal Pa02 50 70 mmHg with an 0 2 ~c


saturation of 87-93%. A Pa02 up to 80 m~ptablc in tenn
infants
14.2.3 Normal PaC02 :
• 35-45 mmHg
• Acceptable upper limit: Acute st. ge: 50 mmHg, chrome (>72 h of
ventilation): 55 mmHg (assuming a corresponding pH of ~7.2)

14.2 CLINICAL CLUES FOR DIAGNOSIS: Shown in Table 14.1


Table 14.1 Clinical clues for diagnosis of respiratory distress

Clues Diaenosis
Prematurity (<34 wks),
No. inadequate antenatal steroids,
APH, maternal DM, Rh
RDS
isoimmunization, a suggesti,·e
gastric aspirate shake test (see
section I-3)
Risk factors of EOS (see section
24.3), PMN in gastric aspirate (>5
Congenital pneumonia
per hofl
Evidence of fetal distress, decreased sphyx1al lung damage
fetal movements, abnormal FHR (Secondary surfactant
patterns (see section 1.2. l 0), MSL, c:eficiency/dysfunction). PPHN.
cord UA blood acidosis MAS
$evere RDS, congenital
Prolonged IPPV, need for high rneumonia, pleural effusion,
inspiratory pressures, difficult to pulmonary hypoplasia,
rise chest (immediate postpartum pneumothorax. airway
and in the first 24 h) ma! formations
PPV, asynchronous breathing
efforts, underlying disease causing
A 1r leak syndromes
air trapping (e.g. MAS), sudden
( ~neumothorax , PIE,
onset hypoxia and hypercarbia,
prleumopericardium)
chest hyperinnation, reduced air
entry II
116

Clues Dia~nosis
Polyhydramnios, single UA, Esophageal atresia with/without
excessive frothing from mouth, trachea-esophageal fistula (see
absent stomach bubble on AXR, section 35.2.2)
scanhoid abdomen
Oligohydramnios, Potter facies, Pulmonary hypoplasia
limb deformities
CDH, congenital cystic
Polyhydramnios, antenatal hydrops adenomatoid malformation,
fetal is pleural effusion (uni/BIL)
Scaphoid abdomen, heart sounds
over the right chest, bowel sounds CDH (See section 35.2.1)
over the thorax
Abnormal presentation (breech,
brow, face), difficult delivery (large
Diaphragmatic paralysis, pain
baby, shoulder dystocia, forceps
(due to brachia! plexus injury,
extraction) especially in a female
fracture humerus or clavicle)
neonate, asymmetric Moro's reflex
on clinical examination
Unexplained sibling death,
unexplained metabolic acidosis and
!EM (see section 33.4)
hypoglycemia, seizures, abnormal
odor (bodv/urinc)
Risk factor for breathing-
swallowing in-coordination such as
asphyxia, CNS malformations,
Aspiration pneurnonitis
gestation <34 wks, poor feeding
technique, anatomical defects (clef\
nalate, ~lossontosis)
Tachypnea, stridor, Upper airway pathologies
suprastemal/supraclavicular (laryngomalacia, vascular
recessions, little oxygen malformations, subglottic
reauirement stenosis)
Metabolic disease (hypoglycemia,
Isolated tachypnea (usually no
!EM), CNS disease, CHD
oxygen requirement)
Polvcvthemia, anemia, pain
Antenatal ACE inhibitors, post-
term, asphyxia, MAS, severe
cyanosis (not responding to 0 2),
PPHN
extreme !ability especially on
handling, tricuspid systolic murmur,
differential saturation
Post term infant, hyper inflated
Amniotic fluid aspiration
chest, other causes ruled out
117

14.3 INITIAL EXAMINATIOJ\ OF A NEONATE WITH


RESPIRATORY DISTRESS
• Respiratory
o Record RR, retractions, grun., cyanosis and stridor
o Check the need for supplemental 0 2 (use pulse oximeter)
o Observe- chest expansion and chest wall movement with
respirations
o Hear-air entry/breath sounds (BIL)
o Transillumination B/L (baseline )-use a cold light source J
o Patency of upper airways in suspected upper airway obstruction_]
(inspiratory stridor, supraclavicular and/or suprastemal
recessions; a history of increase in distress while feeding). Pass
8-10 F catheter through both nares.
• Non-respiratory
o Abdomen:
• Contour (scaphoid, distended) /
• Bowel sound (absence/diminished)
• Palpate liver and spleen (hyperinflation, CHF, !EM)
0 CVS:
• Heart sounds (intensity, location), bowel sounds
• Systolic murmur in tricuspid area, loud P2, parasternal
heave
o Miscellaneous:
• Fontanel, sutures separation (lVH)
• Skin - color (pallor, plethora), mottling, meconium staining
• Tone, pupils, alertness
Algorithm for approaching to diagnosis is shown in Figure 14.1

14.4 INITIAL MANAGEMENT OF A NEONATE WITH


RESPIRATORY DISTRESS: Shown in Figure 14.2

14.5 ASSESSMENT OF SEVERITY OF THE RESPIRATORY


DISTRESS:
Assessment includes continuous monitoring of vital signs. respiratory
distress, air entry, oxygen saturation, Fi0 2 requirement and chafige5 in
ABG ~ ~

Two important scoring systems available are the Downe's score and the
Silverman-Anderson retraction score
14.5.1 Downe's score: Shown in Table 14.2
14.5.2 Silverman-Anderson score: Shown in Table 14.3
118

Figure 14.1: Algorithm showing approach to diagnosis based on


gestation & age of onset
I Pretenn I

I <6h I ' 6-24 h I I > 24 h I

•HMO • Cong. Pneumonia •


!
Acquired pneumonia
• Cong. Pneumonia • Aspiration syndromes • Patent ductus arteriosus
• TTNB • Patent ductus arteriosus • Aspiration syndromes
• Lung malfonnations • Shock* • Pneumothorax
• Pneumothorax • CHD (duct dependent) • Pulmonary hemorrhage
• Lung malformations • CHO (duct dependent)
• Pneumothorax • Shock*

*Shock: lrrespe{;tive of etiology


Tenn

- - - - - -

I < 6h I I 6-21 h I I > 24 h l

• TINB • Aspiration syndromes • Acquired pneumonia


• Cong. Pneumonia - Meconium, amniotic • Pneumothorax
• Postasphyxial lung fluid, blood • Pulmonary hemorrhage
dysfunction • Cong. pneumonia • CHO (duct dependent)
• Aspiration syndromes • CHO (duct dependent) • Shock*
- Meconium, amniotic
fluid, blood
• Pneumothorax
• Lung malfonnations
• Polycythemia
• Lung malfonnations
• Cong. pleural effusion • Cong. pleural effusion
• HMD (associated
asphyxia, IDM
• Pneumothorax
119

Figure 14.2 Initial management of a neonate with respiratory


distress
Titrate inspired oxygen concentration
Administer oxygen* according to Sp02 (target: 87-93o/o),
Attach to a vital signs monitor check Fi02 with oxygen analyzer

Apply suction while withdrawing.


Maintain neck in sniffing position Suction pressure should never
Clear the aif'Vlay (if secretions+) exceed l 00 mmHg

Locate the pathology


Examine for the features of Assess severity with Downc's I
respiratory distress Silverman's score (see section 14.5)
Send call for CXR

Place vascular accesses


Assess circulation (HR, pulse .••••.... , Send ABG (if feasible)
volume, CFT, skin color) Stabilize circulation.

Start supportive measures


• Temperature maintenance
• Correct hypoglycemia
• Assess fluid & electrolyte status
Pretenn infant Near term/ and correct if abnormal
(<34 wks) term infant

• EarlyCPAP • Poor respiratory efforts


• If RDS suspected, (respiratory failure)? No Start CPAP
administer surfactant • Worsening shock? (5-7 cm H10
(INSURE) • PPHN?
• Consider sending • Massive pulmonary
blood culture and hemorrhage?
• Worsening respiratory
starting antibiotics • Malformations (CDH)? distress
(See Chapter 24) • Collapse with apnea and • Metabolic acidosis (pH
fails to respond to BMV? <7.2 with BE<-10)
Yes • Respiratory acidosis
(PaC0 2 >55 mm Hg with
Failure of CPAP* Mechanical pH <7.2)
ventilation • Worsening ABG

*Presence I worsening of respiratory distress and I or hypoxemia (Pa02 <50 mm Hg) on a


CPAP of 7 cm H20 and 70o/o Fi02 should be considered as failure of CPAP. 'A lower
threshold to start mechanical ventilation may be used in ELBW infants and those with
multi-organ dysfunction.
120

Table 14.2 Downe's score

Parameter 0 1 2

RR <60 60-80 >80


(per min)
Cyanosis Absent In room air In 40% oxygen
Audible with a Audible with a
Grunt Absent naked ear
stethoscope
Retractions Absent Mild Moderate - severe
Air entry Good Diminished Barely audible

Table 14.3 Silverman-Anderson score


Si ns 0 1 2
Lags on See-saw
Upper chest Synchronized
inspiration respiration
Lower chest No retraction Just visible Marked
Xiphoid
None Just visible Marked
retractions
Nares
None Minimal Marked
dilatation
Expiratory Stethoscope
None Naked ear
runt onl
*A score of >6 indicates impending respiratory failure and warrants
mechanical ventilation

14.5.3 Assessment of gas exchange (non-clinical):


• Alveolar-arterial Oxygen gradient (A-aD02)
• a/A ratio
• Oxygenation Index (01)
Calculation and interpretation:
A-aDO,:
A-a D02 = PA02 - Pa02 (ie p Alveolar - Parterial oxygen tension)
= [(P 8 -Pw) x Fi0 2 - PaC0 2/RQ] -Pa02
= [(760-47) x Fi0 2 - PaC02/RQ] - Pa0 2
Example: Assuming Fi0 2 of 40%, Pa02 of 60 mmHg, PaC0 2 of 50
mm Hg
A-aD0 2 = [(713 x 0.4)-50]-60
= [285.2 - 50] - 60
= 235.2 - 60
= 175
121

lnterprerat10n:
• Normal range in a newborn: 5 - 15
• Abnormal: 15-40
• Definitely abnormal: >40
a/A ratio:
Ratio of Pa01 to PA02. Consider..d to be a better indicator of gas
exchange as the ratto is less affected oy changes in Fi0 2
Interpretation:
• Greater than 0.8: Nonna!
• Less than 0.6: need for 0 2 tberaty
• Less than 0. 15: severe hypoxem a
Oxyge11ation Index (OJ):
Recommended in babies who are rrechanically ventilated as this score
includes MAP
OJ = (MAP x Fi02) Pa02
Interpretation:
• 01 25 - 40: severe respiratory fa lure; monality risk is 50 60%
• 01 > 40: Mortality risk is >80%

14.6 CXR FINDI~GS OF SPECIFIC RESPIRATORY ILLNESSES:


Shown in Table 14.4

Table 14.4 CXR findin s ofvariou res iraton illnesses · X·


......;:c..:;.:;:..:..:....::.....;.~.=:.;:.;:..:...:...;.;.;.;;.;:.:.;::.a;:....=..::....:..;::::...:..:....::.o;.....:..:..::i:c.:..:..::..:...:..:...;....:.=::...:..:c::..::..::..._~~---!;

Disease CXR fiodio s


• Low lung volum *
RDS • Reticulo-granular shadows, air bronchogram,
ound lasso at ities, whitened out lun s
Transient • Normal/hyperinflated• lungs /
tachypnea • Prominent minor interlobar fissure
of newborn • Mild cardiomega /
0

• Prominent hilar d ulmona vascular markin s


MAS • Hyperinflation (lc>cali1cd or generalized) j
• Areas of atch acelectas1s
Congenital • Low to normal v" lume lungs /
pneumonia • Patch atelectasi
• Pulmonary oligelllia
PPHN
• Features ofundetl I
Air leaks • Pleural air
• Medtastinal shift
•Low lung volume: Less than 7 posterior mt<Yeostab spaces <7 /
' Hyperinnauon: Greater than 8 posterior inteltostals spaces / ~D J.~
·' Cardiomegaly: Card10 ~ratio >65% /•
'Pulmonary oligemiu. Di se yperlUcency 1f the lungs assoc1uted with a rcducuon m the
caliber of the pulmonary arterial tree.

-
-

- -
122

14.7 MANAGEMENT OF RESPIRATORY DISTRESS:


This mcludes oxygen therapy, surfactant and ventilation (both non-
inrns1ve & mechanical)

14.8 OXYGE~ THERAPY


14.8.1 Indications.
• Clinical central cyanosis
• Hypoxemia(n1 saturation <87%* and or Pa01<50 mmHg in room
air)
• Presence or respiratory distress irrespective or02 saturation
*Lower limit or normal levels of saturation is sttll under research.
Pending further evidence, 87% should be considered as the lower limit.
However, healthy term and preterm babies have median Sp0 2 val ues 98-
99% with I 0th centile values around 95%. -
Note: In babies with isolated tachypnea and a normal 0 2 saturation, a
short trial or supplemental oxygen is warranted to assess the response of
tachypnea.
14.8.2 Commonly used oxygen delivery systems in neonates:
Low now systems are commonly available and used tn neonates. These
systems provide a vanable Fi02 depending upon the msp1rato..!l now rate
generated by the neonate (see Table 14.5). ".. ,__
14.8.3 Precautions while administering Oxygen:
• Prewarm and hu~the oxygen especially at now races > 2 L mm
• lliygcn saturation should never cross_J_~ aS/ 0 Z
hyperoxia leads to wide spread free radical injury __.J l _,,
• RFR should never be crossed as excessive flow can cause turbulence


in the airflow and inadvertent uncontrolled PEEP delivery apart from
causing local airway injury
Use oxygen analyzer to check the Fi02 when 0 2 therapy is begun,
l
whenever a change in the oxygen now rate is made or a change in
the respiratory status of the neonate has occurred. ,;
14.8.4 How to administer appropriate oxygen concentration?
Air-Oxygen blender )
These mechanically blend pressurized oxygen and arr, and are the ideal
way to provide appropnate delivered Fi01 • 0 2 concentration and flow
rate are set as per the manufacturer's protocol.
Indigenous air-oxygen mixing.
• Mix oxygen and air at pre-decided flow rates using a ·y· piece to
achieve target Fi02 (see Table 14.6)
123

Table 14.5: Comparison of oxyge11 delivery systems

( i02
Landmar
(•/.)
ks for the RFR
(at an Complication Remarks/precautio
Type depth of (Lim
avera s ns
insertion in)
(in ems)
g
RFR)

Nares to Crust mg,


the inner septa! trauma,
~asal ,(1
I -2
2$ - Alternate between
JfL,
cann~
margin of
the
4
erosion,
nares every 12 hJ
J1n9 eyebrow
I
inadvertent
PEEP -
r
~ Alae nasi
Crusting,
septa! trauma,
Nasopharyng Alternate between
to the I-2 4S-60 septa! erosion,
eal cannula nares every 12 h
tragus inadvertent
PEEP

Read the
product
insen for Short, binasal
Crusting,
Nasal prongs selection I -2 25 45 prongs are
erosion
of recommended
appropriate -
orong I
I RFR should be at
least 4 nmes that of
Oxygen hood -- 2-4 30~ --- the - minute
70_..o ventilation. Lesser
-ct
flow rates carry risk
-=-- ofC02 retentiOil-
Incubator 0 2
,- - - -- --
system - 7-v
1-
Note:
• Short binasal prongs are currendy available for 0 2 administration
alone which can be attached to the humidification system to provide
heated and humidified 0 2
• Oxygen hoods are available with occludable port holes in the sides.
Occlusion of these holes increases the 0 2 concentration by
preventing air entrainment. Apprdximate Fi02 delivered:
o With one port hole opened - J0-50%
o With both the port holes opened - 30-40%
o With both port holes closed - 80-90% (at 0 2 flow rate 10-1 5
L/min)
124
Table 14.6: Air and oxygen flow rates required to achieve desired
FiO' l
01 AIR (Umin)
(LI
mi 4 s 6 7 8 9 10
0 I 2 J
o)
0 • 10.8 20.8 20.K 20.8 20.8 20.8 20.~ 20.8 208 20.8

I 100 S'l.S 47 41 38 34 32 30.5 28 21.S 16 5

2 100 74 59 53.S 4M 44 41 JR.S 35.S 34 32

3 100 R2 70 60.5 56 51.5 48 43.S 40.5 39.5 38

4 100 86 74 66 60 51 54 48.S 45 44 42

5 100 88 78 71 66 59 57 53 4Q.5 4R 46

6 100 90 82 74 70 65 59.S 56 H SI 49.S

7 100 92 84.5 77 72.5 68.5 64 60.S 56 54 52


8 100 93 86 71i.5 75 71.5 67 62 59 57 55
9 100 '14.5 87 82 765 73 69.S 64 62 60 57

10 100 % 8X 84 78 75 71 66.5 64 62 60.5

X axis air; Y axis - oxygen

Nasal canula1
Regression equation for estimating nasal cannula Fi02 at flO\\ rates of
I 3Lmm
Approximate Fi0 2= (02 flow x 0. 79) -t- [(0.21 x VF.) (VF .,, 100)]
Note: VE= minute ventilation (TV x RR), 0 2 flow - mL min
TV assumed: 5-6 mL kg; equation directly applicable for infants < 1500 g

Air e11trainers (Fischer-Payke/):


Air entrainers work by the Venturi principle where based on the si7e of
the vent, amount of air entrained into the reservoir changes and thereby
changes the 0 2 concentration. The opening of the vent 1s adjustable and
corresponds to graded markings of Fi02•
14.8.5 Humidification of gases:
Minimum recommended gas temperature at the level of nostrils: 33 °C.
Recommended humidity: at least 33 mg/L of absolute humidity with a
· J
relative humidity of 70- 100%. 3 (See Table 14.7). _,.

14.9 SURFACTANT THERAPY (See PGJMER video on neonatal


procedures):
14.9.l Indications. ~
Prophylactic: Pretenn infants of <28 wks gestation. Administered within
the mitial 15-20 mm of life before the onset of respiratory distress but
definjtely after initial resuscitation and stabilization.4 Although evidence
125

Table 14.7: Commonly available I umidifiers and recommendations·


Stand alone
Feature Cold water
humidifiers RM E/HMEF*
humidifier
(Fischer-Paykel)
Temperature 18-23 36-38 --
Absolute
15-20 42-44 27-36
humidity
60-80% (at
amb ient temp
Relative
humidity
27-30 °C, 100% --
flow 3-8
L/mi n)
Electrical,
Debris
General safety Gas leakage equipment
blockage
damage
Reservoir &
Microbiological Reservoir
safety contamination
circuit --
contamination
•HME/HMEF: heat and moisture ex '.hanger/filter
Note: Stand alone humidifiers shouk be used wherever possible.

from deve~op~d e
countries suggests a cut-off
cosl-effecttve in our set-up.
w~it
/
may nOl be

Early rescue: Preterm infants' :S3" wks of gestation with respiratory


distress. All infants in this group are assumed to have surfactant deficient
lungs as the dominant path~lounlc:ss proven otherwise. Administration
is typically within the initi 2 h] of life filld snould preferably be given
munediately after the onse o 1stre s irrespective of the venti lato~ and
oxygen requirement.5 Administration in pretcrm Infants >34jvks where a
diagnosis of RDS is contemplated mJst be discussed with the consultant
oncall. - -
Late rescue: Administration in ~ preterm infant with established
respi ratory distress who is requiring respiratory support (CPAP O.J MV)
with a Fi01 requirement of> 30?10 . A' ministering the first dose of
late rescue surfactant beyond 24 h of 11fe (e.g. babies referred from
outside) may not be very effective. Discuss with consultant is such
situations.
Repeat dose of s urfactant: Retrcatment with surfactant should be
flexible and determined by the baby' condition. A well infant who is not
ventilated and a ventilated infanti \I ho requires no more than 30-40% .
oxygen, docs not require re-treatm ent. ff a baby who is ventilated
appears to deteriorate having shown improvement after a_prc;,vious dose
of surfactant, early retreatment sho dd be considered and not delayed
126
until a set time period has elapsed. The threshold for retreatment should
be lower m imants ·who have RDS that is complicated by sepsis or
asphyxia. Evidence suggests that no more than 2 doses are generally
required 7 On occasion a third those may be beneficial. _
CXR 1s not a necessary prerequisite for initiatmg early CPAP or for
administration of the first dose of surfactant. Digital palpation of the tip
of the ET tube in the suprastemalnotch is a useful way to assess correct
1
placement. 8 Management around the time of administering surfactant~
shown m Figure 14.3.
14.9.2 Administration of surfactant
• Bring surfactant to room temperature. Technique: Keep vial between
the palms for 8 mm or keep at room temperature for 20 mm. Do not
shake the vial vigorously as this causes bubble formation.
• Cut the ET tube to a length of 13 cm. Intubate and confirm the tube
position climcally. Do not wait for CXR to confirm tube position.
• Measure the length of the ET tube (in a previously intubated infant).)
Total length of the feeding tube to be cut = ET length -. 1.0 cm (for
adapter). --
• Fill the syringe with required quantity of surfactant
• While maintatning the infant in supme position, briefly dtscontmue
the baby from ventilator. Insert the feeding tube and adrnm1ster
surfactant.
• Not more than 2 aliquots of surfactant are required. There 1s no need
to change posit~
• Between the aliquots attacb the baby to the ventilator or hand bai \

J
gently. Look for adequate chest rise & oxygenation "_)
14.9.3 Precautions:
• Do not heat the vial with artificial heating methods
• Do not suction the baby for at least 4 h after administering surfactant

• -
unless indicated by an emergency ...__
Do not leave the baby unattended after the procedure
14.9.4 Failure of response to surfactant: -
• Teclrnica/ flaws:
o ET tube displacement leading to inadvertent admm1stration into
the stomach
o ET tube too high or too low in the trachea
• Alternative pnmary diagnosis
• Complicated HMO: Pneumonia, PDA. sepsis. PPHN, air leak
syndromes (PIE, pneumothorax)
14.9.S Surfactant preparations available in India (as of 2009) (see
section D 120): Shown in Table 14.8
127
Figure 14.3: Algorithm for management around the time of
administering surfactant
Prctcrm mfant wuh re:.pmuory
diotIC"

If early (.'PAP has b.:en tnitmtcd before


Intubate for surfactant. clinically 'wiilctant 1dmim.>trat1on, rcwn the
ch«l ElT pc»ih"n & .ecurc n nasal prong. "hik in1uba1100

Adnunistcr ~urfactant over 3-5 mtn


Hand \cn11latc in between aliquob

\\'atGh for 5-10 min


Short term side ctTccts:
.__dc;atur1t1on.
________ bradycardi1
_, J
1
So d"a1ura11on. bradycardia
Good rcspmuory effort>
Cie«Ulllon >27 wk>
Ye.. Extubate (INSURE). commuc on
i-----~ nasal CPAP. Watch for re'p1ratory
wor-ening
D
'-----r-------' L - - -

Continue on mcdwmcal ,·cntilauon -g


Table 14.8 Surfactant ore >arat1on1 ava1·1 a blem
. I ndi a
Cone. lnlerval
Brand Source Vol. (per
Dosage
between
Max.
(recommended) dose:.
mL) do-c~
II
8 mL
SurV1n ta Bovine lmL 2 100 mg per kg
& 4 6h 2
(Abbot) minced 5ms,1; = 4 mlJkg
ml
200 mg per kg
C urosurf
Porcine lmL 8 (first)·• 2.5 mlJkg
(Nicholas/ l.5mL 12 h 2
minced Omg I 00 mg per lg
\bbot)
$0 ,·(reneatpl .25 mL'ka
I
5 ml
"leosurf BO\IOC lmLe 2 135 mg per lg
& 12 h 2
(Cipla) lavage
3mL 7mg "
l ...
1: (5 mLJkg)
128

14.10 CPAP:
Application of continuous distending pressure throughout the respiratory
J
cycle in a spontaneously breathing infant
14.10.1 Indications of CPAP ~
• Respiratory distress in pretenn neonates~ (early use reduces
mortali~ or oxygen therapy at 28 d even in neonates between 25



28 wks)
Post-cxtubation
,,-

After surfactant administration and extubation to ~SURE "


,-
J
• AOP {see section 13.9)
• Pulmonary edema and pulmonary hemorrhage]
• PDA (sec chapter 30)
• Tracheomalacia and airway instability
• MAS (in selected cases- where hyperinflation does not dominate the
clinical picture)
• PPHN
14.10.2 Devices for administration of CPAP (See PGIMER video on
neonatal procedures, for setting up CPAP circuit)
• Continuou~jlow devices
o Bubble CPAP
o Venulator CPAP
o Indigenous bubble CPAP
Note:
o There are very limited data comparing, head to head. different
types ofCPAP.
o As the CPAP and the Fi02 delivered by indigenous CPAP are
unreliable, application of this method should be for short
durations only. Whenever used, the gas should be heated and
humidified by passmg through a humidifier, and blended either
by a standalone blender or a Y-piece.
o The exact technique of application of different CPAP's is
beyond the scope of this handbook. The reader is referred to the
video demonstration of procedures
• Variable flow devices - Infant flow devices (flow drivers) and
devices using Benveniste valve. Even though variable flow CPAP
devices have been shown to cause less airway pressure fluctuations
and resultant physiological changes, evidence 1s still lacking to
recommend one over the other. Currently a CPAP device using a
Benveniste valve 1s also used in our unit.
14.10.3 Types of patient interfaces:
The following CPAP interfaces should be used in decreasing order of
preference
• Short bi-nasal prongs
o Fisher Paykel, Hudson, Argyle
129

• Single nasop/1aryngea/ prongs


o For all practical purposes, this 1s an ET tube inserted through
one nostril, up to the nasopl arynx.
For selecting appropriate sizes of m.sal CPAP prongs see Table 14.9. It
has been observed that the sizes recommended by Hudson turn out to be
slightly larger for Indian babies at .he lower end of the corresponding
weight range.

Table 14.9 Appropriate nasaJ CPAP prong sizes


A) Fisher Paykel
Nasal pron2 No. Diameter of nares Width of septum
BC3020- I 0 3020 IO/bx 3.0mm 2.0mm
BC3520-l 0 3520 IO/bx 3.5mrn 2.0mm
BC4030- I 0 4030 IO/bx 4.0mm 3.0mm
BC4540-10 4540 IO/bx 4.5mm 4.0mm
BC5040- I 0 5040 I 0/bx 5.0mm 4.0mm
BC5050-10 5050 IO/bx 5.0mm l 5.0mm
BC5550-I 0 5550 I Olbx 5.5mrn 5.0mrn
BC5560-10 5560 IO/bx 5.5mrn 6.0mm
BC6060- I 0 6060 I 0/bx 6.0mm 6.0m.rn
BC6070- I 0 6070 IO/bx 6.0mm 7.0mm
BC6570-10 6570 IO/bx 6.5mm 7.0mrn
I
B) Hudson
Cannula System Set Cat.
Weight range
size Cat. 1'o. No.
<700 g 0 1683 1690
700- 1250 g I 1685 1690
1250- 2000 g 2 1686 1691
2000- 3000 g 3 1687 1692
>3000 g 4 1688 1693

C) Arl!Vle
Size Equivalent to Hudson size
Extra small Outer diam <Hudson 0 size
Small I
Large 3 l
14.10.4 How to start CPAP:
• lnitial pressure: Level of CPAP should be individualized to the
baby's disease. As a general guideline start CPAP at:
o Lung disease: 5 6 ems H20
o Central problems (apnea): 4 ;ms ~
.1 ,
1
7
130

• Initial Fi02: Depending upon the oxygenation status. As a rule of


thumb, the Fi02 requirement should go hand in hand with the
distending pressure (e.g. 30-40% at 4 ems H20. 40-50% at 5 ems
H10 and so on)
14.10.5 Titration ofCPAP: Shown in Figure 14.4

Figure 14.4 Titration of CPAP

Start on CPAP

Evaluate after 20 minutes


• Evaluate chest mnauon
~
• Blood g3\ analysL~

!
Feature• of uodcrinfla11on
• Per;1Stent. wol"\Cned
w 'or grunt
retra<llOrt>
l
Features of adequate
inflation
,..__ _ _ _ _ ____.
l
Features of ovcrinOation
• Chest wall bypennOauon
- .....,

• High to high nonnal PaC01


• Low to low normal oxygenation "'1th w11bout lov. o•ygcnetion
v.uh / without PaC01>45 mmllg • C\R - hypcnnOauon [./
• CXR low volume I collapse

l
lncrea<c CPAP b> I cm 11,0
l D
Dccrc:bt CPAP by I cm 1120
incmncnL' decrements

Watch for clinical improvement


Repeat ABG (as ~hnically tnd1cated)

Improved

\1cchan1cally ventilate .--C-on_L_m-uc_as_·_pc_r...:c-hn-ic_a_Ii-nd-1-ca-tio_n_,l " \

Vote: CXR give:. a good indication of adequacy ofCPAP. Management doe~ nol depend on
CXR alone as it ma} not always be a\'ailable.

14.10.6 Judging the adequacy ofCPAP:


• Disappearance of grunt and intercostal retractions
• Infant should look comfortable with good chest excursions
• Reduction in Fi02 requirement
• Normalization of Pa02 and PaC02 in blood gas
• CXR normal lung expansion
131

14.10.7 Precautions while admioistc~iog CPAP:


• Watch for any nasal skin blanchi1 g while adrninistcnng CPAP. Also
inspect if there is a crease fo med at the dorsum of the nose
suggesting excessively pinched up narcs after CPAP prongs
application.
• Insert an OG tube immediately ard keep the end open to decompress
the stomach. This helps in avoic.ing the risk of gastric distension,
which can hamper ventilation due to diaphragmalte comprc~nd
may also lead to Oa'iigerffiiScompl cations like gastnc perforation.
• Watch for signs of over distension like signs of mndequat;zard1ac
output. -
• Try positioning the neonate prC¥te and with the neonate's hand
tucked under the chin to help kct!p the mouth closed~ Use of roll
under the neck or under the chc t may also facilitate keeping the
airway patent, thus allowing the pressure to reach the lungs.
• Use of comfort measures, such a. swaddling, and decreasing;; l'ght
and noise stimulation. will aid w th keepmg the nasal CPAP from
being displaced from excessive m vement.
• Local irritation due to patient i terface may lead to septa! and
mucosa! dama~ Remove the m erface every ~hiTe prO\ idc
supplemental blow by oxygen for 1eonatcs receiving more than~q_
inspired Fi02 while on nasal CPAI>. Inspect the narcs for asymmetry
and crusts. -
• Suction each nostril gently with a soft cal cter 1 the exterior narc.
Do not insert suction catheter m"°e than 5 mm · n each narc. This
frequency may be reduced in cute ventila on where loss of
distending pressure is a concern. It the suction catheter does not pass
easi ly past the narcs there could be nasal stcnosis. -
• If narcs show Visible crusts, remo\e them with saline soaked gauze,
apply NS drops and reapply the intt'rface every 6 hourly. )
14.10.8 Weaning from CPAP:
As a general guideline. CPAP can be removed, if the following are
satisfied.

1
• CPAP: 5 ems 11 20 (or 4 ems, in case ofapnea) at an Fi02 :5 30%
• Clinically stable .;lo ,_ ~ ...
• Good respiratory efforts
• Apnea and bradycardia free in the rrevious 24 h

14.11 NIPPY:
N IPPV provides IPPV via a nasal or nasopharyngeal interface device. If
a ventilator is available, NIPPV is preferred over CPAP for the 3
indications mentioned bcloW.--- -=-
14.11.1 Indications
132

• Early NIPPV as a primary mode for RDS in preterm babies in place


of early CPAP. The superiority of N IPPV over early CPAP is
particular apparent in those who do not receive surfactant and those
$30 wks gestation. rn -
1
• Post extubation mode. ]
12
• AOP.
14.1 J.2 Initial settings:
Primary mode in RDS:
• Peak inspiratory pressure (PIP): 15-16 cm ofH20
• Peck end expiratory pressure (PEEP): 5 cm ofH 20
• Ti: 0.3- 0.35 s.
• Fi02 : Adjusted to maintain normal oxygenation
• Flow: 6-7 L/min
Post-extubation: Keep NIPPV rate the same as the lMV rate before
extubation. Increase PIP by 2 to 4 cqi H20 but start at PEEP of :55 cm
H20; adjust Fi02 to maintain oxygen saturations al 87% to 93% on pulse
oximetry.
AOP: PIP 14-15 cm H 20, PEEP :55 cm H 20, Rates 20-30/min, Fi02 -
21%
14.11.3 Adjustment of NIPPY settings are done according to the
c linical and blood gas parameters to keep them within normal limits.
14.11.4 Failure of NIPPY:
Presence I worsening of respiratory distress and I or hypoxemia (Pa0 2
<50 mml lg) at a PIP of 26 cm H20 (24 in ELBW infants), PEEP of 6,
Frequency of60/ min and Fi02 of>60-70%
14.11.S Weaning of NIPPY:
While weaning from N IPPY, the setti ngs are tapered to PfP of 14, PEEP
of 5, rates of 30 and Fi02 <30% before removal. Infants <2 kg may be
given a trial of nCP AP for few hours before removal.

14.12 INVASIVE VENTILATION (See PGIMER video on neonatal


procedures, for setting up ventilator circuit):
The oro-tracheal route of intubation is preferred because of the ease of
lhe procedure.
14.12.1 Indications: see lower portion of figure 14.2
14.12.2 Initiation of mechanical ventilation: Shown in Figure 14.5
133

Figure 14.S Initiation of mechanical \'entilation

Intubate, check tube poo1tion. Atn:p1ne 20 µg.\g u\a I mm+ fentanyl 2 µg.lg
SC..'Ul'e anJ documem O\~ ~ aun (or I\' morphine 0.1 mg kg a. a •lo"'
bol'1-~) JO minutes pnor to intubation (except in
INSURE technique)
\fanuall> 'cnt1late to achie•e
adequate chc-t r1>e & detennme
the appropriate PIP

Set the PEliP auording to the dlsea)e patlrolog)'


• Stiff lung (HMO) S cm H10
• Palchy atclcctasts (pneumonia, MAS) · 4 cm 11,C
• Ml\S with hypcnnfla11on, apnca: 3 cm H,O
Set F/01 according ttJ tire Attnch to tc't lung check for
• PEEP rcqu1rcment (rule oftbumb{!f.EP • FiO ventilator funcuon
• O•ygen •aturat1on (117-93'10)
Set 1·entifator rate: '0-60 bpm
• Stiff Jung, low time co~tant . 60 bpm
• Air trapping (MAS): 40 bpm
'111/nt11in /:£ r11tio: 1:1

Ob>erve lnf11nrfor
• Chest "all mo\emc:nt - adeqwq
• lnterca,,tal rctract1on' - presence I worsening I
ab.cnce
• Inflation of the chest - signs ofo•erinflation
• Chmcal C)11""'L>
lfotch the monitor for
• Saturauon t;irgct M7-93'9
• lleart rate tachyciltd1a (fighting neonate),
bradycardta (hypoxia)
A u1cultate for
• Breath ;0und> (ad«juaC) & S)~try)
• Added sound~ (rhonch1 airway spasm)

Chc't rise inadequate Persistence ofrc1ract10~

Jn.;rcase PIP by 1-2 cm 11,0


e\ay 2 minutes till adequate
\Cnt1lation u; e.tablt>hcd lncrcas< PEF.P by I cm 11,0

Oxygenation u; madcquate

lncrca>e Fi(), by 5°'. increments 1111 Place arterial line (if not done>.
saturation is nonnalizcd Draw bk>ud for ASG
134

14.12.3 Assessment of ET tube position


Clinical
• Direct visualization (while intubation)
• Air entry (BIL axilla) with absence I reduced air entry in the
epigastrium
• Improvement in HR & Sp02.
• Formation of mist in the ET tube
• Digital palpation of tip of ET tube in suprasternal notch while
intubating. This method is unreliable in an already intubated baby.8
No11-c/i11ical
• CXR: Tip of ET tube 1.5 - 2 ems above carina or a l T2 - T3 level.
0
14.12.4 Modes of mechanical ventilation: Shown in Table 14.10

Table 14 10 Common modes of mechanical ventilation


Mode Features Indications Remarks
SIMV lnspiration of • Primary and It is the
(available in baby weaning preferred
Drager, Bird, synchronized to mode of default mode in
Puritan ventilator breath ventilation theNICU
Bennett. and allows • Asynchrony
Sophie) spontaneous on
breathing conventional
between ventilations
mechanical despite
ventilations sedatives

Assist control Infants triggers • Primary and Enables patient


(A/C) ventilator to weaning mode to be ventilated
(available in cycle with each of ventilation al low pressures
Drager, Bird, breath • Asynchrony
Puritan on
Bennell, conventional
Sophie) ventilations
despite
sedatives
Volume Hybrid mode- Not yet Advantage -
assured breath begins in established Ensures
pressure pressure-I imited delivery of al
support mode but if set least set amount
(VAPS) tida l (volume of volume
not reached, it Disadvantage -
converts to a No auto-
tlow-cvcled weaning of
135

Mode Features I 1dications Remarks


mode by pro- pressures
longing the Ti

Pressure Volume control Not yet Allows control -~


regulated -with upper limit e tablished. of PIP to avoid _ i.-

volume for PIP. Adjusts L.send in PIE barotraumas


control PIP (up to 5 cm Following
( PRVC) H20 below max snrfactant iN(j)
limit) to target a•lmmistratton.
set volume Conditions
based on re-quiring high -
previous breath P~EP -
It presence of -
bronchosoasm ·
Pressure PS provides an • Weaning from Requires
support inspiratory ventilation reliable
ventilation pressure boost after respiratoi
(PSV) during improvement effort
(available in spontaneous m lung
Bird, Puritan breathing to pathology
Bennett. overcome the • Weaning from
Sophie) imposed work long tenn
of breathing. ventilation
• Weaning of
infants with
BPDTo
promote
respiratory
muscle
training
Volume Target TV and • Useful in • No more than
guarantee
(VG)
I pressure limits
set inspiratory
situations of
rapidly
130°,,o ofTV
delivered
(not available and expiratory changing lung • Better than
in any of our flows measured dynamics. PRVCas in
ventilators at ET level • Able to adjust PRVC
I
currently) Adjusts PlP for ET leak. volume
until set target changes m measurement
TV reached. lung & circuit is at exp side
dynamics and not at
• Allows auto- wyc piece as
weaning in VG
136

14.12.5 Typical initial settings for common diseases requiring


ventilation: Shown in Table 14.11

Table 14.11 Initial settings for various respiratory diseases

VR
PIP PEEP Flow
Disease Ti (s) (per
(cm H20) (cmH 20) (L/min)
min)
HMD 16 - 18 5-6 0.3-0.35 60 7-8
Pneumonia 14- 16 3-4 0.35-0.4 50-60 6-8
MAS 14- 16 3-4 0.35-0.4 40-50 5-7
Apnea 12 -14 3 0.35 20-30 5-6
Air leak 14 - 16 3 0.3-0.35 60 5-6
BPD 15-20 4-5 0.4-0.7 20-40 5-6

14.12.6 Adjustment of ventilator settings according to ABGs:


• Oxygenation depends on MAP and oxygen concentration (Fi0 2). A
decision of increasing the MAP to normalize the oxygenation may
be an acceptable alternative to increasing Fi0 2
MAP is given by the formula:
MAP~ [k* (PIP x Ti)+ (PEEP x Te)] I Ti+ Te
*'k' is a constant that depends on the flow rate and the type of
waveform generated. Generally, 'k' is 'l' for a square wave and
approximately '0.8' for a sine wave
• PEEP has the maximum influence on MAP. But before increasing
PEEP, the underlying disease process for which ventilation has been
initiated has to be considered
• Ventilation depends on the driving pressure ( "- P), which is the
difference between PIP and PEEP. TV is dependent on the "- P.
• PaC02 is inversely proportional to the minute ventilation, which is
given by the product of TV and ventilator rate.
14.12.7 Recommended adjustments in ventilator settings based on
blood gases and clinical examination: shown in Table 14.12
137

Table 14.12 Recommended adjustments in ventilator settings based


on blood as.
Pa0 2 Paco, Possible change Remarks
(mmHg) (mmHg)

<50 normal • j Fi02 in 3-5% PEEP change may be


increments considered if associated
• j PEEP by I cm chest retractions are
H20 observed
<50 >50 • i PIP (by 1-2 Consider i Fi02
cmH20) appropriate for PEEP
• j PEEP (if chest
retractions+~
<50 <40 • i Fi02 in 3-5% PAH may present with
increments purely oxygenation
difficulty; do not
hvnerventilate
50-80 >50 •
i ventilator rates PIP change may be
(by 5-10) considered if Pa0 2 is low

j PEEP (if chest normal
retractions +)
50-80 <40 L PIP by 1-2 ems
• Consider Lrates if Pa0 2
H20 is low normal as change
Lventilator rates
• in PIP will L MAP
(by 5-10)
>80 <40 •
L Fi02 in 3-S% Consider weaning at this
decrements point
• L PIP by 1 - 2 ems
H 20
PAH - pulmonary artery hypertens10n (persistent or secondary)
Note:
• Always compare the blood gas parameters with the previous gases to identify a trend.
A normal blood gas may still show a trend which may help in further management.
• Changes in Fi02 (especially while weaning) may be done by monitoring the SpO:i
alone provided the ventilation is adequate
• HypOcarbia of less than 30 mmHg has been shown to be associated with PVL and a
poor long term neurodevelopmental outcome. Hence, target a low nonnal TV (- 4-5
mUkg) to avoid over ventilation
• In stiff lung (due to HMD), PEEP can be increased up to 7 ems H 20, keeping the
driving pressure (.AP) constant to maintain a TV of 4-5 mUkg. To achieve this,
simultaneous manipulation of PIP and PEEP may be necessary. This is based on the
accumulating evidence that atelectotrauma is the prime culprit in illllg injury.

14.12.8 Weaning of a baby from mechanical ventilation:


Weaning is the process of gradual, measured reduction of ventilator
settings to a minimum point at whi~h risk of ventilator induced lung
138

injury is the least and from where the infant can be safely taken off
ventilator support. This depends on the underlying disease for which the
infant was ventilated and the mode of ventilation from which he/she has
to be weaned off
14.12.9 Prerequisites for weaning from acute ventilation (up to 7 d of
ventilation):
• Clinically & hemodynamically stable
• Effective respiratory efforts
• Basic lung pathology I disease improving
• Associated illnesses are improving (e.g. active PDA)
• Optimum blood gases
• Complications due to ventilation are taken care of (air leak, collapse
etc.)
14.12.10 Prerequisites for weaning from chronic ventilation(> 7 d of
ventilation):
• All the above features for acute ventilation, plus
• Adequate and consistent Wt gain (over the last 5 d)
• Normal serum electrolytes (especially potassium)
• Acceptable blood Hb I PCV levels (PCV > 35%) (see section 17.6)
14.12.11 General principles of weaning:
• Decrease the most potentially harmful parameters first (PIP & Fi0 2)
• Limit changes to one parameter at a time
• Avoid changes ofa large magnitude
• Document the infant's response to each change in the ventilation
chart
14.12.12 Weaning from A IC mode:
• In NC mode, all the infant breaths are supported with the preset PIP
and hence weaning is different with this mode
• Weaning is done by reduction in the PIP and Fi0 2. As all the breaths
are supported, reduction in the ventilator rates will have no effect as
long as the spontaneous rates arc more than the control rate. As the
underlying disease process improves, spontaneous rates reduce,
thereby reducing the ventilator rates (auto weaning of the ventilator
rates)
• Alternatively, dependency on the ventilator breaths can be reduced
by decreasing the sensitivity of the trigger sensitivity function (assist
sensitivity in VIP-BIRD). This may help in the conditioning of
respiratory musculature
• While weaning, be careful to provide adequate TV, as the infant may
increase his/her RR to increase the minute ventilation which can lead
to autotriggering
14.12.13 Weaning from (S)IMV mode: Shown in Figure 14.6
139

Figure 14.6 Weaning from SIMV mode


May! by 2 ems H 20 if PaC02 <35
I Decrease PIP (by 1 cm Repeat ABG after 20 min of every 2
H20 till 20 cm H 20) small changes or I major change
Caution: SP02 may drop as PIP is !
I
Decrease Fi02 by 3-5o/o decrements
and rates by 5 to reach 40% of Fi02
and 40 bpm

I
Reduce PIP, PEEP and Fi02 by Minimum PIP:
alternating each other to reach 12- • <IOOOg-12
1613130% • I000-2000g- 14
• PIP by 1-2 cm H20 each time • >2000 g-16
• PEEP by 1cm H20 each time r-----+ Minimum PEEP
• Fi02 by 5o/o • <1500g-3
Correspondingly! rates by 5 till 30 • >1500 g- 4

I
I EXTUBATE I
Alternatively:
• At low rates (20-30), SIMV can be
combined with pressure support
(PSv)
• PSV provides moderate support to
the SIMV unsupported patient
breaths and thereby helps in
reduction of work of breathing

14.13 HIGH FREQUENCY VENTILATION:


High frequency ventilators deliver breath rates between 6 to 60 Hz
(1Hz=60 breaths per min). They deliver very small TVs equal to or even
lesser than the anatomical dead space. In our unit. the Sophie and some
of the Drager ventilators have HFOV facility.
14.13.1 Indications:
Traditionally HFOV has been used as rescue therapy where conventional
mechanical ventilation has failed or the baby has developed
complications, such as air leaks, due to conventional ventilation,
although evidence from controlled trials is lacking.
The recent Cochrane update 2009 13 reports that elective HFOV in
preterm infants with RDS results in reduction of BPD among survivors
of borderline significance. Subgroups of trials showed a significant
reduction in BPD with HFOV when no surfactant was used. Pulmonary
air leaks occurred more frequently in the HFOV group. There is no data
from RCTs supporting the use of rescue HFOV in term or near term
infants with severe pulmonary dysfunction.
140

The following are some pragmatic indications of rescue HFOV:


• Persistent hypercarbia (>55 mm Hg) during acute stages of
ventilation (initial 3 d of life), in spite ofa high MAP (:o>IO ems H20)
• Presence of a pulmonary air leak [typically a PIE and
pneumothorax]
• PPHN requiring high settings: HFOV reduces the risk of
volutrauma.
14.13.2 Parameters in high-frequency ventilation
• MAP: MAP is directly proportional to the oxygenation and is the
most important parameter to titrate to take care of Pa0 2 . MAP is set
using the PEEP knob in many ventilators.
• Amplitude: Depth of oscillations around the MAP (expressed
variably; expressed in % in Drager 8000 plus and Sophie). It
primarily affects the ventilation (PaC0 2). Ranges from 0-100% and
is adjusted to get vibrations visible up to the umbilicus.
• Frequency: Number of oscillations per min. Expressed in Hertz (Hz)
where I Hz~ 60 breaths per min.
• Non-modifiable parameters: Ti, and gas flow rate
14.13.3 Initiation and titration of HFOV Operator selectable
parameters: MAP, amplitude, frequency, and Fi0 2 ; apart from these, all
the other parameters are generally pre-decided by the manufacturer
• Initial settings:
o MAP: 2 cm H20 greater than that in IMV (to enhance alveolar
recruitment).
o Frequency: 8-10 Hz (480-600 breaths/min). 10 Hz is
recommended for ELBW babies (<1000 g) and those babies
with severe RDS whereas 8-9 Hz for more mature babies
o Amplitude: Decided based on the adequacy of chest vibrations;
if adequate- should be visible up till the umbilicus
o Fi0 2: Same as that of!MV
• Titration:
o MAP: Chest inflation assessed clinically and by X-ray chest (8
posterior ribs), oxygenation assessed by Pa0 2 and I or Sp02
o Amplitude: Based on chest wall oscillations, and PaC0 2
o Fi0 2 : Based on oxygenation assessed by Pa0 2 and/or Sp0 2
o Frequency: Generally not changed during the weaning process
14.13.3 General guidelines for HFV:
• Increments I decrements in MAP should not be > 1 ems H 20 at a
time
• Avoid ET suctioning as far as possible while baby is on HFOV.
Detaching from the ventilator during suctioning leads to rapid
alveolar de-recruitment. Re-recruitment in HFOV takes a long time
due to very low TVs delivered in HFOV.
141

• CXR: Send call for CXR one<: the decision for starting HFOV is
taken. A check CXR immed 1ately after initiation of HFOV is
essential to know the adequacy of chest inflation. Further CXR's are
warranted in 4-6 hourly interv.ols until the optimal MAP has been
identified
• ABG: Every 2 h during the acute I titration phase; 4-6 hourly and
'SOS' once stabilized
• Spontaneous breathing should be encouraged even on HFOV.
Hence, routine sedation and neuromuscular paralysis is not
indicated. Nevertheless a fighting baby on a HFOV may make the
HFOV inefficient and hence may require sedation. Decide after
discussion with the consultant
14.13.4 Weaning and extubation from HFOV:
• Start weaning Fi0 2 first. Once Fi02 reaches 0.6, then reduce MAP in
I cm H20 decrements
• Reduce amplitude in 5% decrements simultaneously with MAP
based on the PaC0 2 and chest oscillations.
• Frequency is usually not adjusted during the weaning process
• Bigger babies whose lung pathology has resolved may be directly
extubated to a non-invasive mode of ventilation or even to hood
oxygen. A recent study showed that extubation of preterm infants at
MAP below 8 cm H 20 with an Fi0 2 below 0.30 is feasible during
HFOV, with a 90% success rate", showing that direct extubation can
also be done in preterm infants.
• Typical settings from which HFV can be discontinued:
o MAP 7-8 ems H20
o Amplitude 25-30%
o Fi0 2 25-30%

14.14 EXTUBATION AND POST-EXTUBATION CARE:


Extubation is the final end point of the weaning process. It depends on
the natural h/o the disease, gestation and Wt of the infant and associated
complications (air leak, PDA etc)
14.14.1 Plan fOr extubation (from any mode):
• Anticipate and plan extubation at least 2-3 d in advance
• Taper and discontinue morphine at least 12 h prior to the planned
extubation. Tapering may not be required if morphine is given for a
period of <3 d
• Check for spontaneous respiratory efforts. Trial of ET CPAP prior to
extubation to assess the respiratory efforts is not recommended due
to the risk of increased work of breathing and subsequent failure of
extubation. Alternately, ET CP AP can be combined pressure support
(PS) to allow spontaneous breathing with minimized resistance due
to the ET tube
142

• Stop feeds 6 h prior to extubation. Aspirate all the gastric contents


to prevent aspiration
• Adjunctive therapies:
o Methy/xanthines 15 (see sections D7, Dl23)
• Target group: VLBW babies. Among them, the maximum
benefit is likely to been in ELBW babies who are less than
I wk old.
• Administration: Aminophylline IV 5 mg/kg loading
followed by 1.5 mg/kg IV every 8 hourly with the first dose
at least 8 h prior to a planned extubation attempt; total
duration - 48 h (6 doses); or caffeine 20 mg/kg IV 8 h prior
to planned extubation followed by 5 mg/kg oral OD for
total 48 h.
16
o Peri-extubation systemic steroids
• Target group: Infants with repeated attempts for intubation;
traumatic intubation; prolonged intubation (> 14 d); infants
with stridor following extubation
• Administration: Dexamethasone IV 0.25 mg/kg for three
doses administered at 8 hourly interval with the first dose at
least 8 h before planned extubation attempt. (see section
D39)
o Respiratory support:
• Babies weighing ;>2000 g: Extubate directly to room air or
hood oxygen (depending on the oxygen requirement).
Rescue CP AP could be used in these babies in case of
respiratory distress after extubation.
• Babies weighing <2000 g may be extubated electively to
non-invasive ventilation. Lighter babies (e.g. < 1250 g) are
likely to be benefited more than heavier babies. Non-
invasive support decreases the risk of extubation failures at
<14 d of age, but its efficacy beyond 14 dis unproven.
• Post-extubation support: NIPPY is preferred over nasal
10
CPAP. Non invasive ventilation is continued for 24 h post
extubation before removal (see earlier section on CP AP for
removal criteria).
o Peri-extubation chest physiotherapy 17: Elective chest
physiotherapy is not recommended in the peri-extubation period
in mechanically ventilated infants as it has not been found to
reduce the risk of post extubation collapses. Active chest
physiotherapy may be useful in case of:
• Segmental or lobar collapse
• Infant with BPD or cystic fibrosis
• Viscous secretions that does not drain out with routine
suctioning
143

• Check ABG parameters on the pre-weaning ventilator support (see


section 10.5)
• Do gentle ET and oral suctionin.~just prior to extubation
• Technique of removal of the ET tube:
o Continue PPV while pull in~ the tube
o Pull the ET tube while giving a positive pressure breath with an
inspiratory hold if feasible (this reduces the risk of post
extubation collapse)
14.14.2 Post-extubation care:
• Risk of extubation failure is very high in the first 6 h from
extubation. Hence, close monitoring is mandatory. The following
precautions help to reduce post-extubation collapse:
o Oxygen administered should be adequately heated and
humidified by passing it through a stand-alone humidifier.
o Prone positioning: This improves diaphragmatic excursions
o Change of position every 4-6 hourly and adequate clearance of
airways (suctioning) aids successful extubation
o Avoid feeding for up to 6 h following extubation. The duration
may be decreased in stable babies or those with chronic
conditions (e.g. BPD).
• Watch/or the following signs:
o Evidence of upper airway obstruction (stridor, suprasternal I
supraclavicular retractions)
o Evidence of parenchymal involvement (tachypnea, intercostal
retractions, j Fi0 2 requirement)
o Evidence of poor respiratory drive (apnea etc.)
• Postextubation stridor: This is usually due to sub-glottic edema and
is often associated with repeated or traumatic intubations. A short
course of IV dexamethasone may be helpful (see section 14.14.1).
There are no suitable RCT s evaluating nebulized racemic
epinephrine in newborns during the post extubation period. 18 It must
not be used as a routine prophylaxis after extubation. It may be
considered- after discussing with the consultant- if stridor develops.
• Routine postextubation CXR is not warranted. CXR should be done
only if child shows clinical deterioration.
14.14.3 Procedure of chest physiotherapy (see PGJMER video on
procedures in neonatology):
• Identify the area to be drained based on the X-ray (antero-posterior
& lateral views).
• Position the infant for drainage as per standard recommendations
(refer video). Start percussing and move towards the major bronchi.
Avoid percussion babies less than 32 wks gestation. In infants <32
wks, gentle vibratory movements of 2 fingers placed together should
suffice.
144

• Chest wall vibrators are not recommended as the complication rate is


very high. Instead, tooth brush vibrators may be used in difficult
cases
• Postural drainage, particularly head down position, is not
recommended in preterm infants due to unknown effects on cerebral
blood flow and autoregulation
• A void physiotherapy in the immediate postfeed period. -
14.14.4 ET suction (for detailed demonstration refer to PGIMER video
on procedures in neonatology):
Routine suctioning should not be practiced when there is no clinical
indication
• Suction pressure should be <! 00 mmHg. Do suctioning while
withdrawing
• Note the infant's HR, RR and 0 2 saturation values in the monitor
• Increase the Fi0 2 5-10% above the baby's current level 5 min before
procedure.
• Record type and amount of secretions and baby's response to
suction.

14.15 PPHN:
PPHN is dealt with as a special case because it poses many peculiar
challenges. It is characterized by persistent elevation of the PVR at birth.
It mimics the fetal circulation with suprasystemic pulmonary pressures
and right to left shunting through foramen ovale and I or PDA.
Pulmonary artery hypertension secondary to various systemic illnesses
like sepsis and pneumonia occurring beyond the transitional period of life
are not classified under PPHN; rather they are rightly termed as
secondary pulmonary artery hypertension (PAH)
14.15.1 Diagnosis:
• Clinical setting: A typical clinical setting is in a term/post-term
neonate born through MSL and is asphyxiated. Nevertheless, PPHN
should be a differential diagnosis in all centrally cyanotic neonates
irrespective of GA
• Physical examination:
o Prominent precordial impulse
o Single or a narrowly split and accentuated second heart sound
o Systolic murmur consistent with TR
• ABG: Simultaneous prcductal-postductal gradient of Pa0 2 of at least
20 mm Hg in the absence of a structural heart disease (Preductal-
right UL; postductal: LL)
• Pulse oximetry: Preductal-postductal Sp02 gradient of~ I 0% in the
absence of a structural heart disease
Note: Pa0 2 and Sp0 2 gradient is observed due to ductal right to left
shunting of blood. Absence of ductal shunting does not rule out PPHN as
145

in a sizeable number of babies, sh mting occur only at the level of the


foramen ovale
• Echocardiography:
This is the diagnostic investigation of choice and mandatory in all
centrally cyanotic infants espe<ially so where a diagnosis of PPHN
is suspected. The findings are: dilated RA and RV, flat inter-
ventricular septum, paradoxical septa! motion and TR. More specific
features are as below:
o Major criteria:
• Peak velocity of TR (mis). Normal TR velocity up to 4 mis.
Peak RV to right atrium pressure drop (mmHg). This is
determined using the modified Bernoulli's equation [p=4v 2;
p=pressure drop (mmHg), v=velocity (mis)]. Normal RV
pressure = 4v 2 + RA pressure (5-10 mm Hg). This
parameter has an excellent repeatability and accuracy.
o Ductal flow velocity (mis) & quantification of the direction of
shunt. Normal ductal flow velocity changes 0 - 3.5 mis.
• Hyperoxia +/-hyperventilation test (see section 28.5.2)
• ECG: Features ofRVH and 'p' pulinonale
14.15.2 Management of PPHN: Shown in Figure 14.7
• Avoid the following:
o Excessive handling. Cluster all activities together wherever
possible
o Noise (bedside discussions, alarms)
o Bright over head light.
o Temperature disturbances (hypo I hyperthermia)
o Metabolic abnormalities: H)poglycemia, hypocalcemia
o Hematologic abnormalities: Polycythcmia, anemia
o Metabolic acidosis: Correct the inciting factors causing
metabolic acidosis to maintain pH ?:}.25. Routine metabolic
alkalinization (with sodium bicarbonate) is not recommended
due to associated side effects.
o Agitation/ pain. Start morphine infusion 10-20 µg/kg/hour to
block the stress induced catecholamine release and resultant
increase in PVR. Paralysis may be considered but is not
recommended routinely. (see sections 086, 096, Dl 30)
• Administer supplemental oxygen to keep Pa02 in high normal range.
• Hemodynamic support
o Target a mean arterial pressure of 45-50 mm Hg
o Volume expansion with 0.9~0 NS if associated shock is present.
Refractory cases may require inotropic support
o Dopamine >I 0 µg/kg/min and epinephrine >0.5 µg/kg/min may
paradoxically increase the PVR as they arc not systemic
circulation specific.
146

• Ventilator support
o ~to create respiratory alkalosis (PaC0 2 <30
• mmHfil. is not recommended due to associa~
b3rotrauma as well as long term adverse effects due to
hypocarbia (poor neurodevelopment and hearing defects in term
infants)
• Si/denajil citrate: Start sildenafil if the strategies mentioned above
fail. 1 m_g!kg/dose evei:y 6 h; increase to]. mg_lk_gidnse every 6 h if
no improvement i~ Two smalt RCT's from resource
limited settings, in term and near term babies~at sildenafil
significantly increased oxygenation" (see section DI 14)
• iNO (see c ap er 5).
147
Figure 14.7: Management algorith o for PPHN

Suspected PPH " Confinn the diagno is by


Echocardiography

Monitor oximeter 02 satura ion both pre


& post ductal concurrently

Stan I OO"o Fi02 & titrate blsed on Sp02

Fcorrect hypothermia, hyp<>glycemia,


~ polycythemia, and hypocalcem1a

Check blood gas for a; 1dosjs

Intubate and mechanically ventilate ( fpre & post ductally


bypoxemic despite I 00% Fi01 - - -

Ven ti la ti on strategy Pulmonary specific therapy

l'ion-aggressi\e \enlllatioo
Targets:





pH 2:7.25
Pa01: 50-70 mm Hg
PaCOi: 40-60 mm Hg
Rates : 40-60 breaths/min
PTP : Adequate chest rise
J Eligible for iNO

• Ti . 0.4-0.45 s Administer as
per 1\:i.Q_
protocol

High-frequency
(ifCMV fails)
ventilation~ No rei.por se by the next 12@ (ChaptCi'T5)

Options a' rlable (efficacy less promising):


a) I. V. t. agnesrum sulphate (if no
hypottnsion) 200 mg/kg loading
dose, followed by 20-50 mg. kg'h
b) lnfusu,m Mrlnnone (see section 085)
148

REFERENCES:
1. National Neonatology Forum of India. National Neonatal Perinatal
Database - Report for 2002-2003.
2. Finer NN. Pediatr Pulmonol. 1996;21 :48.
3. International Organization for Standardization. Respiratory tract
humidifiers for medical use -- Particular requirements for respiratory
humidification systems. ISO 8185, 2007.
4. Soll RF. Cochrane Database Syst Rev. 2001
5. Yost CC. Cochrane Database Syst Rev. 2000.
6. Stevens TP. Cochrane Database Syst Rev. 2007.
7. Soll R. Cochrane Database Syst Rev. 2009.
8. Ashwin S.MD Thesis. 2009
9. Morley CJ. N Engl J Med. 2008;358:700.
10. Sai Sunil Kishore M. Acta Paediatr. 2009; 98:1412.
11. Davis PG. Cochrane Database Syst Rev. 200 I.
12. Lemyre B. Cochrane Database Syst Rev. 2002.
13. Cools F. Cochrane Database Syst Rev. 2009.
14. van Velzen A. Pediatr Crit Care Med. 2009; I 0:71.
15. Henderson-Smart DJ. Cochrane Database Syst Rev. 2001.
16. Davis PG. Cochrane Database Syst Rev. 2001.
17. Flenady VJ. Cochrane Database Syst Rev. 2002.
18. Davies MW. Cochrane Database Syst Rev. 2002.
19. Shah PS. Cochrane Database Syst Rev. 2007.
149

15. INHALED NITRIC OXIDE

Inhaled nitric oxide (iNO) is a sele•.:tive pulmonary vasodilator used in


m~nagement of term and near term neonates with hypoxemic respiratory
failure and PPHN (see section 14.15).

JS.I WHOM TO TREAT 1


Candidates satisfying all the following criteria are eligible
• GA 2>34 wks
• <: 14 d of postnatal age •
• On mechanical ventilation
• Hypoxemic respiratory failure (Pa02 <50 mm Hg on Fi0 2 of 1.0
with PaC02 <50 mm Hg)
• Post ductal 01'2>25
• Clinical and/or Echocardiographic evidence of PPHN (see section
14.15. l)
*Discuss with consultant in charge in case of babies with postnatal age>
14 d or gestation <34
• OI ~(MAP x FiO,) I Pao,

15.2 NEED FOR ECHOCARDIOGRAPHY PRIOR TO


INITIATION OF TREATMENT
It is highly desirable but not mandatory to get an Echo done prior to
initiation of therapy. Echocardiography is done to
• Confirm the presence of pulmonary hypertension
• Rule out underlying structural heart disease
• Assess left ventricular function
• Obtain baseline parameters suggesting pulmonary hypertension
enabling serial assessment of response to therapy
15.2.1 Situations when echo is mandatory
• Whenever there is clinical suspicion of underlying CHD.
Contraindications to nitric oxide therapy include
o CHD with duct-dependent right-to-left shunt
(CoA, critical AS, aortic arch interruptions, HLHS etc).
o CHD with severe left ventricular dysfunction. Decreased PVR
would increase left ventricular preload and overwhelm the LV
leading to worsening CHF
o TAPVC
• In neonates with CDH (To assess LV function)
• In non-responders: Those neonates who do not show clinical
response to nitric oxide (increase in Pa0 2 2> 20 mm Hg or decrease in
OI by 2> 20%) within 60 min of initiation of therapy (underlying
heart disease should be ruled out)
150

15.3 PRECAUTIONS BEFORE INITIATION


Nitric oxide administration should be considered only as a part of overall
clinical strategy in managing these neonates. (See section 14.15.2).
Before initiating nitric oxide therapy, ensure
• Presence of a postductal arterial cannula (UAC preferred whenever
possible)
• Adequate alveolar recruitment (Get CXR as early as possible- lung
margins should contain at least 7 visible intercostal spaces)
• Maximum Fi02 ( 1.0)
• Methemoglobin measurement facility is available and is in working
state (see section 15.7.1)

15.4 ADMINISTRATION OF iNO


15.4.1 Nitric oxide circuit
In PGlMER we use the sensor NOx from Sensorrnedics (model no.-REF
FIL 5800)
The main components of the circuit are
• NO cylinders (containing 920 ppm NO)
• Two stage regulator with two manometer gauges - first one
displaying cylinder pressure and second one the in- line pressure
• iNO flow meter (Oto 1 Umin) with magnified reading scale
• NO delivery line (Black colored) - from flow meter to Inspiratory
limb of ventilator circuit
• NO/N0 2 sampling line (Transparent) with water trap- from
Inspiratory limb close to wye to monitor-Sensor NOx
• NO!N01 monitor - Sensor NOx (a combined Nitric Oxide
(NO)/Nitrogen Dioxide (N0 2) monitor based on electrochemical fuel
cells. lt pumps a constant gas flow of 250 mL/min through to obtain
a measurement)
15.4.2 Initial setup instructions:
• Make sure the ventilator is functioning with the circuit attached to a
test lung
• Mount the NO flow meter on a level surface.
• Connect regulator outlet to the NO flow meter gas inlet using the
black hose with the quick connect adapter.
• Check that the valve on the flow meter is closed.
• Attach the black delivery line to the female Luer connector on top of
the NO flow meter. Tee the other end of the delivery line into the
patient breathing circuit at least 30-40 cm upstream of the sampling
site.
• Transparent sampling line from inspiratory limb close to wye to be
connected to the monitor (with a water trap)
• Tum on nitric oxide gas supply.
151

• "Flush" the system according I< suggested "flush" procedure below.


This procedure flushes the delivery portion of the NO system of
hannful oxides of NO, such as N0 2.
• You are now ready to deliver NO gas.
15.4.3 "Flush" procedure for the delivery portion of the iNO system:
• Set up the NO circuit for delivery as outlined in above; see "Initial
Set-Up Instructions"
• Hook up the ventilator to a test lung
(patient should be manually ventilated during this procedure).
• Tum on the NO gas flow to 1 Umin by turning the knob on the
precision metering valve. Allow the gas to flow into the ventilator
circuit.
• Watch the N0 2 values displayed in the monitor. As soon as the N0 2
value has dropped to a stable level, allow the gas to run for an
additional 3 s and then adjust the NO flow to the desired level (see
Calculations for NO Delivery to detennine flow required for desired
NO concentration).
• The calculated NO flow should be compared with the analyzed NO
dose to confirm accurate NO dosing. Should the actual NO flow
differ from the calculated NO flow by more than 10% beyond
published specifications, the cause must be determined and corrected
immediately.
• Once the desired NO concentration has been reached, ensure that
N0 2 level is acceptable for patient administration. The table below
will give you the approximate N0 2 values for a given NO
concentration and ventilator flow at Fi0 2 of 1.0 (See Table 15.1).

Tablel5.l: Approximate N0 2 values (ppm) for given NO


concentrations and ventilator flows at Fi0 2 of I 0
Ventilator Flow llnml
[NO]
5 10 15 20
5nnm 0.5 0.1 0.1 0.1
JQnnm 0.5 0.2 0.2 0.1
JOnnm 0.5 0.3 0.2 0.2

The table above is for reference only. Factors such as the accuracy of the
ventilator flow, percent error in delivery apparatus, human error, and
accuracy of calibration of the NO may all affect the actual delivered
concentrations of NO and N0 2 •

Once prescribed dosage is achieved (as per measured NO) alarms in


SensorNox should be set as
a. High/low NO dosage+/- 5 ppm
b. High NO, 2 ppm
152

2. Connect the patient to the ventilator and monitor according to


protocol.
Remember, the flush procedure must be performed each time NO therapy
is started. This includes initial therapy starts, tank changes and re-
starting therapy after trials off NO.
15.4.4 Calculation of dose and titration of NO
• The dose can be easily calculated on continuous flow ventilators
using the following formula. (Use the inbuilt facility in monitor -
Sensor NOx to do this calculation). The continuous flow of gas
ensures that the concentration of iNO will remain constant and will be
unaffected by all changes to ventilation, except changes of ventilator
flow rates.
• Initial NO flow (L/min) =
(Ventilator flow (L/min) x Desired NO (ppm)]/ 920 [source tank NO
(ppm)]
Example:
Minute volume, or ventilator flow= I 0 LI min
Nitric oxide source tank= 920 ppm
You want to deliver 20 ppm to your patient.
Initial NO flow (L/min) =
(IO L/min x 20 ppm desired N0] / 920 ppm (tank NO)= 0.21 Limin
Ready reckoner
• The Table below was developed using the calculations above (See
Table 15.2). You may use it as a starting point for setting your NO
flow rate. Please note that these are reference points only. The actual
dose delivered must be measured by the independent analyzer.
• Factors such as the accuracy of the ventilator flow, percent error in
delivery apparatus, and human error, may all affect the actual
delivered patient dose. The calculated NO flow should be compared
with the analyzed NO dose to confirm accurate NO dosing. Manual
fine tuning of the NO flow in the flow meter may be required to
achieve the exact required dose.
• Remember that Table 15.2 holds good only for ventilators where flow
is user-adjustable (e.g. Drager) and not for ventilators where flow is
automatically adjusted (e.g. Sophie).

Table 15.2: NO flow in liters/min for given NO concentrations and


ventilator flows

{NO/ Ventilator Flow (L/min


concentration 5 10 15 20
5 1111m 0.03 0.06 0.09 0.13
IOnnm 0.06 0.13 0.19 0.25
201111m 0.13 0.25 0.38 0.50
153

15.5 INITIAL DOSE AND WEAN ING: Shown in Figure 15. l


15.5.l When to stop & how to stop
• Abrupt discontinuation can be oone in non responders (No response
within 60 min of initiation of therapy)
• Abrupt discontinuation should be avoided in responders because it
may cause rebound pulmonary hypertension
• Discontinuation could be done
o When the Fi02 is <0.6,
o iNO dose has been weaned gradually to I ppm and
o Patient remains stable on 1 ppm dose for at least 6 h
• An increase in Fi0 2 of up to 15 °/o after discontinuation of therapy is
acceptable and doesn't warrant reinitiating therapy.
• The usual duration of treatment with nitric oxide is around 5 d.

15.6 MONITORING (also see section 15.9)


• Baseline
o Blood gases
o Platelet Count
• Continuous monitoring of NO & N0 2 levels (displayed in
equipment)
• Blood gases (Post ductal)
o 30 min & 60 min after initiation of therapy to define response
o Before each step in weaning
o 30 min after each weaning slep to ensure stability
o In case of clinical deterioration at any time
• Methemoglobin levels
o Within four h of initiation of therapy and
o Repeated every 24 h.

15.7 TOXICITY
15.7.1 Methemoglobinemia:
• The binding of NO to hemoglobin results in the production of
methemoglobin. This is not in itself toxic, but methemoglobin is not
able to carry oxygen. Therefore high levels of methemoglobin will
reduce the oxygen carrying capacity of the blood
• With doses of iNO of less than 20 ppm you would not expect to see
methemoglobin levels in excess of 2%
• A level of 2% should be considered a warning level, and if
methemoglobin levels rise to 5% iNO dosage should be reduced and
the level rechecked after 1 hour. If the levels have not fallen
substantially, iNO administration should if possible be reduced
further.
154

Figure 15.1 Initial doses and weaning

*Eligibility Criteria ··clinical Response•.i ***Weaning Criteria


•GA 2: 34 wks,:::: 14 d of (Occur in< 60 min) Fi02 < 0.6 and
postnatal age Pa02 j> 20 mm Hg or Pa02 > 60 mm Hg
• On mechanical ventilation !in 01by20o/o
• Hypoxemic respiratory
failure
• 01 > 25 (postductal)
• Clinical or Echo evidence
ofPPHN

; .:;· ·'""""
If Eligibility Criteria•

~1-T
Initial Clinical No Non Responders
•Echo mandatory to rule
out underlying
structural heart disease
• Poor lung recruitment
is the most common
cause of failure
• Continue at 20 ppm until Weaning STOP • Changing ventilator
Criteria••• met NITRIC
strategy will be more
•Wean from 20 to 5 ppm in 5 ppm steps q OXIDE beneficial
2-4 h
• Wean from 20 to 5 ppm within 24 h

Patient stable at
5 ppm?

Reduce in 1-2 ppm steps every 6-12th hourly


Wean from 5 to I ppm over 24-48 h

No
Patient stable at I ppm?

OffiNO

L atient stable off iNO? No


Upton 15% increase
in Fi02 requirement is Yes
acceptable)
155

• If at any time the methemoglotin percentages exceed 10% stop iNO


and consider treatment of met hemoglobinemia with a dose of 1-4
mg/kg I.V. of methylene blue.
M ethemog/obin levels
• < 5% Safe
• 5 - 10% ,!. iNO by 50% and repeat methemoglobin level
• > 10% Discontinue iNO
Methemog/obin levels measurement facility: This facility is available in
PG! (Nehru Hospital, 5" level, OT block, Anesthesia ABG room- no
internal phone available) and at Fortis hospital, Mohali.
The test may be done from Fortis hospital, Mohali only if the facility in
PGI is either not working or not accessible. It must be done with the
permission of the consultant.
The details of the set-up in Mohali •re enlisted below
Correspondence: Fortis Hospital Sector 62, Phase VIII, Mohali 160 062
Tel: 91-172-5021222, 91-172-4692222
Sample: 0.5 mL of arterial blood in a heparinized syringe - to be
transported in ice slush
Test Name: ABG (with methemoglobin level)
Billing for the test will be done at (OPD reception between 0800 - 1830
& In-patient department reception at other times). Both are situated at
ground level.
Cost: ~ 400. After billing, they will be guided by hospital personnel to
surgical ICU, which is at 2nd floor. Test is done at Surgical ICU.
15.7.2 N0 2 :
• Nitric oxide reacts with oxygen to form NO,, the higher the dose of
iNO and/or Fi0 2 the greater the amount ofN0 2 produced.
• N0 2 levels should be continuously monitored and should never be
more than 5 ppm. Reduce the dose of NO and recheck circuit
connections for leak whenever N0 2 level crosses 3 ppm. (Levels
usually remain< 0.5 ppm with nitric oxide doses up to 20 ppm)
N0 1 /eve/s
• < 3 ppm Safe
• 3-5 ppm ,!. iNO by 50% every 15 min till NO,< 3 ppm
• > 5 ppm Discontinue iNO
15.7.3 Platelet dysfunction: NO is an inhibitor of platelet function. It
should be used with caution in cases of underlying thrombocytopenia or
bleeding problem. Ensure platelet count of at least 50,000 and treat any
clinical bleeding due to thrombocytopenia aggressively.

15.8 SPECIAL SITUATIONS (Discuss with consultant before


initiating therapy)
15.8.1 CDH: Patients with severe CDH are poor responders as a group 3.
Available evidence suggests that iNO therapy in patients with CDH
156

should not be routinely used; rather, its use should be limited to patients
with supra systemic PVR after establishing optimal lung inflation and
demonstrating adequate LV performance.
15.8.2 Preterm neonates (<34 wks) with hypoxemic respiratory
failure: Recommendations for routine use of nitric oxide in pretenn
cannot be made based upon the available evidence 4 . It can be considered
in selected subgroups.

15.9 NITRIC OXIDE THERAPY - MONITORING SHEET: Shown


in Figure 15.2. Use a new chart every day.

Fi ure 15.2 Monitorin sheet for iNO thera


BASELINE DATA
Name 01 (post ductal)
Age (Hours oflife) Pa02
Date& Time CXR findings
CR no Echo findings
Gestational age
Diagnosis Platelet count

SENIOR RESIDENT

Hours PaOz NO N02 Methffh


JR in
Time after Fi02 (Post- 0 (ppm) (ppm) Levels
MAP chargt>
initiation ductal) Displayed Displayed (o/o)
0.5
I.

2.
3.

REFERENCES
I. The Neonatal Inhaled Nitric Oxide Study Group. NEJM 1997; 336:
597.
2. FinerNN. Pediatrics2001; 108: 949.
3. Neonatal Inhaled Nitric Oxide Study Group. Pediatrics 1997;
99:838.
4. Barrington K J. Cochrane Database Syst Rev 2007; 18.
157

16. BRONCHOPULMONARY DYSPLASIA

16.1 DEFINITION
The term BPD rather than Chronic Lung Disease (CLD) should be used
as it is clearly distinct from the multiple CLDs oflater life. The definition
of BPD has been revised recently by NICHD 1 (See table 16.l)

Table 16.1: NICHD definition


GA <32 wks >32 wks
>28 d but <56 d of
36 wkPMA or
Time point of postnatal age or
discharge, whichever
assessment discharge, whichever
comes first
comes first
Essential
Treatment with oxygen >21 % for at least 28 d PLUS
criterion for BPD
Breathing room air by
Breathing room air at 36
56 d of postnatal age or
Mild BPD wk PMA or discharge,
discharge, whichever
whichever comes first
comes frrst
Need for>21% but
Need for >21 % but
<30% oxygen at 56 d of
<30% oxygen al 36 wk
Moderate BPD postnatal age or
PMA or discharge,
discharge, whichever
whichever comes first
comes first
Need for ~30% oxygen
Need for ~30% oxygen
and/or positive pressure,
and/or positive pressure,
(PPV or NCPAP) at 56 d
Severe BPD (PPV or NCP AP) at 36
of postnatal age or
wk PMA or discharge,
discharge, whichever
whichever comes first
comes first

16.2 PHYSIOLOGIC TEST


The idea behind this test is to identify babies who may not require
oxygen and hence are wrongly labeled moderate to severe BPD at 36 wks
PMA due to varying unit practices of weaning from oxygen. Neonates
receiving <30% oxygen or oxygen >30°/o with saturations >96o/o undergo
a room-air challenge with continuous observation and oxygen-saturation
monitoring for 30 min. Babies should be continuously monitored for
apnea and bradycardia. Those who maintain saturations ~90% probably
do not have moderate to severe BPD. Weaning is not recommended
based on this test and this is for the diagnosiic purposes only.
158

16.3 CONCEPT OF NEW BPD


The "new"' form often develops in pretenn newborns in the post-
surfactant era, who had needed little or no ventilator support and have
had low inspired oxygen concentrations during the early postnatal days.
It is believed to be due to an arrest in the normal acinar development. X-
ray shows little, but homogenous, lung involvement.

16.4 CLINICAL FEATURES


• Tachypnea, retractions, sometimes paradoxical breathing, rhonchi
and crepitations
• Failure to thrive
• Copious respiratory secretions, aspirations, lung atelectasis
• Chronic hypoxemia- cor pulmonale
• Tracheo-bronchomalacia
• Feeding difficulties, bulbar dysfunction and GER

16.5 SALIENT PULMONARY FUNCTION ABNORMALITIES


Decreased compliance, increased airway resistance, variable time
constants, ventilation-perfusion mismatching and increased PVR are
major changes in the BPD. These must be kept in mind when deciding
optimal ventilation strategy. Other cardiac manifestations include RVH,
LVH, systemic hypertension and development of prominent systemic-to-
pulmonary collateral vessels causing shunting of blood to lungs and
edema.

16.6 MANAGEMENT OF BPD


16.6.1 Ventilatory strategy in established BPD: Pa0 2 should be
maintained 50-70 mm Hg, and the Sp0 2 90-95%, to prevent or treat
pulmonary hypertension and car pulmonale. Minimize further lung injury
by accepting PaC0 2 45-55 mm Hg and pH 7.25-7.35. Use slow rates (20-
40/min), moderate PEEP (4-5 cm H2 0), lowest possible PIP and Ti (0.4-
0.7 s) (see section 14.12.5). This is because BPD is characterized by
hyperinflation, cystic changes and prolonged time constants. Older
infants with BPD and those with diffuse haze and no cysts can tolerate
PEEP of 5-7 ems.
16.6.2 Extubation: Every attempt is to be done to extubate the baby
from the ventilator as early as possible. (See section 14.12.10).
Before extubation:
• Baby should be gaining Wt for at least a couple of days.
• A recent CXR should be available prior to extubation to rule out any
major collapse or consolidation.
• lf the baby has had extubation failures in the past, consider using
peri-extubation Dexamethasone (0.25 mg/kg/dose q 8 hourly for 3
doses, l" dose at least 4 h prior to extubation)(see section D39) 2 .
159
16.6.3 Role of nutrition in BPD
• Fluids: Fluids should be restri ;ted to 150 mL/kg/d. If it interferes
with administration of adequat< Calories a balanced diuretic can be
used to prevent fluid overload.
• Enteral nutrition: The infunts developing BPD require 20% to 40%
more Calories than their age-matched healthy infants. OOP can
compound the problems by increasing the chest wall compliance.
OOP must be managed aggressively (see section 38.6). Provide 120-
150 Cal/kg/d and 3-4 g/kg/d of proteins.
• Fortification: Supplementation of breast milk with HMF is needed
to make up for protein and mineral deficiencies (see section 9.12).
Additional fat (MCT oil) rather than carbohydrates may be desirable
to meet further caloric needs; the metabolism of fat produces less
carbon dioxide than carbohydrates. However, additional fat may be
used cautiously as it slows gastric emptying and may worsen reflux.
• Partial parenteral nutrition (PPN): In difficult situations, PPN must
be used to provide adequate nutrition within the constraints imposed
by the permissible volume (see chapter 32).
16.6.4 Pharmacological Management:
• Diuretics:
o Indications:
• Failure to taper ventilatory settings; with evidence of fluid
inCXR
• Excessive Wt gain in the setting of restricted fluids.
o Dose: Frusemide 0.5-1.0 mg/kg/dose IV or PO bid (once a day
in infants <31 wks corrected age) (see section D55).
o Response to frusemide should be assessed to decide about
continuation of diuretics. For use more than 2 days, shift to a
balanced diuretic combination. Generally, diuretics are not
required for more than 5 days.
o Thiazides have a weak diuretic effect but the risk of electrolyte
abnormalities is less. There are no comparative studies between
frusemide and thiazides in neonates. Dose: Hydrochlorthiazide
1-2 mg/kg/dose PO bid. (sec section D64)
o Monitoring:
• Monitor daily Wt, input output charting 12 hourly.
• Serum electrolytes 24 hourly initially for 1-2 d after starting
diuretics/ if Wt loss is more than acceptable and twice a wk
thereafter.
• ABG/ venous blood gas OD at least or depending on the
clinical condition.
• USG KUB at the end of prolonged diuretic therapy to look
for nephrocalcinosis.
160
Bronchodilators: may be useful in babies with BPD as they have
• increased airway resistance due to smooth muscle hypertrophy and
hyper-reactivity. There is no preventive effect of bronchodilators on
the incidence and severity of BPD. The two most widely used
bronchodilators are salbutamol and ipratropium (see sections DI 13
and D71).
o Indications:
• Increased resistance or prolonged expiration on pulmonary
graphics
• Rhonchi on auscultation
• Prolonged expiration.
• Decreased breath sounds m the setting of lung
hyperinflation.
o Monitoring:
• ECG monitoring.
• Serum electrolytes 24 hourly (salbutamol can cause
hypokalemia).
• BS 24 hourly and in case of polyuria.
o Dose:
• Salbutamol: 0.02- 0.04 mL/kg/dose of 0.5% sol in 2 mL
saline q 4-6 hourly
• Ipratropium: 0.025- 0.08 mg/kg diluted to 2 cc saline q 6
hourly
MDI-spacer and jet nebulizer are equally effective in improving the
pulmonary mechanics and MDI-spacer is a more cost effective option. 3
• Steroids:
o Indication: Routine use of systemic dexamethasone (see section
D39) for the prevention or treatment of BPD is not
recommended.
• Dexamethasone may be used in a clinical setting only under
exceptional circumstances- e.g. failure to extubate from
mechanical ventilation after 1 mth or repeated extubation
failures. Discuss with consultant before use. Informed
consent of the parents must be obtained. They must be
informed about the potential short and long term side
effects.
o For facilitating extubation in ELBW babies who are ventilator-
dependent beyond 7 days of life, dexamethasone can be used in
the following regime: 0.15 mg/kg/d x 3 d; 0.1 mg/kg/d x 3 d;
0.05 mg/kg/d x 2 d; 0.02 mg/kg/d x 2 d. This provides a
cumulative dose of 0.89 mg/kg over 10 d4 .
o There is currently no role of inhaled steroids in the management
ofBPD.
161
16.6.5 Home Oxygen therapy
• Eligibility criteria
o Otherwise growing infants w 1th BPD
5
o Room air Sp02 <95% ·6 , who have mild oxygen requirement <I
L/min.
o On full feeds and do not show any episode of desaturation during
and after feeding.
o No excessive secretions, increased work of breathing or anemia at
the time of discharge.
56
• Target Sp0 2 295% • • The higher end of the range must be targeted in
those with PAH. In neonates who are still at risk ofROP at discharge,
a lower cut-off(>92%) may be accepted.
Skills taught to the family: The family should be taught the following
skills in hospital before discharge.
• Initial steps of resuscitation
• Vital sign monitoring
• Suctioning of oropharyngeal secretions
• Physiotherapy techniques
The case should be discussed with the local pediatrician who is going to
take care of baby once baby is discharged.
Procurement of home oxygen apparatus
• The parents must procure two cylinders of oxygen. These are
available in Chandigarh in Sector 16 market surgical stores, for one
time purchase of< 3500 per cylinder or on rent at < 300 per mth per
cylinder and a refill cost of< 150 per refill (these are year 2009 prices
and may change with time).
• They must also purchase a suction apparatus (foot operated) [Sector
16 market surgical stores, cost < 650] before they go home.
• Alternative for the oxygen cylinder can be oxygen concentrators but
the cost is high (Cost:< 60,000 per apparatus). Oxygen concentrators
can also be rented at approximately < 4,500 per month (contact
Hospital Suppliers, SCO 54-55, sector 16-D, Tel 0172-2770345,
9417449808).
• For monitoring Sp0 2 they must buy a finger pulse oximcter either
through Sector 16 market surgical stores, or contact Mr. Ajay (cell
9988880675) or directly from Bhagirath Place, Chandni Chowk,
Delhi (cost approximately< 6,000).

16.7 LONG-TERM FOLLOW-UP


• Infants receiving home oxygen therapy must come weekly to NFC in
the 1st rnth if distance permits or see a local pediatrician. Sp02
should be kept 295% to ensure appropriate Wt gain.
162

• The usual concerns pertaining to ELBW infants applies to those with


BPD and they must be followed up for growth and neuro-
development, nutrition, hearing, ROP, vision, OOP etc.
• About 50% of all infants with BPD will need to be re-admitted
during early childhood for respiratory distress, often following RSV
or other viral infections. Chest X-ray findings are generally non-
specific and are highly insensitive markers of changes in lung
function. Anti-RSV monoclonal antibodies are not yet available in
India.
• Children with BPD more often develop asthma compared with the
general population. Consultation from Pediatric Pulmonology
division must be sought for infants with features of asthma.
• In NICHD Network study of births <33 wks in 1993 to 1998, BPD
was a significant independent risk factor for moderate or severe CP.

REFERENCES
1. Jobe AH, Bancalari E.NICHD-NHLBIORD Workshop. Am J Resp
Crit Care Med 200 I; 163: 1723.
2. Khemani R G, Randolph A, Markovitz 8. Cochrane Database Syst
Rev 2009; 8
3. Baveja R, Christou H. Semin Perinatol 2006; 30: 209.
4. Doyle et al. Pediatrics 2006; 117: 75.
5. Panitch H et al. In: McConnell MS, Imaizumi SO (eds), Guidelines
for pediatric home health care. Am Acad Ped; 2002. p 323
6. Allen Jet al. Am J Resp Crit Care Med 2003; 168: 356
163

17.ANEMIA

17.1 DEFINITION
Anemia is defined as Hb or PCV value below the expected range for the
gestational and chronological age (see table 17.1 and 17.2).

Table 17.1: Normal Hb values in infancy' [mean (range))

BW(g) A2e (wk)


2 4 6 8 10
800-1000 16 IO 8.7 8 8
(14.8-17.2) (6.8-13.2) (7-10.2) (7.1-9.8) (6.9-10.2)
1001-1200 16.4 12.8 10.5 9.1 8.5
(14.1-18.7) (7.8-15.3) 17.2-12.3) (7.8-10.4) (7-10)
1201-1400 16.2 13.4 10.9 9.9 9.8
(13.6-18.8) (8.8-16.2) (8.5-13.3) (8.4-11.8) (8.4-11.3)
1401-1500 15.6 11.7 10.5 9.8 9.9
(13.4-17.8) (9.7-13.7) ' (9.1-11.9) (8.4-12) (8.4-11.4)
1501-2000 15.6 11 I 9.6 9.8 IO.I
(13.5-17.7) (9.6-14) ' (8.8-11.5) (8.4-12.1) (8.6-11.8)

Table 17.2 Hb change in the postnatal period

Maturity At birth At nadir Time of


1..tdLl lf'idL) nadir
Term 15-22 9.5-11 6-12wk
Preterm (> 1200~) 14-20 8-10 5-10 wk
Preterm (< 1200g) 13-19 6.5-9 4-8 wk

PCV or Hb must be measured on venous or arterial blood. Capillary


blood samples can give a falsely high reading, which can exceed the
correct reading by 12-20%.

17.2 CAUSES OF ANEMIA:


The causes can be broadly categorized into 3 major groups: blood Joss,
increased erythrocyte destruction, or decreased erythrocyte produc!ton.
The common causes m each category include (but are not limited to) the
following (see table 17.3). ----
164

Table 17.3 Common causes of anemia

Etiology Clues on history & Lab investigations


clinical examination
Blood loss
Feta-maternal Obstetric procedures, Kleihauer-Betke Test
bleeding placental on mother's blood
malformations, can
also be spontaneous
Placental causes APH, delivery events, Initial PCV can be
cord prolapse, vasa normal. Falls later.
previa,
pallor/shock soon
after birth
Intracranial bleed Neurologic USG head
Abdominal bleed deterioration, USG abdomen
birth trauma
Sampling loss Bloodletting chart
Hemolvsis
Immune hemolysis Mother Rh -ve, group t reticulocyte count,
(Rh, ABO 0, nucleated RB Cs,
incompatibility) Earlier affected polychromasia,
siblings, DCT+ve
Hcpatosplenomegaly
RBC membrane Family h/o anemia, t reticulocytc count,
defects gallstones nucleated RBCs,
polychromasia,,
osmotic-fragility test,
DCT-ve
Acquired hemolysis Septicemia, NEC, Associated
(sepsis, DIC) cavernous thrombocytopenia
hemangioma ± coagulonathv
Decreased production
Anemia of Usually <32 wks, Low reticulocytc
prematurity more frequent with count,
stormy neonatal Normocytic
period normochromic
Bone marrow failure Dysmorphic features, Pancytopenia, low
syndromes Skeletal defects reticulocyte count,
bone marrow exam
165

17.3 CLINICAL FINDINGS:


Mild anemia may be clinically siknt. Findings associated with severe
anemia include:
• Pallor, tachycardia, wide pulse pressure, hypotension, metabolic
acidosis
• Tachypnea, increased oxygen requirement, apnea
• Poor feeding, lethargy
Findings associated with chronic anemia include poor growth, decreased
activity and limited cardiovascular reserve.

17.4 DIAGNOSTIC EVALUATION OF ANEMIA: Shown in Figure


17.1. Before blood transfusion, take a sample for central lab CBC and 1
extra sample in EDTA vial if further work-up is anticipated. Take
samples for other tests depending on the etiological possibilities.
Figure 17.1 Diagnostic evaluation of anemia

l Hematocrit

Low
Bone marrow suppression
• Congenital syndromes /
• Acquired - parvo B 19

Positive
Immune hemolytic anemia
• ABO & Rh isoimmunization
• Minor blood group
MCV

Low
• Chronic blood loss
• Thalassemias

Normal Abnormal
• Blood loss • Spherocytosis
• Infection • Elliptocytosis
• RBC enzytne defkiency • G6PD deficiency
166

17.5 TREATMENT OF ANEMIA:


Treat underlying cause when feasible, as per results of diagnostic
evaluation. Transfuse PRBC's as required, irrespective of underlying
cause. Blood transfusion and use ofEPO are covered below.

17.6 PRBC TRANSFUSION


17 .6.1 Indications for PRBC transfusion'
• PCV <36% and requiring
o >35% supplemental oxygen
o MAP :0:6-8 cm H20 by CPAP or IMV
• PCV <31%and
o Requiring <35% supplemental oxygen or MAP <6 cm H 20 by
CPAP or IMV
o >9 episodes of apnea and bradycardia in 12 h or 2 episodes in
24 h requiring bag & mask ventilation while on adequate
methylxanthine therapy
• PCV < 40% and
o HR >I 80/min or RR >80/min persisting for 24 h
o Wt gain <10 g/d for 4 d while on I00 Cal/kid
o Undergoing surgery
• PCV <2 I% and
o Asymptomatic with reticulocytes <100,000/µL (2%)
• Hypovolemic shock associated with acute blood loss
Do not transfuse for phlebotomy losses alone

17.6.2 Choice of blood group: Shown in Table 17.4

Table I 7.4 Choice of blood group for PRBC transfusion

Guidelines for ABO-compatibilitv


ABO group ABO status of blood component being transfused
(infant) RBCs/Granulocvtes FFP/Platelets
0 0 0, A, B or AB
A AorO Aor AB
B BorO Bor AB
AB AB, A, BorO AB
Guidelines for Rh-compatibilitv
Rh type Rh status of blood component being transfused
(infant)
RBCs/Granulocytes FFP Platelets
Positive Positive or negative Pos or neg Pos orneg
Negative Negative Pos or neg Negative
167

17.6.3 Volume & duration of blooo transfusion


• In small and sick babies give I' I mL/kg over 4 h. Recheck the PCV
and transfuse another 10 mL/kg if PCV is still below the transfusion
threshold.
• When there is acute blood loss and the baby has features of shock.
blood can be given over 30-60 min.
• In hemodynamically stable preterm transfuse 20 mL/kg over 4 h.
• Routine administration of frusemide with all transfusions is not
recommended. Give frusemide (0.5 mg/kg JV) at the half-way mark
of the transfusion only if the infant is unlikely to tolerate a volume
load (e.g. hemodynamically significant PDA. congestive cardiac
failure, established BPD).
• Volume can also be calculated as per the following equation:
Volume~ (Desired PCV - Patient's PCVl, wt (kg), 80-100 mL/kg
(PRBC PCV)
Where the desired PCV is 45%
• Consider PET in place of simple transfusion in following cases:
o Hydrops with respiratory distress due to anemia
o Severe anemia with CHF and pulmonary edema
• For volume of PRBCs for PET use the following formula:
Volume~ (Desired PCV -Patient's PCV), Wt (kg), 80-100 mL/kg
(PRBC PCV - Patient's PCV)
Where the desired PCV is 30%.
17.6.4 Practical issues related to transfusion
• Two types of stored PRBCs are available in PG!MER blood bank
(CPDA-1 & Additive solution (AS)-1 units). CPDA-1 blood can be
stored up to 35 d and that of AS-I blood up to 42 d.
• Contact JR or SR of blood transfusion department in case of any
difficulty in procuring the required blood group.
• After taking the required volume keep the blood bag inside the
refrigerator (lower shelf). Once opened, blood products can be used
only for 24 h.
• Before transfusion, match the blood bag number, blood group &
patient name written over the blood bag with that of the reaction
form provided.
• Warm the blood gradually to 37 °C by placing inside the incubator.
Do not warm it by placing under the radiant warmer or putting inside
hot water.
• For all transfusions, check PCV 1-4 h after completion of the
transfusion.
• In PGIMER blood bank, blood products are routinely screened for
HIV, HBsAg, HCV, syphilis & malaria.
168

• Use an infusion pump for blood product transfusion. Use of


intermittent pushes of blood is prohibited.
• Use peripheral lines as the risk of clotting and subsequent blockage
of central line is more if given through central line.
• Monitor HR, RR, temperature, BP and Sa0 2 every 30 min during the
procedure. BS should be checked hourly if glucose infusion was
interrupted during transfusion.
17.6.5 Hemolytic reactions
• Infusion should be stopped and the infant evaluated clinically if any
of the following develop during the transfusion:
o apnea, tachypnea, cyanosis;
o tachycardia, bradycardia, or arrhythmia;
o significant change in systolic BP;
o significant increase or decrease (>I °C) in temperature;
o red urine.
• If a hemolytic reaction is noted or suspected, stop the transfusion
immediately and send the blood bag along with tubings and 2
samples of the neonate's blood (1 in plain vial & 1 EDTA vial) with
a "blood reaction form", duly filled, to the blood bank.
Treatment of hemolytic reaction
• Stop transfusion as soon as a reaction is suspected. Examine the
blood to determine if the patient was the intended recipient and then
send the unit back to the blood bank after informing the Transfusion
Medicine (blood bank) JR or SR.
• Continuously monitor vitals including cardiac rhythm.
• Support the airway and administer oxygen as necessary
• Maintain intravascular volume. Administer one I 0 mL/kg NS bolus
in case of shock. Further boluses may be given based on
normalization of vital signs. Start inotropes if shock persists. (see
section 29.6)
• Catheterize the bladder. Monitor urine output
• Send patient blood for SERFT, ABG. Simultaneously evaluate for
evidence of hemolysis (cola colored urine, free Hb in urine,
increased PT, aPTT and Lactate dehydrogenase and decreased
International normalized ratio (INR) and fibrinogen levels). Also
take patient's blood from a site other than the transfusion site, in an
EDT A vial and send to blood bank to be cross matched against the
pretransfusion sample to determine if the correct blood was
administered.
• Frusemide may be administered if urine output < 1mL/kg/h. Low-
dose dopamine (0.5-2 µg/kg/min) may be considered to improve
renal blood flow.
• Treat hypocalccmia with calcium gluconate.
• Fever can be treated with paracetamol (I 0 mg/kg).
169

• In case of evidence of anaphyl axis (flushed appearance, urticaria,


hypotension) administer epinepl rine 0.0 l mg/kg, maximum 0.3 mg
dosage SC or IM q 5 min until rc:sponse. In case of no response after
3 doses, administer IV epinephrine infusion 0. I µg/kg/min. Also
consider diphenhydramine 1-2 mg/kg and ranitidinc l mg/kg as a
second line agent in case of non response to epinephrine.
Methylprednisolone (l-2 mg/kg up to 125 mg) is administered to
prevent protracted and recurrent anaphylaxis. For bronchospasm
refractory to epinephrine administer inhaled salbutamol 0.5%
solution (0.1 mL in 2 mL of NS) over 20 mins and to be repeat as
necessary· 3

17.7 OTHER ISSUES WITH REGARD TO NEONATAL


TRANSFUSION
17.7.1 Reducing the number of donor exposures: In addition to
reducing the number of transfusions, reducing the number of donor
exposures is important. This can be accomplished be assigning a specific
unit of blood (to make satellite bags), which may suffice for treatment
during the neonate's entire hospitalization and limit exposure to a single
donor. Contact blood bank and speak to a Transfusion Medicine
consultant on day 1 of admission of a baby who is expected to receive
multiple transfusions. Fill the following in the proforma (titled - satellite
bag request from Neonatal unit): Patients name, CR no, volume required
(mL), whether irradiation required. Give a combined request for all the
ELBW infants in the unit for that day. The request should reach the blood
bank latest by l 0 am.
17. 7.2 Hyperkalemia & acidosis: Concerns, that stored blood might
increase serum potassium levels or decrease pH, are unfounded as long
as the transfused volume is low. However for large volume transfusion
(>25 mL/kg) and DVET, fresh blood(< 5 d old) should be used.
17.7.3 Transfusion associated GVHD: It occurs when viable T
lymphocytes contained in a transfused blood product engraft in the
recipient and react against the recipient's tissues. The signs and
symptoms include fever, generalized erythematous rash, diarrhea, liver
dysfunction and pancytopenia. Irradiated blood must be transfused to
prevent GVHD. Because of the risk of potassium leakage after
irradiation, RBCs should be transfused within 24 h of irradiation. This
facility is available only during morning hours (9 am to l pm) atlcr
discussion with the transfusion medicine SR. Irradiation of blood
products to prevent GVHD is recommended for the following groups
• Neonates who had required IUTs & who require transfusion
postnatally
• Neonates with known or suspected cellular immune deficiencies
• Fetus requiring IUTs (of relevance to obstetricians)
170

• Recipients of cellular blood products from first-degree blood


relatives
Leukocyte reduction filters do not prevent GVHD and are not a suitable
method (see section 36.6.2).

17.8 RECOMBINANT EPO FOR ANEMIA OF PREMATURITY


EPO is not accepted universally as a standard therapy for treatment of
anemia of prematurity (see section D49). While EPO cannot prevent
early transfusions, modest decreases in the frequency of late PRBC
transfusions have been documented. Meta-analysis' of RCTs shows
marginal benefit with both early(< 8 d) and late (2: 8 d) EPO after birth,
but with increased risk of stage 3 ROP with early EPO administration. At
present there is no agreement regarding timing, dosing, route, or duration
of therapy. When the family has religious objections to transfusions, the
use of EPO is advisable. Dose of EPO is 200 - 250 units/kg administered
3 d/wk. 6 mg/kg/d elemental iron must be started along with EPO. It is
not routinely administered in PGIMER. Discuss with a consultant before
administering.

17.9 PREVENTION OF ANEMIA


Strategies include
• Monitor and record phlebotomy losses daily
• Order laboratory tests judiciously
• Send the minimum amount of blood necessary for laboratory tests
(see chapter on investigations for details)
• Remove umbilical lines and arterial lines as soon as possible
• Replace the dead space fluid after sampling from umbilical or
arterial lines
• Start iron therapy in all preterms after 2 wks of life (see section
9.11.1).

REFERENCES:
l. Stockman JA 3rd. Am J Dis. Child 1980; 134:945.
2. Shannon KM. US Multicenter Erythropoietin Study. Pediatrics.
1995;95: I ..
3. Lieberman P. American academy of allergy, asthma and
immunology guideline, 2005.
4. Aher SM. Cochrane Database Syst Rev. 2006.

.
171

18. POLYCYTHEMIA

18.1 DEFINITION
Polycythemia is defined as venous "'CV equal to or more than 65% (fur
both term and preterm newborns) or arterial PCV ~63% By default, the
worcr'PCV" refers to venous PCV mly and wheil'ineilsured by the spun
method, and not by automated cell counter because spun PCV is higher
than automated cell counter me1sured PCV and it shows better
correlation with viscosity in v'tro. 1 he capillary tub.f should be filled to
3/4~of its length and spun a 11 ,000 rpm for 5 mi!Vn a m1crocentri fuge
(see section 1-3). - - ·
18. J.I Dynamic definition of polycythemia:
The PCV shows a physiological change over time in the initia l hours of
life. Thus, the upper limit of venous PCV can be de fi ned as ~70% at 2 lt
of lif~~6~o/!.&§ h of life and ~G5% thereafter in neonatal lifer.

18.2 RISK FACTORS FOR POLVCYTHEMIA


Risk factors are shown in Table 18. l

Table 18.1 : Monitorin in the r es1•nce of risk factors


These babies must be actively Individualize cases and monitor if
monitored for polycythemia required (to be decided by SR)

oidism /
Maternal use of propranolol /
Perinatal as h ia /
Suspected TORCH infection

Lookin lethoric I

18.3 MONITORING: Indications sl'own in Table 18.1


• Cord clamping time should be n ted. (whether >3 min or not).
• lf possible, do cord PCV o · all term newborns- at risk of
polycythemia. T here is a good cc rrelation in term newborns between
cord PCV ~~and developmeit of polycythemia at 2 holl!:_ of life.
There is no significant difference found between~ or VV PCV ..1

• Monitor PCV at 2 hour of life. ( o further monitoring is required if


2 h PCV is :S56% in term babit;il
• In all oth~s, monitor PCV of cord blood, 2 h, 6 h,

-
and 12 h & as clinically indicatec.
172

18.4 SYMPTOMS
There are a large number of symptoms. Only those, which requires PET,
are mentioned here.
CNS:
Lethargy (14.5%) I
Hypotonia (7-9%) I
Irritability (13%) I
Tremors (7%) j
Seizures (1.2%)
Stroke
One or more CNS findings (27%)
Metabolic:
Hypoglycemia (11-40"/o)
Symptomatic hypocalcaemia (1-11%)
CVS:
Tachypnea (16-27%)
Respiratory distress (9%)
I
Tachycardia
Cyanosis (7-14.5%)
Apnea (4%)
Pleural effusion
CHF
GIT:
Poor feeding (7-20. 7%)
Feed intolerance (22%)
lieus
NEC (l-3.7%)
Renal:
Oliguria
ARF
Renal vein thrombosis
Hematologic:
Symptomatic Thrombocytopenia (1-30%)
Significant Hyperbilirubinemia (2-22%)
Misc:
Peripheral gangrene

18.5 TREATMENT
18.5.1 Hemodilution (by fluid supplementatio
d
Hemodilution must not be done as there is no vidence available in
literature to support fluid supplementation for asymptomatic moderate
(PCV 65-75%) polycythemia. An RCT done in our unit in asymptomatic
babies of"'.34 wks of gestation showed no difference in the need for PET
between the fluid supplemented and non-supplemented group. 2
173

18.5.2 PET:
Indications:
• All asymptomatic newborns witl PCV >75%
• All symptomatic newborns with PCV ~65%
Blood vessels used: (in order of preference)
Use radial artery, ulnar artery or po .erior tibial artery. Avoid UV as far
as possible because of tile risk ofNEr In polycythemia.
Fluid used: -
NS (Q.9% NP.9) 1s the preferred flud. There 1s no clinically important
difference among plasma, 5% alb1.~ NS, or Ringers solution in
reducing PC'{ NS IS cheai,readil) available, and does not carry the
potential risk of transfusion associated infection. Viscosity depends on
plasmayroteins which is higher in adult_plasma. Hence, after PET with
adult plasma, the PCV may fall but viscosity may still rema~n high.
Calculation offluid volume:
Exchange volume- <Observed PCV -. Desired PCV) x blood volume
Obser' ·ed PCV
Where desired PCV 1( 55% /
Calculation of blood volume:3 ShO\\.T in Fit,'Ure 18. 1
I
Figure 18.1 Blood volume according to weight (Reprinted from Journal of
Pediatrics. volume IOI, Rawlings JS, Penen ~ •• Wiswell Th, Clapper J, Estimated blood
volumes m poly9them1c neonates as a fuoe1 on of b1nh weigh~ page~ 594-9, copyright
1982, '~1th perr111ss1on from Elsevier)
110

~
lDO
Jf

>
-
::::,.
so
::::i

cO

"
...lu

E~

Birt!" , ..eigl" 1gmsj


174

Monitoring
Monitor PCV 2 h after PET and then every 12 hourly for 48 h or as
clinically indicated.
18.5.3 Algorithm of management of polycythemia;.-Shown in Figure
18.2

Figure 18.2 Algorithm of management of polycythemia


At risk for polycythemia/

i
Monitor as per schedule j
i
Symptomatic Polycythemia -+ Asymptomatic
J
l
PET
l
PCV>75% /
l
PCV<75% I
l
Monitor/

l
Nonna!PCV /

18.6 SEQUELAE AND FOLLOW-UP


A PET reverses the physiological abnormalities associated with
hyperviscocity syndrome. There is no convincing data to suggest that
PET improves long term outcome in patients with polyS)'lh~mia. It is
possible that the underlying etiology, the symptomassoClatea or the
complication encountered is the important determinant of ultimate
outcome than treatment or polycythemia per se. Definitive data on long-
term outcome with treatment is still unavailable in infants with
symptomatic polycythemia 4• All babies with symptomatic~
should be followed up in NFC and further follow-up of these babies
should be scheduled as per either the symptom associatecfOrihe
complication encountered (see section 42.2).
175

REFERENCES
I. Shohat M, Reisner S H, Mimour i F, Merl ob P. Pediatrics 1984; 73:
11.
2. Mangalabharathi, Dutta S. DM t11esis PGIMER; Chandigarh: 2009
3. Rowling JS et al. J Pediatr 1982: IOI: 594.
4. Michael S. Schimmel M S, Bromiker R, Soll RF. Clin Perinatol
2004; 31: 545.
176

19. BLEEDING NEONATE

Neonates, especially preterms, are at higher risk of bleeding due to


decreased activity of certain coagulation factors and impaired platelet
function. Bleeding is a common problem in sick neonates and can be life
threatening.

19.1 PREVENTION OF BLEEDING


• Give 1 mg Vit K IM at birth to all babies > 1.5 kg and 0.5 mg to all
babies Sl.5 kg. (sec section D 131)
• Give I mg Vil K weekly to babies on TPN, broad spectrum
antibiotics and sick neonates.
• Give 10 mg Vit KIM/IV to mothers 24 h before delivery, who are
on drugs like phenobarbitone, phenytoin, anti-tubercular drugs or
coumarins.

19.2 CLINICAL APPROACH TO A BLEEDING NEONATE


The following questions must be addressed:
• Was the baby sick or well at the onset ofbleeding 9
• Was Vit K given to the baby?
• Is the bleeding generalized or localized? (generalized bleeding is
almost always due to coagulopathy or thrombocytopenia or both).
• Is there a family h/o bleeding? (more relevant in a well baby with
bleeding)
• Is there a h/o maternal thrombocytopenia, connective tissue disease,
PIH or intake of barbiturates, phenytoin, aspirin, rifampin, JNH or
warfarin?
• What was the age of onset of bleeding? (immune thrombocytopenias
present usually in first 24 h, classic Vit K deficiency bleeding
between 2 to 4•h d of life)
• Is the bleeding petechiael with small mucosa! hemorrhages
(generally indicates thrombocytopenia) or are the bleeds large
(indicates coagulopathy)?
• Are there coexisting signs like jaundice, organomegaly, signs of
sepsis or erythroblastosis?

19.3 INVESTIGATIONS:
Platelet count, coagulogram and peripheral smear must be done in all
cases and the rest of the investigations should be individualized.
19.3.1 Platelet count: Thrombocytopenia is defined as platelet count less
than l 50,000/mm 3 and severe thrombocytopenia as< 50,0001 mm 3.
177

19.3.2 Coagulogram: Normal valu.:s may vary between laboratories (see


Table 19.1 ). PT :O:l 7 s is abnormal in both term and preterm. APTT of
>45 s in term and >55 s in preterm is generally considered to be
abnormal.

Table 19.1 Normal coagulation parameters in term and preterm


neonates
Test I Dav I I Day 5 I Day 30
Tenn neonate - values in mean± 1 S.D 1
PT (s) I 13.o± I.43 I 12.4± I.46 I 11.8± 1.25
APTT(s) I 42.9 ± 5.80 I 42.6 ± 8.62 I 40.4 ± 7.42
Pretenn neonate - values in mean and 95% C.I 1
PT (s) I 13.0 (I0.6-16.2) I 12.s (I0.0-15.3) I II.8(10.0-13.6)
APTT(s) I 53.6 (27.5-79.4) I 50.5 (26.9-74.I) I 44. 7 (26.9-62.5)
Blood drawn from a heparinized catheter should not be used. Normal
ratio of blood: anticoagulant should be 9: I in the vial. If there is
polycythemia, inform the lab so that quantity of anticoagulant in the vial
is adjusted accordingly (blood: anticoagulant ratio should be 19: I). If the
sample is clotted, it should not be assumed that neonate's coagulation
profile is normal, but one should send another coagulogram.
19.3.3 Peripheral smear: This is useful for
• Rough estimation of platelet count: Count the number of platelets in
IO oil immersion fields and multiply by 15,000. If platelet count is
needed in emergency, talk to the hematology emergency lab
technician or Hematology SR personally for a manual count.
• The size of platelets can be estimated and fragmented RBC's can be
seen in case of DIC.
19.3,4 Apt test- This is used to rule out swallowed maternal blood. This
should be done if the baby has only gastro-intestinal bleed & otherwise
clinically well. The blood is swallowed during the delivery and onset will
be within the first 3 d of life. Mix I art of astric aspirate/stool/vomitus
with 5 parts of distilled wat~r. entrifuge it and separate the clear pink
supernatant. Add I mL of I% NaOH to 4 mL of the supernatant. A
sample contammg maternal blood wtll tum brown while fetal blood
remains pink. Run simultaneous controls with maternal and fetal blood.
19.3.5 d-Dimer assay is required to confirm DIC. A 5 mL vial is
provided by the coagulation lab for fibrin degradation products & d-
dimers. A minimum of 3 rnL blood is required for this. Discuss with the
hematology SR before sending, if you send only 3 mL.
19.3.6 PIVKA (Protein Induced in Vit K Absence)- for confirmation of
vit K deficiency. This can be done even up to 72 h after Vit K
administration. This need not be done routinely. (Currently not available
in PGI)
178

19.3.7 Antiplatelet antibodies for immune thrombocytopenia (not


available in PGI currently).

19.4 APPROACH TO DIFFERENTIAL DIAGNOSIS: Shown m


Table 19.2

Table 19.2 Approach to differential diagnosis

. Clinical Diagnosis
Platelets PT
: condition
rsick
neonate N
N i Liver disease
N N Stress bleed
............'.......•........•..
Well Immune
neonate thrombocytopenia,
N N Kasabach-Meritt
syndrome, bone marrow
_hypojJlasia
Vit K deficiency ·
N i i bleeding
Hereditary clotting
N N i fact(}r~eficiencx ..
Swallowed blood,
trauma, qualitative
N N N
platelet defects, Factor
.......................................................x........m.... ~ei1cie11cy·............................. j

19.5 TREATMENT:
19.5.1 General principles of treatment of a bleeding neonate
• Give Vit K 1 mg IV if it has not already been given in the preceding
week.
• Keep cross matched blood ready for emergency transfusion and for
further transfusions.
• If there is hypovolemic shock/blood loss > I 0%, give equal volume
of whole blood and plasma expander.
• Look for the underlying cause and treat it.
19.5.2 Platelet transfusion
Indication for platelet transfusion: 3.4
• Count <50,000 µL in
o any preterm infant (<33 wks) in l" wk oflife
o clinically unstable term infants in l" wk oflife
o any neonate undergoing invasive procedure (e.g. ventricular tap)
179
o preterm neonate who h" to be started ibuprofen or
indomethacin or who has re<:ent-onset grade Ill/IV IVH
• Count <20,000 µL in all stable infants beyond l" wk of life without
active bleeding. There is evident e from pediatric oncologic literature
that a count> 10,000 µL is safe lor performing a LP in an otherwise
stable, non-bleeding infant.
• Count <100,000 µL in presence of allo-immune thrombocytopenia
(see section 19.7.1 for more details)
• Count <100,000 µLin presence of active major bleeding
• Qualitative platelet defect with bleeding with any platelet count.
Blood group for transfusion: Shown in Table 19.3. Platelets are less
antigenic than RBC's; hence more flexibility is available in terms of the
group.

Table 19.3 Blood 2rouo for olatelet transfusion


Baby Platelet group
group 1st preference 2°0 preference
0 0 B
A A AB
B B AB
AB AB B or A

Instructions related to platelet transfusion


• Transfuse 10 ml/kg of PC over 1 hour. This will raise the platelet
count by approximately 60,000/mm 3.
• The PCs must be kept in room temperature only.
• Start transfusion as early as possible after arrival of PC from the
blood bank because of the risk of aggregation.
• Gently swirl the bag before starting transfusion.
• Avoid transfusion through a central line, due to the risk of
thrombosis.
19.5.3 PRP: PRP is obtained by centrifuging anti-coagulated blood at
room temperature. PRP has less concentration of the platelets when
compared to PC (approximately 4 times less). The concentration of the
coagulation factors is also unreliable after the first 24 h of collection.
When there is thrombocytopenia and coagulopathy, transfusion of PC
and FFP is to be preferred over PRP.
19.5.4 FFP/ Single donor plasma (SDP)
Indications:
• Coagulopathy with bleeding
• Coagulopathy and invasive procedure planned
180

• Factor replacement when concentrates are not available (factor 11, V,


X and XI)
• At the initiation of heparin therapy.
5
Which group? : Shown in table 19.4

Table 19.4 Blood group for FFP transfusion


.
Baby FFP group
.
group
1si preference 2" preference
11

0 0 A,B,AB
A A AB
B B AB
AB AB -
Instructions related to FFP transfusion
• Transfuse FFP l 0 mL/kg over 2-3 h. With active bleeding one may
need to raise the concentration of the clotting factors to 20% of the
normal. This can be done by repeating l 0 mL/kg.
• FFP/SDP can be stored temporarily in the freezer compartment of
the refrigerator for less than 12 h.
• Once thawed, transfuse immediately and do not refreeze.
19.6 Vitamin K deficiency bleeding: Shown in Table 19.5

Table 19.5 Vitamin K deficiency bleeding

Tvoe Age Typical site of bleed Cause


Early <24 h lntracranial, gastro- Maternal drugs*,
intestinal, intra- Inherited
abdominal coagulooathv
Classic 2-7 d GIT, mucosa!, Missing the dose of
umbilical stump, Vit K at the birth
injection sites
Late 1-3 mths Intracranial, GIT, Cholestasis, diarrhea,
skin idiopathic
(*- m this group, do cord blood coagulat10n profile & 1f abnormal give 10
mL/kg FFP)

19.7 IMMUNE THROMBOCYTOPENIA:


Autoimmune thrombocytopenia is due to the antibodies directed against
an antigen on mother's own platelets. Allo-immune thrombocytopenia is
due to the antibodies directed against paternal platelet antigens
(commonly Human platelet antigen (HPA)-la). Immune
181
thrombocytopenia should always "'' suspected in an otherwise well
looking neonate with isolated severe thrombocytopenia. There can be a
history of affection of a pn vious sibling. In autoimmune
thrombocytopenia, the mother would have thrombocytopenia.
Alloimmune thrombocytopenia can present with prenatal intracranial
bleed.
19.7.1 Postnatal management:
• Screen the baby's platelet count soon after birth if born to a mother
with immune thrombocytopenic purpura (ITP)
• In case of alloimmune thrombocytopenia, give washed PC of the
mother resuspended in plasma or from a donor who is HPA-la
negative. Administer when neonate has counts <30,000 per µL
irrespective of bleeding; 30,000 to 49,000 per µL if minor bleeding:
and 50,000 to 99,000 if major bleeding.
• IVIG: 0.4 g/kg/d for 5 d or I g/kg1d for 2 d. (see section D68)
• Prednisolone 2 mg/kg/d (see section D l 03)

19.8 DIC:
• Treat the underlying cause
• GiveVitKl-1 mg JV
• Platelets and FFP are given as needed to keep the platelet count
above 50,000/µL.
• Consider DVET, if bleeding persists.
• In case of thrombotic DIC, give heparin@ 30 U/kg IV stat, followed
by I 0 U/kg/h to keep APTT 1.5-2 times of the normal. LMWH is
preferred in neonates over unfractionated heparin'. If LMWH is
used, the dose is 1.5 mg/kg/d SIC q 12 hourly.

19.9 MANAGEMENT OF ISOLATED ALTERED GASTRIC


ASPIRATE:
• Give stomach wash with NS.
• If altered aspirate continues, send platelet count & coagulogram.
• If platelet count and coagulogram are normal or stress bleeding is
suspected, give IV ranitidine 0.5 mg/kg/dose BID for preterm and
1.5 mg/kg/dose q 8 hourly for term babies. (see section D l l OJ

19.10 PROACTIVE MONITORING OF PLATELET COUNT/


COAGULOGRAM:
In the following conditions the JR must send the laboratory
investigation even without overt bleeding:
19.10.1 Platelet count
• NEC
• Those receiving ibuprofen/ indomcthacin (see section D66, D69)
182

• Mother received drugs like aspirin in analgesic dose, warfarin


• Intra-uterine infections
• Large hemangiomas (Kasabach- Meritt syndrome)
19.10.2 Coagulogram
• Cholestasis, liver disease. (see section 20.17)
• Mother received drugs which can cause coagulopathy

REFERENCES:
1. Andrew M. Blood. 1987;70:165.
2. AndrewM. Blood. 1988;72:1651.
3. D.J. Cassandra. Transfusion of neonates and pediatric patients. In:
Blood Banking and Transfusion Medicine: Basic Principles and
Practice Ed 2, 2007, 510.
4. Saxonhouse MA. Neoreviews, 2009.
5. Transfusion guidelines for neonates and older children. British
Committee for Standards in Haematology (BCSH). 2004.
183

20. JAU "DICE

20.1 DEFINITION OF PATHOLOGIC OR NON-


PHYSIOLOGICAL JAUNDICE
• Clinical jaundice in first 24 h of life
• TSB > 15 mg/dL in the I" wk of life
• TSB .more than 95<h percentile for the postnatal age in hours (see
section NI 9)
• TSB increasing by> 5 mg/dL/d
• Conjugated hyperbilirubinemia (direct bilirubin level >I mg/dL
when the TSB is < 5 mg/dL or> 20% of the total if the TSB is > S
mg/dL)
• Clinical jaundice (serum biiirubin >7mg/dL) persisting for more than
14 d oflife in term and 21 d oflife in preterm
However, in preterms, TSB of even I 0-12 mg/dL may cause neurological
damage if not treated. Hence therapeutic definition (i.e. jaundice likely to
need treatment in order to avoid neurological damage) is more relevant
for clinical practice.

20.2 EVALUATION OF A JAUNDICED NEONATE


The history and examination are directed towards assessing the severity,
complication and the etiology of jaundice.
20.2.1 Severity of jaundice
• Clinical jaundice becomes apparent at TSB levels of 5-7 mg/dL.
Jaundice in newborn progresses in a cephalo-caudal direction and
hence dermal staining of bilirubin may be used as a clinical guide to
the level of jaundice (See Figure 20.1).
• The newborn should be examined in good daylight. The skin should
be blanched with digital pressure and the underlying color of skin and
SC tissue should be noted. The reliability of clinical assessment of
jaundice can be affected by many fuctors: experience of the examiner,
lighting condition of the room, clothing of the baby, skin
pigmentation, gestation, postnatal age and PT exposure.
• TcB must be used for routine monitoring of bilirubin and for
measurement of pre-discharge bilirubin for babies who are in
postnatal and labor wards. TcB should be measured over forehead. If
the value falls within 2 mg/dL of PT zone or above, the value should
be confirmed with a capillary TSB. Once the baby is started on PT,
TcB cannot be used unless a photo-opaque patch is applied. TcB is
less reliable when the TSB i,. >IS mg/dL, in preterms and in
pathological hyperbilirubinemia.
184
Figure 20.1 : Correlation between icteric dermal .iones (Kramer ) and
serum bilirubin ' alues

Dermal Mean ± SD
zone (mg/dL)
I 5.9±0.3
2 8.9 :I: 1.7
3 11.8 ± 1.8
4 15 :I: 1.7
5 > 15

20.2.2 Evaluation of complications


• Look for evidence of ABE by domg a complete neurological
examination especially of the muscle tone. cry, and mental status (see
Table 20.1 ). The tenn "kemicterus" should be reserved for the
chronic and permanent clinical sequelae of b1hrubin toxicity. Stage
the encephalopathy, if any.
• The b1lirubm-induced neurological dysfunction (BIND) score enables
one to decide on the urgency of intervention (see Table 20.2). A total
BIND score o f 7-9 represents severe ABE and urgent DVET is
required to possibly minimize further brain damage. A total score of
4-6 represents moderate ABE and is likely to reverse with DVET. A
total score of 1-3 represents mild ABE and wi ll usually reverse with
DVET. These three ranges of BIND scores roughly correspond to
what were earlier called the "initial", "intermediate" and "advanced"
stages of ABE.

20.2.3 Evaluation of etiology


The time of onset of jaundice may give some clue to underlying
diagnosis {See fable 20.2) Detailed history and clinical examination is
warranted m all neonates with suspected pathological Jaundice (See
Table 20 3 and 20.4).
M H c 185

f Table 20.1 Bilirubin-induced neur >logical dysfu1 on score

Mental
Severity Score Muscle tone Cry pattern
status
None 0 Nonna( Normal Normal
Sleepy,. Neck stiffn~ss,
High
Mild I poor mild
pitched
feeding JI hyper/hvootonia
Arching neck,
Lethargic,
Moderate 2 retrocollis, Shrill
irritable·
arching trunk ·
Semi-
coma, Bowing trunk,
Severe 3 Inconsolable
seizures. opisthotonus .
coma
,\ote: The 81?\D o;corc holds good for late wctenn and term infant>. Pretenn babies may
not ~ho" the abo~c evolution of ABE. -

Table 20.2: Age of onset and comn on underlying cause

<24 h I 24-72 h 3-7 D >7 0


Breast Milk
Rh Incompatibility Idiopathic
I Jaundice
ABO Incompatibility
G6PD Deficiency
Sepsis
.
Minor Blood Group
Incompatibility
RBC Membrane Defect
I Enclosed Hemorrhage
I lncreaseJ Enterohcoatic Circulation
Hypothyroidism
Intestinal
Obstruction

Table 20.3: History inn jaundiced infant

History Relevance
Blood group incompatibility (Rh.
Previous sibling with neonatal ABO), G6PD deficiency,
jaundice or family h/o anemia, spherocytosis, Cnglcr-NnJjar.
~~~e~am~1 ___--------~~U~G~1~~~a~r\a~n~~~~~~~---'
186

History Relevance
Maternal illness with fever and
JUI
rash during pregnancy
Asphyxia, trauma, use of oxytocin,
Labor and delivery events
delayed cord clamping
Maternal drugs (sulfonamides, Hemolysis in a G6PD deficient
nitrofurantoin, antimalarials) infant
Galactosemia, a-1 antitrypsin
Liver disease in the family
deficiencv
Prolonged parenteral nutrition Cholestatic jaundice

Table 20.4: Physical examination in a jaundiced neonate

Physical examination Relevance


SGA Polycythemia, JUI
Microcephaly IUJ
Pallor Hemolytic anemia, extravasation of blood
Bruises, cephalhematoma Increased bilirubin formation
Petechiae IUI, sensis, en"hroblastosis
Hepatosplenomegaly Hemolytic anemia, JUI, liver disease
Chorioretinitis IUI
Urine staining diapers and
clay colored stool Cholestasis

20.3 LAB INVESTIGATIONS


20.3.1 Level of jaundice
TSB should be done when pathological jaundice is suspected or when
there is a doubt in visual estimation of jaundice or when TcB is ~15
mg/dL. Once under PT, TSB should be repeated every 4-12 hourly. More
frequent assessment of jaundice is done when-hemolysis is suspected or
the TSB value is near DVET zone.
20.3.2 Investigations to determine etiology of jaundice
Any neonate whose TSB is high enough to require PT must undergo
investigations to determine the etiology.
• Blood grouping and DCT. This should be done only if mother's
group is 0 or Rh negative or if a minor blood group incompatibility
is strongly suspected.
• G6PD enzyme activity
• CBC for evidence of hemolysis (increased reticulocyte count -
reticulocyte count is normally as high as 6.5% in I" wk of life which
187

falls to 2% by the end of 2"' wk of life), fall in PCV, peripheral


smear for spherocyte (both mi 'ro- and macro-), elevated nucleated
RBC count (> 1000 nRBC/mm 3), anisopoikilocytosis and
polychromasia)
• Conjugated bilirubin fraction must be assayed at least once if
jaundice persists beyond 5 days and/or when cholestasis is suspected
• If history and or presentation suggest sepsis, investigate for sepsis
20.3.3 Prediction of severe hyperbllirubinemia
Neonates- born at :::36 wks and :::2000 g with no risk- getting discharged /
at <72 h age should have their bilirubin measured by TcB and assessed
for the risk of developing severe hyperbilirubinemia on Bhutani's hour
specific bilirubin nomogram (see Table 20.5; section NJ 9).

20.4 ACTION BASED ON PRE-DISCHARGE BILIRUBIN 1 : Shown


in Table 20.5

Table 20.5 Action based on pre-discharge bilirubin in neonates :::36


wks and :::2000 g without risk factors

Pre-discharge TSB Discharge


Action
value a~e

Don't discharge, plot TSB in


In high OR high
< 72 h PT chart & start PT if
intermediate risk zone
reauired
In low intermediate or < 24 h Review at 48 hours following
low risk zone OR was 24-48 h discharge
not done 48-72 h

20.4 MAJOR RISK FACTORS FOR SIGNIFICANT


HYPERBILIRUBINEMIA IN INF ANTS :::35 WKS GESTATION
• Clinical jaundice observed in first 24 h of birth
• Previous sibling received PT
• Cephalhematoma, subgaleal bleed or significant bruising
• Nonoptimal sucking/nursing
• GA 35 to 36 wk
• Blood group incompatibility with +ve DCT, incidentally known
hemolytic disease

20.6 TREATMENT
The two main treatment modalities arc
• PT
• DVET
188

20.6. l Parameters to be taken into account while deciding about


treatment:
• Gestation of the baby
• Wt of the baby
• Postnatal age of the baby in hours
• Level of jaundice
• Presence of risk factors

'"""" 20.7 GUIDELINES FOR NEWBORN INFANT 2' 35 WKS OF


GESTATION
• AAP published charts for PT and DVET for newborn infants 2'35
wks of gestation in the year 2004 (see section N20. l, N20.2). They
have 3 action lines based on the risk- low, medium and high risk.
Indian babies have many risk factors like lower serum albumin,
higher bilirubin production rates, higher G6PD prevalence, and
unrecognized asphyxia and also our PT units are sometimes unable
to provide intensive irradiance. Hence, the PGIMER unit follows
only the medium and high risk lines in the AAP chart; and we ignore
the low risk line.
o Medium risk line- 2' 38 wk and no risk factors
o High risk line- 2' 38 wk+ risk factors or 35-37 6"
Risk factors- isoimmune hemolytic disease, G6PD deficiency, asphyxia,
significant lethargy, temperature instability, sepsis, acidosis, albumin <3
g/dL.
• Use total bilirubin for decision making. Do not subtract direct
reacting or conjugated bilirubin unless it is more than 50% of total or
5 mg/dL.
• Immediate DVET is recommended ifthe infant shows signs of ABE.
• By default, PT means intensive PT (irradiance in blue-green
spectrum of at least 30 µW/cm 2 per nm and delivered to as much of
the infant's surface area as possible).

20.8 PRETERM INFANT< 35 WKS OF GESTATION


• There is a lot of controversy about the cut-off values for PT and
DVET in preterrn babies. The general guide is to start PT when TSB
is 0.75% and to do a DVET when TSB is 2'1 % of the body Wt in
grams (see Table 20.6).
• The following cut-off values are currently followed in PGl 2 • Perform
a DVET at the lower end of the range in the presence of isoimmune
hemolytic disease, G6PD deficiency, asphyxia, significant lethargy,
temperature instability, sepsis, acidosis and albumin <3 g/dL.
189

T a bl e 20 6 T reatment l uidelines in infants <35 "'ks of 2estation


Wt 'T DVET
< 1000 g Visible jaundice 10-12
1000-1500 g -_9 12-15
1500-2000 g 10-12 15-18
2000-2500 g 13-15 18-20

20.9 PT
20.9.J Practical points
• Commo11/y used light sources are
o Special blue tube lights (Phalips TL52, 20W)
o Special blue CFL lamps (Philips l 8W or Osram 18 W)
o High intensity gallium nitride blue light emitting diodes (LED)
2
• Dose: Minimum of 15 µW/cm2/nm. Ideally 30 µW/cm /nm. The
higher the 1rradian~e. the bette· 1s the effect. Io increase the dose,
sc the following methods
Most importantly, measure the irradiance and if it is below 15
µ W 1cm2tnm. change the tubes.
Consider double surface PT (place lights both above and
below). Double surface and multiple PT should be used if:
• TSB rises rapidly (>0.5 mg dL h)
• TSB is within 3 mg/dL of the threshold for DVET
• TSB fails to respond t) single surface PT within 6 h (i.e.
e ot a or con mi..cs o n
lfTSB falls to a eve > m ~dL below the threshold for DVET.
step down to single surtacc 1 .
o Distance between tubes and baby can be decreased to 10-15 cm
o Add additional PT units see indications above, for double
surface PT)
o Sides of bassinet. incubator or warmer can be lined with
aluminum foil or white she ts taking care to sec that the hot air
vents arc not blocked.
• SR of each area should check irradiance of all the PT units
belonging to his her area every f >rtnightly (i.e. on I" & 16th of every
month) and ensure that the lights and protective covers are clean.
• While under PT, the baby's eye should be securely covered (put an
opaque paper in between layers pf bandage) w11hout undue pressure
on the face and nose. Commerc ally available PT goggles may also
be used. They generally come in 2 sizes- 2 cm x 9 cm and 3cm x 12
cm
• The mother should be encourag.!d to remove the baby from under
the lights, uncover the eyes and breastfeed every 2-3 h. During
breastfeeding, switch off the Pl unit. If the TSB is rising at >0.5
190
mg.dLh or the TSB is within 3 mgdL of the threshold for DVET,
the mother must be told to minimize the stoppages of PT as far as
possible.
20.9.2 Monitoring a baby receiving PT
• Clinical assessment of jaundice in babies under PT may be
fallacious. Hence, monitor TSB level every 4-12 hourly, depending
on proximity ofTSB to the cut-off value for DVET.
• Babies under PT may develop hyper or hypothermia. Monitor
axillary temperature every 2-4 hourly.
• Record Wt daily; ensure that baby passes adequate urine (6-8 times
per day).
• Some degree of loose green stools are fairly common during PT.
Sometimes, a skin rash may develop. Mother should be reassured
about the transient and benign nature of these conditions.
• Check skin color. PT if used in infants with conjugated
hyperbihrubmemta can cause bronze discoloration of skm.
20.9.3 Stopping PT
Stop PT once you obtain 2 TSB values at least 4 h apart that are at least 2
mg 'dL below the PT cut-ofT (see section N20. I). Take the natural course
of the cause of jaundice into account while stoppmg PT. Check for
rebound nse in TSB after 8-12 h in neonates with GA <35 wks, BW
<2000 g, G6PD deficiency or hemolytic diseases. In all others, check
rebound by TcB.

20.JO DVET
20.10.1 Indications for DVET:
• Hydrops: Perform DVET as soon as possible after birth, once the
baby is stabilized. (initially only PET may be done to increase PCV
if baby cannot tolerate double volume exchange)
• I-Vo previous sibs requiring DVET because of Rh isoimmunization
and the index patient 1s born with pallor, hejiaiOsplenomegaly and
positive OCT.
• Cord Hb < I 0 g/dL and/or ord TSB > 5 m dL
• Rate rise o SB > mg/ Uhour despite PT or rate of rise ofTSB
> 0.5 mgtdLhour despite PI 1f Hr>is between I 0-12 g dL -
• Any TSB > 12 mg/dL in first 12 h a"ffit any I SB 5 2umg, dL m the
neonatal period in the setting of hemolysis.
• Jn DVET zone as per modified AAP charts for near tc and term
babies (see section N20.2) ...- y
191

20.J0.2 Which blood group to ask for? Shown in table 20.7


Table 20. 7 C hoice of blood group for DVET

I' 1 choic ·: Rh-negative blood of baby's ABO


type
Rh isoimmunization 2"" choic.!: 0-ve whole blood
If under~one intrauterine or DVET earlier
with 0-\ e blood, 0-ve blood has to be used
c1.: · tlv -
I"' choice: g +ve cells suspended in AB
ABO
incompatibility
plasma _- --
2nd choicC-o +ve whole bl~

For other babies Baby's blood group I

20.10.3 Practical points about reqoisitioniog blood


• Donor blood must also be cross 'Tlatched against maternal plasma.
• Ideally, the age of the blood nust be 5 d or less. If the baby is
otherwise healthy, one could use older blood.
• Check the pH of donor blood from the blood bag (not from the
tubing). If pH <7, ask for a fre!>h ahquot of blood. Correction of pH
to physiological level by addition of buffer solutions is not indicated.
• Check G6PD status of donor blood. The result 1s unlikely to be
available before the DVET bu G6PD deficient donor blood may
explain unsatisfactory fall or paradoxical rise of TSB after the
DVET.
• Use CPDA stored blood [Do not use SAGM (Saline-adenine-
glucose-mannitol blood as it co1Lains mannitol].
• Irradiation is mandatory if the infant has had previous IUT (sec
section 17 7.3)
• In PGIMER blood bank, blood products are routinely screened for
HIV, HBsAg, HCY, syphilis & malaria. In an emergency situation
where the requisite blood group is not available in PGIMER, and if
blood is issued from another blood bank, always check the screening
status. Blood banks in the Tric11y area include Government medical
college and hospital (GMCH)-3 ~. GMSH-16, Rotary, Fortis, Mohali
civil hospital, Panchkula civil heispital.
• Warm the blood gradually to 37 °C by placing inside the incubator.
Do not warm it by placing under the radiant warmer or putting inside
hot water.
• Do not massage or shake the bag
• Ideally, reconstitution of packe( cells and plasma in a ratio of 7:3
(PRBC: FFP) should be done in blood bank itself and not in the unit.
192
Talk to the SR or consultant of Transfusion Medicine to get pre-
mixed "'hole blood.
20.10.4 Procedure of DVET (Also see PGIMER video on neonatal
procedures)
• Volume requirement· 2 x infant's blood volume 50 mL extra (for
dead space) (also see figure 18.1)
Blood volume= 80 mL kg in infants> 2 kg
90 ml.Jkg in infants 1-2 kg
I 00 mL. kg in infants < I kg
• Explain the procedure and its risk to the parents and take their
informed consent.
• Ensure the stomach is empty.
• Check and match the bag number on the bag and the reaction form.
• Monitor HR (ECG monitor), temperature (thermistcr probe) and
Sp01 continuously and RR every 10 mm during the procedure.
• The aliquot volume should not exceed 3-5°'0 of the blood volume of
the baby. The sacker and smaller the baby, smaller should be the
ahquot.
• Durmg the DVET keep moving the bag intermittently to prevent
RBC's from settling.
• To a\'Otd air embolism, always keep the synnge vertical w1th nozzle
facing down and never leave the umbilical catheter end open.
• lJsc the 4-way DVET stopcock
• Do not be in a hurry to finish the exchange; it should take at least I
hour.
• An otherwise healthy neonate does not require IV Calcium during
the DVEl.
20.10.5 Blood samples to be drawn during DVET
• The first aliquot w.ithdrawn from the baby should be used for thJ
purpose of various investigations (CBC, G6PD, DCT)
• The last aliquot wuhdra\~O discard dead
space volume) should be used for future cross matchi~
20.10.6 Post-OVET instructions -
• Give vit K and repeat all medications the baby ""as recel\ mg
• Watch for bleeding from umbilical stump
• Monitor RR, HR. color and temperature 1'2 hourly for 2 h
• Check BS, TSB & PCV at 2 h followmg DVET -
• Oral feeds can be started after l-2 h if baby 1s well ~
• There 1s no need for routine antibiotics after a DVFT (even after
multiple transfusions), unless there has been a breach of aseps1s or
the umbilicus looks unhealthy.
193

20.11 FLUID SUPPLEMENTAT ON: Shown in Figure 20.2


• ln a study conducted in PGIMER on term neonates with severe non-
hemolyuc Jaundice (TSB >20), fluid supplementation decrea!ied llie
. neecrtor tlv £I ' even tn infants who had no O\Crt features of
dehydrallo!{ Tlte fluilfJN/5 in ~ 0/o Dextr~ shOuid be g1veO-ov<:E!__
('1. h (50 mUg + 20 mL kg PT al owance ., •, of 8 hour maintenance

-
0
til\ .W
1."1~
f_

o
t1µ1d requirement). A simple brmula to calculate ' this 8-h fluid
requirement 1s. Fluid volume= [340 .f xm6, "h~e x 1s that day's
maintenance fluid requirement(e~pressed m ml.kg,d) and Wt IS
expressed m kg)
• lt may also work in hemolytic Jaundice and preterm neonates, but
evidence is still awaited. pie should consider giving fluid
suppl ementation in all cases of evere n~:J1emolytic Jaundice (TSB
> 18) and in Ifie waiting phase b fore DVE'T m cases w1lh hemolytic
J~
Figure 20.2~ Algorithm for fluid supplementatiot>

Tenn neonaL!~ with


TSB "'ithin mg!dL of
DVET zone r more

TSB >25 mgldl or rss 25 mg ·dL & No


bllirubm encephalopathy b1lirubin encephalopathy

Give Omd tart fluids & rpt TSB after 4 h


supplementauon till blood for
DVET is available

Rpt TSB m exclrutge Rpt TSB below


zone exchange zone

Do DVE1 Continue fluids for


4 mnri> h
194

20.12 IVlGs (see section D68)


!VIG given in the dose of 0.5-1 g/kg can prevent repeated DVETs in
jaundiced babies due to Rh isoimmunization or proven ABO
incompatibility4 . It should be administered to all Rh ·isoimmunized
neonates soon after birth if DVET is not imminent an}I immediately after
the first DVET.

20.13 PHENOBARBITONE (see section D99)


It induces hepatic conjugating enzymes and in an unblinded trial, was
shown to reduce the need for DVET and duration of PT in VLBW babies
if started on day I of life 5 . It takes 2-3 d to induce the enzymes and has a
limited role if jaundice is already at its peak. There are concerns about its
effect on long term neurodevelopment. Prophylactic phenobarbitone does
not help in G6PD deficiency. Do not use without discussing with
consultant.
Approach to jaundice in non-isoimmunized neonates and to a baby born
to an Rh -ve mother are shown in Figure 20.3 and 20.4 respectively.

20.14 DISCHARGE AND FOLLOW UP


• Do a thorough neurological examination and record any abnormal
findings in the discharge summary. Make sure the cause of jaundice
has been ascertained.
• Give a list of drugs to be avoided in G6PD deficient babies to the
parents. Tell parents of G6PD deficient neonates to avoid use of
naphthalene balls for storing clothes.
• Hearing screening (see section 41.2). BERA is used for screening.
Increased inter-peak latencies I-III and 1-V indicate bilirubin induced
auditory neuropathy. BERA can promptly improve (completely or
partially) after a DVET, with latency of wave I and amplitudes oflll
and V showing maximum recovery. OAE must not be used to screen
or follow-up ABE.
• MRI
o Indication: Any baby with evidence of stage 1 bilirubin
encephalopathy with developmental delay and all the babies
with bilirubin encephalopathy of stage ~2. To be done at ~6
mths of age.
o Schedule examination after discussion with consultant.
o For details of taking appointment, refer to section 42.4.
o Findings in kemicterus: MRI shows changes of kemicterus
within the l st wk of the illness. In acute kernicterus, only T 1-
weighted images show bilateral symmetrical increased signal
intensity in the globus pallid us and sub-thalamus in about 2/3 cd
of cases. After the neonatal period, T 1 hypcrintensities fade
away and are replaced by hyperintensities in the same areas on
195

Ti-weighted images with or without hyperincensitics m the


putamen and thalamus.
• SPECT (Single Photon Ernissio1 Computed Tomography)
This modality is helpful if the c 1ild 1s bctng rnvestigated for the first
time beyond infancy, because MRI findin s become less clear.
SP CT shows asa ganglia.

Figure 20.3: Approach to jaundice In non-isoimmunized neonates

Newborn • Can discharge


Infant (:>:35 w) • Advise to follm~ a~ m
table 20.5
+
,,1
Assess for jaundice
8-12 hourly

!
ls jaundice __N_o--t• ls newborn read Yes Any major nsk factor•
present'> for discharge? - - - - . . . . ANDagc <72 h

! Yes

• ls age <24 h
• Appears excessive for age
J No lYb
• Measure TSB
• Doubt about degree of
• Plot in nomogram &
jaundice decide funhcr
iv~
Measure TSB &
interpret by age in
hour

Ko Is TSB 75• Don't di~chargc.


lsTSB m PT
percent le ------!~ Re\iew by
wne'>
12-24 h

! Yes
• Evaluate cause • Can discharge'
• Stan PT • Advise to foll was m
• Repeat TSB in 4-12 h table 20.5
*Note: Major risk f1ctors
• Clinical Jaundice S 24 h
• Pre\ious sib received PT
• Cephalhcmatoma, subgaleal bleed or sign 1cant bruising
• Nonoptimal sucking/nursing
• Gestauonal age 35 to 36 wk
• su~nect hcmolvt1c d1sca.~c
196
Figure 20.4: Approach to a baby born to an Rh ~ve mother
Mother Rh negative

i
H/o previous sib involvement
Isoimmunized in this pregnancy
• Rising ICT titer+
• Hydrops fetalis
• Fetal anem1·a
Yes

SR to attend
No

Cord TSB/PCV/DCT

Is immediate DVET
No Monitor TSB/PCV 4 hrly
required? -------~ Start IVIG if features of

l
Do DVET
Yes
isoimminization

Start PT ifTSB
Give IVIG • Is in PT zone
Intensive PT • Rising by> 0.5 mg/dl/h

1 1
Do DVET ifTSB > 12 mg/dL in !' 24 h or> 20 mg/dL subsequently
Can repeat TVIG 12 hrly
Do conjugated TSB & subtract it from total only if> 50o/o of the total

Table 20.8 Drugs to be avoided in case of G6PD deficiency

Drugs definitely Drugs that may produce


No
producintz hemolvsis hemolvsis
Antimalarials
I Primaquine Chloroauine
2 Quinacrine Hvdroxychloroauine
3 Quinine
4 Mepacrine
/

197

Drugs definitely Drugs that may produce


No
oroducine hemolvsis hemolvsis
Sulfa dru1s
I Sulfanilamide Sulfadiazine
2 Sulfapyridine Sulfaohenazole
3 Sulfathiazole
4 Sulfasalazine
5 Sufamethoxazole
Sulfones
1 Dapsone
Nitrofurones
I Nitrofurantoin
2 Furazolidone
3 Nitrafurazone
Antipyretics & analgesics
I Antipyrine Aspirin
2 Mephenemic acid Ibuprofen
3 Phenylbutazone Probenecid
4 Oxyphenbutazone Phenacetin
Antibiotics
1 Nalidixic acid Chloramphenicol
2 Nitrofurones Norfloxacin
3 Ciprofloxacin
4 T rimethoprim
ATT
l PAS Pyrazinamide
2 !NH
Miscellaneous
l Naphthalene
2 Vit K 2 & K3
3 Quinidine

20.14.1 Drugs to be avoided in case of G6PD deficiency: Shown in


table 20.8
• Repeat G6PD activity after 1 mth if it was deficient earlier. Mutation
analysis for major G6PD mutations can be done after seeking
appointment from Dr Reena Das. Hematology.
• Do neurodevelopmental evaluation at 3, 6. 9 and 12 mths (see
sections 43.1, 43.2).
198
20.15 PROLONGED JAUNDICE
Visible jaundice (serum bilirubin >7 mg/dL) that persists beyond 14 d of
life in term and 21 d of life in preterm infants. Persisting jaundice is more
common in breastfed infants than artificially-fed infants. At least 9% of
breastfed infants are jaundiced at 28 d of age. Approach to a case of
prolonged jaundice is shown in Figure 20.5
20.15.1 Causes of prolonged jaundice
• Hemolytic disease
o Blood group incompatibility
o G6PD deficiency
o Hereditary spherocytosis
• Hypothyroidism
• Breast-milk jaundice
• UT!
• Malaria
• Pyloric stenosis
• Extravascular blood
• Crigler-Najjar syndrome
• For causes of conjugated hyperbilirubinemia see section 20.17.
Consult Pediatric Gastroenterology SR or consultant, if conjugated.
Gilbert syndrome in isolation is not a common cause of jaundice in
neonates, but it may exacerbate the jaundice when it is present concurrent
with G6PD deficiency or breast milk jaundice.

20.16 BREAST MILK JAUNDICE


• Jaundiced breast-fed infants who are well are unlikely to have
serious disease. Breast milk jaundice is a diagnosis of exclusion,
after investigating as above.
• If TSB is > 15 mg/dL, recheck the bilirubin within 1-2 d to ensure
that it is not increasing. Otherwise repeat weekly or less often as
indicated by clinical examination. If persistent, recheck the
conjugated fraction.
• Parents would need reassurance that the jaundice itself is not
harmful.
• Although temporary cessation of breastfeeding may reduce or
eliminate prolonged jaundice associated with breast milk, we do not
recommend this, as the evidence implicating breast milk as a
causative factor is weak; cessation of breast milk may stigmatize the
mother and increase the risk of GIT infections.
199
Figure 20.5: Approach to a case of prolonged hyperbilirubinemia

Prolon;ed Jaundice

i
Direct & Total Bilirubin

I
+
Predominantly +
Conjugated
Unconjugated Evaluate for causes of cholestasis

i
History- hemolytic disease, jaundice
(see Figure 20.6)

Examination- signs of hypothyroidism


Investigation
• Blood grouping, DCT
• Retie count, peripheral smear
• G6PD activity
• Thyroid profile
• Urine for reducing substance
• Urine routine/microscopy & c/s

i
If all work up negative & jaundice
persisting (>15 mg!dL), Give
phenobarbitone 5 mg/kg/day for 7 day
and re-evaluate (only after discussion
with consultant).

20.17 APPROACH TO CONJUGATED HYPERBILIRUBINEMIA:


shown in Figure 20.6
Conjugated hyperbilirubinemia is defined as direct bilirubin level > l
mg/dL when the total bilirubin is < 5mg/dL or > 20% of the total
bilirubin if > 5mg/dL. Neonatal cholestasis is defined as conjugated
hyperbilirubinemia + dark yellow urine ± pale stools.
200
Figure 20.6 Approach to conjugated hyperbilirubinemia
Jaundice,
dark urine± acholic stool

Give vitamins in
Conjugated hyperbilirubinemia - - - - . enhanced doses''!'
Do LFT, PT, INR

Sick or clinical setting* Not sick & no specific


Urine for non-glucose clinical clues
reducing substance, GAL Ts Look for stool color for 3d
Blood and urine culture Abdominal uso"
CBC, malaria parasite
TORCH serology Pale stools
AFP, urinary succinylacetone
Pigmented stoo! GB: sma\l/non-
Serum ferritin •----USG: nonnal visualized
IEM work up ifnecessary
Gallbladder (GB) Triangular cord sign+


Liver biopsy if indicated
Urgency: Biliary
Atresla
Liver biopsy

Liver biopsy± HIDA

Neonatal hepatitis: giant cell Biliary atresia on liver biopsy


transformation, lobular disarray Biopsy equivocal and no excretion on HIDA
Bile duct _pauci~ (Hepatobillary lmino-Diacetic Acid)
Storage disorder Laparotomy and preoperative cbo\angiography
Kasai portoenterostomy or Hepaticojejunostomy

1
"· Vit A (Aquasol-A) 50,000 IV IM monthly, Vit D (Arachitol) 40,000 JU IM monthly, Vit K 5 mg JM
monthly, Vit E 15-200 mg/d PO. Water soluble vitamins: twice the RDA. Continue fat soluble
vitamins for 3 mths after resolution of jaundice.
* fndividualize investigation,*'" surgery ifcholedochal cyst on USG
~ Stop milk feeds till galactosemia is ruled out
• may need bone marrow testing

REFERENCES
I. Subcommittee on Hyperbilirubinemia. Pediatrics 2004; 114: 297.
2. Cloherty J P, Eichenwald E C, Stark A R. Manual of neonatal care
2007. Lippincott Williams and Wilkins 61h edition; chapter 18.
3. Karthik B, Praveen K. M.D. Thesis PGIMER; Chandigarh: 2008.
4. Hammerman C. Acta Pediatr 1996; 85: 1351.
5. Kumar R. Indian Pediatr 2002; 39:945.
201
21. INTRA-CRANIAL HEMORRHAGE AND
PERIVENTRICULAR LEUCOMALACIA

21.1 MAJOR TYPES OF INlRACRANIAL HEMORRHAGE:


Shown in Table 21.I

Table 21.1 Major types of intracranial hemorrhage

Type of Maturation of Relative Usual


hemorrhage infant frequency clinical
severity
Subdural Tenn > pretenn Uncommon Serious
Primary Tenn > preterm Common Benign
subarachnoid
Intracerebellar Preterm > term Uncommon Serious
Intraventricular Preterm > term Common Serious
Intra-cerebral Term > preterm Uncommon Variable

21.2 WHEN TO SUSPECT INTRACRANIAL HEMORRHAGE:


• Catastrophic deterioration- Baby suddenly becomes very sick
showing signs of brain stem compression viz. stupor, coma, ataxic
respiration, bradycardia, absent doll's eye movements, skewed
deviation of eyes, unequal pupils, nuchal rigidity, ophistotonus, tonic
posturing, hypotonia.
• Acute unexplained deterioration while on ventilator
• Seizures
• Apnea
• Signs of hydrocephalus- raised fontanel, loss of pulsatility of
fontanel, irritability, lethargy.
• Asymptomatic babies: showing bloody CSF tap with three tube test
negative.
''Three Tube test': this test is used to differentiate SAH/IVH from
traumatic tap. Collect the CSF 0.5 mL in the first vial and then
sequentially in two other vials and see for the color of the CSF and
microscopic examination on NC. In case of progressive clearing of
CSF in the vials (positive test) it is likely to be a traumatic bleed. In
cases ofIVH/ SAH the CSF should appear similar in the 3 vials. The
same cell count in the first and third vial also suggests IVH/SAH
while progressive clearing suggests a traumatic tap.
202

21.3 NEURO-IMAGING MODALITIES: Shown in table 21.2

Table 21.2 Types of intracranial hemorrhage and their diagnosis

Type of Common Common sites Usual


hemorrhage pathologies of collection Diagnostic
modalitv
Intra ventricular Origin Ventrolateral USG-
subependymal lateral Procedure of
germinal ventricles, choice.
matrix, extends choroid plexus, CT- To detect
in ventricles, parenchyma complicating
peri-ventricular lateral to lesions e.g.
hemorrhagic ventricles Subdural
infarction hemorrhage
(SDH), post.
fossa bleed,
communicating
hvdroceohalus
Subdural Tentorial Most often CT- Best.
laceration infratentorial MRI: Infra-
Faix laceration Longitudinal tentorial bleeds.
cerebral fissure USG- Insensitive
Convexity Surface of Skull
Subdural cerebral radiograph- for
hematoma convexity skull fracture
Primary Leptomeningeal Cerebral CT- Best.
subarachnoid arterial/ convexity MRI- for
bridging veins posteriorly, infratentorial
bleed posterior fossa bleeds.
USG-
Insensitive.
CSF- Incidental
diaQnosis
lntracerebellar Primary Cerebellar CT- Best.
Intracerebellar, fossa MRI- IfCT fails
Venous to pick.
infarction, USG-
extension from Interpretation
IVH/SAH, difficult as
laceration vermis echo2:enic
203

21.4 GRADING OF IVH (ON US<;): 1


• Grade 1: Germinal matrix hemorrhage or minimal IVH (<I 0%
ventricular volume)
• Grade 2: IVH occupying 10-50% of the ventricular area on
parasaggital view.
• Grade 3: IVH occupying >50% of the ventricular area on
parasaggital view which usually distends the lateral ventricle (at time
of diagnosis of IVH).
• Peri-ventricular hemorrhagic infarction: The presence of bleed in the
cerebral parenchyma adjoining lateral ventricle e.g. in
periventricular white matter on parasaggital view.

21.5 MANAGEMENT OF IVH: Shown in Figure 21.l

Figure 21.1 Management of IVH


r Catastrophic deterioration CSF done to rule out High index of suspicion-history of
meningitis showing asphyxia, abnormal presentation,
blood instrumentation during delivery,
difficult delivery, prolonged or
l precipitous labor.

l
Three vial test -ve

1
I Look for signs ofbrainstem herniaJion, do USG Head I

I ! l
Bleed with signs Bleed without
No Bleed of brain stem signs of brain
herniation stem herniation

'
1
l
Vitals.& ~NS
mon1tonng
I

Surgical
decompression
I



i
Medical management
Maintenance of cerebral perfusion- maintain
normal BP. Refer to Chapter 29.
Avoidance of fluctuating/raised BP, hyper-
osmolar solutions, rapid bolus
Trc-atment of acidosis, pneumothorax,
seizures, !CO, 10, (optimize ventilator
Monitor OFC and settings).
fontanelle daily, serial • Follow up USG scans (see section 21.8) .
USGq7d
204

21.6 SCHEDULE OF USG SCANNING:


• Asymptomatic preterm infants- All preterm infants S33 wks of
gestation and <J 500 g BW should undergo cranial USG on day 4 of
life (as 90% present by that age), on day 7-14 of life (almost 100%
present by then) and at 36 to 40 wks PMA (PHH, ventriculomegaly
and porencephalic cysts are identified). For neonates <28 wks,
perform an additional USG within 24 h as well, to prognosticate and
decide on aggressiveness of treatment (Modification of the
2
American academy of neurology practice parameter, 2002)
• Symptomatic babies- USG scan is done whenever child becomes
symptomatic.
• Follow up USG- If IVH is detected; the scan should be repeated
after 3-5 d as 20-40% extends in that duration. For further follow up
see section 21.8.
21.6.1 CT and MRI
• CT scan must be done to detect hemorrhagic lesions in the
encephalopathic term infant with a hlo birth trauma, low PCV, or
coagulopathy.
• If CT findings are inconclusive, MRI should be performed between
2 and 8 d oflife to assess the location and extent of injury.

21.7 PREVENTION OF IVH:


• Newborn resuscitation
o A voiding rapid fluids infusion- Give saline over 10 min and do
not give fast IV pushes esp. in preterrn babies.
o Preventing hypoxia and hypercarbia
o Avoiding excessive pressure on the infant's face during
interventions like bag and mask ventilation
• Sedatives and muscle relaxants
o Opioid infusions are often used in infants receiving IMV who
show asynchrony with ventilators (see section 086). A meta-
analysis3 of six studies revealed no significant effect (RR ~
0.84; 95% CI, 0.60 to 1.17) on all IVH or severe IVH, however
in the NEOPAIN trial neonates receiving regular infusions
without any open-labeled morphine had significantly higher
incidence of IVH. The neonates receiving only open labeled
morphine developed the composite outcome of death, IVH and
PVL significantly more often. Hence, there is no indication for
the routine use of opioids and they should be given only with
specific clinical indications based on pain scores (see section
44.5.1).
o The use of muscle relaxants is not recommended as it has many
4
adverse effects that over-ride its benefits. (see section 096).
205

• Other precautions preventing major hemodynamic disturbance-


o Gentle handling and mininal stimulation.
o Gentle tracheal suctioning (see section 14.14.4)
o Preventing rapid infusions of colloids and blood products
o Gentle pushes during DVET.
o Avoiding high venous pressures like prompt treatment of
myocardial failure, high PEEP, gentle ventilation strategy
preventing pneumothorax. (see section 14.12.5)
o NaHC0 3 infusions (if at all used) must be diluted to 4.2% and
administered as a slow infusion.
• Pharmacological interventions
No preventive medicine has been convincingly demonstrated to
reduce the incidence of IVH. These include Phenobarbitone,
Indomethacin, Ethamsylate, Vit E.

21.8 PHH
21.8.1 Definition and diagnosis
PHH- is defined as IVH followed by progressive enlargement of cerebral
ventricles witil the ventricular width at the intraventricular foramen
exceeds 4 mm over the 97th centile for GA.' (see section N8) Ventricular
Index is the distance between midline and border of lateral ventricle in
the plane of third ventricle in coronal view. The incidence of PHH
increases with the severity of IVH- grades I & 2: 5-12%, grades 3 & 4:
PHH up to 75%. Ventricular Index is preferred over Ventriculo-
hemispheric ratio (VHR).
21.8.2 Management of PHH: Shown in Figure 21.2
21.8.3 Indication for therapeutic LP (See PGIMER video on neonatal
procedures):
LP is therapeutic only ifthe hydrocephalus is communicating. lfthere are
signs of raised ICP or the ventricles gradually enlarge beyond the 97th
centile +4 mm limit, LP is done to drain IO mL/kg of CSF (measured at
bedside with the help of sterile graduated disposable syringe) and sent for
analysis (see section NS). After LP and draining CSF USG is done to
find the ventricular width. If it crosses the 97th centile +4 mm limit, the
LP is repeated.
21.8.4 Pharmacological management of PHH:
Acetazolamide and frusemide (see sections DI and D55) are not
routinely recommended in the management of PHH. 6 Their role in other
forms of hydrocephalus is not clear.
21.8.5 Indications for Ventriculo-peritoneal (VP) shunt
• Progressive ventricular dilatation > 4 wks despite serial CSF taps.
• Rapidly progressive ventricular dilatation (head growth >2 ems/wk,
moderate or severe ventricular dilatation)
206

Figure 21.2 Management of PHH

~
+
I No (65%) •
I Slow (30o/o) progression I
progression
I I

l Continued • Spontaneous Rapid (5o/o)


No further I dilatation
(35%) (>4 wks)
Arrest (65o/a)
(>4 wks)
progression (<4
wks)
I treatment
!
Serial LP I Shows features oflCP, rapid
ventricular head growth(> 1.5 cm/week),
drainage apnea, altered scnsorium, full
fontanel, separated sutures >Srrun,


Cessation I Contd
J.

I of dilation dilation I Serial LP (Appxox 10 ml/kg)


VP Shunt
Pediatric
If not possible-ventricular drainage,
should do from both sides.

Surgery
F/up

J. 1
Cessation of Contd
dilation dilation


Ventricular drainage

I
J.
Cessation of
dilation
l 1
Contd
dilation

Monthly observation for 3 months and then 2 monthly for I year VP Shunt
Pediatric
Surgery
F/up

External ventricular drains may be tried as temporary procedures in


infants < 1500 g and with CSF protein > 200 mg/dL pending VP
shunting.
207
21.9 PVL:
PVL refers to necrosis of white mi,tter in the region dorsal and lateral to
the external angles of lateral ventr cles. Incidence of B/L cystic PVL is
around 10-13% in 23-27 wks, 4 7% in 28-32 wks and overall 5%.
Echodensities have an incidence of I0-18%, 4-9% and 8% for
7
corresponding gestation. . lt may present soon after birth in case the insult
occurs in utero but usually takes 2 wks to develop.

21.10 RISK FACTORS OF PVL:


Prematurity, hypoxic ischemic injury, chorioamnionitis, hypotension,
large PDA, apnea, hypoxia, hypocarbia and EOS.

21.11 TYPES OF PVL: Shown in Table 21.3

Table 21.3 Tunes of PVL


Tvne Focal Diffuse
Site oflesion Near trigone of Diffuse involvement in
lateral ventricle and periventricular area
around foramen of
Monro.
Cells affected All cells lying in Precursors of
affected area oligodendrocvtes
Frenuencv More common Less common
Nature of insult Near total ast>hVYia Lesser degree
Diagnostic modality USG MRI preferred; USG
insensitive
Clinical correlates Spastic diplegia Cognitive and behavioral
oroblems associated
Appearance on Cysts in Decreased white matter,
imaginP neriventricular area ventriculomegalv.

21.12 TIMING OF APPEARANCE OF FINDINGS ON IMAGING:


• 24-48 h- after the insult, increased echogenicity is visible
(Periventricular flare; Transient- for 48 h, persistent- >7 d).
• 2-3 wks - cystic changes appear (cystic PVL)
• 2-3 mths- Cysts resolve and ventriculomegaly ensues.

21.13 GRADING OF PVL ': Shown in Table 21.4

Grade I
Grade II
Grade III sts
Grade IV
208
2
21.14 TIMING OF USG/MRI FOR PVL
• First USG at 7- 14 d
• Follow up with monthly USG for evolution
• USG at 40 wks PMA or prior to discharge
• Indications of doing MRI: Premature baby on follow up presenting
with cognitive, motor and/or sensory impairments.

21.15 FACTORS DETERMING PROGNOSIS OF PVL


• Any CP
o Lesions in the parieto-occipital region are more prone to causing
CP than those in the posterior frontal lobe
o Larger the area involved, greater are the chances of CP
9
• Type ofCP
o Quadriplegia: associated with diffuse lesions in frontal, parietal,
and occipital lobes of both hemispheres.
o Diplegia: associated with periventricular lesions confined to the
parietal or occipital lobes
• Cognitive dysfunction, especially an Intelligence quotient (IQ) <70:
directly proportional to the size and extent of white-matter
echolucencies.

21.16 STRATEGIES FOR PREVENTION OF PVL


• Promptly correct hemodynamic disturbances
• Avoid
o Hypoxia
o Severe hypocarbia (<25 mm Hg)
o Severe hypotension
• Early treatment of PDA
• Prevention and aggressive management of sepsis, especially EOS
• Gentle ventilation strategies

REFERENCES:
I. Volpe JJ. Clin Perinatal. 1989;16:361.
2. Ment LR. Neurology. 2002;58: 1726.
3. Bellu R. Arch Dis Child Fetal Neonatal Ed. 2009 Jun 15. [Epub
ahead of print].
4. Cools F. Cochrane Database Syst Rev. 2005.
5. Levene MI. Arch Dis Child. 1981 ;56:905.
6. Whitelaw A. Cochrane Database Syst Rev. 200 I.
7. Larroque B. J Pediatr. 2003;143:477.
8. de Vries LS. Behav Brain Res. 1992;49: 1.
9. de Vries LS. Neuropediatrics. l 993;24:263.
209

22. SEIZURES

22.1 BACKGROUND
Seizures are the most common neur(•logical emergency in newborns. The
incidence of seizures in the neonatal period is greater than in any other
time of life. with most seizures occurring within the I" wk of life.

22.2 CLASSIFICATION OF NEONATAL SEIZURES: Shown in


Table 22.1 (adapted from Volpe)
Table 22 1 Classification of neonatal seizures
Seizure
Occurs in Manifestations
tvne
Subtle • Preterm > Ocular movements- eye deviation (term),
(50%) Terrn fixed stare (preterrn), nystagmus. Others are
oral buccal- lingual movements; limb
movements, including rowing, swimming,
bicycling, pedaling, and stepping; changes
in HR and/or respiration; apnea; and BP
changes.
Clonic Term> • Rhythmic with I to 3 jerks per second,
(25 - 30%) Prctenn with a slow decline in rate as the seizure
Focal persists.
• Involves one body side. May spread on
Multifocal same side. Indicates underlying focal or
metabolic cause.
• Migratory in nature
Focal Tonic Preterm > • Rigid posturing of one limb or
(5%) Terrn asymmetrical posturing of the trunk or
Generalized neck.
tonic • Sustained posturing resembling
"'decorticate," opisthotonic, or
"decerebrate" rigidity
Myoclonic Rapid speed of the jerking and the tendency
(15-20 %) to affect flexor muscle groups.
Focal • Involve tlexor muscles of the upper
Multifocal extremities.
Generalized • Asynchronous twitching of several body
parts.
• B/L jerks with flexion of upper and,
sometimes, lower extremities.
*Apnea alone rarely represents a seizure unless tt occurs in the context of
other clinical seizure activity.
22.3 NONEPILEPTIC BEHAVIORS OF NEWBORNS
22.3.1 Jitteriness versus seizures: Shown in Table 22.1
210

T a bl e 22 2 J'tt · ess Vs Seizures


I er1n
Clinical Manifestation Seizure Jitteriness
Dominant movement Clonic jerking Tremor
Ocular abnormalities Yes No
Passive restraint halts activity No Yes
Autonomic changes Yes No
Stimulation induces activity No Yes

22.3.2 Benign neonatal sleep myoclonus is another neonatal seizure


mimic in which there are BIL or U/L, synchronous or asynchronous
myoclonus that occur during active sleep and is not stimulus-sensitive

22.4 ETIOLOGY OF SEIZURES


Neonatal seizures usually have an underlying etiology (See Table 22.3).
Only a small percentage (2%- 5%) of neonatal seizures is idiopathic

Table 22.3: Etiolouv of seizures and outcomes


EtioJouv Term Preterni Outcome
HIE (50-60%). Any seizure
Most common. Common Variable
t·-e
Common.
IVH Uncommon As tonic Poor
seizures.
Common.
SAH (severe) Healthy in
Uncommon Good
between
seizures
Subdural (associated with birth
trauma)
Common uncommon Good
Hu... oulvcemia Common Common Variable
Hvnocalcemia Uncommon Uncommon Good
Intracranial infection
Common Common Variable
(5 -10%1
Cerebral dysgenesis
(Dysmorphic features,
Common Common Poor
microcephaly, or cutaneous
lesions suauestive)
DruQ' withdrawal Uncommon Uncommon Variable
Neonatal epilepsy syndromes
(most common is benign Uncommon Uncommon Variable
familial neonatal seizures)

22.5 ETIOLOGY OF SEIZURES BY PEAK AGE OF ONSET:


Shown in Table 22.4. Metabolic abnormalities (Hypoglycemia,
hypocalcemia, hypomagnesemia and hypo/hypematremia), focal
211

ischemic necrosis (stroke) I sinus thwmbosis and cerebral dysgenesis are


common causes of seizures that m.1nifest anytime during the neonatal
period.

Ta ble 22.4: E.
tiolo"" of seizures bv a2e of onset
< 24 h 24-72 h 72 h-1 wk I wk-4wks
IVH in Bacterial/Fungal Bacterial/Fungal
HIE premature sepsis and sepsis and
newborns Meningitis Meningitis
Benign
SAH, Laceration Cerebral idiopathic Herpes simplex
oftentorium or contusion with neonatal encephalitis
falx SDHand SAH seizures (fifth
day fits)
Storage disorders
Scalp local Drug (rare): GMI
Bacterial sepsis
anesthetic withdrawal gangliosidosis
and meningitis
injection type I, Gaucher's
disease tvoe 2
Benign familial
IEM: Pyridoxine Tuberous
neonatal Kemicterus
dependency sclerosis (rare)
seizures
Rare: sepsis and IEM: Glycine
meningitis IUI, encephalopathy, IEM (rare): Organic acidemias, Urea-
Direct drug Urea-cycle cycle disturbances
effects disturbances
Others (rare):
Drug Others:
withdrawal, Intracerebral
incontinentia hemorrhage,
pigrnenti, Tuberous
Tuberous sclerosis
sclerosis

22.6 DIAGNOSIS
22.6.1 History and examination
• Maternal history- history that supports TORCH infection, maternal
PIH, fetal distress, maternal infection/chorioamnionitis.
• Delivery history for type of delivery, any use of local anaesthetics
for the mother and did they not take effect? (Suggesting perhaps not
injected into her but into baby), antecedent events, instrumentation,
Apgar score and cord pH.
• Postnatal history- Age of onset, feeding history, sleep and activity
prior to seizures. A h/o tremulousness may suggest drug withdrawal
or neonatal hypocalcemia. Lethargy and temperature instability may
suggest an infection. Hiccups may suggest nonketotic
hyperglycinemia.
212

• Family h/o seizures: genetic syndrome and IEM's (see sections


33.6.1 and 34.5).
• Detailed neurological examination, examination of scalp for in utero
needle injuries, Inspection for skin lesions and assessment of
fontanels.
• If there is doubt about occurrence or nature of the seizure and it
happens to occur in front of you, it would be worthwhile to
videograph the seizure using your personal mobile phone. It can be
transferred to the NSR computer using Bluetooth.
22.6.2 Laboratory investigations
• Serum glucose, calcium (QoTc interval on ECG), magnesium, pH,
SERFT, PCV and bilirubin (if baby significantly icteric).
• LP should be performed to determine the presence of infection.
• Neuroimaging: Perform USG cranium to look for intracranial bleeds
and malformations (often inadequate). Once the infant is stable,
computed tomography or MRI is essential.
• Others (to be done in specific situations)
o Thrombophilia evaluation if evidence of stroke or venous
thrombosis. Defer evaluation by 1-2 mths to avoid falsely
reports.
o IEM (sec section 33.7):
• Blood ammonia and lactate, serum aminoacidogram, TMS
• Urine metabolic screening, urine aminoacidogram
• CSF:serum glycine > 0.08 suggests non-ketotic
hypcrglycinemia. CSF lactate and pyruvate for
mitochondrial cytopathies. CSF: serum glucose <0.5 in the
presence of low CSF lactate levels suggests Glucose
transporter (GLUT)-! deficiency syndrome.
o Investigation for congenital viral infections
22.6.3 Electroencephalography
A characteristic feature of neonatal seizures is the phenomenon of
electroclinical dissociation: seizures can be electro-clinical,
electrographic (subclinical) or clinical only. The EEG is analyzed for
ictal activity (focal or multi-focal spikes or sharp waves and focal mono-
rhythmic discharges) and for background activity (see Table 22.5).

22.7 MANAGEMENT (also see sections 020, D79, D99, OIOI, 078):
Shown in Figure 22.1
22.7.1 Practical points:
• During the initial management every seizure episode should be
treated. When seizures become unresponsive to maximal doses of
phenobarbitone and fosphenytoin only frequent (>3/hour) or
prolonged seizures (>3min) or those associated with clinically
significant changes in cardiovascular stability should be treated.
213

Table 22.5: Association of clinical seizure tvnes and EEG


Clinical seizures - El.,ctroencephalo11raphic seizures
Common Uncommon
Subtle" +
Clonic focal, multi-focal +
Tonic focal +
Tonic generalized +
Mvoclonic focal, multi-focal +
Myoclonic generalized +
Only specific vanet1es of subtle seizures are associated with simultaneous EEG
seizure activity (ocular movements and apnea- Term; chewing - Pretenns)

• Ensure BS and calciuf9i.5aiormal during the treatment of seizures .


Levels of BS and calciuM'Way reduce during the course of treatment
making the seizures refractory to further treatment. Re-measure them
in case seizures are refractory to phenobarbitone and fosphenytoin.
• Phenobarbitone clearance is decreased by 50% in asphyxiated
neonates' but a total dose up to 4ff mg/kg is tolerated well without
adverse effects
• Pyridoxine IV preparation (see section 108) is not easily available in
India and an IM preparation may be used instead. (I mL of
Aristoneurol has 100 mg pyridoxme. I mL may be administered in
the anterolateral thigh).
• Lignocaine (see section D75) can be administered in a tapering
regimen. Start with 4 mg/kg/h IV on the I" d; reduce by I mg/kg/h
on each subsequent day till stoppage.
• Diazepam (see section D41) is to be used only if Lorazepam is not
readily available. Dilute to I mgimL. Give 0.25 mg/kg slow IV
followed by infusion of0.3mg/kg/hour in case ofreftactory seizures.
• Advantage of fosphenytoin over phenytoin:
o can be given rapidly as it has much less cardiotoxicity
o compatible with all IV solutions
o less purple-glove syndrome
• Lorazepam has the following advantages over diazepam: a less rapid
redistribution (with longer anticonvulsant activity) and less sedation
and respiratory depression.

22.8 LONG TERM TREATMENT


• Long-term treatment is directed against the specific cause of
seizures. For disease specific treatments refer to the appropriate
protocols.
• Maintenance dose of Phenobarbitone (3-4 mg!kg!d OD) and
Phenytoin (4-8 mg/kg/d OD) should be started 24 h after the loading
214

Figure 22. l : Flowchart for acute management of neonatal seizures

"leonatc with seizure

I0% dextrOSe 2 mlJlcg


Ensure TABC•:
DextrOSU"< value bolus. then continuous
Ensure IV access; - - -• infusion ~· 6 mg/leg min
Do BS <40 mg/dL

f-
(Avoid Hyperglycemia)
i BS>40

Do ioniled calcium b)' ABG If ionized calcium < 0.6 mm~IL!...,ond seizures
anal}'7er Give~alcium persist rpt Calci1Ii¥1 dose anctii' no response
gluconate ~ mUk,.; TV over 5-10

Sci7Ures persist.
Ca - "lormal
!
m1ns - .. l
give 50% Magnesium Sulphatc~IP mUkg IM ~

Se11.11rcs persist

Give [nJ. Phcnobarbitone~gllc~~over


persist after 15 mins consider I0 m
15 mms. lfselZUJ'C50
botiiSeSup t<A:tO m.s/kg,.
Assess ~1zurc control .after every
t
m1ns of end '!'ii't>Olus "T
Se•~orcs persist
Gne fo phenytoin 20 mg/kg JV Infuse over 10 mins
lfphen)10in is used give same dosage at rate of I ml!lkg. mm.
Assess seizure control after 30 min;----;
:J
Seizures persist + Consider mtubauon and

dive Lo~~am 0.05 mg'kg over 2-5 mtns..


mech vcnula11on

Assess control after mins. Rpt dose once if seizures persist


J
Seizures persist i
Consider alternate drug.~
(after discussion with consultant)
ALTERNATE DRUGS (see sections D 108, 084, 075)
Pyndoxme 100 mg TV
Folinic acid 2.5-5 mg
Midazolam 0. 15 mg/kg TV bolus. followed by continuou.' infusion (lµg.•Jcg.min)
increasing by 0.5 to I µgllcg1mm every 2 min until a favorable response or a maximum
of IR µg/kgfmm
Lignocaine: load mg dose 2 mg 'kg followed by IV infusion of 6 mg'kg'hour.
Topuumate (30 to 40 mg'kgiday TID)
Valproate: Can cause hyperammonem1a and neuroto:uc1ty to developing brain. Use
only for hi~hlv refractory setzUres.

*T ABC- temperature, airway. breathing, c1rcularion


215
dosage. Benzodiazepines are 1YJ ically not used for maintenance
therapy.
• Monitor serum drug levels in the following circumstances
o Refractory seizures
o Patient on polytherapy
c Suspected drug toxicity
o Hepatic or renal dysfunctio11
• In any mfant with medicall, refractory seizures, treat with
pyridoxine 15 mg/kg/d for l to 2 mtbs to determine 1f pyridoxine
dependency is the etiology for th1• seizures.

22.9 PROGNOSIS :;)


22.9. l Good prognosis: A normal interictal EEG in a term newborn (not
preterms), transient metabolic derangements (typically late-onset
hypocalcemia), SAH and hereditary neonatal convulsions.
22.9.2 Variable prognosis: Symptl)matic hypoglycemia, mtracraniaU
infection and TEM.
22.9.3 Poor prognosis: Early-onse seizures, frequent or prolonged
seizures that arc refractory to multiple anticonvulsants, cerebral
dysgenesis, moderate or severe IIIE, isoelectric, low-voltage, or
paroxysmal burst-suppression bad ground activity and myoclonic
encephalopathies.

22.10 WEANING AED: Shown in F gure 22.2


216

Figure 22.2: Flow diagram on weaning and duration of AED -

Newborn on AED

l
Transient metabolic problem - stop AED.
If non-transient etiology, stop all AED
except Pb* when seizure controlled

Normal
l
Assess neurological Discharge on Pb.
status at discharge Repeat neurological
Abnormal
examination at 1 mth

Do EEG

Stop Pb
,I Abnormal

Abnormai '----~
Reassess at 3 mths of life Taper & stop Pb
Normal over 2 wks.
and repeat sequence.
Switch to
carbamazepine/valproate
Taper & stop Pb
over 2 wks

* Pb = Phenobarbitone

References
l. Volpe J J. Neurology of Newborn 5th edition 2008; Philadelphia
Elsevier: Chapter 5.
217

23. ASEPSI~ ROUTINES

23.1 DEFINITIONS
The single most important intervention to reduce sepsis in a newborn unit
is hand hygiene. Hand hygiene is defined as any method that removes or
destroys microorganisms on hands. The following definitions are
relevant to hand hygiene:
• Hand hygiene: A general term that applies to hand washing,
antiseptic hand wash, antiseptic hand rub, or surgical hand
antisepsis.
• Hand washing: Washing hands with plain (i.e., non-antimicrobial)
soap and water.
• Plain soap: Refers to detergents that do not contain antimicrobial
agents or contain low concentrations of antimicrobial agents that are
effective solely as preservatives. They may be bar soaps or liquid
soaps.
• Antimicrobial soap: Soap (i.e .. detergent) containing an antiseptic
agent.
• Antiseptic hand wash: Washing hands with water and soap or other
detergents containing an antiseptic agent.
• Alcohol-based hand rub: An alcohol-containing preparation
designed for application to the hands for reducing the number of
viable microorganisms on the hands (usually contain 60%-95o/o
ethanol or isopropanol)
• Antiseptic agent: Antimicrobial substances that are applied to the
skin to reduce the number of microbial flora. E.g. alcohols,
chlorhexidine, chlorine, hexachlorophcne, iodine, chloroxylenol,
quaternary ammonium compoW1ds and triclosan.
• Antiseptic hand rub: Applying an antiseptic hand-rub product to all
surfaces of the hands to reduce the number of microorganisms
present.
• Decontaminate hands: To reduce bacterial counts on hands by
performing antiseptic hand rub or antiseptic hand washes.
• Visibly soiled hands: Hands showing visible dirt or visibly
contaminated with proteinaceous material, blood, or other body
fluids (e.g., fecal material or urine).

23.2 HAND WASHING PROTOCOL


23.2.1 Perform hand washing for 2 min:
• At entry/re-entry into any newborn care area
• If hands are visibly soiled (see definition in section 23.1)
• Before performing any invasive procedure (Inserting vascular lines,
bladder catheterization etc). A 2 min hand wash with soap is
218

required even if one would be wearing sterile gloves for the


procedure.
• After touching soiled items, body fluids or excretions, mucous
membranes, non-intact skin, and wound dressings, even if hands are
not visibly soiled.
• If moving from a contaminated body site to a clean body site of the
same patient during patient care.
• After touching any baby with culture-proven sepsis. This includes
fomites attached to or in the vicinity of the baby- e.g. tubes, lines,
baby linen, cot, incubator, radiant warmer, devices attached to baby,
files, charts of baby, items dedicated to baby- e.g. measuring tape,
stethoscope, BP cuff etc.
• After removing gloves.
• Before & after eating and after using the toilet.
Jn all other situations, alcohol based hand rub is superior to hand
washing. All hand washing must be followed by drying and by
application of an alcohol hand rub.
23.2.2 Pre-requisites for hand washing
• Ideally, hands must be washed with liquid soap from a dispenser and
with running lukewarm water from an elbow operated tap. Avoid
using hot water, because it destroys the superficial layers of the
epidermis and promotes colonization.
• Once the liquid soap finishes, the dispenser must be emptied,
cleaned thoroughly and filled afresh. Do not simply "top up" the
liquid soap. Without periodic cleaning, the dispenser may develop a
biofilm with bacteria.
• If liquid soap is unavailable, one may use a bar soap. It must be
ensured that the bar soap either hangs so that the water drips off, or it
is kept in a rack with holes at the bottom for drainage. It is the
responsibility of the sister-in-charge to get the rack thoroughly
scrubbed and cleaned in each shift. It is dangerous to use a bar soap
that is lying in a stagnant pool of water.
• If the tap is not elbow operated, it must be closed using a sterile
paper towel that is used for hand drying. Do not touch the tap
directly.
23.2.3 How to perform hand washing:
• All personnel who handle newborns must keep their nails short.
• First roll up the sleeves till above the elbow. Remove wrist watch,
rings, bangles etc (this must be adhered to irrespective of marital or
religious status or the prevailing fashion)
• Wet from finger tips to the elbow under running water, apply soap
on the wet areas and rub to create lather.
• Then follow the 6 steps of hand washing taking care that it occupies
2 min. Look at a clock. Two min is longer than you think!
219

(1) Palm to opposite palm, fingers interlocking


(2) Palm to back ofopposite hand, fingers interlocking
(3) Knuckles rubbed again,! opposite palm
(4) Hand encircling opposi1e thumb
(5) Finger tips to centre of palm
(6) Hand encircling opposite wrist
• Wash hands and forearm under running water, keeping them upright
under the tap.
• Stay in this position for a few seconds until excess water drips off
23.2.4 Drying
Wet hands transfer pathogens much more readily than dry hands.
• Always dry hands immediately after washing using sterile paper
towels and discard the sheets in the waste bin. Mop hands on paper
towels for l 0 s and repeat it with another set of paper towels.
• Never use a common towel meant for multiple users.

23.3 ALCOHOL-BASED HAND RUB


23.3.1 Use alcohol based hand rubs:
• After drying hands following hand washing
• Before and after every routine patient contact.
Remember: Alcohol based hand rubs have been shown to be definitely
superior to soap and water hand washing in reducing bacterial colony
counts of the hands. Hence, application of alcohol-based hand rubs must
be preferred over hand washing for all routine contact.
It is equally important to remember: Alcohol-based hand antiseptics are
not effective on hands that are visibly dirty or contaminated with organic
materials. Hands that are visibly dirty or contaminated with organic
material must be washed with soap and water, even if hand antiseptics
are to be used as an adjunct measure.
The term "patient contact" is not restricted to direct contact with a
patient. It includes (but is not limited to) the following:
• Perfornling any kind of non-invasive procedure
• Recording any patient parameter
• Touching baby's clothes/linen
• Handling baby's incubator/warmer/devices attached to baby
• Handling baby's probes/BP cuff
• Handling baby's IV tubings/syringes
• Handling baby's milk tubings/ syringes
23.3.2 Technique of applying alcollol-based hand rubs
• Apply product to palm of one hand (one press on 500 mL
Sterilium® bottle pours -1.5 mL of sterilium) and rub hands
together, covering all surfaces of hands and fingers.
• Wait until hands are dry. Do not touch the baby with wet hands.
220

23.4 ASE PSIS ROUTINES FOR INDIVIDUAL BABIES


• Maintain adequate supply of disposables. If the patient's family has
financial difficulties, it is preferable to invest in disposables than
buying expensive items like !VIG, surfactant etc.
• Use triple swab technique before any procedure that involves skin
break
• Change dressings as soon as they get soiled
• Ventilator tubings used for a single baby need not be routinely
changed. Change once they are visibly contaminated.
• Remove all lines (IV or arterial, central or peripheral) as soon as
they are not required.
• Change all the tubings for parenteral fluids OD in the morning shift
and immediately if they are visibly contaminated.
• Autoclaved linen should be used for placing, wrapping or cleaning
the baby.
• All linen should be changed once daily and immediately if they are
visibly soiled.
• Parents must be instructed about hand hygiene measures as soon as
they enter the NICU and they must be supervised a few times.
• Supporting staff from other departments (including doctors,
radiographers, ECG technicians, etc) must be instructed about hand
hygiene measures as soon as they enter the NICU and they must be
supervised. Do not assume that they remember the hand hygiene
protocols from their previous visits.
• All babies receiving intensive care must have their individual
resuscitation tray, resuscitation equipment, stethoscope, measuring
tape, spirit swab bowl, betadine swab bowl, thermometer, saturation
probe, BP cuff and Sterilium bottle. Sharing of these items is
prohibited.
• Babies in non-intensive areas should be sponged daily with
individual autoclaved cotton using a personal bowl. Babies must not
be bathed.
23.4.1 Policy for vascular catheters'
• Use vascular catheters made of polyurethane, silicone elastomer or
Teflon; and not polyvinyl chloride or polyethylene.
• For peripheral cannulas, hand hygiene by use of an alcohol-based
hand rub or hand washing with an anti-bacterial soap followed by
the use of a pair of fresh, clean (not necessarily sterile) gloves is
recommended. The insertion site must not be touched after
disinfection. A small sterile drape for placing the articles is
sufficient. Sterile gloves are necessary while inserting arterial
catheters. The tip of the glove covering the index finger may be cut-
off to allow better palpation.
221

• The insertion site must be disir fected by applying spirit followed by


povidone-iodine. Povidone-iodine must be allowed to remain for at
least 2 min or longer if it has nut air dried by that time.
• For CVC's and PICCs, maximal sterile barrier precautions are
required- surgical scrub, cap, mask, sterile gown, sterile gloves and a
large sterile drape. All subsequent handlings of the CVC or PICC
that involve breaking the line must be performed with the same
attention to maximal sterile barrier precautions as the initial
insertion.
• A transparent, semi-permeable polyurethane dressing is preferable to
standard gauze and tape dressing as it permits secure fixation,
visibility and protection from wetness. Gauze may be preferable in
case of oozing of blood.
• Brachia) and jugular veins are preferred for PICCs as thrombosis
rates are less. The use offemoral lines is prohibited.
• In-line filters must not be used. The only possible indication is pre-
existing phlebitis or use of a drug highly likely to cause phlebitis, in
which case it may be used after discussing with the consultant.
Never use in-line filters along with lipids, blood, dextran and
mannitol.
• Anti-microbial impregnated vascular catheters are currently not
available in India.
• Do not apply any antibiotic/antiseptic ointment at the insertion site
of peripheral catheters, CVC's or PICC's and umbilical catheters.
They increase emergence of resistant organisms, promote fungal
colonization and might affect the integrity of the catheter material.
Do not use prophylactic systemic antibiotics or antibiotic lock
solutions as they promote antibiotic resistance.
• Use heparin prophylaxis (dose 0.5 IU/kg/h) in patients with short-
term CVC's to reduce the risk of blockage [typical RR 0.28, 95% CI
0.15, 0.53, NNT 5, 95% Cl 3, 8]. The infusion must run at a rate
;o.0.5 mL/h (for neonates < 30 wks GA and :o>l mL/h for neonates ;o.
30 wks. 2 For umbilical arterial catheters, use heparin in a dose of 0.5
to I IU/mL.
• Peripheral venous and arterial catheters need not be changed
electively at fixed intervals. This is unlike adults, where the change
of peripheral venous catheters is recommended every 72 h.
• CVC's and PICCs need not be electively changed. If a change is
mandated due to malfunction, a useful method is to insert a guide
wire and change the catheter over the guide wire. However, this
must not be done in case of suspected catheter related blood stream
infection (CRBSI).
• Administration sets through which lipids or blood products have
been given must be changed within 24 h. Studies in adults show that
222

it is safe and effective to change administration sets of routine fluids


every 72 h. However, given the lack of data in neonates and the high
rates of sepsis in India, it would be safer to change all administration
sets every 24 h.
• There is no convincing evidence that needleless connector systems
(Clave", local agent- Sudarshan Sharma- 9814602436) decrease
sepsis or phlebitis in neonates. They may reduce the risk of needle
stick injuries. In a pilot RCT in PG!, there was a trend towards
longer intervals till the first episode of sepsis in the needleless
connector group. Needleless connectors may be used after
discussion with the consultant on a case-wise basis.
• The use of a common stock solution (e.g. Heparin, saline) for
multiple patients is prohibited. The use of a common multi-dose vial
of a drug for multiple patients is prohibited; however, it can be used
for a single patient repeatedly. The use of a single-use vial
(generally they contain no preservative or bacteriostatic agent) on
multiple occasions is prohibited.
• UAC's must be placed in the high position (See PGIMER video on
neonatal procedures and section N22). Remove and do not replace
umbilical arterial or venous catheters in case of CRBSI, vascular
insufficiency, or thrombosis.
• UAC's should not be left in place >S d. Umbilical venous catheters
should be removed as soon as possible when no longer needed but
can be used up to 14 d ifmanaged aseptically.

23.5 EQUIPMENT DECONTAMINATION AND


HOUSEKEEPING ROUTINES: Shown in Table 23.1 and 23.2.

Table 23.1 Equipment decontamination

Item Activity Periodicity


In use: detergent & In use: once daily
water
Incubators and open
Not being used:
care systems Not being used:
dismantle weekly and
2% cidex
clean with 2o/o cidex
Clean with moist
Ventilator body Once daily
cloth
Infusion pump and Clean with moist
Once daily
monitors cloth
Dismantle,
Resuscitation bags and 2% cidex for After each use
accessories 30min
Dismantle, 2% Once weeklv
223

Item Activih Periodicitv


cidc> for 6 h
Rubber & plastic
2% cidex for 6hr Once daily
tubings
Humidity bottles,
Clean with
Suction bottles and 0 2 Once daily
detergent
hoods
Clean with spirit After each use
Laryngoscope 2% cidex for 30
Once daily
min
Before and after each
Thermometer Wipe with spirit
use
Stethoscope, Before and after each
Wipe with spirit
measuring tapes use
Wipe with moist
Weighing machine Once daily
cloth
Use disposable in
-
intensive areas
Saturation probes
In CLR nursery: Before and after each
wipe with spirit use
Use disposable in
BP cuff -
intensive areas
Procedure sets Autoclave After each use

T a bl e 232H ouse k eeo1ne: rou f 1nes


Item Activity Periodicity
Floors Mop with phcnvl Thrice daily
Wipe with
Walts Thrice Daily
detergent/carbolic acid
Fans Wipe with detergent Fortniohtlv once
Basins Clean with detergent Thrice daily
Manually clean and
Linen After each use
then autoclave
Wash with detergent,
Feeding utensils Before each use
boil for 20 min
Wipe with
Shelves Thrice daily
ohenvl/carbolic acid
Teleohone Wipe with moist cloth Once daily

23.6 ENTRY RESTRICTIONS


• Encourage parents to visit their baby. Mother should be allowed to
visit at any time in all areas. Father can visit the baby nursed in
224

intensive areas during 5 pm to 7 pm. However, timings for fathers


may be relaxed on request.
• There are no visiting hours for other relatives and well wishers in the
NJCU or NNN. They may visit during the permissible visiting hours
in the Maternity ward, Gynecology ward or private wards only.

23.7 UNIVERSAL PRECAUTIONS


23.7.1 Universal precautions apply to blood and to other body fluids
containing visible blood. Universal precautions also apply to tissues and
to the following fluids: CSF, synovial fluid, pleural fluid, peritoneal
fluid, pericardia! fluid, and amniotic fluid.
23.7.2 Universal precautions do not apply to feces, nasal secretions,
sputum, sweat, tears, urine, and vomitus unless they contain visible
blood. The risk of transmission of HIV and HBV from these fluids and
materials is extremely low or nonexistent.
23.7.3 What do universal precautions mean?
• Always wear sterile gloves for heel stabs, phlebotomy and insertion
of vascular catheters. Wearing gloves appears cumbersome for the
beginner, but one soon gets used to it. A small window can be cut at
the region of the finger tip of the index finger of the dominant hand,
to aid palpation of veins and arteries.
• Wear gloves while handling any kind of body fluids. It is a basic
right of every doctor to have a pair of sterile gloves provided by the
hospital for every procedure that involves possible contact with
bodily fluids that require universal precautions.
• Do not recap used needles by hand
• Do not remove used needles from disposable syringes by hand
• Do not bend, break, or otherwise manipulate used needles by hand
• Destroy needles using the needle destroyer provided in every ward
• Dispose scalpel blades and other sharp items in puncture-resistant
containers for disposal.

23.8 BABIES WITH THE FOLLOWING CONDITIONS REQUIRE


ISOLATION
• Diarrhea
• Pyoderma
• Discharging wounds
• JUI (see chapter 26)

23.9 STAFF MEMBERS WITH THE FOLLOWING ILLNESSES


SHALL NOT CARE FOR BABIES
• Fever
• Diarrhea
225

• Pyodenna
• External infected wounds
• Conjunctivitis
• Ear discharges
• Viral exanthems
Those with upper respiratory infections may work wearing a mask at all
times.

23.10 BIOMEDICAL WASTE DISPOSAL: Shown in Table 23.3

Table 23 3 Biomedical waste disposal


Color Codine; Waste
• Human anatomical waste (human tissues, organs,
body parts),
• Microbiology & biotechnology waste (wastes
from laboratory cultures, stocks or specimens of
Yellow (solid micro-organisms live or attenuated vaccines,
infectious) dishes and devices used for transfer of cultures),
• Solid waste (items contaminated with blood and
body fluids including cotton, dressings, soiled
plaster easts, line beddings, other material
contaminated with blood)
Solid Waste (waste generated from disposable items
Red (solid non-
other than the waste sharps such as tubing, catheters,
infectious)
IV sets etc.)
Waste Sharps (needles, syringes, scalpels blades,
Blue (sharps) glass etc. that may cause puncture and cuts. This
includes both used & unused shams)
• Discarded Medicines and Cytotoxic drugs (wastes
comprising of outdated, contaminated and
Black (other discarded medicines),
solid waste) • Chemical Waste (chemicals used in production of
biological, chemicals, used in disinfection, as
insecticides, etc)

REFERENCES
I. O'Grady. MMWR 2002; 51: I
2. Shah PS. Cochrane 2009
226

24. SEPSIS

24. 1 DEFINITIONS
"Jeonatal sepsis 1s defined as the presence of generalized systemic
features of sepsis associated with pure growth of bacteria from one or
more sites.
Probable sepsis: clinical and laboratory findings consistent with bacterial
infection without a positive culture.
Severe Sepsis: Sepsis associated with organ dysfunction, hypoperfusion
abnormalities, or hypotens1on. Manifestations of hypoperfusion include
but are not limited to proloQged CFT, lactic acidosis, oliguna or an acute
.a!!,eration in scnsorium.
Septic Shock: Sepsis-induced hypotension despite fluid resuscitation (sec
chapter 29).
\fODS· Presence of altered organ functions in an acutely 111 patient such
that homeostasis cannot be maintamed without intervention.

24.2 PRESENTATION ACCORDING TO T IME OF ONSET


• Early-onset (<72 h)
• Late onset (""72 h).
EOS presents with prominent respiratory signs while LOS has more
vaned presentations.
24.2.I Clinical signs associated with sepsis
The possib1hty of sepsis must be considered with any clinical
deterioration unless the event is readily explained by other causes. The
studies that have addressed the issue of clinical signs in nosocomial
sepsis, including one from PGl, 1 have by and large arrived al the
following signs: lethargy/h otonia taeh · abdominal
distension, increase sptrates, retractions runtin h otension/dela
cap1 ary re 1 . pa lor, jaundice al a nea, abnormal skin
~r. ra year ta an increased venrilator requirements. _
Late chmcal Signs are indicative of severe septicemia: sclcrema. shock.
~catures of DIC, pulmonary hemorrhage, collapse)

24.3 APPROACH TO EOS


There is no rationale for performing a "sepsis screen" in suspected EOS.
The~ 1s too low to confidently rule out fOS.>23
24.3.1 Symptomatic neonates
Neonates who tum symptomatic within 72 h must be climcally assessed
for probability of sepsis. 20% of symptomatic neonates in PGI suspected
to have EOS arc biOOCrtUTriire pQ2itiv)l -
• The following neonates need not be immediately started on
antibiotics but their clinical course must be carefully monitored:
227

o Those who are born with<. ur any of the known risk factors of
sepsis [preterm, pPROM, ~ROM > I 8 h, duration of labor > 24 h,
spontaneous pretenn onse1 of labor. clinical chorioammomus.
foul smelling liquor, uncl ·an vaginal exanunations. maternal
fever, maternal urinary or other systemic infections, frequent
(>3) per vaginal examina ions in labor, pennatal asphyxia].
AND r '
o Chest X-ray not suggestive .>fpneumonia AND
o Have alternative reasons to ·xplain the symptoms.
Note: contrary to popular practice in India, the corr ev1at1on
for 'preterm premature rupture of membranes' is pPROM and not
PTPROM. -
• Symptomatic neonates with any of the known risk factors listed or
who have a CXR suggestive c. f pneumonia or do not have any
alternate explanation for the sigas, must be immediately started on
antibiotics after drawing a bloo I culture. LP for CSF examination
must be performed m symptomatic neonates, with the exception of
premature neonates presenting \.\Ith respiratory distress at birth with
no risk factors for sepsis.4..s
24.3.2 Presence of risk factors for s psis in as)mptomatic babies
• All neonates. especially those who are premature. must be evaluated
for presence of risk factors of E)~k score was generated in
PGI and was later validated in RCT." All neonates <35 wks of
gestation, who remain asympton 1 ~ life}areassessed
for the risk of EOS using the following pennatal risk score.
r °"Kisk factor Seore
IP per vaginal examinations ?. 6
Clinical chorioammonitis• 6
BW < l.5kg 3
Male gender 3
Not received IP antibiotics•• 2
Gestation 5 30 wks 2
• mica! chorioamnionitis: JP ever (>37.8°C) with ~of the
following features: fetal tachycardia, uterine tenderness, malodorous
vaginal discharge, maternal leucocytosis (TLC > 15,000).
••Antibiotics started <4 h prior tD delivery also classified as "Not

-
received antibiotics" -
o Neonates with a score of C-6 must be carefully monitored_
clinically for a period of at teast'72 h for signs of sepsiS.-A score
0-6 is not a justification for I avmg the baby unmonitored with
the mother m the ward. Etern I vigilance is the pnce one has to
pay for a restrictive antibiotic policy. Sepsis screen and CSF
must not bc pertormed. Thos who remain asymptomatic until
72 h need not be actively mon torcd further, but the mother must
228

be instructed to bri ng any unusual sign to notice within the fi rst


7 d. Occas1onally, EOS may be as'Yfuptomat1c in the ~
~present late. especially if the mothernacf receive ~-
partum antibiou~
o Neonates with a score of~7 must be §biected)o a blood culture
and prophylactic empirical ant1b1ot1cs must be started. Sepsis
screen must not be performed. CSF examination must NOT be
performed to begin with as it is not re uired m asymptomatic _M.:
nsk neonates7•8, but must be per ormed if the neonate turns
symptomatic or the blood culture is reported positive.
c Neonates with extreme risk factors (a) very prolonged rupture of
membranes (~72 h), (b) very prolonged labo~4 h), (c) foul
smelling liquor. (Cl) unclean per vagi nal exammat1ons. (e)
maternal Scpti'Cemia or other systemic Infections, must be
started on empirical prophylactic antibiohcs, irrespective of the
score.
24.3.3 A ntibiotic treatment of EOS
There 1s generally no distinction m the choice of empincal antibiotics. be
tt suspected EOS or suspected LOS (see section 24.8)
24.3.4 Adjunctive therap) : Supportive and adjunctive therapy in EOS is
similar to LOS (see sections 24.9 and 24.10).

24.4 A PPROAC H TO LO
• Neonates who become symptomatic afler 72 h must be evaluated for
LOS. The clinical signs m section 24.2TCan be used as a guide.
Overall. 30°'0 neonates clinically suspected to have LOS in PGI
NJCU have culture proven LOS. 1
• A single episode or transient presence of one of the above signs may
not warrant any action. The more persistent the sign the more likely
ll 1s associated with LOS.~
• Based on clinical assessment the neonate must be categon1cd into
low probability of sepsis or high probability of sepsis. "Low
probability'' represents situations where the clinician woul~
Wliiii1gtc>\\1thhold antibioucs if the sepsis screen is negative
• Those with low probability of sepsis (e.g. single episode of apnea,
but otherwise well) should undergo a sepsis screen The purpose of
the sepsis screen is to rule out sepsis rather than to rule m sepsis. The
sepsis screen consists of: CRP. ANC. ITR and micro-erythrocyte
sedimentation rate (µ-ESR).
o CRP: It is done by quantitative ELISA or by a bedside semi-
quantitative latex agglutination kit. More than I 0 mg/L is
positive.
o ANC: It must be read off Manroc's charts, Schelonka 's chart or
Mouzinho's chart, depending on whether it is a tcnn baby or a
229

pretcrm baby respectivelj 10·11 (sec section NIO, NI l, N12).


For term neonates in the 1 1itial hours of life, Schelonka's chan
is more accurate than Mmroe's. For neonates born m high
altitudes in Himachal P;alesb, take care to use Christensen's
nomograrns (section N 12).
o ITR: Value above 27% in term babies is considered positive. 11
For prctcrms, it is consider ·d to be 20%. !TR 1s defined as
Immature PMN <band forms. metamyelo & myelocytes)
Mature + immature neutrophils
o µESR. Value (in mm m fiht hour) > '·3+age in days" m the J ' 1
wk of II fe or > I0 thereafter is considered positive.
• Two systematic reviews on sepsis screens reached the same
conclusions- that there is no iueal test or combination of tests. 12•13
Among the various tests, quant tative CRP is the best, followed by
qualitative CRP and ITR.
• If all the parameters of the sepsis screen are negati\'e in a neonate
assessed to have low probab1l ty of LQ§, an11biot1cs may not be
started and the neonate must he monitored chrucally. The screen
must be repeated after 12-2 h. Two consecutive completely
negative screens are sugge'SITVe>fno sepsis.2
• Smee CRP 1s the key paramet ·r in the sepsis screen, a pragmattc
approacnis that if the CRP alo ie is positive or any two parameters
of the sepsis screen are positive a blood culture must be drawn and
empincal antibiotics must be s artcd. A CSF exammation must be
performed. Meningitis (non-cultJ~roven) occurs in 3.4°,,o cases of
suspected LOS & 25% cases of u!!ure positive LOS 8 ·-
• Neonates assessed to have a his h clinical probability of sepsis may
not be subjected to a sepsis sere n, because a negative screen would
not alter the decision to start ant biotics. A CSF exammatton must be
performed.

24.S BLOOD CULTURE


• Inoculate I to 3 mL venous blood in a Pediatric BACTEC culture
bottle. tn.S bottle Jias an antil 1otic neutralizing medium [for aTI
antibiotics except\~openem-:- lnupenemJ) hence it gives more
reliable results than conventton'ff culture ·even if the patient 1s on
antibiotics. Blood cultures sent tctween 9 am and 9 pm arc directly
put into the BACTEC machine; whereas those sent between--2...£.m
and 9 am are kept in an incuba or in Emergency overnight before
being put in the BACTEC mach1 'le.
• Do not use umbilieal venous catheters, indwelling arterial lines or
capillary blood samples for culture because of nsk of contamtnation.
If catheter-associated sepsis 1 suspected, a culture should be
obtained through the catheter as veil as peripherallj.
230

• The following are suggestive of contamination: growth in only one


bottle, mixed growth of doubtful significance, known contaminants
(aerobic spore bearers, proj)TOnibacteria et<.:), delayed onset of
growth (>72-96 h) in the absence of prior antibiotics. Some non-
fcrmenters are known to have delayed onset olgroWrtl un~ormal
circumstances.

24.6 CSF ANALYSIS


• In an unstable neonate the LP can be deferred until stabilization is
achieved. The cellular and"'61ochem1caf86ii0rmalities persist for up
to 3 d. Gram positive bacteria clear in 36 h of appropriate therapy
whereas gram negative bacteria may take up to 5 d.
• In a neonate with meningitis not showing clinical recove!)!.. after
institution of antibiotics, LP should be repeated after 48 h
• If the LP 1s traumatic tfir"CSF should be sent for gram stain and
culture. The concentration of glucose is not significantly altered by a

l
traumatic LP. Nothing much is gained by using the various formulas
for adjusting the WBC count m a traumatic CSF, based on the RBC
counts. Adjustment merely results in a loss of sensitivity with
14
marginal gam in specificity.
• The WBC cell count must be performed w1t!lm 30 mio of drawing
the sample, m the Neonatology lab by the lab technician during
office hours and by the JR (to be confirmed by the sRt'iift'Cr office
hours. CSF WBC and glucose rapidly fall- with time, g1\ ing spurious
results. 5 - -
24.6.1 Interpretation of CSF findings
• Apart from culture and gram stain, 4 parameters are commonly
evaluated: total WBC count (per µL), percentage neutrophil count,
glucose and protein. The traditionally used cut-offs are unacceptable
because they are based on 2 SD values of normal populations. T~ere
is surprisingly little data on the hospital-based mcidence of culture-
proven meningitis among cases of suspected sepsis in developing
countnes. Based on a hospital-based study from Bangladesh a
prevalence of 5°/o among cases of suspected nosocomial sepsis can
16
be assumed. Based on a multi-centric study from Asia, a
prevalence of 13% among cases of culture-proven EOS and 17%
7
among cases of culture-proven LOS can be assumed.
• Among preterm infants (<34 wks), none of the above CSF
parameters was shown to be satisfactory for the rapid diagnosis of
meningitis (n= 4,632 infants). 18 Similarly, none of the above CSF
parameters was shown to be satisfactory for the rawd diagnosis of
meningitis in infants 2:34 wks {n= 9111 infants). 9 However, for
want of a better alternative, these parameters arc still used.
231

• Revised guidelines were genorated (see Table 24.1) using the


likelihood ratios generated from the above large studies and making
the following assumptions
o Prevalence of meningitis in suspect sepsis= 5%
o Prevalence of meningitis in proven sepsis= 13-17%
o Threshold for empirically treating as meningitis is at a
probability of20% (as approximately one-third of neonates with
meningitis die and half have moderate to severe disability at 5
yrs- also see section 42.2.1 and chapter 43)
o Post-test probabilities for India can be re-calculated using
Fagan's nomogram
o Decision for treating as meningitis can be reviewed after culture
report becomes available as the interpretation of CSF
parameters differs, based on culture positivity

Table 24.1 Revised guidelines for empirical treatment of meningitis


based on CSF parameters

Among neonates
Among neonates with
with blood culture
suspected sepsis
proven sepsis
Preterm babies
• WBC>25AND •WBC>lO
protein > 170 OR
OR • Glucose< 25
• WBC> 100 OR
Cut-off OR • Protein > 170
values to • Glucose < 25
diagnose Term babies
meningitis • WBC>21 • WBC>8
OR OR
• Glucose < 20 • Glucose < 20
OR
• Protein > 120
1Vote:
I. Have very low threshold for treating as meningitis in proven gram -ve LOS as the
prevalence is highest in this sub-group (-30o/o).
2. CSF parameters may not qualify for a diagnosis of meningitis when sepsis is initially
suspected, but the same parameters may qualify for a diagnosis of meningitis once
culture report becomes available (Table 24.l). In this case, switch over from anti-
meningitic to meningitic doses of antibiotics with plan to treat for 21 d.
3. There is no need to do a blood glucose
232

24.7 LRINE ANALYSIS


• The signs of UTI are nonspecific and varied. The common clinical
signs m cases of UTI m neonates are - failure to thnve (50%), fever
(39%). vomiting (37%). diarrhea (25%), cyanosis (23%), Jaundice
( 18%) and irritability & lethargy ( 17° 0).
1

• Urine culture must not be routinely performed.20•21 Neonates with the


above clmical signs. or who are VLBW or have known urinary tract
anomalies or have had previous or on-going bladder cathetcnzation
or visibly turbid unne should be investigated for UTL
• Routine urine microscopy has poor correlation with culture and must
not be relied upon for diagnosing UTI. More accurate microscopic
analysis of unccntrifuged urine can be perfonned with a
hemocytometer and reporting cells per cubic millimeter (cut-off~ I0
WBCstmL). Urine culture mulLalways be performed on a sample
obtained by a supra-pubic as iration SPA or by a freSh bladdei
catheter. In neonates, use of ~ g:11idanc1: s1mp ities S A and
impro\es the d1agnoSTic rjeld. SPA is a more painful procedure and
has lower yield of urine compared to bladder catheterization

24.8 t\NTTBIOTIC T REATMENT


24.8.1 Starting empirical antibiotics for nosocomial sepsis

following policy 1s currently followed:


• First line: C.iprofloxacin + Amikacin (covers - 75% isolates) (see
0
Based on the blood culture sensitivity repons of a recent I -yr period, the

sections 030. 05). lf.m_eningitis is suspected, replace Ciprofloxacin


[{><
by_Cefotax1me-sulbactam (see section 024) ' '>""
• Second line: Vancomycin + Piperacillm-Tazobactam (covers - 90% H ? ~
isolates) (see sections 0129. 0102) '(
• Third line: Vancomycin + Meropenem (covers - 95-100%) (see (\
sections 0129, 081) ~7
The antib1ot1c policy 1s reviewed periodically and may change after the
next renew. Cephalosporins rapidly induce the production of extended
spectrum ~-lactamases. cephalosporinases and fungal colonization. and
hence, are best avoided as empirical antibiotics.
24.8.2 Lpgradation of empirical antibiotics
• Empmcal upgradation must be done if the expected clmical
improvement with the ongoing line of antibiotics docs not occur. A
minimum of 48-72 h of observation should be allowed before
declaring the panicular line as having failed. The duration may be
longer for Vancomycin compared to the Penicillin group and
Aminoglycosides because Vancomycin has a low log-kill of
bacteria.
233

• In case the neonate is extremely sick or deteriorating very rapidly


and the treating team feels that the neonate may not able to survive
48 h in the absence of approrriate antibiotics. a decision may be
taken to bypass the first line of antibiotics and start with the second-
hne of antibiotics m consultatto t with the consultant on call.
24.8.3 Antibiotic therapy once culture report available
• If the ~wth is a non-contaminant, the antibiotic sensitivity must be
assesse to decide whether an ibiotics need to be changeCI or not.
The following guidelin~ must le adhered to:
o If the organism 1s sens1t1 ·e to an antibiotic with a narrower
spectrum or lower cost, ti crapy must be changed to such an
antibiotic. even if the neon tc was improving with the empirical
antibiotics.
o If possible, a single sen. 1tive antibiotic must be used, t h J
exception bcmg Pse__g_do!!_lQ 1as for wh ich 2 sensitive ant1b1otics
must be used. Twosens tive antibiotics (a Pcnicillm + an
Aminoglycoside) may also be used for S aureus and Efecalis.
o "rt the empmcai antibioti ;s are reported sensitive, but the
neonate has worsened on these antibiotics. it may be a case of m
vitro resistance. AntibiotKs may be changed to an alternate
sensitive antibiotic with the narrowest spectrum and lowest cost.
c If the empirical antibiotics re reported resistant but the neonate
has improved clinically, it -nay or may not be a case of in-i•ivo
sensitivity. In such cases 1 careful assessment must be made

J
before decid ing on contin 1ing with the empirical antibioticso
One must not continue w1til antib1ot1cs with in vitro resistance
in case of Pseudomonas, K ebsiella and MRSA; and m cases of
CNS infections and deep-sc.ated infections.
o If no ant ibiotic has been re >orted sensitive, but one or more has

l
been reported 'moderately cnsitivc' , therapy must be changed
to such antibiotics at tht highest perrmssible dose. Use a
combination, in such cases.
24.8.4 Duration of antibiotics
• Culture positive sepsis: A sensi ive antibiotic for toLal duration of 14
d. Staphylococcus aureus se sis invariably requires 14 d of
antibiotics. In those neona cs who arc infected by non-
Staphylococcm aureus orgamsms. w1thout menmg1t1s or deep-seated
infections, and who rapidly be ome completely asymptomatic, one
may consider a shorter duratioc of antibiotics after discussing with
the consultant. 22 Qyantjtativ.e CRP assay (<10 mg/L) could be~)
as a guide to decide on stoppagL of antibiotics. 23 ~
• If the blood culture is rcpo11cd sterile at 48 h, the followmg

r
~ guidelines must be adhered to:
o Asymptomatic neonate at mk of EOS: stop antibiotics
234

o Suspect~S or Los)nd the neonate becomes completely


asymptomatic: stop antibiotics
o Suspected EOS or LOS and the neonate improves but does not
become asymptomatic: repeat a CRP assay and re-evaluate the
clinical course
• IfCRP +ve (>10 mg/L): antibiotics for 7-d course
• If CRP -ve and clinical course not suggestive of sepsis:
consider sto in antibiotics
o Suspected OS or LO ; an the neonate has not improved or
has worsened: upgra e antibiotics as per the empiric antibiotic
policy. Simultaneously, alternative explanations for the clinical
signs must be actively so-ughtr<lr:-- - -
or culture-proven meningitis, gram stain-proven meningitis o~

a

eningitis suspected on CSF examination: give total of 21-d course
f parenteral antibiotics that cross uninflamed meninges. Anti-
eningitic doses must be used throughout the course.
o For culture-proven meningitis, only antibiotics with proven in
vitro sensitivity must be used. .._
o .... Morutonng protocol follo;fng diagnosis of meningitis:
• Twice weekly OFC
• Daily 110 m
.-

n and Wt monitoring, twice weekly


J
serum Na~ (for SIADH (see section 8.8.2) .___
• wice week y neurological examination (focal neurological
deficits).
• Hearing screen after 4-8 wks (see section 41.2. l)
• USG head in t~ 1st wk and at the end of antibiotic therapy
(look for ventricular size, ventricular wall enhancement,
• midline shift, i~ventricular debtj_§J,Ventriculitis requires
6 wks of im_tibiotics,, (See PGIMER video on neonatal
- procedures, for ventricular tap).
• Contrast enhanced comg!:!te~oarae_hy (CEC_D head
may be required- in case of rapidly risi'!Lor~ with
suspicious USG, focal ~e~es, focal neurolog1ca eficits
or infectio~ Citrobacter and Enterofi'CiCm.
• UTI may be treated for 7-14 d. Start empincal treatment with
Cefotaxime/Ceftriaxone plus Amikacin (see sections D24, 026, 05),
and modify as per culture report. Nalidixic acid or nitrofurantoin
should not be used to treat UTJ in neonates since they do not achieve
therapeutic concentrations in the renal parenchyma and blood
str fter nt all proven ust be started on

4 Amoxicillin 10 mg/kg (or Cc halexin) OD oral rophy ax


section me that a rena
are performed to exclude reflux (See Figure 24.1).
, MCU an
235

Figure 24.l: In vestigation of UTI

~~
liSG :F.xam

t i
NonnaI Abnonnal

t
II
! i l
<2 yr 2-5 yr
I I >S yr
MCU&
DMSA
MCU& DoDMSA No test
DMSA DoMCU
only if scar
on DMSAor
D\iSA not
possible

• Proven bone or joint infection must be treated for at least 6 wks.


Start empirical treatment with : 1oxac11lin or Vancomycin (plus an
ammoglycoside for first 1-2 w~ s) and modify as per culture report
(see sections 034, D 129). Of his, at least 4 wks must constitute
parenteraJly administered antib otics. The remainder of the course
may be enterally administered.

24.9 SUPPORTIVE CARE OF Sl('K SEPTIC NEWBORNS


The survival of a sick septic newborn often depends upon aggressive
supportive care.
Neonat~s shou!i~!{5ed .in thermo-neutra environment taking :are
to avoid DlYP---~-~enm~ there ng ox en consum tto
Aggressive nutritional support is m:eded to combat t e cata oltc state
associated with~-
• Oxygen saturation should be maintained in the normal range and
mechanical ventilauon may be required in case of increased work of
breathing (see sections 14.8, 14. 0 and 14.12).
• Anemia.1. thrombocyto_penia, an (i2!a
are treated with appropriate
transfusions. Packed red cells a 1d FFP might have to be used (see
secltons i7:6 and 19.5). - - -
• Septic infants should be scrCC'1ed ror(£ypoglycem(;) and treated
appropriately (sec section 11 .4).
236

24
• Management of Septic Shock (see section 29.6)
Fluid resuscitation with isotonic boluses (up to 2 boluses of 10-20
mL kg over 20-30 min each) should be accomplished (see section
29.6). ln addition, hypoglycemia and hypocalcjmia should be
corrected. Hypocalcemia must be treated with slow IV
administration of calcium gluconate at a dose of 2 ml/kg (see
section O~f shock persists, central venous ancrartemrt'-access
should be obtained and vasoactive agents should be started, with
dopamine as a first-line ag~t (see section D45). If after the first
h our c1rcufati"on is not restored with further pressor support. concern
for adrenal insufficiency sh.ould be raised and hydrocortisone
therapy should be considered.

24.lO ADJUNCTIVE THERAPfES


24.10.1 IVIG:
The currently available evidence does not support the use of TVIG. IVIG
may be used in a difficult siruation, after discussion with the consultant.
Dose: Pentaglobin 5 mUkg/d for 3 d (IgM 6 mg, IgA 6 mg and lgG 38
mg/mL) (see section 068)
Among patients with clinically suspected infection, the reduction of
mortality with IYIG is of borderline significance [typical RR 0.63 (95%
CI; 0.40, 1.00)]. In cases of subsequently proven infection the reduction
in mortality is statistically significant but has very wide Cl (typical RR
0.55 (95% CI; 0.31. 0.98)].25
24.10.2 Colony stimulating factors (see sections 058, 059)
There is currently no evidence to support the use of colony stimulating
factors. From the Cochrane review, there is no evidence that the addition
of G-CSF or GM-CSF lo antibiotic therapy in pretcrm infants with
suspected systemic infection reduces mortality. 26 Prophylaxis studies
have not demonstrated a significant reduction in mortality in neonates
receiving GM-CSF [RR 0.59 (95% Cl 0.24, I .44)).
24.10.3 DVET
OVET has been used as a modality for managing sepsis for several
decades, but large, well-conducted RCTs are still lacking. In a case of
deteriorating sepsis with sclerema, DVET may be performed after
discussion with the consultant. 17 In unstable babies, a single volume
exchange may be done.

24.11 FUNGAL SEPSIS


24.11.l Risk factors: The following are risk factors:
• Prematurity especially gestation < 28 wks
• Very lowBW
• Use of broad spectrum antibiotics especially third generation
ccphalosporins
237

• Prolonged ET intubation
• Receipt of parenteral hyper alimcntation
• Presence ofCVCs
• Surgical procedures especially abdominal and cardiac
• Prolonged hospitalization
• Administration of corticosteroids and H2 receptor blocking agents
• Hyperglycemia
• NEC
24.11.2 Diagnosis
• Fungal sepsis must be suspected in sick newborns with any of the
above risk factors or any sick neonate who has received up to the
third line of empiric antibiotics or sepsis developing beyond 7 d of
life. A smoldering course with persistent thrombocytopenia or
unexplained hyperglycemia or high CRP is typical of fungal sepsis.
• Culture: Candida sp grows in routine blood culture media, but if
other fungi are suspected, a fungal culture medium should be used
(special biphasic media containing BHI broth with agar). Although it
is recommended that cultures should be monitored for 10 d to ensure
adequate growth of slower growing Candida species and other fungi,
results can be available as early as 72 h. For neonates with
indwelling central lines, samples must be obtained from both
catheter and venepuncture.
• CSF: CSF examination for cells, biochemistry, smear for fungal
elements and fungal culture must be performed because this affects
the choice and duration of antifungals. Culture of the CSF is
important in diagnosing fungal meningitis in VLBW infants since
CSF cell counts and chemistries may be normal.
• Suprapubic urine examination for fungal hyphae. Report is available
on the same day (call Mycology lab or Dr Arunaloke Chakrabarti).
• Microscopic examination of huffy coat by centrifugation of blood in
microhematocrit tubes can be used for rapid diagnosis of fungal
invasion in blood.
• If disseminated candidiasis is suspected based on clinical features or
if a positive fungal blood culture is obtained, perform the following:
o Indirect ophthalmoscopy - Endophthalmitis begins as a
chorioretinal lesion that gradually elevates and breaks free in the
vitreous, appearing as a white fluffy ball. These solitary or
multiple white lesions are most often seen in the posterior retina
(zone 1) and vitreous. Contact Ophthalmology JR or SR.
o Abdomen USG for renal mycetomas and hepato-splenic
abscesses
o Neuroimaging to look for ventriculitis or abscess
o Echo for fungal endocarditis
238

24.11.3 Treatment
Empirical treatment:
• First line: Fluconazole (see section D52)
• Second line: Plain Amphotericin B (see section D 11 ). This can be
started if there is no response after 5 d of fluconazole treatment.
Treatment ofproven fungal sepsis:
• If sensitivity report is available, follow the report. Use the simplest
and least expensive anti-fungal (in most cases Fluconazole).
• If sensitivity report is awaited, follow these guidelines:
o For uncomplicated systemic fungal infection, use Fluconazole
o For CNS fungal infection, use plain Arnphotericin B + 5-
flucytosine (see section D53)
o For hepato-splenic or pulmonary: use Amphotericin B Lipid
Complex
o For C glabrata: Use Voriconazole
o For':C parapsilo!tt-imd C tropicalis, use higher doses of
Amph~
o ~use Am~otericin B J
o For endocarditis or Candida refractory to fluconazole ~
Arnphotericin B: use Micafungin
The role for liposornal Amph~ very limited in neonatal fungal
sepsis. Oc21ls1onal c~esOfCNS f'ltilga1 infection may require j t - - - -
~4 Duration of anti-fungal treatment ----
Fluconazole: 7-10 d if uncomplicated, 10-14 d if funguria or mycetoma
(do not go by USG ffodings- they~ to disappear).
Arnphotericin B: Cumulative dose of 20-25 mg/kg. In neonates, there is
no need to give test dose or to build ~

REFERENCES
1. Singh S.A. J.Trop.Pediatr. 2003; 49: 235
2. Benitz W.E. Pediatrics 1998; 102: E41
3. Mahale R. Am.J.Perinatol. 2009;
4. Eldadah M. Pediatr.lnfect.Dis.J. 1987; 6: 243
5. Weiss M.G. J.Pediatr. 1991; I 19: 973
6. Dutta S. Arch.Dis.Child Fetal Neonatal Ed 2009;
7. Fielkow S. J.Pediatr. 1991; 119: 971
8. Kumar P. J.Paediatr.Child Health 1995; 31 : 8
9. Kudawla M. J.Trop.Pediatr. 2008; 54: 66
10. Mouzinho A. Pediatrics 1994; 94: 76
11. Schelonka R.L. J.Pediatr. 1994; 125: 603
12. Da Silva 0 . Pediatr.lnfcct.Dis.J. 1995; 14: 362
13. Fowlie P.W. Arch.Dis.Child Fetal Neonatal Ed 1998; 78: F92
14. Greenberg R.G. Pediatr.lnfect.Dis.J. 2008; 27: 1047
239

15. Rajesh N.T. Arch.Dis.Child Fetal Neonatal Ed 2009; Aug 10: Epub
ahead of print
16. Ahmed A.S. Indian Pediatr. 2002; 39: 1034
17. Tiskumara R. Arch Dis Child F & N Ed 2009; 94: F 144
18. Smith P.B. Am.J.Perinatol. 2008: 25: 421
19. Garges H.P. Pediatrics 2006; 1I7: 1094
20. DiGeronimo R.J. Pediatr.Infect.Dis.J. 1992; I I: 764
21. Tamim M.M. Pediatr.Infect.Dis.J. 2003; 22: 805
22. Chowdhary G. J.Trop.Pediatr. 2006; 52: 427
23. Couto R.C. Braz.I.Infect.Dis. 2007; 11: 240
24. Carcillo J.A. Crit Care Med. 2002; 30: 1365
25. Ohlsson A. Cochrane.Database.Syst.Rev. 2004; CD001239
26. Carr R. Cochrane.Database.Syst.Rev. 2003; CD003066
27. Sadana S. Indian Pediatr. 1997; 34: 20
240

25. EPIDEMIC OF SEPTICEMIA

25. I DEFINITION
Epidemic is defined as the occurrence of cases greater than the expected
number. Strictly speaking, for labeling as epidemic, baseline prevalence
is necessary and the unexpected rise has to be statistically proven.
Practically speaking, the investigation & control measures should be
initiated with any unexpected sharp increase of a specific infection.

25.2 MANAGEMENT
The steps are provided below:
25.2.1 Get organized:
• To get the services of the division of hospital infection control, meet
Dr. Manisha or Dr. Malkiat Singh. Microbiology has got a vital role
in the investigation of an epidemic. A multidisciplinary team should
quickly be constituted to handle the epidemic- consisting of unit
consultants, area SR, sister-in-charge of the area and hospital
infection control team.
• Additional support may be required from hospital administration,
sanitation and biomedical engineering after the initial investigation.
The consultant-in-charge must contact the relevant support staff.
• A formal meeting should be conducted in the unit to define the case
and plan the evaluation and management.
25.2.2 Defining a case:
• This should be formulated by the members of the team in the
meeting. The definition should include time, place and person. E.g.:
I. "any NICU baby who has grown MRSA from any body site after
l" Nov 2007." This allows the members of the unit to understand
what should be called as a 'case' and it ·can be used prospectively to
identify more cases.
25.2.3 Confirm the outbreak:
• Compare the past unit data, preferably of that season with the
infection rate of the presumed outbreak. The SR in charge of the area
should obtain the previous unit data for that specific infection.
25.2.4 Rapid identification of the existing cases:
• Send the cultures of all the babies admitted in that area. Do focused
clinical examinations. Keep low threshold for suspicion of sepsis
and investigation.
25.2.5 Prevent further spread:
• Strengthen the asepsis routine.< including hand hygiene and
housekeeping practices (see sections 23.2, 23.5). Area SR should
sensitize all the staff of the area (including sanitation staff) regarding
the outbreak and should take efforts to improve the compliance with
asepsis routines.
241

• Isolation: Physically isolate the affected babies. General measures


of infection control like contact isolation and droplet isolation
precautions must be taken. Shift the babies to the isolation room of
the respective area ifthe number of the babies permits.
Barrier nursing: neonates infected with the same organism must be
cohorted and segregated from rest of the neonates. Dedicated nurses
and residents should be appointed for the affected neonates, and they
should not participate in the care of other babies.
25,2.6 Determining the source:
• The area consultant, SR and JR's must review all the case records of
the affected babies to find out the source. This should be critically
analyzed e.g. whether all the babies got shifted from a single place
or in a particular transport incubator or babies getting shifted to a
particular bed are getting infected.
• Common sources are contaminated !VF, TPN, formula milk,
incubators (including transport incubators), humidification
chambers, drugs, shared BP cuffs, stethoscopes, ventilation circuits,
resuscitation equipments, soaps and antiseptic solutions. The s;ourcc
may be outside the unit, e.g. from the labor room.
• The spread of infection can occur through the hands of the personnel
involved in the care of the baby or through the fomites. The health
care personnel can also be reservoir of the infection or carriers.
• Surveillance cultures: Snrveillance cultures often help in identifying
the source. Cultures need to be taken from environmental sites, from
neonates and from the staff(See Table 25.1).
For identifying colonization of neonates take the swabs from a) nose
b) inguinal region c) axilla d) umbilicus.
• Detailed microbiological characterization should be done.
Antibiogram, biotyping, scrotyping and phage typing help in
identifying the type of the strain. Molecular typing [like PFGE
(Pulsed field gel electrophoresis), (RAPD) Randomly amplified
polymorphic DNA or DNA finger printing) is necessary for further
characterization of the strain. Above mentioned tests are available in
Dept of Microbiology on request. For characterization of bacterial
and fungal strain, contact Dr. Pallab Ray and Dr. Arunaloke
Chakrabarti respectively.
• If culture is positive ft-om an employee, he/she may have become
transiently colonized after contacting the affected infant and need
not be a persistent carrier. If culture positive, take repeat cultures and
from other body sites to know whether they are the persistent
carriers. Preserve the confidentiality of the staff members who are
assessed, cultured and treated.
242

Table 25.l: Cultures for identifyin~ the source o f various or2an1sms


Cultures to be given
Organism Comments
special emphasis
These are the common
Skin, nasal smears of
Staphylococcus sites of colonization in
NICU personnel
persistent carriers
Povidone iodine and Can grow in antiseptic
Pseudomonas other antiseptics, solutions, also grows in
humidifiers, nebulizers humid environment.
Candida & TPN, !VF, mucosa! Fungi like Malassezia
other fungi membranes are lipophilic
Enterobacteriaceae are
Klebsiella, Stool, oral secretions,
colonized in the gut and
Enterobacter, umbilical cord of
transmitted through hand
Enterococci neonates
of health care workers.
Coagulase
negative
Skin, invasive catheters Rule out contamination
Staphylococcus
aureus (CONS)
Environmental
Acinetobacter, (mattresses, air These are generally
Alkaligenes conditioners, ubiquitous.
ventilation tubings)

25.2.7 Tracking the epidemic:


Perform "line listing" of the cases & construct an epidemic curve. Keep
the serial record of the neonates developing the infection and tabulate the
following information:
S. No.
Name
A-No. I 1-No/O-No
Gestation
Wt
DOB
Date of transfer to area
Date on onset of symptoms
Date of sending culture
Interventions done prior to sepsis
Culture report
Doctors who handled
Nurses who handled
Outcome
243

Use the information from the line listing for determining the type of
outbreak. If the outbreak is due to a point source, it will have one major
peak, and if it is propagating outbreak it will have multiple peaks.
25.2.8 Antibiotic policy
Check the sensitivity pattern of the implicated organism and consider a
change of antibiotic policy, if necessary (see section 24.8.1).
25.2.9 Other administrative measures
• Limit the new admissions into the area only for unavoidable
admissions.
• Involve the Obstetrics department and try to transfer waiting high
risk mothers to other hospitals for delivery.
• Avoid transfer of the residents from one area to another area in the
unit.
• Tackling the source:
o Point source- like drugs, !VF, formula feeds must be discarded.
If a particular batch no. of IVF is responsible then notify the
hospital administration.
o If the source is equipment like incubators, disinfect it. Do not
use until two consecutive cultures are negative.
o If the source is a health care personnel acting as persistent
carrier, treat the carrier state if treatment available. He/she is to
be allowed to participate in the care of the babies, only if two
consecutive cultures are negative. Persistent carriers may have
to be permanently shifted out "fthe area.

25.3 FOLLOW UP:


All measures should be continued until the last colonized baby with that
specific strain, is discharged. Follow up surveillance must be done to
ensure that the measures are effective. A formal meeting is to be
conducted once the outbreak is under control to present the summary of
the epidemic and to congratulate the staff for their co-operation and
efforts.
244

26. TORCH INFECTIONS

This chapter does not cover HIV. See chapter 27 for HIV.
26.1 SUSPECT AN IUI IN THE FOLLOWING SITUATIONS
• Maternal h/o contact with a known infected case or h/o non-
vesicular rash (Rubella, Parvovirus) or vesicular rash (Varicella and
Herpes) during pregnancy
• PDA in a near tenn/term infant
• Clinical stigmata (unexplained severe SFD, hepatosplenomegaly,
blue berry muffins, microcephaly)
• Late onset neonatal cholestasis
• H/o recurrent abortions in mother -- suspect syphilis

26.2 GENERAL INVESTIGATIONS TO BE DONE IN ALL


BABIES WITH SUSPECT IUI
• Placental histopathology in newly born babies with suspected intra-
uterine infection.
• Send the baby's venous blood for lgM and IgG levels for the
suspected infection- plain vial 1-2 mL (cord blood analysis must not
be done as contamination is possible with maternal blood)
• CBC and platelet count
• USG/CT brain for hydrocephalus and intracranial calcification.
• LFTs
• If maternal TORCH titers are not available, send 2 mL of maternal
blood simultaneously with the baby's blood.
• Ophthalmoscopy (except in case of suspected TB and congenital
syphilis)

26.3 GENERAL MEASURES (modified from AAP Red book & CDC
guidelines)' ·2
• Contact isolation in a separate room in NNN. It is preferable but not
absolutely required to isolate incubator-confined patients. Also limit
transport and movement of patients outside of the room.
• Early discharge to be planned if isolation is not feasible.
• Wear a new gown at entry and thoroughly hand wash while entering
and leaving. Wear gloves while handling patient.
• Napkins, beddings and other materials that are exposed to the
infant's body fluids should be bagged and sterilized.
• Ensure that rooms of patients on contact precautions are prioritized
for freqiient cleaning and disinfection with a focus on frequently-
245

touched surfaces and equipment in the immediate vicinity of the


patient
26.4 CONGENITAL TOXOPLA~MOSIS
85% of cases are asymptomatic at birth. The classic triad of
chorioretinitis, hydrocephalus and intracranial calcifications is rare
26.4.1 Diagnosis
Specimen required - Blood, urine and CSF
• Toxoplasma serology battery: Send 1-2 mL clotted blood for ELISA
(lgM, lgG and IgA) to Parasitology Lab. A major problem with
Toxoplasma serology is lack of sensitivity and specificity of
individual tests, which improves when tests are combined. The lgM
lmmunosorbent agglutination assay (JSAGA) is a more sensitive and/
highly specific test (currently not available in PG!MER and priv'!I<{
labs in Chandigarh).
• In case of lgM negative and lgG positive cases use of IgG/IgM
western blots of mother-infant pairs can prove useful. This is not
routinely done in PGI. Discuss with Parasitology SR about
availability of these tests. Maternally transferred IgG antibodies
usually decline and disappear within 6-12 mths. Detection of rising
IgG titer in sequential sera is suggestive of infection.
• Isolation of T. gondii from body fluid by mice peritoneal inoculation
is available in the Parasitology dept. Report is available in I mth.
• Detection of organism in CSF. blood and urine by PCR. Discuss
with Parasitology SR about availability of these tests. Treat PCR
positive cases.
26.4.2 Additional investigations to be done in proven cases
• Urine analysis - to rule out proteinuria
• G6PD screen before starting Sulfadoxine
• A11ditory brainstem response
26.4.3 · Management of an infant with suspected congenital
toxoplasmosis: shown in figure 26.1
26.4.4 Treatment
A previously undiagnosed untreated case can present anytime from
infancy through adolescence with ocular (chorioretinitis) or neurological
(seizures, hydrocephalus) sequelae. Hence treat all cases irrespective of
appearance of symptoms.
• Since Pyrimethamine and Sulfadiazine are not easily available in
India, use Sulfadoxine-pyrimethamine (Available as Susp.
Pyralfin/Saligo- 25mg Pyrimethamine and 500mg Sulfadoxine I 5
mL) (see section Dl09, Dll9). Dose: 1.25 mg/kg pyrimethamine
and 25 mg/kg Sulfadoxine every 15 d + Folinic acid 5 mg once a wk
for 2 yrs. Folinic acid is available as Tablet Recovorin 15 mg. Make
246

Figure 26.l Management of an infant with suspected congenital


toxoplasmosis

Patient with suspected


congenital toxoplasmosis

lgM/lgAIJgG -ve

! Toxoplasma Serology Battery No treatment required* I


(ELISA lgM, IgA and IgG)

I IgM +ve/ IgA +vc I I IgM +ve/ IgA -ve I I OnlylgG+ve I

Normal Suggestive
CT/ophthalmoscopy CT/ophthalmoscopy
·>
Send blood and urine to Parasitology
____, Dept for isolation of T gondii by
mice peritoneal inoculation after
discussion with Parasitology SR Normal
CT/ophthalmoscopy

• Do not start treatment immediately

Suggestive
+ve • Do 3 monthly ophthalmic evaluation
for appearance of retinitis and start
CT/ophthalmoscopy treatment if positive.
• Do follow up IgG every 6 weeks.
_I Treat as congenital
Start treatment if lgG titers are rising
I toxoplasmosis at 6 weeks

Note;
• Suggestive CT findings are periventricular white matter and basal
ganglia calcification and hydrocephalus.
• Suggestive ophthalmoscopic findings are focal necrotizing retinitis
with macular involvement

Folinic acid OD if ANC <IOOO and consider stopping


Pyrimethamine if ANC < 500.
• Prednisolonc (see section DI03) I mg/kg is added when CSF protein
is > 1 g/dL or when active chorioretinitis threatens vision. Continue
until resolution of signs and symptoms.
• Do CBC monthly.
247

• Do SGPT, creatinine and urinalysis every 3 mths to monitor


Sulfadoxine toxicity.
• After treatment, resolution of clinical findings may take up to I mth.
26.4.S Follow up
• Ophthalmology (visual impairment occurs at 5 yrs even with
treatment in 85% of patients with severe disease and 15% with mild
disease at birth)
• Neurosurgery (if ventricular dilatation is suspected or proven)
• Neurodevelopmental follow up.

26.S CHICKEN POX


The timing of maternal varicella influences the nature of neonatal illness.
Elective delivery should be avoided until 5-7 d after the onset of
maternal rash to allow for the passive transfer of antibodies from mother
to child.
26.S.I Maternal infection and neonatal manifestations: Shown in
Table 26.1

Table 26 I Maternal varicella and neonatal manifestations


Maternal infection Neonatal manifestation
First 20 wks Fetal varicella syndrome characterized by one or
gestation more of the following: skin scarring in a
dermatomal distribution; eye defects; hypoplasia
of the limbs; and neurological abnormalities
28 wks gestation till No fetal or neonatal effect other then the
4 wks prior to development of herpes zoster in the first few
de liven• vears of infant life
1-4 wks prior to 23% develop clinical varicella (50% infected);
delivery symptoms are mild due to transfer of maternal
antibodies.
Infection 1 wk prior Severe infection
to and after deliverv

26.S.2 Diagnosis
• Presence of typical vesicular rash and maternal h/o peripartum
varicella is itself diagnostic.
• Antigen detection by indirect fluorescent antibody test: Obtain a
special slide for this test from the Virology department Room no
107, level I, Research A block. Take scrapings from the base of the
lesion and apply to the well of the slide (A dermatology consultation
can be sought for obtaining the skin scraping). Transport promptly to
lab. Results are available in 24 h.
• Infant 1-2 mL blood for Varicella zoster virus lgM: rarely required
248

26.5.3 Management: Shown in Tables 26.2 and 26.3

Table 26.2: Seoaration of mot her an db a b>y


Situation Seoaration of babv and mother
Maternal rash onset> 5 d before Not required. Isolate dyad from
birth or> 2 d after birth other infants. Send dyad home once
mother is non-infectious (lesions
dried & crusted, approx. 5-7 dafter
onset) and baby is asymptomatic
Maternal rash within approx 5 d Required until maternal lesions
of birth to 2 d after birth have dried and crusted (approx. 5-7
dafter the onset of rash). Separation
not required if the infant develops
clinical varicella. A mother and/or
her baby with active vesicles should
also be isolated from other mothers
and babies.

Table 26.3 Guidelines for VZIG administration

Situation Treatment to neonate


Onset of maternal rash from 5 d before to VZJG (Varitect CP) I
2 d after birth mL/kg (25 JU/kg) IV.
Non-immune exposed neonates (mother Infuse at 0.1 mL/kg/h for
has no h/o of chicken pox infection or I 0 min and if well tolerated
vaccination) increase to maximum of l
All preterm <28 wk and < I kg who are mL/kg/h. VZIG should be
exposed to chickenpox in the first 28 d of given to the baby as early
life. as possible, but must be
within 72 h of
exposure/delivery. (see
section Dl33)

• VZIG may prolong the incubation period of the virus for up to 28 d


and therefore exposed neonates that are given VZIG should be
monitored for signs of infection for this time period
• Maternal shingles around the time of delivery is not a risk to the
neonate because of protection by transplacentally acquired maternal
antibodies. This may not apply to the baby who delivers before 28
wks or weighs less than I kg who may require treatment with VZIG.
• Expressed breast milk can be given even if mother-infant dyad is
separated. Breast feeding can be allowed once mother is
noninfectious.
249

• IV Acyclovir (60 mg/kg/d g•h hourly IV for 5-7 d) should be


administered to any neonate wh J develops chickenpox whether or
not they received VZlG (see section 02).
• Neonatal ophthalmic examination should be organized afte; birth in
case of suspected congenital vari< eHa syndrome

26.61'!EONATAL HERPES SIMPLEX INFECTION


• Transmission routes are intrauterine (5%), peripartum (85%), and
postnatal (I 0% ).
• Three presentations occur- Skin eye and mouth (SEM) disease-
45%; CNS disease (30%); disseminated disease (25%). Patients with
disseminated or SEM disease present to medical attention at I 0 to 12
d of life (or earlier if there is ruprure of membranes), while patients
with CNS disease present somewhat later, at 16 to 19 d of life.
26.6.1 Diagnosis
• DNA PCR of blood and CSF: Case to be discussed with virology
SR. 2 mL of blood/CSF must be drawn in a plain vial and sent
immediately to lab for processing. Sensitivity 67-100% and
specificity 70-100% for both blood and CSF.
• Serologic studies have limited role in diagnosis due to low
sensitivity and specificity. Specimen- Conjunctiva! and throat
swabs, CSF, urine and clotted blood (1-2 mL). Specimen is sent to
Virology department for indirect IF.
• Antigen detection by indirect fluorescent antibody test: Obtain
special slide for this purpose from the Virology department. Take
scrapings from the base of the lesion and apply to the well of the
slide (A dermatology consultation can be sought for obtaining the
skin scraping). Transport promptly to lab. Results are available in 24
h
• CNS imaging: MRI with gadolinium is superior to computed
tomography (CT) scans for the diagnosis of CNS herpes. Imaging
procedures may reveal focal abnormalities in the temporal Jobes,
insular cortex, gyrus rectus that manifest with a low signal on T 1
weighted spin echoes and a high signal on T2 weighted spin echoes
• EEG -Periodic lateralized epileptiform discharges (PLEDs) and
'"multifocal periodic pattern" are suggestive of herpes encephalitis.
Paroxysmal discharges in the newborn period are generally
generalized and need not be confined to the temporal region as in
older age groups.
26.6.2 Management
• Baby can be delivered by LSCS if mother has active genital lesion
and duration of rupture of membranes <4 h
250

• Acyclovir: 60 mg/kg/d 8'h hourly IV if infection proven (see section


D2)
• Duration of therapy - 21 d for Disseminated or CNS disease; 14 d for
SEM.
• Patient with eye involvement should receive topical ophthalmic
agents (Acyclovir 3% - Zovirax ophthalmic ointment) in addition to
parenteral therapy.
• Patients with CNS HSY involvement should have a repeat CSF PCR
analysis at 2 l d; and then stop therapy if negative. If PCR is
positive, continue acyclovir and do weekly PCR till negative, when
acyclovir can be stopped
• Monitor the ANC and renal function twice weekly throughout the
course of therapy. Consider decreasing the dose of acyclovir or
administering granulocyte colony-stimulating factor if the ANC
remains below 500/µl for 48 h.

26.7 NEONATAL CMV DISEASE


The fetus and infant can either be infected via viral transmission through
the placenta, during delivery (via cervical secretions and blood) or from
the mother via breast milk.
85-90% has subclinical infection. Cytomegalic inclusion disease (CID) is
characterized by involvement of multiple organs, in particular the
reticuloendothelial and CNS, with or without ocular and auditory
damage.
26. 7. l Diagnosis
The first 3 tests mentioned below must be sent in all cases where CMV
inclusion disease is a possibility.
• 1-2 mL Clotted blood for CMV lgM: Positive lgM at <2 wks of age
(only 70% of the neonates with congenital CMV have lgM
antibodies at birth) indicates congenital infection and appearing for
the first time at > 4 wks of life indicates perinatal infection. Send
sample to Virology department Room no 109. Sensitivity and
specificity ranges from 70-90 %.
• Send blood in EDT A vial for pp65 antigen detection on Tuesday or
Friday to Virology department Room no 107.
• Ask for special vial (alcohol containing) for urine microscopy from
virology lab and send urine to look for owl eye (intranuclear)
inclusion bodies - Virology department.
• Identification ofCMV-DNA by PCR in urine, blood and CSF. Done
only after discussion with virology SR.
• CNS imaging: findings include multifocal lesions predominantly
involving deep parietal white matter, ventriculomegaly, intracranial
calcifications, brain atrophy and destructive encephalopathy, with or
251

without gyral abnormalities. l he presence of abnormalities in the


anterior part of the temporal lo Je increases the likelihood that CMV
infection is present.
• Ophthalmic and hearing assessment.
26.7.2 Treatment
• Follow general measures (see section 26.3)
• Ganciclovir treatment for congenital CMV with CNS involvement
may be considered after discussing with consultant (see section
D56). A phase IJl RCT 3 had shown that there was improved hearing
compared to co11trols after 6 mths follow-up. but there was no effect
on long-term neurodevelopmental or other sequelae. Single reports
of improvement in infants with cholestasis and chorioretinitis after
IV ganciclovir therapy have been published. Oral valganciclovir
(Valcyte, Roche/Ranbaxy) at 16 mg/kg had been found to be simlTa:r
in efficacy to 6 mg/kg IV ganciclovir.4

26.8 RUBELLA
When rubella infection occurs during pregnancy, especially during the
first trimester, the risk of fetal infection may be as high as 90%. The most
common manifestations of CRS are sensorineural hearing loss, cataracts
and heart defects. PDA is the most common defect and may occur as the
sole manifestation of congenital rubella. Eye defects include cataracts
and a 'salt and pepper' retinopathy.
26.8.1 Diagnosis of CRS (any one positive test required)
• Demonstration of rubella-specific IgM antibody before 3 mths of
age. In some instances, IgM may not be detected until at least 1 mth
of age. So infants with symptoms consistent with CRS who test
negative shortly after birth should be retested at l mth of age.
• IgG that persists at a higher level (i.e., titer that does not drop at the
expected rate of a twofold dilution per month) and for a period of>
6 wks.
• PCR for Rubella DNA
Serology is available in PG! at room no 109, Dept of Virology. PCR is
currently not available in PG! but could be done in private labs and
should be done in infants with symptoms consistent with CRS who have
persistent lgM seronegativity. Ophthalmic testing and hearing assessment
should be done in all proven cases.
26.8.2 Treatment
Follow general measures stated in introduction. There is no specific
treatment. Non-immune pregnant staff members must be shifted to other
areas. The family must be told that non-immune pregnant family
members or well-wishers must be asked to stay away.
252

26.9 HEPATITIS B
The prevalence of HBsAg positivity in pregnant mothers in various
Indian studies ranges from 0.6%-5.0%. 70-90% of newborns born to
mothers who are HbsAg and HbeAg positive acquire infection during the
perinatal period and 90o/o of these newborns become chronic carriers. 5o/o
of newborns born to HbsAg +/ HbeAg - mothers become chronic carriers
5
26.9.1 Management of infant born to HbsAg +ve moth er : Sh own m .
Table 26.4

Table 26.4 Management of infant born to HBsAg +ve mother

Maternal Intervention
status I
Gestation and
Wt ofbabv
HbsAg Administer Hepatitis B vaccine (see section 5.2.6) and
positive (Term HBIG (0.5 ml) lM at Sl2 h of birth (efficacious up to
baby of any 72 h) (see section D63). Administer at different
Wt) injection sites. Repeat vaccine doses at I and 6 mths
(85%--95% efficacy). If patient cannot afford HBIG
administer vaccine first dose Sl2 h of birth with repeat
doses at I and 6 mths (70-90% efficacv)
HbsAg Same as above. Initial vaccine dose (birth dose) should
positive not be counted as part of the vaccine series. 3
(pretenn baby additional doses of vaccine (for a total of 4 doses)
or< 2000 g of should be administered beginning when the infant
any gestation) reaches age I mth.
Mother with Ensure administration of vaccine at Sl2 h of birth. If
unknown mother turns out to be HbsAg positive later, administer
HBsAg status HBIG as soon as possible but no later than age 7 d
after birth.

• Postvaccination testing for anti-HBs and HBsAg can be performed


after completion of the vaccine series, at age 9-18 mths. HBsAg-
negative infants with anti-HBs levels 2:10 mIU/mL arc protected and
need no further medical management. HBsAg-negative infants with
anti-HBs levels <l 0 mlU/mL should be revaccinated with a second
3-dose series and retested 1-2 mths after the final dose of vaccine.
• Infants of HBsAg-positive mothers should be breastfed beginning
immediately after birth.
• HBsAg-containing combination vaccines may be used tOr infants
aged 2:6 wks born to HBsAg-positive mothers to complete the
253
vaccine series after receipt of a b rth dose of single-antigen hepatitis
B vaccine and HBlG.

26.10 HEPATITIS C
Approximately 5% of all infants born to HCV infected mothers become
infected. Risk factors for MTCT include maternal HIV co-infection, high
maternal HCV viremia, IV drug use.
26.10.1 Management
• Allow breastfeeding
• PCR tests for HCV-RNA at 2 mths or Anti-HCV testing at 12~
18 mths of life. These investigations are not currently available in
PG!.
• There is no specific management

26.11 HEPATITIS E
Studies have shown that Hepatitis E is responsible for 40-60% of acute
viral hepatitis in pregnancy. 20% of women can develop fulminant
hepatic failure. Preterm delivery rates are higher. Vertical transmission
rates up to 75% in various studies. Neonatal manifestations include
anicteric, icteric and fulminant hepatitis. Send blood for lgM anti-HEY
antibodies by ELISA assay and HEV-RNA to confirm diagnosis (the
latter is currently not available in PG!).

26.12 PERINATAL TB: Shown in Figure 26.2


Symptoms may be present at birth but are usually seen in the second and
third wks. Common clinical manifestations include hepatosplenomegaly
(76%), respiratory distress (72%), fever (48%), lymphadenopathy (38%),
abdominal distension (24%), lethargy and irritability (21 %), ear
discharge ( 17%), and skin papules (14%).
26.12.1 Investigations
Send tests for AFB, culture to Mycobacterial lab No: 217, Dept of
Bacteriology, level 2, Research A block.
• Do CXR in all cases. CXR is abnormal in all cases of congenital TB
and in 50o/o cases a military pattern is seen.
• Send 3 gastric aspirates for AFB staining and culture only if CXR
suggestive.
• Placental tissue for Histopathological examination and culture.
• CSF for AFB stain and culture
• Lymph node biopsy and bone marrow aspirate can be done if
available and diagnosis is otherwise uncertain after above
investigations
• Consider HIV testing (mandatory if TB confirmed)
254

26.12.2 Treatment (see sections 072, DI 11, 0107, 050, 0108)


• Separate the infant and mother if mother has active TB or evidence
of recent infection (abnormal X-ray; Mantoux positive) and when
infant is not started on ATT (preventive or therapeutic).
• Once infant is on ATT, allow breast-feeding
• Also isolate mother from baby if Multidrug resistant (MDR) TB
suspected or if mother is noncompliant or has received ATT for <2
wks
• EBM can be allowed even if mother and infant are separated.
• BCG should be administered to all infants before hospital discharge.
Special !NH-resistant BCG is not required.
• When infant is on ATT administer pyridoxine 5 mg/kg OD (see
section DI 08)

Figure 26.2: Management of an infant born to mother with TB


ATT Dosages Mother with active TB or evidence of recent infection
Isoniazid (H) - 5 mg/kg
Rifampicin (R) - 10 mg/kg
P zinamide Z) - 25 m

Start prophylaxis with HR in Ensure treatment. of mother and promptly


bab and allow breast feedin screen household and close contacts.

Examine baby for perinatal TB, CXR,


Gastric juice for AFB if CXR +ve, CSF

Baby infected Baby not infected


2 HRZ/7-10 HR Continue prophylaxis with HR

Give HR
prophylaxis for 9
mths ( 12 mths if Mantoux at 3 mths
Hrv positive) +ve ·Ve

2 HRZ/7-10 HR Stop prophylaxis


If the mother is o e with nd sputum, or
asymptomatic with sputum negative once ATT received for 2 wks:
observe baby and mother, and screen contacts.
255

26.13 SYPHILIS 6
26.13.1 Diagnosis
• If mother is seroreactive, evaluate baby with a quantitative non-
treponemal serologic test (VDRL). Conducting a treponemal test is
not necessary.
• Examine thoroughly for evidence of congenital syphilis (e.g.,
nonimmune hydrops, jaundice, hepatosplenomegaly, rhinitis, skin
rash, and/or pseudoparalysis of an extremity).
26.13.2 Management
Scenario I: Infant with an abnormal physical examination that is
consistent with congenital syphilis
Evaluation
• Do blood VDRL
• CSF analysis for VDRL, cell count, and protein
• CBC and differential and platelet count
• Other tests as clinically indicated (e.g., long-bone radiographs, chest
radiograph, liver-function tests, cranial USG, ophthalmologic
examination, and auditory brains tern response)
Treatment: Aqueous crystalline penicillin G 100,000-150,000 units/kg/ct
(see D98), administered as 50,000 units/kg/dose IV every 12 h during the
first 7 d of life and every 8 h thereafter for a total of 10 d (3 wks if CNS
involvement) or Procaine penicillin G 50,000 units/kg/dose IM in a
single daily dose for 10 d. lf>l d of therapy is missed, the entire course
should be restarted. Data are insufficient regarding the use of other
antimicrobial agents.
Scenario 2: Infants who have a normal physical examination and VDRL
titer the same or less than fourfold the maternal titer, and the
1. Mother was not treated, inadequately treated, or has no
documentation of having received treatment;
2. Mother was treated with nonpenicillin regimen; or
3. Mother received treatment <4 wks before delivery.
Evaluation
• CSF analysis for VDRL, cell count, and protein
• CBC and differential and platelet count
• Long-bone radiographs
Treatment
Crystalline penicillin G (see dose above, section D98) or Procaine
penicillin G (see dose above) or Benzathine penicillin G 50,000
units/kg/dose IM in a single dose (use latter only if evaluation is normal
and follow up is certain).
256

Scenario 3: Infants who have a normal physical examination and VDRL


titer the same or less than fourfold the maternal titer and the
1. Mother was treated during pregnancy, treatment was appropriate for
the stage of infection, and treatment was administered >4 wks before
delivery; and
2. Mother has no evidence of reinfection or relapse.
Evaluation: No evaluation is required.
Treatment: Benzathine penicillin G (see dose above). No treatment is
required if mother was treated adequately before pregnancy and is VDRL
non-reactive during pregnancy
26.13.3 Infection control
Baby is not infectious 24 h after penicillin therapy. So there is no need to
isolate baby after 24 h of penicillin therapy.
26.13.4 Follow-Up
• In sero-reactive babies do follow-up VDRL every 2-3 mths until the
test becomes non-reactive or the titer decreases fourfold. VDRL
should normally decline by 3 mths and should be non-reactive by
age 6 mths if adequately treated. If these titers are stable or increase
after age 6-12 mths, the child should be retreated with a 10-d course
of parenteral penicillin G.
• Infants whose initial CSF evaluations are abnormal should undergo a
repeat LP every 6 mths until the results are normal. A reactive CSF
VDRL test or abnormal CSF indices that cannot be attributed to
other ongoing illness requires re-treatment for possible
neurosyphilis.

REFERENCES:
1. Guideline for Isolation Precautions: Preventing Transmission of
Infectious Agents in Healthcare Settings 2007, CDC
2. Isolation Precautions. AAP Red Book 2009: 149-158.
3. Kimberlin DW. J Pediatr. 2003;143:16.
4. Kimberlin DW. J Infect Dis. 2008;197:836.
5. Hepatitis B treatment guidelines. CDC 2006
6. Evaluation and treatment of infants during the first month of life.
Congenital syphilis treatment guidelines. CDC 2006.
257

27. HUMAN IMMUNODEFICIENCY VIRUS <HM INFECTION

27.1 HIV MTCT


27.1.l Rates of transmission
Mother-to-child transmission of the HIV-I continues to be a major global
health problem. Vertical transmission (mother to child) is the main cause
of childhood HIV infection (See Table 27.1 ).

Tab le 27. l: Risk of oerinatal transmission


Time period Risk
During Pregnancy 5-10%
During labor and delivery 10-20%
During breast feeding 5-20%
Overall without breast feeding 15-25%
Overall with breast feeding to 6 mths 20-35%
Overall with breast feeding to 18-24 mths 30-45%

27.1.2 Epidemiology of perinatal transmission of HIV-I


Following are the important risk factors for matemo-fetal transmission:
• Maternal plasma viral load- is the strongest independent predictor of
both intrauterine and IP transmission of HIV-I, although
transmission can occur rarely, even at low or undetectable viral
loads.
• Advanced maternal HIV-I disease.
• Low CD4 count or percentage (<200).
• STDs.
• Primary HIV- I infection.
• Greater than 4-hour duration of membrane rupture, chorioamnionitis.
• Vaginal delivery.
• Premature delivery.
• Breast feeding. Most transm1ss1on of HIV-I through breast milk
occurs during the infant's first few months of life. with a lower but
continued risk remaining thereafter. Risk factors for breast milk
transmission of HIV-I include:
o Women seroconverting during lactation
o Detectable HIV-I RNA level in breast milk
o Bleeding or cracked nipples
o Subclinical and clinical mastitis, and breast abscesses.
258

27.2 COUNSELING AND TESTING OF MOTHERS


NACO advocates that all women of childbearing age should receive
preconception HIV counseling and that all pregnant women should be
offered HIV testing as part of routine primary medical care, regardless of
risk factors and the prevalence rates of HIV in the community. A woman
has a right to refuse testing if she does not think it is in her best interest.
The antenatal testing and counseling is done in PG! in the Gynecology
OPO 2"' floor, New OPO between 9 am to I pm.
Testing of women before or during pregnancy is comprised of initial
screening with ELISA followed by confirmatory testing of reactive
samples with a supplemental test (e.g., Western blot). If the first
encounter with a pregnant woman is late in pregnancy or during labor,
either an expedited ELISA or rapid testing is used to establish the HIV
status of the woman so that an Anti-retrovirus prophylaxis regimen to
prevent perinatal transmission can be initiated immediately. A "rapid
test" is a kit designed to test a single specimen for HIV-I antibodies;
results are available within minutes to 2 h. The sensitivity of these tests is
100% and specificity is in range of96.8-l00 %. Kits in PG! are provided
free of cost by NACO.
27.2.1 Counseling procedure followed at PGIMER: Shown in Figure
27.1

Figure 27.1 Counseling of HIV+ve mother at PGIMER

I Not ready for

Counseling r
screening __..,..Re-counseling

Repheat Twice - - Infected


wit card test
L Ready for
screening --ELISA
L Patient not
infected

27.3 PROPHYLAXIS REGIMES TO REDUCE MTCT: The WHO


2010 guidelines are shown in Figure 27.2. (Also see sections 091, 0132)

27.4 MODE OF DELIVERY


Studies performed before the advent of HAART (Highly active
antiretroviral therapy) showed LSCS done before labor and rupture of
membranes reduces perinatal transmission of HIV-I by 50 to 87 percent,
independent of the use of ART or ZOV prophylaxis 3. Whether elective
LSCS would offer any additional benefit in women successfully treated
with HAART who have very low or undetectable viral load is unclear.
259
Figure 27.2: Approach to prevention of MTCT of HIV

Establish HIV status of


pregnanl women

Known HJV infection and HIV test positive HIV test negative
already receiving ART

+
Continue ART Determine ART
I eligibility* I
I

Eligible for ART*"' •
Not eligible for ART; requires
I I ARV prophylaxis I
+
Give one of the recommended 3-
drug ART regimes to mother in

Option A: Maternal
AZT prophylaxis

Option B: Triple
ARV prophylaxis
antenatal period** starting from 14 starting from 14
weeks of gestation weeks of gestation

•• + + +
I Continue ART in labor I Sd-NVP at the start
of labor and AZT +
Continue triple ARV

3TC twil:e daitY


I prophylaxis in labor

Breastfeeding or replacement Breastfeeding


+ Breastfeeding
i
feeding Mothers: Contmue AZT+ :'\fothers; Continue triple
Mothers: Continue ART 3TC until I week alter delivery ARV prophylaxis unt1l l
Infants: Daily NVP or twice- Infants: Daily NVP from birth week after complete cessation
daily AZT from birth until 4-6 until 1 week after all exposure of breastfeeding
weeks of age (Irrespective of to breast milk has ended, or, if Infants: Daily NVP from
mode of infunt feeding) breastfeeding stops before 6 twice-daily ACT from birth
weeks, for a minim11m of 4 to 6 until 4 to 6 weeks of age.
weeks following bin:h

Replacement feedi•g only Replacement feeding only


Mothers: Continue AZT+ "1others: None
3TC until I week after delivery Infants: Daily NVP or twice-
Infants: Daily NVP or sd- daily AZT from birth or as
NVP plus twice-daily ACT soon as feasible until 4-6
from birth until 4-6 weeks of weeks of age.
'g'

*Start ARV prophylaxis while waiting to determine ART eligibility


**Avoid use of EFV in first trimester; use NYP instead.
#If AZT was taken for at least the last 4 weeks before delivery, omission of the maternal
sd-NVP and accompanying tail (AZT+ 3TC) can be considered.
260

Elective cesarean delivery is recommended if


o HIV-I -infected women who present late in pregnancy on no ART
• High viral load

27.5 DISINFECTION PRACTICES IN DELIVERY ROOM


• Resuscitation takes priority even in the absence of proper protective
devices.
o All the reusable devices like delivery instruments and resuscitation
equipments which came in contact with body fluid should be
disinfected before reuse by using the following disinfectants with a
contact time of at least 20 min. [(Glutaraldehyde based formulations
(2%) or Stabilized hydrogen peroxide (6%)]
• Environmental surface germicide effective against HIV is a solution
of sodium hypochlorite (I part household bleach to 99 parts water or
1/4 cup bleach to I gallon of water) prepared daily. Bleach,
however, is corrosive to metals (especially aluminum) and should
not be used to decontaminate medical instruments with metallic
parts.

27.6 MANAGEMENT OF HIV-I-EXPOSED INFANTS IN


DELIVERY ROOM
The initial assessment of the HIV-I-exposed infant begins in the delivery
room.
• Maternal medical and obstetrical history should be reviewed.
• Records of HIV-infected pregnant women should be checked for co-
infections, such as other TORCH infections and infants should
undergo further evaluation accordingly (see chapter 26).
• Resuscitation of the baby should take priority even in the absence of
proper protective devices.
• The universal precautions are the same as for any other procedure
(see section 23.7).
• The JR must procure the kit designed for HIV +ve mother's delivery
available with the SLR staff on duty (cap, mask, gown, shoe covers,
goggles, and polythene cover for disposal).
• The baby's mouth and nostril should be wiped as soon as head is
delivered
• All maternal secretions and blood should be washed off from
infant's body (sponge the baby with lukewarm water within a couple
of hours of birth)
• The cord must be clamped early. Do not milk the cord; and cover
cord with gloved hand to avoid splashing.
• CBC with differential count must be done at birth, as a baseline
investigation
261

• Start ART as in section 27.3 ab.we

27.7 MONITORING ART IN THE NEONATE


• CBC with differential at birth . 4 wks, and 8 wks to monitor for
ZDV-associated hematologic toxicity
• Adverse effects of ZDV- Severe anemia or neutropenia, lactic
acidosis, severe GIT intolerance.
• Adverse effects ofNVP- Hepatitis, hypersensitivity reaction, Steven
Johnson (SJ) syndrome.

27.8 FEEDING HIV-EXPOSED NEONATES


Mother should be counseled in the antenatal and postpartum period
regarding breastfeeding. NACO emphasizes exclusive replacement
feeding in situations of AF ASS- acceptable, feasible, affordable,
sustainable and safe. In case replacement feeds is not feasible give
exclusive breast feeds for initial 6 mths with rapid cessation' (within 2
wks ). The chances of MTCT are highest with mixed feeding practice'.
The HIV-free survival at 18 mths is same when exclusive breast feeding
is combined with AZT prophylaxis for 6 mths and when exclusive
formula feeding is given with I mth of AZT prophylaxis'.

27.9 FOLLOW UP: Shown in Table 27.2

T a ble 27 2 F OIIOW-UD 0 f a HIV exposed neona t e


• History and physical examination (including Wt,
Ht, and OFC)
• Assessment of growth and development
Routine Care • Routine childhood immunizations
• Psychosocial support
• Monitor compliance to treatment
• Monitor for infections, especially TB, on oach
visit

Pneumocystis • All HIV exposed infants should get Trimethoprim/


Sulfamethoxazole prophylaxis from 4 to 6 wks
carinii
and continue till HIV-I infection is reasonably
pneumonia
excluded or till 5 yrs of age irrespective of
(PCP)- more
immune status (see section D36).
correctly
Pneumocystis • Dose: 5 mg/kg/d as a single daily dose .
jiroveci • Alternatives: Dapsone (2 mg/kg OD), [check
G6PD levels before instituting therapy]
prophylaxis
• Refer to NACO guidelines for detailed indications
in oediatric age group
262

o HIV-I DNA PCR within 48 h, 2 wks (optional),


1-2 mths, and 2-4 mths of age
• HIV-I antibody testing at 12-18 mths
HIV- I testing
(if serial HIV-I DNA PCR negative at 4 mths of
age)
to document H IV-1 sero-reversion and definitively
exclude infection.

27.10 VARIOUS TESTS DONE TO CONFIRM MTCT: Shown in


table 27.3 and figure 27.3

27.11 RECOMMENDATIONS FOR IMMUNIZATION IN HIV


INFECTED CHILDREN
IAP recommends the normal vaccination schedule for the asymptomatic
infants exposed to HIV. Always check the clinical status for HIV/AIDS
disease before administering a live virus vaccine. Other vaccines not
within the normal EPI schedule- including Hepatitis, Japanese B
encephalitis and Chicken pox- can be given.

27.12 HIV-I TESTING OF FAMILY MEMBERS


Because children with perinatally acquired HIV-1 may remam
asymptomatic for several years, all siblings previously unevaluated for
HIV infection should be tested regardless of age.

27.13 CLINICAL MANIFESTATIONS IN NEONATES


The clinical manifestations of HIV-I infection in infants are highly
variable and often nonspecific. Infants with perinatally acquired HIV-I
infection often are asymptomatic, and physical examination usually is
normal in the neonatal period. The median age of onset of any HIV- I -
related symptom or sign is about 5 mths. Growth delay can be an early
sign of untreated perinatal HIV-1 infection, and the linear growth is most
severely affected in infants with high HIV-1 RNA levels. Other features
of infection in early infancy could include lymphadenopathy,
hepatosplenomegaly, oral candidiasis (often recurrent & difficult to
treat), developmental delay and dermatitis.

27.14 PEP FOR MEDICAL/NURSING PERSONNEL


These should be followed as soon as possible.
• First aid should be given immediately after the injury: wounds and
skin sites exposed to blood or body fluids should be washed with
soap and water, and mucous membranes flushed with water. Do not
squeeze.
263

Table 27.3 Tests to confirm MTCT


When
Results What results
Test name Indications What it does performed & Advantages Disadvantages
reported as mean
Time required
+ve means sensitivity 96o/u
To diagnose HIV Detects the First 48 h, then
infected and specificity Less sensitive for
infection early presence of viral Qualitative 4-6 wks, 3 mths
HIV-I If -ve twice, 99"/o (for HIV identifying non-B
When antibody DNA in positive or &6 mths
DNA PCR' including once subtype B at I subtype virus
status not mononuclear negative
after 2 mths- not mth)
informative cells by PCR 7-14 d
infected
Positive test
To assess HIV Detects and Quantitative- Whenever need Wider Not good for
means infection
HIV-I activity in babies measure amount No of copies to quantify viral availability. diagnosis and not
butt negative test
RNA PCR known to be of viral RNA in ofRNNmL replication Faster turnover recommended for
does not rules out
infected plasma of plasma 3-10 d Quantitative screening.
infection ---
Detecb.
For diagnosis replicating HIV Long turnaround
Qualitative Has replaced by +ve means
when antibody in infants PBMC Very low false time
HIV culture positive or PCR infected
status not co-cultured with positive False negative
negative 30-40 d
informative donor results reported
lymphocytes
To confinn Detects antibody. Sero-reversion
HIV-I Qualitative -vc results at 18 May be false
negative HIV Reflects infant's 12 & 18 mths. remains gold
Antibody positive or mths means no positive if done
status at 12 & 18 exposure but not 1-2 d standard to rule
test negative infection. <12 mths of life.
mths. infection status out infection.
a- Cord blood specimen should not be used because of possible contammahon with ntatemal blood. P24 Antigen assay-This test 1s not recommended for
screening purposes because of poor sensitivity. The detection sensitivity of the p24 antigen !CD assay is Oo/o with cord blood samples, 38% from infants under 3
mths of age and 58% overall (Specificity 88-91°io) 7 .
264

Figure 27.3 Algorithm for establishing diagnosis in neonate

Neonate delivered to HTV +ve mother

Family can afford. Routine policy


Early confirmation desired.

HIVDNAPCR P24 assay

+ve -vc +ve

Repeat Repeat ELISA at 9 or 12 mths (74%


immediately at6m & 96o/o specificity
respectively).

tve -ve
-ve

HIV HIV
confirmed reasonably HIV
excluded unlikely

ELISA at 18 mths, 2
times, different kits

HIV HIV
confirmed excluded

• The exposure should be evaluated for potential to transmit HIV


infection (based on body substance and severity of exposure) (Figure
27.4 and 27.5).
• PEP for HIV should be provided when exposure to a source person
with HIV has occurred (or the likelihood that the source person is
infected with HIV).
• The exposure source should be evaluated for HIV infection. Testing
of source persons should only occur after obtaining informed
consent, and should include appropriate counseling and care referral.
Confidentiality must be maintained.
265

• Clinical evaluation and baselin" testing of the exposed health care


worker should proceed only after informed consent.
• Exposure risk reduction educat10n should be held with counselors
(New OPD, 2"' floor, room no 2019) reviewing the sequence of
events that preceded the exposure in a sensitive and non-judgmental
way.
• An exposure report should be made. There is no specific form.

Figure 27.4: EC of hospital person•el Algorithm

ls this source material blood, body fluid, other potentially infectious material
(OPIM) or an instrument contaminated '"'ith one of these substances?

No PEP relquired+----No
i yri
OPIM,
blood/bodv fluid

+
LP
Jntact skin Type of exposure?

Mucus membrane/ .s k 1 L J ercutaneous


'Iegnty comprmmld exposure

Small volume
(few drops)
Large volume
(several drops/major
splash)/longer duration
(several minutes or more)
j
More severe (large bore

l
hollow needle, deep
Less severe (solid puncture, visible blood
needle, superficial or needle used in pt.
scratch) artery or vein)
EC 1 EC 2

+
EC2
EC 3
266

Figure 27.5: Determining HIV SC

Source
HIV HIV status of the exposure
unknown
source

l l
negrve

No PEP HIV Status


i
HIV SC
required positive unknown unknown

11 +
Low titer High titer (advanced
(asymptomatic/ AIDS, primary HIV
high CD4 counts) infection/high viral load
or low CD4 counts)

1
HIV SC 2

HIV SC I

EC HIV SC PEP Recommendation


1 1 PEP may not be warranted
1 2 Consider Basic Regimen
2 Recommend Basic Regimen
(most exposures are in this category)
2 2 Recommend expanded regimen
3 1 or 2 Recommend expanded regimen
213 Unknown If setting suggests a possible risk
(epidemiological risk factors)
and EC is 2 or 3, consider basic regimen

Basic regimen: AZT 600 mg in divided doses (300 mg twice a day or


200 mg thrice a day for 4 wks + 3-TC 150 mg twice a day for 4 wks.
Expanded regimen:
Basic regimen + Indinavir 800 mg thrice a day or any other protease
Inhibitor.
267

REFERENCES
I. Ministry of Health & Family Welfare, Government of India. ART
Guidelines for HIV-Infected Adults and Adolescents Including Post-
exposure Prophylaxis; May 20<l7.
2. The International Perinatal HIV Group. NEJM 1999; 340: 977.
3. Marina M de Paoli, Ntombizodumo B M, Richter L M, Rollins N.
Acta Pediatr 2008; 97: 1663.
4. Babat R, Moodley D, Coutsoudis A, Coovadia H. AIDS 1997; 11:
1627.
5. Thior I et al. JAMA 2006; 296:794.
6. Lewis DE et al. Clin Diagn Lab Imrnunol !995; 2: 87.
268

28. CONGENITAL HEART DISEASES

28.1 COMMON SCENARIOS WHERE CHD's SHOULD BE


SUSPECTED
• Antenatally diagnosed CHD
• An asymptomatic neonate presenting with the following
o Murmur
o Differential pulses on palpation
o Cardiomegaly seen on CXR
• Presentation with shock and acidosis after an apparent period of
normalcy.
• Central cyanosis from birth.
• Fetal or neonatal arrhythmia
• Neonate v,rith suspected genetic syndrome known to be associated
with CHD. Example: Down, Edward, Patau, Turner, Noonans,
Williams and cri-du-chat (sec chapter 34).
• Maternal illness/drugs associated with CHD: Diabetes (especially
when poorly controlled during pregnancy is associated with heart
disease in 30% of babies born), PKU, rubella, anticonvulsants,
alcohol, lithium

28.2 GENERAL MEASURES AND FURTHER EVALUATION


• Delivery room management: Newborns \vith antenatally diagnosed
CHD are unlikely to be symptomatic in the delivery room due to
persistence of the fetal connections. Follow general NRP guidelines
during resuscitation.
• Assess for presence of dysmorphic featores and other extra-cardiac
malformations
• Assess HR and color (cyanosed or pale); look for signs of respiratory
distress
• Palpate brachia! and femoral pulses: Discrepancy between right and
left brachia! pulses or weak femoral pulses suggests the possibility
of an aortic arch abnormality.
• Take four limb BP (see section 29.2.1): In the normal neonate the
BP in the thigh should be 5-10 mm Hg higher than that in the arm, a
lower value in the legs raises the possibility of an arch abnormality.
Note: The value of four limb BP measurements in the neonate is
questionable with differences of as high as 20 mm Hg having been
identified to be more likely to be due to random variability in
measurement than to aortic arch abnormalities. Also a normal value
does not exclude the conditions, particularly if the femoral pulses are
269

of low volume or impalpable. It the evaluation of the femoral pulses


suggests possible coarctation, then echocardiography is clearly
indicated.
• Palpate for hepatomegaly: An tnlarged liver indicates heart failure
or elevated right heart pressures.
• Auscultate for murmurs
Murmurs in newborn period arc mostly innocent murmurs but there
is a relatively high incidence of structural heart disease in neonates
presenting with asymptomatic cardiac murmurs (50-75%).
• Auscultate for bruits: cerebral or hepatic arterio-venous
malformations.

28,3 CAUSES OF HEART MURMURS IN THE NEONATAL


PERIOD: Shown in table 28.1

Table 28.t Causes of heart murmurs in neonatal period

Innocent or nhvsiolo2ical
Physiological pulmonary Ejection systolic character, grade I to 2,
branch narrowing low pitched and extends till or just beyond
S2. Maximal in pulmonary area,
transmitted throughout the chest. Resolves
bv 6 mths.
TR Confused with VSD clinically. Resolves
as PVR falls by day 2 -3.
Transient systolic closing Audible at left upper sternal border on day
PDAmurmur I.
Patholo2ical murmurs
Obstructive lesions AS and PS
(producing turbulence in a
great artery)
Regurgitant valves Mitra! and tricusoid regurgitation
Shunting Small VSD and PDA

Generally innocent murmurs are grade 1-2. The following indicate a


pathological murmur: Grade more than 2; diastolic murmur or
continuous murmur.

28.4 INVESTIGATIONS
28.4.t CXR: Shown in Table 28.2
28.4.2ECG
Ask for 13-lead electrocardiography - includes V3R or V4R. Normal
EXG findings are shown in Table 28.3
270

Table 28.2 CXR findings in different cardiac abnormalities

Information obtained on CXR


Radiological Abnormality Disease condition
feature
Heart apex Right Dextrocardia may be a
position isolated or associated with a
range of cardiac defects
Abdominal situs Inversus, Suggestive of heterotaxy
ambi ITTlOUS
Aortic arch Right Associated with TOF
Thymic shadow Absence Absence - DiGeorge
Heart size Cardio-thoracic Cardiomegaly due to any
ratio > 60o/o * cause. Massive cardiomegaly
seen with Ebstein's anomaly,
pericardia! effusion, DCM.
Heart contour Boot shaped TOF
Egg-on-side shaped TGA
Snowman Suoracardiac TAPVC**
Broncho vascular lncreased HighPBF
markings Decreased Low PBF
Skeletal Spinal Syndromes, e.g. Alagille's or
abnormalities abnormalities V ACTERL (Vertebral
anomalies, anal atresia,
Rib anomalies cardiovascular anomalies,
tracheo-esophageal fistula,
esophageal atresia,
renal/radial anomalies, limb)
association
Trisomies
*Large thymus may be mistaken for cardiomegaly. Three rad10log1cal
signs aid in diagnosing a thymus:
Sail sign: a triangular projection on either or both sides of the
mediastinum
Notch sign: a indentation at the junction of thymus with heart
Wave sign: a rippled thymic contour due to indentations caused by the
anterior rib ends
**Obstructed TAPVC often clinically and radiologically mimics HMD.
271

Table 28.3 Normal ECG findings (figures are ranges with means in
brackets)
Measure 0-1 d 1-3 d 3-7 d 7-30d
Term neonates 1
QRS axis + 59 to +64 t•l +77 to +65 to
+193 (135) +197 (134) +187 (132) +150(110)
PR interval (s) 0.08-0.16 0.08. 0.14 0.08- 0.14 0.07 - 0.14
(0.11) (0.11) (0.10) (0.10)
QRS duration 0.02 - 0.08 0.02 - 0.07 0.02 - 0.07 0.02 - 0.08
V5 (s) (0.05) (0.05) (0.05) (0.05)
RV! mm 6.5-23. 7 7.0-24.2 5.5-21.5 4.5-18.1
(13.5) (14.8) (12.8) (I 0.5)
SY! mm 1.0-18.5 1.5-19.0 1.0-15.0 0.5-9.7
(8.5) (9.5) 16.8) (4.0)
RV6mm 0.5-9.5 0.5-9.5 1.0-10.5 2.6-13.5
(4.5) (4.8) (5.1) (7.6)
SV6mm 0.2-7.9 0.2-7.6 0.2-8.0 0.2-3.2
(3.5) (3.2) (3. 7) (3.2)
Preterm neonates '
QRS axis +75 to +75 to +75 to +17 to
+194 (]27) +195(121) +165 (117) +171180)
PR interval (s) 0.09-0.10 0.09 -0.10 0.09 - 0.10 0.09- 0.10
(0.10) (0.10) (0.10) (0.10)
QRS duration 0.04 0.04 0.04 0.04
V5
RVl mm 2.0-12.6 2.6-14.9 3.8-16.9 6.2-21.6
(6.5) (7.4) (8.7) (13.0)
SY! mm 0.6-17.6 1.0-16.0 0.0-15.0 1.2-14.0
(6.8) (6.5) (6.8) (6.2)
RV6mm 3.5-21.3 5.0-20.8 4.0-20.5 8.3-21.0
(11.4) (11.9) (12.3) (15.0)
S V6mm 2.5-26.5 2.6-26.0 3.0-25.0 3.1-26.3
(15.0) (13.5) (14.0) (15.0)

ECG features in a preterm baby < 35 wks


• Relative L V dominance, less RV dominance
• P and QRS axis directed more left
• Shorter P, QRS, QT intervals
• Smaller R in VI, taller R in V6
• Taller T in V6
Chamber hypertrophy in ECG: Shown in table 28.4
272

Table 28.4 ECG findings in chamber hypertrophy

RA hvnertrophy P wave peaked (>3 mm in any lead)


LA hypertrophy • P wave duration >0.08 s
• Notched P waves in limb leads
• Bivhasic P waves in VI
RVH
• S wave in I> 12 mm
• Monophasic R wave> !Omm VI
• R wave in VI> 25mm or aVR > 8mm
• Upright T wave in VI after 3 d
• RAD with QRS axis>+ 180"
• qR pattern in VI (normally seen m 10%
newborns)
LVH • LAD or relative LAD <+60°
• R/S progression in precordial leads resemble
adult progression
• RV 6 >17 mm in !st wk (>25mrn in !st mth)
• SV 1 >20mrn
• SV 1 + RV 6 >45mm
• QV 5 or V6 >5mm with tall symmetric T
Biventricular • Abnormal voltages over Rand L chest leads
hypertrophy • Prominent mid-precordial voltages

T ab Ie 28 .5 CHD present1n2 wit


"h neonata cyanos1s
Right-to-left Admixture lesions Transposition of the great
shunts arteries
Cyanosis ± Cyanosis ±heart Cyanosis ± Cyanosis ±
collapse failure heart failure collapse
Tricuspid Total anomalous With VSD/ Without
atresia pulmonary venous persistent ventricular
drainage ductus septa! defect/
Pulmonary Truncus arteriosus artcriosus PDA
atresia
Critical Double inlet/outlet
pulmonary ventricle
Stenos is
TOF HLHS
273

28.5 APPROACH TO A CYANOflC NEONATE


Always examine the baby in a tht:rmo-neutral environment and ensure
that the peripheries are wanni to rule out acrocyanosis. Confirm clinical
cyanosis with pulse oximetry. A~proach to a neonate with central
cyanosis is shown in Figure 28.1
28.5.1 CUD presenting with neonatal cyanosis: Shown in Table 28.5
28.5.2 Hyperoxia test:
ABG should be obtained (do not use pulse oximeter). Obtain a right
radial artery blood gas in room air. Give near to 100% oxygen (through a
nasopharyngeal tube at 5 Umin) and 15 min later obtain another ABG
(Table 28.6).

Table 28.6: Interpretation of hyperoxia test

Disease At F 10 2 = 0.21 At F102 = 1.00


Pa02 (Sa02 ) Pa0 2 (Sa02)
Normal 70 (95) >200 (100)
Pulmonary disease 50 (85) >100 (100)
Cardiac disease
Separate circulation .. <4-0 (<75) <50 (<85)
Restricted PBF <40 (<75) <50 (<85)
Complete mixin~ without 50 (85) <150 (<100)
restricted PBF"
..
*D-transpos1t10n of the great artenes (d-TGA) with mtact ventncular
septum.
**Tricuspid atresia with PS or atresta; pulmonary atresia or critical PS
with intact ventricular septum; or TOF.
***Truncus, T APVC, single ventricle, HLHS, d-TGA with VSD,
tricuspid atresia without PS or atresia.
Note:
• PPHN is often difficult to distinguish from congenital cyanotic heart
disease clinically. In PPHN, differential cyanosis may be seen if
ductal shunting is present but this finding is absent if shunting occurs
at the atrial level (see section 14.15). Echo is the confirmatory
investigation.
• Duct depending aortic arch anomalies can occasionally present with
differential cyanosis with saturation in right hand more than I Oo/o
greater than saturation in LL. Cardiomegaly on CXR is suggestive
and Echo is confirmatory.
274

Figure 28.1 : Approach to a neonate with central cyanosis


I Newborn ~j~h clinical c;~

IMaternal history, antenatal USG and physical findings like cardiomegaly, murmurs, clearly audible
bilateral breath sounds on auscultation and/or lack of respiratory distress suggest a cardiac cause

Fi02 21% - Pa0 2<50 mmHg


Fi0 2 100% - Pa02 < 50 mmHg
+---[ Do hyperoxia test ~
Fi02 21 % - Pa02 <50mmHg
Fi02 I00% - Pa01 > 150 mmHg

Fi02 21 %- Pa02 <50mm Hg


CCHD
Separate circulation Fi02100%-Pa02 50-150 mm Hg
Pulmonary cause of cyanosis likely j
I: Restricted PBF

CCHD with complete mixing Confirm pulmonary cause


without restricted pulmonary ___, with CXR. Another clue is the
blood flow or pulmonary cause presence of hypercarbia
! Look forpreductal (right +--
, hand RH) and postductal
I (lower limb LL) saturation
No di!T
saturation
Di ff saturation >I 0

t
F;GEll
: RH>LL I I LL>RH I DoCXR [
l
Do CXR and Echo.
Echo confinns
PGEI [
I
· diagnosis of PPHN [ Start O!igemic non oligemic \
I and CXR confirms
lung field lung fields
associated lung
disease with PPHN
r Pulmonary outflow obstruction
TGV with either I
PPHN
Aortic arch abn
I
Complete mix.mg with I
unrestricted ASD
275

28.6 PGE 1 (See section 0105)


28.6.l Indications for starting PGE 1 infusion
• Cyanotic newborn (see figure under section 28.5)
• Reduced or absent femoral pulses in an unwell infant.
• Presentation with shock in first 3 wks of life when associated with
other cardiac abnormalities
• Echo proven duct dependent cardiac lesions
The more clinically unwell the infant, the lower the threshold for starting
PGE,. If in doubt and echocardiography is not immediately available,
one may try a 30 to 60 min trial of PGE 1 followed by reassessment.
Assess for signs of improvement like increased blood oxygenation with
cyanotic heart disease (minimum of 20 mm Hg); and improved BP, blood
pH, and urine output for acyanotic heart disease.
28.6.2 Dose: The initial starting dose is usually 50 nglkg/min (Note:
nanograms). This dose may need to be increased by 50 ng/kg/min
increments. Doses as high as 4 µg/kg/min may be occasionally be
required. Once therapeutic effect is achieved, taper to as low as 10
ng/kg/min. Left sided obstructive lesions generally require higher doses.
28.6.3 Deterioration on PGE 1 infusion
Some cardiac conditions actually worsen after starting PGE 1•
• HLHS with a restrictive foramen ovate or intact atrial septum.
• Variants ofmitral atresia with a restrictive foramen ovale.
• TGA with intact ventricular septum and restrictive foramen ovale.
• T APVC with obstruction of the common pulmonary vein.
Always intubate before shifting a baby for cardiac surgery, when the
baby is on PGE 1 infusion.

28.7 APPROACH TO NEONATE WITH HEART FAILURE AND


COLLAPSE
28.7.1 CHD presenting with collapse in the neonatal period
• Due/us-dependent systemic circullltion (Collapse +heart failure)
HLHS, Coarctation of the aorta, Interrupted aortic arch, Critical AS,
Aortic atresia
• Due/us-dependent pulmonary circulation (Collapse + cyanosis)
Tricuspid atresia, Pulmonary atresia, Critical PS
• Parallel circulations (Collapse + cyanosis)
TGA without VSD/PDA
28.7.2 Management
• Maintain airway and temperature; establish umbilical venous access;
establish arterial access.
• Correct metabolic acidosis if pH <7.2; correct hypoglycemia and
hypocalcemia.
276

• Intubate and ventilate.


• Reduce pulmonary overload by ventilating with a modest PEEP (4 -
6 cm H 20) and initially in room air to maintain systemic saturations
75%-85%
• Avoid respiratory alkalosis. Maintain PaC0 2 37 - 45 mm Hg.
• Sedate with morphine.
• Start PGE 1 at rate sufficient to maintain ductal patency if required
(see section D 105)
• If signs persist, review PGE 1 dose, consider volume expansion and
correct anemia. Discuss need for low dose inotrope or nitroprusside
(if BP will allow) with consultant (see section D93). High dose
inotrope in this situation may increase systemic vascular resistance
and worsen systemic blood flow.
• Treat congestive cardiac failure

28.8 CHD PRESENTING WITH CONGESTIVE CARDIAC


FAILURE: Clinical clues and approach are shown in Figure 28.2 & 28.3
Heart failure in neonates manifests by a collection of signs that result
from excessive PBF and inadequate systemic blood flow.
28.8.1 Clinical signs:
Poor feeding, sweating and breathlessness arc eommon prwenting
features. Respiratory distress, tachycardia and hepatomegaly ""' fotlnd
on examination. Edema is rare unl~Sii antenatal heart failuFe pr-000eM
hydrops fetalis.
• Left-sided obstruction (Heart failure +col~
HLHS, Coarctation of the aorta, Interrupted aortic arch, Critical AS,
Aortic atresia
• Admixture lesions (Heart failure + cyanosi.\)
T APVC, Truncus arteriosus, Double inlet/outlet ventricle, Double
outlet ventricle
• Left-to-right shunts (Heart failure)
PDA (most common), VSD, Arteriovenous malformations (llepatic
and cerebral), Endocardial cushion defect
Of the above lesions, left-sided obstructive lesions, TGA, T APVC and
large arteriovenous malformations can present with cardiac failure in the
1st wk of lite.
The non-struct11r.a.l causes of neonatal heart failure are metabolic
disorders like hypoglycemia and hypocalcemia, primary myocardial
disease, asphyxia! cardiac injury, severe anemia, myocarditis and
arrhythmias.
Note: Clues to left sided obstructive disorders are single and loud S 2,
increased right ventricular activity on precordial palpation and abnormal
postductal pulse oximetry reading. Decreased femoral pulses often are
277

not present at this stage because the ductus usually is large. Room air
pulse oximetry in the lower extremities (postductal saturation) may be
helpful. A value above 96% Of •17% rules out a completely ductal-
dependent left heart obstruction ( hypoplastic left heart or interrupted
aortic arch).

Figure 28.2 : Clues to diagnosis of CHF

Neonate with clinical


findings s/o heart failure

1
I Detailed history

Infant of diabetic mother Asymmetric septa! hypertrophy and structural heart diseases; metabolic
causes (hypoglycemia and hypocalccmla) and polycythemia
Birth asphyxia Asphyxia! oardiac injury and metabolic causes
Pretenn neonate Fluid overload and PDA
Maternal rubella virus or Myocarditis and PDA respective! y
Parvovirus infection during
pregnancy

i
Clinical findings
I Hydrops Indicates antenatal cardiac failure· arrhythmias, myocarditis, severe
anaemia, Jarge AVM's
I Associated BPD Chronic right heart failure (cor pulmona!e)
Abnormal rhythm Arrhythmias
' Abnonnal bruits AVM's
I Rash, weak pulses, distant Viral myocarditis
heart sounds, gallop rhythm
Sepsis Seps1$ induced cardiac dysfunction
Cyanosis Common mixing lesions
I Presentation with shock and Left sided OOstructive lesions
collapse

28.8.2 Oxygen therapy in congestive heart failure


• Oxygen (maintain saturation > 90% except in case of critical left
sided obstructive lesions where Sp02 of 75% - 85% might not need
oxygen administration)
28.8.3 Management: Approach
• Maintain thermoneutral environment (see section 7.2.l); correct
acidosis (see section 10.9.3), hypoglycemia (see section 11.4) and
hypocalcemia (see section 8.8.6)
• Maintain PCV of> 36%
278

Figure 28.3: Approach to management of cardiogenic pulmonary


edema

Neonate with acute cardiogenic pulmonary edema I


!
Administer oxygen and IV frusemide. Treat infection with antibiotics.
I Maintain hematocrit ~ 36% I
!
Blood pressure, HR I
!
1
SBP > 101h centile
I Arrhythmia SBP <101h centile

IV Morphine
1 l
I Refer to arrhythmia flow chart I
IV Nitroglycerine
(caution with Dopamine 4-20 µg/kg/min
valvular stenosis) Adrenaline up to 0.05-2.5 µg/kg/min
Correct hypoglycemia, hypocalcemia
and acidosis

Improved
No improvement Improved 1
• Increase diuretic Taper medication BP still < 101h
dosage Switch to oral centile
• Low dose dopamine medications I
Oral
(2-4 µg/kg/min)
medications
• Dobutamine

Improved No improvement

l
Oral medications
l
I Consider I
Oral frusernide 2-3 Milrinone I
mg/kg/day
Oral digoxin (no need for
loading dose)
Consider ACE inhibitors
279

• Restrict fluids to 213" maintenance requirements and institute tube


feeds in case of respiratory disrress. Start diuretics to decrease pre-
load, but use cautiously in case of shock. Increase Calorie input by
25% in case of chronic CHF
• Inotropes and IV vasodilator~ to be considered in severe and
decompensated cases.
• Elective ventilation should be considered early in case of acute
decompensated failure
• Continuous infusion offrusemidc (0.1-0.4 mg/kg/h) is used to avoid
hypotension and brisk changes in serum electrolytes produced by
intermittent bolus therapy (see section D55). A continuous infusion
produces more physiological and controlled diuresis as compared to
intermittent boluses. 3
• For mild cardiac failure and after improvement of severe cases,
o Start oral frusemide. Add spironolactone if long duration of
therapy likely (see section DI 18).
o Obtain a baseline ECG and then start digoxin elixir (see section
D42). An oral maintenance dose without loading dose is
adequate for digoxin and steady state digoxin levels are
obtained in 5-8 d.
o Consider ACE inhibitors (see section D46) in dilated
cardiomyopathy and large L to R shunts causing CCF. Use with
extreme caution in preterm babies as it may precipitate ARF.

28.9 APPROACH TO A NEONATE WITH ARRHYTHMIA


28.9.1 ECG: Obtain a 12-lead ECG. ECG findings in different
arrhythmias is shown in Table 28.7

Table 28.7 Various arrhvthmias and their ECG findin!!s


Dia!!nosis Findin2
Narrow comolex tachvarrhvthmia
Atrial flutter • "Saw tooth"
flutter waves

.J-~~A~-·~M+
..,. •1·~-IJ..~, .... ..,. •
• Atrial rate up to
500 in
newborns

AV reentry tachycardia (commonest) • Regular R-R


interval, with
rates greater
than 230 beats/
in and usuallv
280
260 t-0 300
beats/min.
• P follows QRS,
typically on
upstroke of T
• AV block
terminates
tachycardia
• Pre-excitation
(delta wave)
and short PR
interval seen
post termination
in Wollf-
Parkinson-
White WPW.
AV nodal reent tach cardia • P wave usually
not visible,
superimposed
on QRS.

Atrial fibrillation • "Irregularly


irregular"
•No two RR
intervals
exactly the
same
• P waves
difficult to see

Sinus tachycardia • N onnal P wave


axis
• P waves
recede QRS
Wide complex tachyarrhythmia

VT • Often with AV
dissociation
11
• Capture" or
"fusion 11 beats
diagnostic.

VF • Chaotic rh thm
281

• Rapid and
irregular
rhythm

Brad arrh hmias


Sinus bradycardia • Slow atrial rate
with normal P
waves
• I: I conduction
Com lete AV block • AV dissociation

• ,~·,,J,,
• Regular R-R
intervals

~! = ,...
•&Yr
. . l-.a 0 • Regular P-P
intervals
• Atrial rate >
ventricular rate

2nd degree AV block • Progressive PR


Mobitz type I (Wenckebach) interval
prolongation

't ,~--
L-'rl'& ... !
followed by a
blocked beat
• Usually
indicates block
in the AV node
Mobitz type II •No
characteristic
PR

1+'4'4
• =• prolongation as
seen in type I.
• Usually not
reversible with
medications.

28.9.2 General treatment principles for all arrhythmias


Always review blood gases, glucose, electrolytes (Na+, K+, iCa++, Mg++).
Management of SVT is shown in Figure 28.4 and management of wide
complex tachyarrhythmias is shown in Figure 28.5.
28.9.3 Direct current (DC) cardioversion with defibrillator
Indications for cardioversion:
SVT with hemodynamic instability
282

Indication for defibril/ation


• Pulseless VT
• VF
Figure 28.4 : Management of SVT

Neonatal SVT

Hemodynamically stable Hemodynamically unstable

IV adenosine
I Vagal maneuvers I
l
DC Cardioversion 0.5-1 J!kg.
Double the dosage if no response
l !'-Jo response
Consider IV adenosine if no response

I IV amiodarone I
after 3 shocks

1 No response
Evaluate cardiac function
No response

IV Esmolol or Mctaprolol
IV Flecainide/propafenone/
procainamide

Method
• Consider intubation and ventilation before cardioversion
• Switch power on the defibrillator and turn the selector switch to
"defib".
• Select energy setting by using the up/down arrows.
• Apply a liberal amount of gel on both paddles or use gel patches.
• The sternal paddle is placed immediately to the right of the sternum
just below the clavicle and the apex paddle is placed between the tip
of the left scapula and the spine to place as much heart mass as
possible between the two paddles. The paddles should be applied
firmly against the chest wall to avoid arcing and skin burns.
• Press the charge button on the front panel or on the apex paddle
handle.
• When a tone appears clearly say "One, I'm clear' Two - you 're
clear! Three - everybody's clear!". Using the thumb simultaneously
press both the shock buttons on the paddle until energy is delivered.
• Repeat the above steps if needed.
• If conversion to sinus rhythm is not achieved after two attempts,
drug therapy should be initiated before attempting cardioversion
again.
283

• Although cardioversion can restore sinus rhythm, it cannot maintain


sinus rhythm. Therefore, ic is always prudent to have a
pharmacologic agent available to maintain sinus rhythm after
conversion.
28.9.4 Vagal maneuvers for SVT
• Apply icepack (place crushed ice inside 2 plastic bags) over face;
avoid eyes and do not hold for too long. Always cover baby with
towel and perform under ECG monitoring to document reversion.
• Oropharyngeal suctioning or gag with spatula.
• Do not put pressure on eyeballs as this can result in retinal
detachment; do not use carotid sinus massage as this may
compromise cerebral circulation and airway.
28.9.5 IV adenosine (see section D3)
• Babies should have continuous ECG monitoring throughout
administration of adenosine
• Adenosine can be given in a starting dose of 0.05 mg/kg, with doses
increasing by 0.05 mg/kg up to 0.25 mg/kg. Need to wait 2 min
between doses and check patient's vital signs.
• Adenosine should be given very quickly and as proximally in the IV
set-up as possible. A three-way should be used so that the adenosine
can be quickly flushed with NS. When the volume of adenosine is
small it should be diluted with NS so that the drug has the chance to
reach the body.
• The recorded strip immediately after conversion to sinus rhythm has
occurred should be saved and inspected for concealed pre-excitation
which may be revealed during the first few beats after conversion to
sinus rhythm.
• After a patient has been reverted a 12 lead ECG should be performed
to look for pre-excitation and other abnormality.
28.9.6 Maintenance drug therapy In SVT
• No pre-excitation - use sotaloL'propanolol or digoxin (see sections
D42, DI 17, Dl04)
• If pre-excitation present- use sotalol/propanolol
• If no response to Esmolol in acute management - use class IA drugs
(quinidine, procainamide, disopyramide). Class IC drugs (flecainide,
propafenone) can be considered in case of non response
• If decreased ventricular function - consider digoxin or amiodarone
(see section D8)
28.9. 7 Duration of treatment:
Treat for about 6 to 9 mths, adjusting dosage for size, and subsequently
allow the patient to outgrow the drug dose by about I yr of age and then
stop.
284

Figure 28.5: Management of wide complex tachyarrhythmias


I Wide complex tachycardia
I
l Pulsatile VT:
l
Pulseless Ventricular tachycardia I
Amiodarone 5 mg/kg over 20-60 min
ventricular fibrillation
IV or
i Procainamide 15 mg/kg over 30-60 min
Start CPR-follow NALS guidelines IV.
1
Give J ' shock I -2 J/kg. Polymorphic pulsatile VT (torsade
de points):
Magnesium sulphate 25-50 mgfkg IV
l VT/VF

I 2nd shock 4 J/kg I


1 Consider and correct reversible causes*

If still VT/VF give


Adrenaline 0.1 ml/kg 1: 10000 soln and
3rd shock 4 J/kg

1 VT/VF persists
Give Amiodarone 5 mg/kg and 4th shock 4J/kg
Consider lignocainc if amiodarone is not immediately
available. Also consider Magnesium 25-50 mg/kg slow
IV ifTorsadc de pointes
i
Continue giving shocks every 2 min. Give
adrenaline immediately before every other shock
until return of spontaneous circulation.

Note: Uninterrupted cardiopulmonary resuscitation (CPR) is vital during pulseless VTNF


management.
The follov.ring are the reversible causes*
Hypoxia, Hypothennia, Hypokalemia!hyperkalemia, Hypoglycemia, Tension
pneumothorax, Drugs and toxins, Pericardia! tamponade, Metabolic acidosis

28.10 APPROACH TO A NEWBORN WITH A MURMUR: Shown


in figure 28.6
285

Figure 28.6 Approach to a neonate with murmur

I Neonate with murmur detected on routine examination I


!
I Do a complete cardiac examination I
i
• Munnur grade more than 2; diastolic murmur or continuous
murmur
• Associated abnormal cardiac ~xamination findings related to
dysmorphic features, abnonnal S2, pulses, BP, saturation, CXR or
ECG.
• Abnormal hemodynamic status

Yes I No

i 1
Echo to be done If murmur persists Periodically reassess baby
during hospital fix an appointment till I wk. In case of early
stay with PCC (Thur 2 It-- discharge, call to Children
pm, Advanced OPD at I wk for
Cardiac Centre). An reassessment
Echo will be decided
at follow up in PCC

28.11 COUNSELLING
Having a sibling with CHD confers a 2% risk on a subsequent child. A
mother with CHD has a 6% risk of having an affected offspring and a
father a 2% risk overall and if there are two affected first-degree
relatives, the recurrence rate ofCHD is 3% to 12% (Table 28.8).

Table 28.8: Recurrence risk if a first-degree relative is affected

First degree relative with % affected


CHD
HLHS 19.3
COA 9.4
AV seotal defect 8.8
AS 1.2
PS 2.8
VSD 2.9
Ebstein's anomaly 4.0
286

If a neonate is born who has a first degree relative (parent or sibling) who
has been diagnosed with HLHS, coarctation, or bicuspid aortic valve do a
complete cardiovascular examination at birth and investigate
immediately if suspicious findings; and refer babies with a normal
examination to the PCC (Advanced Cardiac Centre, Block IC, Thur 2
pm) at 2 wks of life.

REFERENCES:

I. Davignon A. Pediatr Cardiol. 1980; I: 123.


2. Sreenivasan W. Am J Cardiol. 1973;3 l :57.
3. Singh NC. Crit Care Med. 1992;20:17.
287

29.SHOCK

29.1 DEFINITION
Shock is a clinical state of acute circulatory dysfunction resulting in
insufficient 0 2 and nutrient deliv~ry to satisfy tissue requirements.
Hypotension, frequently but not always. accompanies shock.
Hypotension refers to a BP that is lower than the expected reference
range (see sections Nl4, Nl5, Nl6). During the first postnatal day, the
numerical value of mean arterial BP is approximately equal to the
numerical value of the patient's GA.

29.2 MEASUREMENT OF BP
29.2.I Noninvasive BP monitoring (oscillometric method): (See
PGIMER video on neonatal procedures, for NIBP measurement).
Oscillometry is the only reliable and accurate way of measuring BP
indirectly. To minimise errors the following guidelines are recommended
• Use appropriate cuff size. The width of the air bladder should be 45-
55% of the circumference or 125 -155% of diameter of the arm (or
calf). Three sizes of neonatal cuffs are available; size 1 (arm
circumference 3-6 cm), size 2 (arm circumference 4-8 cm) and size 3
(arm circumference 6-11 cm).
• Place the cuff so that the artery is aligned with the mark
• Wrap the cuff snugly around the infant's limb
• Obtain BP measurement during quiet or sleep state
• Obtain average of two or three measurements if making management
decisions
• Use MBP to monitor changes (less likely to be erroneous)
Fallacies with osci/lometric method
• Movement artefact
• May overestimate BP measurements in hypotensive pretenns
29.2.2 Invasive BP monitoring (See PGIMER video on neonatal
procedures for peripheral arterial line and UAC insertion): Considered
gold standard. Invasive BP monitoring must be done in all sick babies
requiring frequent BP monitoring even if there is no hypotension. To
minimise errors when using in-dwelling arterial lines, the following
factors should be noted
• Keep the transducer at the level of heart (mid-axillary line)
• Dicrotic notch must be clearly visible on the arterial waveform trace
• Air bubbles in the system results in excessive damping (decreases
SBP & increases DBP). If dicrotic notch becomes distorted or
absent, one should suspect overdarnping and look for the presence of
air bubbles in the catheter transducer system.
• Tubing should have low compliance and shortest possible length
(long length decreases both SBP, DBP)
288

29.3 CAUSES OF SHOCK: Shown in Table 29.1

Table 29.l Causes of shock

Etiopathology Causes Clinical clues


Blood loss (placental
APH, delivery events,
bleed, IVH, pulmonary
pallor, revealed bleed
hemorrhage, DIC)
Hypovolemia Plasma loss (low oncotic Hydrops, suspicion of
oressure, caoillarv leak) NNEC, seosis
ECF loss (insensible Extreme prematurity,
water loss, oolvuria) excessive Wt loss
Obstructive (AS, CoA) Onset towards end of l" d
Myocardial dysfunction
(asphyxia, SIRS, Asphyxia, infant of
myocarditis, diabetic mother, sepsis,
Cardiogenic cardiomyopathy)
' HR >220, in ECG rhythm
Arrhythmia
disturbances
Others (high PEEP, Hyperexpanded chest,
tension pneumothorax, ,J,ed air entry, C0 2
cardiac tamponade) retention
Peripheral vasodilatation
Abnormal (sepsis, drugs, Wide pulse pressure
vasoregulation neurogenic)
Vasoconstriction (I" 24 h in ELBWl
Suggestive clinical
Mixed Sepsis
features

29.4 GENERAL CLINICAL FEATURES


29.4.1 Early compensated phase:
• Prolonged CFT (> 3 >) checked over sternum or forehead
• Pallor in presence of normal PCV
• Mottling of skin
• Cold extremities in absence of environmental factors
• Tachycardia (new onset), or bradycardia in preterms
• Decreased urine output
29.4.2 Decompensated phase:
• Hypotension (narrowing of pulse pressure may be noted early)
• Lethargy or obtundation
289

29.5 INVESTIGATIONS
• pH, BE, lactate, PCV, BS, calcium, Na, K, urea, creatinine (in all
cases)
• Sepsis investigations, if sepsis 's suspected (see sections 24.4, 24.5)
• Serum cortisol for inotrope res.istant hypotension defined as
dopamine requirement 2: 20 µg/kg/min (cortisol < 5 mg/dL is
suggestive ofrelative adrenal insufficiency)
• ECG, CXR if cardiogenic cause suspected (may help in diagnosis)
• Echo: perform whenever cardiogenic cause suspected. Look for
cardiac contractility and ejection fraction. Also helpful in diagnosing
PDA (look for flow through PDA, Left atrium/ aorta (LA/Ao) ratio,
LV filling pattern - El A ratio and diastolic steal in peripheral arteries
like mesenteric, celiac, renal and MCA) and PPHN (look for TR jet,
pattern of flow through PDA and ventricular septa) position). It
should also be considered in inotrope resistant shock of any etiology
( doppler USG of peripheral arteries may be performed to have an
idea of peripheral resistance, presence or absence of PDA, superior
vena cava (SVC) flow and cardiac contractility parameters) to fine
tune the inotropic requirement. The LVO can be quantified to guide
the management ofhypotension (Table 29.2).
o If the LVO is normal or high and PDA is not evident, a
vasopressor (e.g. dopamine) can be instituted. If a
hemodynamically significant PDA is diagnosed, additional
treatment should be directed toward the PDA.

Table 29.2: Normal values for LV output1

BW mL/min mL/kg/min
750-1249 275 ± 37 262 ± 31
1250-1749 388 ± 60 261±36
1750-2249 522 ± 92 259 ± 35
2250-2749 602 ± 85 244 ± 27
2750-3249 737 ± 128 247 ± 37
3250-3749 902± 120 257 ± 35
3750-4249 924 ± 119 229 ± 31
4250-4750 987 ± 67 221±15

o If the LVO is low (<120 mL/kg/min) and the LV is underfilled,


volume expansion is the first line of management.
o If the LVO is normal and the contractility of the LV is impaired,
dobutamine should be the initial choice.
o Quantification of SVC flow in newborn infants has been
reported to be a marker of cerebral perfusion.
290

29.6 TREATMENT (Figure 29. l)


Despite efforts to use all the available evidence. management often
remains empiric. It is important not to be treating a number but to
consider the BP in the context of the infant's total clinical condition.
Frequent evaluation of vital signs, BP, perfusion, urine output, acid-base
balance, and neurologic status are used to guide the interventions.
29.6.1 Volume expansion:
Volume expansion should be a part of initial circulatory support but
should not be repeated unless there is a convincing response to treatment
(improving BP and falling HR) or strong evidence of hypovolemia.
Dose: l 0-20 mL/kg of NS over 20-30 min.
29.6.2 Dopamine: (see section 045)
Usually stated at 5 µglkg/min & gradually increased by 5 µg/kg/min
increments every l 5 min up till 20 µg/kg/min. Dopamine affects all 3
major determinants of cardiovascular function (i.e., preload, myocardial
contractility, afterload), however the effect on peripheral vascular
resistance (afterload) and myocardial contractility are believed to be the
most important factors in raising BP.
29.6.3 Dobutamine: (see section 043)
It is often used in combination with dopamine to improve cardiac output.
Is more potent in increasing cardiac output and decreases systemic
vascular resistance (SVR) hence should be considered early when there is
poor myocardial contractility and increased SVR (post asphyxia! cardiac
dysfunction). Doses are same as that of dopamine.
29.6.4 Adrenaline: (see section 04)
Add once maximum dose of dopamine .and dobutamine has been
reached. However in vasodilatory shock where there is decreased SVR,
adrenaline should be stated once maximum dose of dopamine has been
reached. ln addition, it should be started as first line inotrope in post
cardiac arrest state. Usually started at 0.05 µg/kg/min and hiked up by
0. l µg/kg/min until 2 µg/kg/min.
29.6.5 Hydrocortisone: (see section 064)
Consider when there is poor response to 20 µg/kg/min of dopamine.
Send cortisol levels prior to stating therapy. Start with hydrocortisone 1-3
mg/kg 8 hourly, continuing for l -3 d depending on the response.
Perinatal asphyxia, sepsis, ELBW; and concurrent refractory
hypoglycemia and hyperkalemia are situations where adreno-cortical
insufficiency is likely. Use only after discussion with consultant.

29.6.6 Milrinone: (Milicor®) (see section 085)


A phosphodiesterase-JI! inhibitor improves diastolic myocardial function
and decreases PVR. In term neonates with CHO, presenting with low
cardiac output following cardiopulmonary bypass and cardiac surgery it
has shown promising results. Dose: 0.5-0. 75 µg/kg/min after loading
291

with 0.1 mg/kg over 15-30 min Use only after discussion with
consultant.
29.6.7 Vasopressin: (Pitresin, CpreS<in®)
In a recent study', the authors concluded that vasopressin might be a
promising rescue therapy in catecholamine-resistant vasodilatory shock
in ELBW infants with acute renal injury. Dose: 0.3-2 mU/kg/min. Use
only after discussion with consultant.

29.7 WEANING FROM INOTROPES


Decrease inotropes gradually (Adrenaline to be tapered first and then
Dopamine/Dobutamine) every 1-2 hourly once there is nonmalization of
tissue perfusion. Generally, a 6-h period of nonmal BP and perfusion or
any episode of hypertension would be considered cues for weaning
inotropes. Take natural course of the underlying disease in to account
while deciding about rapidity of tapering.
292

Figure 29.l: Approach to management of shock

Shock
(Poor tissue perfusion± low MBP)

Volume correction with 10 mUkg of NS over 30 min

No improvement
Improvement {.l- HR andt BP)
• Can repeat bolus in confirmed cases of
• Continue monitoring perfusion
hypovolemia
• Can repeat bolus if perfusion still
• When in doubt, establish CVP to help
impaired
decision making
• But do not v.aste time in inserting CVP line;
go to next step if required

• Start inotropc and treat underlying condition


1
Choice of inotrope based on clinical scenario
o Low SHF without vasodilatation!hypotension (prctcnn < 24 h, large PDA,
PPHN, asphyxia): Start with Dobutamine (5-20 µg!kg/min) 4Dopamine
(5-20µg/kglmin) --+-Adrenaline (0. l-0.Sµg!kg/min). Add dopamine earlier if
BP drops with Dobutamine
o Low BP with vasodilatation/hypotension (sepsis, adrcnocortical
insufficiency): Start Dopamine (5-20µglkglmin) -+Adrenaline (0.1-
lµg/kg/min)
• Treat underlying cause
o PDA (fluid restriction/lbuprofen/indomethacin)
o Sepsis (antibiotics, IVIG, DVET)
o PPHN (minimum handling. ventilation, iNO)
o Duct dependent circulation (prostaglandin infusion)
o Hypoglycemia, hypocalcaemia, hypoxia, metabolic acidosis (pH <7 .20)

REFERENCES
1. Walther F J. Pediatrics 1985; 76: 829. Pediatrics 1985; 76: 829
2. Meyer S, Loffler G, Polcher T, Gottschling S, Gartner L. Acta
Paediatr 2006; 95: 1309
293

30. PATENT DUCTUS ARTERIOSUS OF PREMATURITY

30.I BACKGROUND:
The ductus arteriosus is patent in all newborns at the time of delivery.
Functional closure begins l 0-15 h after birth. It is closed functionally by
48 h after birth in almost all infants delivered at 0".40 wks gestation and
by 72 h after birth in 90% of infants delivered at 0".30 wks gestation. 25%
of infants with BWs 1,000-1,500 g will have a PDA at 72 h, and 70% of
these will require treatment. 65% of infants with BWs <I ,000 g will have
a PDA at 72 h, and 85% of these will require treatment.

30.2 CLINICAL SETTING:


PDA must be suspected under the following circumstances
PDA with little or no lung disease may occur in bigger premies (> J 500g)
• Systolic murmur: starts at 24-72 h age, becomes progressively
louder and longer.
• Usually do not develop severe CHF in neonatal period.
PDA in infants (l000-1500 g) with lung disease:
• Most common group.
• Clinical setting: Babies with respiratory illnesses on tapering
ventilation who suddenly worsen. L to R shunt becomes obvious as
PVR falls.
PDA in ELBW babies with severe lung disease
• Associated with a high incidence of PDA (>80%) - silent dangerous
ductus
• May only present with deterioration of vcntilatory status, with no
signs of PDA.

30.3 CLINICAL FEATURES:


• Murmur- systolic or continuom. Among neonates, the murmur is
usually systolic.
• Hyperdynamic precordium
• Bounding pulses/wide pulse pressure (PP > y, of corresponding
systolic BP)
• Increased oxygen &/or ventilatory requirements
• Features ofCHF
o Tachycardia (HR >160 beats/min)
o Tachypnea
o Hepatomcgaly
o Dependent edema
• Features of poor systemic blood flow (when ductal shunt > 50% of
LV output)
o Metabolic acidosis
o Oliguria
294

o Feed intolerance
30.3. l Utility of 3 major clinical signs at different days of life '" '
Shown in Table 30.1

T able 30.1 Utilitv of clinical si2ns in PDA


Clinical features lsensitivitv I soecificitv)
Day of
Hyperdynamic Bounding
life Murmur
precordium oulses
I 0 I0 50 / 73 10 / 70
2 30190 70 / 65 40 / 73
5 78 I 91 78 I 81 78 I 76
7 79 I 94 I 00 I 78 100 I 76

• Reliance on clinical signs leads to a mean diagnostic delay of 2 d,


with a range of 1 to 4 d. The most reliable combination of signs is an
overactive precordium and a munnur with a PPV at best of 77o/o. 2
Echocardiography is recommended in all ELBW infants in the first
24 h oflife irrespective of the symptoms.

30.4 ECHOCARDIOGRAPHY
PDA is confirmed on color Doppler echocardiography. An Echo must be
performed on all ELBW babies within 24 h of life and in all other babies,
whenever clinically indicated. SRs are authorized to perform a basic
Echo but they must get the findings confirmed by a Pediatric
Cardiologist. The hemodynamic significance of the PDA must always be
assessed and reported.
30.4.1 Features of hemodynamic significance on echocardiography: 3
Shown in Table 30.2

30.5 TREATMENT OF PDA


30.5.1 Indications of treatment:
All clinical and echocardiographic hemodynamically significant PDA's
must be treated pharmacologically and with supportive care.
30.5.2 Non-pharmacological & Supportive care:
• Fluid restriction (2/3'' maintenance) - to be guided by strict input
output monitoring
• Monitoring of Wt at least twice daily.
• Serum electrolytes and renal functions are to be monitored twice
daily.
• Frusemide when clinically indicated (see section D55)
• Avoid digoxin and ACE inhibitors, unless recommended by the
Pediatric Cardiologist in consultation with the Consultant
Neonatology.
295

Table 30.2 Features of nemodynamic significance on


echocardiography in PDA

Modality
Feature and
quantified position of
NoPDA Small Moderate Large
samole eate
Characteristics of ductus arteriosus
Transductal 2-D short
0 . <l.5 1.5-3 >3
diameter (mml axis view
PWDat
Ductal velocity
pulmonary 0 >2 1.5-2 <1.5
Vmax (emfs)
end of duct
PWDwithin
Antegrade PA left
diastolic flow pulmonary 0 <JO 30-50 >50
(cm/s) artery

Pulmonan overcirculation
M-mode
Left atrial/aortic long axis 1.13±0.23 <1.4:1 1.4-1.6: I >l.6:1
view
M-mode
Left
long axis 1.86±0.29 - 2.15±0.39 2.27±0.37
ventricular/aortic
view
transmitral
E/A <I <I 1-1.5 >1.5
Donn!er
PWD
between <35
!VRT (mis) <55 46-54 36-45
mitral and
aortic valve
M-modeof
LVSTI 0.34±0.09 - 0.26±0.03 0.24±0.07
aortic valve
S stemlc ffu,,_.,r erfusion
Retrograde CWDof
diastolic flow descending JO <30 30-50 >50
(%) aorta
PWOofLV
LVO >314
outflow 190-310
(mUkg/min)
tract
CWD- continuous wave Doppler, IVRT- Isovolumetnc relaxation ttme, LVSTI- Left
ventricular systolic time integral

30.5.3 Pharmacotherapy:
Pharmacotherapy is permissible if the age of the neonate is less than 3
wks, if the neonate has not already received 2 courses of medication and
if there is no risk of a ductus dependent disease. An Echo prior to starting
pharmacotherapy is desirable, but not mandatory. The situations in which
an Echo is mandatory are: gestation > 32 wks, absent femoral pulses.
shock, atypical location of the murmur, cyanosis that does not improve
on oxygen and malformations. Response to pharmacotherapy can be
monitored clinically. It is not essential to perform a check Echo.
296

Ibuprofen (see section D66)


IO mg/kg/dose OD orally for 3 d or I 0 mg/kg/dose on day I followed by
two doses of 5 mg/kg/dose OD at 24-h intervals.
Contraindications
• Blood urea > 60 mg/dL
• Serum Creatinine > 1.8 mg/dL
• Urine output< 0.6 ml/kg/hour
• Platelet count <60,000 /cu.mm
• NEC or stool hema test> 3+
• Active bleeding
• IVH grade III/IV or progression of IVH demonstrated from an
earlier cranial USG
• Coagulation defects
Jndomethacin (.'ee section D69): Short course is shown in Table 30.3

Table 30.3 Short course of indomethacin

Age at first First dose Second dose Third dose


dose (mg/kg/dose (mg/kg/dose (mg/kg/dose
IV) IV) IV)
<48 h 0.2 0.1 0.1
2-7 d 0.2 0.2 0.2
>7d 0.2 0.25 0.25

Long course
0.1 mg/kg/dose IV/oral 24 hourly interval for 5-7 d
Contraindications - similar to Ibuprofen
30.5.4 Repeat course:
If ductus reopens after the first course, second course can be given (no
data to support superiority of prolonged second course versus short
second course). A maximum of 2 courses may be tried.
30.5.5 Surgical closure:
Surgical closure is indicated if
• There is a contraindication to medical therapy
• The patient has not responded to 2 courses of medical therapy
• The age of the patient is >3 wks and the disease is either clinically or
echocardiographically of hemodynamic significance.
The CTVS SR must be contacted if surgical closure is contemplated. A
detailed Echo by a Pediatric Cardiologist is mandatory before the patient
is operated.

30.6 FOLLOW UP OF PATIENTS WITH PDA


30.6.1 Patients who had PDA that responded to pharmacotherapy
297

Such patients should be followed up mly in the NFC (see section 42.2)
30.6.2 Patients who had PDA that was operated
Such patients should be followed Lp at least once in the CTVS OPD
(Advanced Cardiac Centre, ground f;oor) of the concerned consultant; in
the PCC, Thursday, 2 pm, Advanced Cardiac Centre, ground floor as
well as in the NFC.
30.6.3 Patients who had an echo confirmed PDA that was not
hemodynamically or clinically significant, but persisted at the time of
discharge
Such patients must be followed up in the PCC and in the NFC. They
must be monitored for signs of chronic CCF and episodes of pneumonia.
Surgery is indicated in such patients if
• Signs of CHF appear
• There is even a single episode of pneumonia
• Echo confirmed features of pulmonary artery hypertension
• PDA persists at age >!yr and Wt >8 kg

REFERENCES:
I. Skelton R. J Paediatr Child Health. I 994;30:406
2. Davis P. Arch Pediatr Adolesc Med. 1995;149:1136
3. Sehgal A. Eur J Pediatr. 2009; 168:907
298

31. NECROTJZING ENTEROCOLITIS

31.1 RISK FACTORS


• Prematurity
• Rapid increase of feeds
• Perinatal asphyxia
• Shock
• AIREDF
• UAC
• Maternal hypertensive disorders
• PDA
• lndomethacin I Ibuprofen
• Aminophylline ±steroids
• Polycythemia
• Hypothermia
31. 1. I Prevention
• Avoid the preventable risk factors mentioned above
• Prophylactic probiotics reduce severe NEC by 66%, all-cause
mortality by 59% and time to reach full feeds by 5 d 1• All regimes of
probiotics irrespective of time of onset, dose, duration, or species
have been sho\\11 to be beneficial. Probiotics are beneficial in ELBW
babies as well as in an Indian setting. Once enteral feeds are
tolerated, start probiotics (Darolac®, Aristo Pharma) in a dose of I
sachets (I billion cells) 12 hourly for 21 d for all neonates weighing
<1250 g at birth or 1250-1500 g with AIREDF on antenatal doppler.

31.2 CLINICAL FEATURES AND STAGING


NEC is typically suspected in a preterm infant <32 wks gestation who
develops abdominal distension, coffee ground aspirates and constipation;
and looks sick. Rarely, the infants may have diarrhea instead of
constipation. In contrast to western literature, data from PGIMER shows
that the peak age for NEC in preterm infants is from the end of the I" wk
of life to the 2"d wk (PG! Annual data, 2008).
31.2.1 Modified Bell's staging for NEC: Shown in Table 31.1

31.3 DIFFERENTIAL DIAGNOSIS


• Septic ileus
• Gut immaturity
• Congenital intestinal obstruction
• Spontaneous intestinal perforation
• Intussusception
• Dysentery
• Campylobacter diarrhea
299

Table 31.1 Modified Bell's sta2in!! for NEC


Stage Systemic signs Intestinal signs Radiologic sings
Increased pre-feed residues. mild Normal or mild
IA- suspected Temperature instability, apnea,
abdominal distension, emesis, stool dilation of intestinal
NEC lethargy, bradycardia, ileus (±)
positive for blood loops
IB- suspected NEC Same as above Bleeding per rectum Same as above
Intestinal dilatation,
Same as above + absent bowel
HA- definite NEC Same as above pneumatosis
sounds
intestinalis
Same as above + abdominal
Same as above + tenderness, ascitis, abdominal Same as above +
HB- definite NEC
thrombocytopenia cellulites or right lower quadrant portal vein gas, asc1t1s
mass
Same as above + hypotension,
I HA- advanced
bradycardia, apnea requiring Same as above +
NEC (bowel Same as above
ventilatory support, acidosis, definite ascitis
intact)
DIC, neutrooenia
HIB- advanced
Same as IIIA+
NEC (bowel Same as IIIA Same as IIIA
pneumoperitoneum
perforated)
Bowel wall edema defined as "Bowel wall thickness> the thickness oftntervertebral dtsc at that level". Dilated bowel loops defined as "Width of bowel loop>
transverse diameter of vertebral body at that level"
300

31.4 MANAGEMENT
31.4.1 On suspicion of NEC
• Keep NPO
• Continuous gastric aspiration
• Antibiotics as per sepsis protocol after taking blood culture (see
section 24.8.1).
• Complete workup for sepsis (see sections 24.4, 24.5, 24.6)
• Platelet count
• Stool for occult blood (APC 3C Pediatric Biochemistry- 9 to 11 am,
except Sundays)
• Blood gas for acidosis
• Serum electrolytes
• AXR (supine as well as lateral decubitus)
• Remove umbilical catheters (arterial & venous)
• Pediatric surgery opinion if suspected perforation
• Attempt feeds once gastric aspirates are nil for at least 24 h with soft
abdomen and good bowel sounds/baby starts passing stools.
31.4.2 Supportive care:
• Treatment for shock (see section 29.6), DIC (see section 19.5),
electrolyte imbalance (see section 8.8), acidosis (see section I 0.9.3),
apnea (sec section 13.4).
• Because of third space loss, patient may require !VF up to 200
mL/kg/d or more. Guide fluid therapy depending on urine output.
serum Na & blood urea.
• Replace gastric aspirates with N/2 saline with KCl (I mL/100 mL
fluid) every 12 h.
31.4.3 Suspected stage 3 disease: Management is shown in Figure 31.1
• Do abdominal paracentesis and send fluid for smear and culture. If
fluid is bilious or exudative, insert flank drainage 2.
• Monitor flank drainage with pre-weighed surgical packs (replace at
least twice daily) or with urine collection bag attached to drain site.
Replace flank drainage with NS every 12 hourly.
• Remove flank drain if drain output is nil for 48 h with improvement
in the patient's intestinal condition. (consider blockage of drain if
drain output is nil but intestinal condition fails to improve). Consult
pediatric surgery before drain removal/replacement.
31.4.4 Monitor progression
Progression of disease is likely during first 72 h after onset, hence
aggressive monitoring is required during that time
• Abdominal girth - 6 hourly
• Hemodynamic monitoring - continuously
• Supine and lateral decubitus AXR- 12 hourly for first 72 h and
thereafter as only as clinically indicated (look for fixed intestinal
301

loops; evidence of pneumatos1s; ascites- compare with previous


AXR)
• Serum electrolytes - 12 hourly
31.4.5 TPN
TPN must be instituted for NEC stage 2'11. (See chapter 32).
31.4.6 Laparotomy
Laparotomy is considered if
• Patient's intestinal &/or general condition fails to improve after 48 h
of insertion of flank drain in NEC stage III.
• Signs of intestinal gangrene appear

31.5 TERM NEC: (- 10% of cases)


• Major risk factors leading to NEC in full-term neonates included
sepsis, SGA, perinatal asphyxia, severe jaundice requiring DVET,
chorioamnionitis, and CHO, such as co-arctation, protracted diarrhea
and maternal pre-ecclampsia.
• Full-term neonates develop NEC earlier than pre-term neonates do.
• Term infants have a better 3-mth survival rate than pre-term
neonates, but surgical complication rates remains the same.
302

Figure 31.1: Approach to case of suspected Stage III NEC

Suspected NEC

!
Nil oral. Continuous gastric aspiration.
Antibiotics. Complete workup for sepsis.
Platelet count
Stool for occult blood
Blood gas for acidosis
Serum electrolytes
AXR (supine as well as cross table lateral)
Remove umbilical catheters

!
Stage 3 disease

Yes
..
l
No
Pediatric surgery opinion and
abdominal paracentesis

+
Perforation

+
lank drainage

No improvement in Lcontinue supportive care in all stages +---..J


next 48 h

Laparotomy

REFERENCES
I. Deshpande et al. PSANZ conference, 2009
2. Moss R Let al. N Engl J Med 2006; 25; 354: 2225
303

32. PARENTER\L NUTRITION

32.1 INDICATIONS
TPN should be reserved for babies m whom significant enteral nutrition
(>60 Cal/kg/d) is not possible. In the PGIMER unit the indications for
starting TPN are
• All ELBW babies (consider staning on day I itself) who are kept nil
per oral.
• Babies with BW 1-1.5 kg & not expected to receive significant
enteral nutrition for more than 3 d.
• Babies with BW > 1.5 kg & not expected to receive significant
enteral nutrition for more than 5 d
• Neonates with NEC (see section 31.2.1), surgical abdominal
conditions (see section 35.3)
• Short bowel syndrome

32.2 NUTRITIONAL GOALS


• To achieve a postnatal growth rate that approximates the intrauterine
growth rate.
• To provide 90-110 Cal/kg/d for optimum growth from non-protein
sources.
• Achieve a ratio of non-protein Calories per g of AA ~ 24-32 or a
Calorie-nitrogen ratio of 150-250, where nitrogen is 0.16 per g of
protein.
• Carbohydrates to provide 60% and lipids 40% of the total non-
protein Calories. For example if we deliver dextrose of 12
mg/kg/min, AA 3 g/kg/d and lipids at 3 g/kg/d, the non-protein
Calories will be 88.7 Cal/kg/d (66% from carbohydrate & 34% from
lipids) and there will be 25.3 non-protein Calories per g of AA
infused.

32.3 COMPONENTS OF TPN


32.3.1 Carbohydrates
• Dextrose is the main energy substrate.
• Energy density of 3.4 Cal per g.
• Start with 6 mg/kg/min (right from birth) and increase everyday by 2
mg/kg/min if there is no hyperglycemia to a maximum of 12-14
mg/kg/min.
• If BS levels are > I 00 mg/dL, do not increase the glucose infusion
rate and if BS levels are> 150 mg/dL decrease the glucose infusion
rate by 2 mg/kg/min.
• The maximum concentration of dextrose that can be used is 12.5%
and 25% in the peripheral and the central lines respectively
304

32.3.2 Proteins
• Crystalline AA solutions provide the protein requirements. Two
types of preparations are available in market: Aminoven (6% &
!0%) and Primene (10%).
• Start from day I of life at 2 glkg/d, as much as possible depending
1
on fluid allowance and access.
• Advance by I glkg/d to a maximum of 3 g/kg/d in term infants and 4
mglkg/d in preterm infants.
• AA yields 4 Cal per g. Do not include protein in the Calorie count.
• A rise in blood urea is not an adverse effect or sign of toxicity; rather
it is a normal accompaniment of increased protein intake. More
often, it is because of fluid deficit and fluid therapy should be
optimized.
• Hyperammonemia and metabolic acidosis are uncommon with
present day AA solutions.
• Restrict protein intake to 0.5-1 g!kg/d when there is oliguria
associated with serum creatinine > 1.5 mg/dL.
32.3.3 Lipids
• Lipid emulsions serve as an energy dense substrate besides
preventing essential fatty acid deficiency. lntralipid (10% & 20%) is
the available brand. I 0% lipid has an energy density of I.I Cal per
mL and 20% lipid of 2 Cal per mL.
• Lipids are usually started at the rate of I g/kg/d beginning within 48
h of life. Gradually increase by I g/kg/d until a maximum of 3
g/kg/d.
• The total amount for the day is to be given as continuous infusion
over 24 h.
• Infusion rate should not exceed 150 mg/kg/h (i.e. 3.6 g/kg/d)
• 20% lipid emulsions is to preferred over I 0% emulsions as higher
phospholipids content in I 0% interferes with TG clearance leading
to higher TG and cholesterol values.
• Clearance is monitored by measuring plasma TG levels. Maximal
acceptable level ranges from 150 to 200 mg/dL. If the value is
between 150 to 200 do not increase the dose and if it is above 200
mg/dL stop it altogether.
• IV lipid emulsions in the recommended infusion rate ( :> 150
mg/kg/h) do not seem to affect platelet number or function and
bilirubin displacement from albumin sites. However, one should
monitor TG level in cases of jaundice nearing DVET level and
severe thrombocytopenia.
• Serum TG value should be checked once lipids of 3 g/kg/d is
reached and subsequently at weekly intervals. It should also be
305

checked ifthe plasma looks vi,ibly lipemic and in presence of severe


sepsis
• In neonates with acute respirat<1ry failure with or without pulmonary
hypertension, lipids should be limited to 2 g/kg/d.
• Lipid emulsion should be protected by aluminum foils or carbon
sheets during PT to decrease the formation of hydroperoxides.
32.3.4 Electrolytes (see section 8.3.3)
Sodium:
• The normal requirement is 3 mEq/kg/d. ELBW infants may need as
much as 5-6 mEq/kg/d because of their poor renal tubular absorption
(see section 36. 7).
• It should be added from day 3 onwards once the cumulative Wt loss
is> 5°/o.
• Is added as NS 0.9% (1 mL~ 0.15 mEq) or 3% NaCl (I mL~ 0.5
mEq).
Potassium:
• The normal requirement is 2 mEq/kg/d.
• It is provided as 15% potassium chloride solution(! mL~ 2 mEq).
Chloride:
The normal requirement is 3-6 mEq/kg/d. this amount is delivered
automatically as constituent of NaCl and KCI.
Calcium:
• Normal dose is 72 mg/kg/d of elemental calcium
• This is given as 10% calcium gluconate injection (I mL~ 9 mg of
elemental calcium) or l 0% calcmm chloride injection ( l mL~27 mg
of elemental calcium).
Phosphorus:
Currently IV phosphate solutions are not available in India.
Magnesium:
• The usual dose is l mEq/kg/d
• Given as 0.25 mL/kg/d of 50% MgS0 4
Trace elements (Zn, Cu, Mn, Se)
• Zinc is required from day 1; others are required after 2 wks. If the
baby is getting partial enteral feeds, these trace elements are not
required.
• Currently l.V. trace elements are currently not available in India.
• In patients with TPN, giving I 0 mL/kg of FFP every 4" d can
provide these trace elements.
32.3.5 Vitamins
MVI pediatric is designed for pediatric use but is currently not available
in India.
• The adult MVI solution is available. The dose is I mL/kg/d. It does
not provide vit K, B 12 , biotin & folic acid.
306

• Administer a weekly dose of vii K (0.5-1 mL/kg J.M.) and vii B12
(10 µg/kg J.M.).
• About 80% of vit A and 30% of vit D and E are lost during
administration owing to adherence to tubings and photodegradation.
Photodegraded MVI increases urinary peroxides. Protect MVI
containing solutions from ambient light by wrapping with opaque
paper. By adding the vit preparation into fat emulsion instead of AA-
dextrose mixture, vit losses can be reduced.

32.4 CHECKLIST FOR STARTING TPN


• Patent central line/ peripheral cannula
• BS, SERFT, Ca, pH, urine for glucose
• Hemodynamic and cardiorespiratory stability

32.5 DAILY CALCULATIONS


• Daily calculations for individual patients can be done with the TPN
program in the computer (two programs are available, one in NDM
v2.0 and the other in Excel sheet in D drive of the NSR and USG
room computers) or else can be done manually with the help of the
TPN worksheet given below. After opening NDM v2.0, click on the
"TPN" button in the toolbar at the top. A window opens up. The
steps are self-explanatory.
• Another person must crosscheck the calculations independently.
• Preserve the daily TPN work sheet for future reference. Maintain a
TPN monitoring chart showing the nutrient intake (Calories, protein,
lipids), clinical and laboratory monitoring parameters.
32.5.1 Steps for calculation of TPN
I. Total fluid intake: _ _ ml/kg/d x _kg _ _ mL/d
Total TPN volume:
I - (Feed vol+ drug vol+ arterial line vol+ ___mL/d
blood products)
II. Fat volume: _g/kg/d x _kg+ 0.1 * _ _ mL/d
(*Lipid concentration per mL of I 0% lipid, use 0.2 if using 20%
lipid)
III. Glucose-AA volume: II - III mL/d
IV. Glucose-AA volume to be prepared: IV x 1.2' ___ ml
(1.2 was multiplied to have 20% extra volume for wastage factor)
V. Additive volume:
a. AA _g/kg/d x _kg x 10 x 1.2 ---
mL

b. Sodium _mEq/kg/d x _kg x 6.6' x 1.2 _ _ml


( 6.6 mL of0.9% NaCl~ 1 mEq of Na, multiply by 2 if using 3%
1

NaCl)
307

c. Potassium _mEq/kg/d x _kg ' 0.5 x 1.2 ___ mL


d. Calcium gluconate 8 mL/kg/d x__ kg x 1.2 ___ mL
e. MgSO, 0.25 mL/kg/d x _kg x , .2 mL
VI. Total additive volume (a+ b + c +- d + e) mL
VII. Dextrose volume: ~ V-VI ___ mL
VIII. Dextrose amount: _mg/kg/min x 60 x 24 x 1.2 --~g/d
IX. Dextrose concentration (VIII + VII) x I 00 ___%
dextrose
X. Calculate the volumes of I 0% & 25% dextrose to make VII volume
with IX cone.
I 0% Dextrose mL
25% Dextrose _ _ _ mL
XI. Add I mL/kg/d of MVI in the fat volume mL
Final TPN order to infuse
Line I: Lipids __ mL/h for 24 h (III+ 24)
Line 2: Glucose-AA _ _ mL/b for 24 h (IV+ 24)

32.6 PREPARATION AND ADMINISTRATION OF THE


SOLUTION (See PGIMER video on neonatal procedures)
• Ensure thorough asepsis while preparing TPN (wear gowns. mask &
gloves).
• Dextrose, AA, electrolytes are mixed to form one solution in glass
bottle. Lipids are drawn in another syringe and vitamins are added.
• Both solutions can be administered through the same IV line by
means of a Y connector.
• Use bacterial filter in the tubing coming from dextrose-AA mixture
just before the Y connector.
• The bottles of AA and lipid solution should not have multiple
punctures. The daily requirements for multiple babies should be
drawn through one puncture and the rest discarded.
• Change the tubing and the bottles after every 24 h.
• Assess the IV site for any extravasations hourly.
• Do not disconnect the bottle containing the TPN solution from the
infusion set.
• Avoid breakage of the line through which the TPN is infused. Use
separate peripheral cannula for antibiotics, blood transfusion or other
drugs.
• The addition of heparin (0.5 units/mL) reduces the incidence of
phlebitis and thrombosis of both peripheral and central lines (see
section D46). Because pf the effects of heparin on stability of
calcium and lipids, it should not be added as a routine.
308

Cover TPN with opaque paper to prevent photodegradation. This



decreases the incidence ofBPD.

32.7 ROUTE OF ADMINISTRATION


• Placement of central line allows the use of more concentrated
solutions but incurs greater risk of infection. It should be considered
in the following circumstances
o when the need ofTPN is expected for more than 5 d
o glucose concentration is > l 2.5o/o
o osmolarity is >900 mOsm/L
• For calculating osmolarity, remember
o Each l % Dextrose = 5 5 mOsm/L
o Each 1% AA = 100 mOsm/L
o Each 1% NaCl = 340 mOsm/L

• Administration of lipids through same IV line offers protection


against phlebitis or potential loss of the access sites.

32.8 MONITORING: Shown in Table 32.1

Table 32.1 Monitoring of a neonate on TPN

Parameter Initiallv 11" wk) Later


Clinical
Wt Dailv Dai Iv
OFC. length Weeklv Weeklv
Urine Outnut 8 hourlv 8 Hourlv
IV Site I Hourly I Hourlv
Laboratoro
Urine Sp Gravity/Glucose Each Soecimen 8 Hourlv
BS 6 Hourly 12-24
hourIv
Serum Na/K, urea, creatinine, Daily Twice
calcium, pH, PCV, Inspection for weekly
lipemia
LFTs, serum proteins, serum TG, Weekly Weekly
ANC/CRP/ urine for funm•s

32.9 COMPLICATIONS
Besides infection and catheter related complications, following are the
important metabolic complications of parenteral nutrition
• Hypoglycemia, hyperglycemia, glycosuria, hyperosmolality and
dehydration are related to low or excessive carbohydrate infusion.
309

• Metabolic acidosis, azotemia, hyperammonemia are related to


protein intolerance.
• Hyperlipidemia, abnormal platelet adhesion, increased risk of
bilirubin encephalopathy are attributed to lipids
• Metabolic bone disease due to phosphorus and mineral deficiency
and trace elements deficiency could occur after prolonged TPN.
• Cholestasis and abnormal liver enzymes. Etiology is multifactorial.
Gamma glutamyl transpeptidase (GGT) and ALP are initially raised
followed by rise in direct bilirubin and transaminases.

32.10 MANAGEMENT OF COMMON COMPLICATIONS


32.10.1 Hyperglycemia: (see sections 11.9, 11.10)
• Rule out possibility of sepsis as a cause
• Decrease or omit drugs which can cause hyperglycemia (if the baby
is receiving) like steroids, aminophylline
• Before parenteral fluid preparation
o BS> 100 mg/dL: do not increase the glucose infusion rate
o BS> 150 mg/dL: reduce glucose infusion rate by 2 mg/kg/min
from previous
• After parenteral fluid preparation for the day
BS >200 mg/dL or glycosuria: start insulin infusion at a dose of
0.05 U/kg/h and gradually increase as required to a maximum of 0.2
U/kg h (see section D54). If BS remains high, stop TPN and start
Isolyte-P with glucose at 4 mg/kg/min.
32.10.2 Cholestasis
• Evaluate for other causes of hepatic dysfunction (sepsis) (also see
section 20.17)
• Prevention: Minimize the duration of TPN
o Start MEN as early as possible and advance as tolerated
o Prevent and treat sepsis
• Decrease AA to l g/kg/d
• Continue lipids and maintain TG < 150 mg/dL
• Start oral Ursodeoxycholic acid (UDCA) (Udiliv®) at 15-20
mg/kg/din 3 divided doses (see section Dl28).
32.10.3 Sepsis
• Limit lipid infusion to 1-2 g/kg/d and monitor TG levels.
• Have low threshold for considering and starting therapy for fungal
infection (see section 24.11)
• Remove CVC if possible. Infectious Diseases Society of America.
2
recommendations state that CVC's can be retained in patients with
fever and mild to moderate disease, if the infecting organism is
CONS, and if there is no suspicion of local or metastatic
complications. Avoid routine cultures of either the catheter segment
310

or blood from catheter. These may be considered in case of


persistent bacteremialfungemia, with the catheter being retained.
• Start antibiotics as per prevailing policy (see section 24.8.1)

32.11 ENTERAL FEEDING DURING PARENTERAL


NUTRITION
Start trophic feeds as soon as the baby is hemodynamically stable (see
section 9.7). Unless contraindicated, attempts should be made to
administer sub-nutritive amounts of oral feeds along with parenteral
nutrition.

32.12 WEANING OF PARENTERAL NUTRITION


• Decrease the rate of TPN in tandem with rate of advancement of
enteral feed to achieve the desired total fluid volume.
• When the caloric intake by enteral feeding is at least 50% of the total
intake, discontinue vitamins, calcium, phosphorus, magnesium, and
proteins in the TPN.
• Subsequently lower the dextrose concentration by 1-2% per day until
glucose infusion rate of 4 mg/kg/min is reached and taper lipid
infusion rate by l g/kg/d.
• Discontinue TPN when 2/3ro of total Calories can be administered
through enteral route.

REFERENCES:
I. Thureen PJ. Pcdiatr Res. 2003;53:24
2. Mermel LA. Clin Infect Dis. 2009;49: I
311

33. INBORN ERROW. OF METABOLISM

33.1 IMPORTANCE OF DIAGNOSING IEM


Prompt diagnosis and high index of suspicion of lEM has a three-fold
signi ficancc.
• These are rapidly progressive a. d cause irreparable brain damage
early in the course.
• Treatment can be effective if co:mnenced early in some cases and
long-tenn outcome may be improred.
• These disorders have genetic implications for the families
concerned, even when treatment LS unsatisfactory. Prenatal diagnosis
in subsequent pregnancies may al ow parents to avoid the recurrence
of a serious disease. -
rt is worth investigating 0 abics <l dia ose one enuine IE . One
must always remember that outcome is directly related to the speed !>L
diagnosis. Currently there is no ~el~tru screening
program m PGIMER. Regular creening for common IEMs,
hypothyroidism etc is likely to be set ti> shortly.

33.2 IEM THAT HA VE ONSET DURING NEONATAL PERIOD:


~~
Table 33.1 IEM that have onset duri 1g n~

Map c syrup urine disease -


Non ketotic hyperglycinemia ..-
Aminoacidopathies
Homocystinuria -
T (!)inemia ,,,
Metl yl ma Ionic aciduria ..,,.
Organic acidemias Prop. onic aciduria
lsov leric aciduria
OTC deficiency -
Urea cycle defects Citrullinemia "'
Ar ·rsinosuccinatc 1 ase deficienc .,,,
Glu<:'->se-6-phosphatase deficiency
Glycogen storage disorders
fructose bis hos hate deficienc
P~.I deficien.£)'
Fatty acid oxidation defects
-Mult le ac 1 CoA deficienc

Congenital lactic acidemias

Peroxisomal disorders
312
3.3 PRESENTATION OF IEM IN NEONATAL PERIOD: Shown in
Figure 33.1

Figure 33.1 Presentation of IEM in neonatal period

IEM

Acute encephalopathy Metabolic Acidemia Hypoglycemia

• Urea cycle disorders -


-!
• Organic acidemias
!
• Galactosemia
• Non kctotic hyperglycinemia .... Fatty acid ~idation • Glycogen storage disorders
• Organic acidemias- Q.efects - • Camitine deficiency
• Maple syrup urine disease ~ • Congenital lactic acidosis• Organic acidemia
• Mitochondrial diseas~- • Fatty acid oxidation defects

33.4 CLUES TO THE PRESENCE OF AN IEM*: Shown in Table


33.2

Table 33.2 Clues to the presence of an IEM

Historical • Previous unexplained neonatal death


• Siblings with known !EM
• Unexplained clinical deterioration after
initiation of oral feeds in an infant who was
well at birth
Clinical • Persistent hiccups
• Unusual body/urine odors
• Cataracts
• Unexolained enceohalopathy and! or seizures
• Unexplained high anion gap metabolic
acidosis/respiratory alkalosis (see sections
Biochemical
10.9.2, 10.12)
• Refractory hvooglycemia (see section 11.7)
*Note: Presence of consanguinity further strengthens the diagnosis.
313

33.5 INHERITANCE PATTERN OF IEM's: Shown in Table 33.3

Table 33.3 Inheritance pattern of IEM's

Autosomal recessive All IEM's except the ones listed below


Omithine carbamyl transferase
X-linked recessive
deficiency
Deficiency of E-l oc sub unit of Pyruvate
X-linked dominant
dehvdrogenase (PDH)

33.6 APPROACH TO IEM


33.6.1 Approach to IEM presenting with CNS changes: Figure 33.2
Figure 33.2 Approach to IEM presenting with CNS manifestations

finitial findings include one or more of the following


• Poor feeding
• Lethargy
• Convulsions & coma-not responding to glucose/calcium
• Vomiting

Metabolic disorder +------,_!_____ __.Infection

+
l
Obtain plasma NH 3 - - - - - - O b t a i n pH and CO,

High

Obtain pH and C0 2
No™'i 1 j
i High Anion gap
acidosis
Normal Anion gap

l
Normal Anion gap
acidosis

l Organic acidemia Aminoaciduria/


Urea eye le disorders Galactosemia

33.6.2 Approach to IEM presenting with hypoglycemia: Shown in


Figure 33.3
33.6.3 Approach to hyperammonemla: Shown in Figure 33.4
314

Figure 33.3 Approach to IEM presenting with hypoglycemia

Hypoglycemia

!
Urine for non glucose reducing substances;
if strong suspicion, send GALT

Presentl lAbsent

Galactosemia Ketones

lHigh

Fatty acid oxidation defect: Glycogen storage disorder


ketogenesis defects Organic acidemia

Figure 33.4 Approach to hyperammonemia

Neonatal hyperammonemia with symptoms with first 24 h oflife

Premature Full-term No
Acidosis
+
THAM PC
+ acidosis

Deficienc Organic Urea


y acidemia cycle
de1cts

Absent Plasma AA

f'"'"'
Urine orotic acid
citrun,.in_e_ _ _ _ _ _c_.irlnine

wj +
Citrulline Citrulline
moderately markedly
CPS OTC elevated ASA elevated ASA
deficiencv deficiencv prtent abtent

Argininosuccinic Citrullinemia
aciduria
315

33.6.4 Approach to metabolic acidosis: Shown in Figure 33.5

Figure 33.5 4 Approach to metabolic acidosis in IEM

Unexplained metabolic acidosis with increased anion gap

Abnormal +---Normal +---- lactate Elevated


organic acids

1
Organic
acidemia
Abnormal +---------
Organic
acid

~
Dicarboxilic!
aciduria Normal

Elevated pyruvate Normal or low


Fatty acid Normal Lactate to pyruvate,
oxidation defects pyruvate ratio Elevated L:P
(L:P) ratio ratio

• Glycogen storage
disease type- I
• Fructose l,6-DP
deficiency,
+-- Present ...,.._ Hypoglycemia
• PEP carboxykinase
deficiency i
Absent
• Respiratory chain defects
• Pyruvate carboxylase

i
• PDH deficiency
deficiency

• Pyruvate carboxylase
deficiency

33.6.5 Conditions presenting without metabolic acidosis &


hyperammonemia: Shown in Figure 3.6

33.7 INVESTIGATION OF A SUSPECTED CASE OF IEM: Shown


in Table 33.4
316

Figure 33.6 Conditions presenting without metabolic acidosis &


hyperammonemia
Nonna! NH 3
No metabolic acidosis

Refractory myoclonic
j
Vomiting, Dysmorphic facies,
seizures/opisthtonus hypoglycemia, hypotonia, seizures,
jaundice, hepatomegaly, blindness
posture
sepsis

l
Non ketotic l l
Peroxisomal
hyperglycinemia Galactosemia disorders

Table 33.4 Investigation of a suspected case of IEM

• Full blood counts


• Urea and electrolytes
• Blood gas analysis
• Blood ammonia levels*
First- line • Urine-reducing substances
investigations • Urine ketones [Multistix®]
• Blood ketoncs [by Optium glucometer-
contact company for calibration]
• BS
• LFTs
• Urine AA
• Urine organic acids
Second -line • Plasma AA
investigations • Blood and/ or CSF lactate and I or pyruvate
• Plasma camitine and acylcarnitine analysis
• Urine orotic acid
• GALT enzvme assav [for aolactosemia]
• Enzyme assays on blood or skin fibroblasts
e.g. Lysosomal enzyme studies DNA
Specialized
mutation analysis
investigations
• Very long chain fatty acid levels
• Plasma and urine AA
317

33.8 GENERAL PRINCIPU:S OF MANAGEMENT OF


NEONATES WITH ACUTE PRESENTATION: Shown in Table 33.5

Table 33.5 Principles of management of a case of !EM during acute


stage

• Admit in NICU
• Establish IV access, arterial line
• Adequate respiratory support
• Correct hypothermia, hypoglycemia &
Supportive care dehydration
• Correction of acidosis with NaHC0 3 [when
pH <7.22 & HC0 3 <14 mEq/L]
• Monitor electrolytes & blood gases
• Start antibiotics if sepsis is suspected
Reduce load on the • Keep NPO [stops exogenous protein]
affected metabolic • Start JV dextrose at 6 mg/kg/min
pathway
• Ensure adequate hydration & adequate
urine output
• Peritoneal dialysis• indicated if
o oliguria/anuria
Removal of toxic
o serum sodium> 165 mEq/L
metabolites
o persistent metabolic acidosis
o hyperarnmonemia > 400 µmol/L
o if no decrease in ammonia after 4 h of IV
benzoatc
•Vitamins [JOO times the daily requirement]:
3 mL ofNcurobion JM, once daily. Split the
Co-factor
dose as volume is too high for neonates.
administration ..
•Oral cam1hne Syrup 100-200 mg/d
[5 mL ~ 250 mg] (see section D22)
*DVET has no role

33.9 SPECIFIC MANAGEMENT OF HYPERAMMONEMIA


IV medication if ammonia > 150 µmol/L
• *Sodium benzoate (IV/ oral) 250 mg/kg/d (see D 115)
• *Sodium phenyl butyrate (IVI oral) 250 mg/kg/d
• *Arginine I 0% 200 mg/kg
• L carnitine (see section 022) I 00-200 mg/kg
*Not available in India currently. Food grade C'ral benzoate (used by bakers) can be used
orally after discussing with parents.
318

33.10 MANAGEMENT OF A NEONATE WITH SUSPECTED IEM


WHO DIES BEFORE DIAGNOSIS
• Take sample on newborn screening card
• 5 mL heparinized blood at 4 °C
• 5 mL plasma at -20 °C
• 10-20 mL urine at -20 °C
• Skin biopsy for fibroblast culture
• Muscle & liver biopsy
• Above samples should be ideally processed within 3 d.

33.11 IEM WITH BETTER PROGNOSIS


Some !EM have a better prognosis with treatment, and every effort must
be made to establish the diagnosis in these conditions. Treatment may
even be started empirically. These are: biotin-dependent holocarboxylase
synthase deficiency, phenylketonuria (when diagnosed pre-clinically, on
screening), tyrosinemia type I, mild variants of maple syrup urine
disease, mild variants of urea cycle disorders and galactosemia.
319

34. GENETIC/ SYNDROMIC ILLNESSES

34.1 BASIC TERMINOLOGY:


Proband: It is the index case through whom a family is found and who
can be used to study the genetics of a particular disorder.
Locus: Specific position on a chromosome, where the gene is located.
Allele: The gene or DNA sequence occupies the same position (locus) on
a chromosome. If both the chromosomes have the same allele occupying
the same locus, the individual are referred to as 'homozygous'. If the two
alleles are different it is referred as 'heterozygous'.
Genotype: Genetic constitution of an individual.
Phenotype: It is the physical appearance and constitution due to the
interaction of genotype with the environmental factors.
Major anomalies: Those anomalies, which have a potential to cause
functional debility.
Minor anomalies: Those anomalies, which are of only cosmetic
significance.
Association: It is combination of anomalies in which individual
components occur together more frequently than would be expected by
chance alone. Ex: V ACTRL, CHARGE (Coloboma, heart, atresia of
choanae, retarded growth, genito-urinary, ear) association
Syndrome: Multiple structural defects that run together and are thought
to be due to a particular chromosomal, genetic, teratogenic or unknown
insult that impairs multiple tissues.
Sequence: A single underlying abnormality gives rise to cascade of
structural changes. Ex: Potters sequence, Amniotic band disruption
sequence.
Complexes: Refer to anomalies of several different structures all of
which lie in the same local body region during the embryogenesis. These
are commonly due to vascular anomaly. Ex: hemifacial microsomia,
sacral agenesis.

34.2 PEDIGREE SYMBOLS: Shown in Figure 34.1

34.3 MAJOR TYPES OF GENETIC DISORDERS:


• Chromosomal disorders: These can be due to numerical or
structural abnormalities. The numerical abnormalities are commonly
aneuploidies Ex: Trisomy 21, 13 and 18. Structural abnormalities
include deletions, microdeletions (Ex: Prader-Willi, Angelman
syndrome), inversions, translocations.
• Single gene disorders: These are result of a single mutant gene
coding for an enzyme or a protein. This leads to deficiency of that
enzyme/ protein in various organ systems of the body. These will
320

follow Mendelian pattern of inheritance 1.e. Autosomal dominant,


recessive and X-linked.
• Polygenic or multifactorial: Caused by the interactions of
variations in multiple genes and environmental factors. Ex: Heart
disease, many birth defects such as cleft lip +/- cleft palate, diabetes
and asthma.

Figure 34.1 Pedigree symbols

D Male 0-0 Mating

0 Female 0+-0 Divorce

() Sex unspecified
O==D Consanguinous mating

,0 ,0 Deceased individuals
db Dizygous twins

••D
Affected individuals

A Monozygous tw·ins

n
Pruband
~

m Individuals
and generations Abortus (remale)

34.4 WHEN TO SUSPECT SYNDROMIC OR INHERITED


DISORDER?
• If baby has more than one dysmorphic feature or congenital anomaly
• If there is family h/o inheritable disorder
• H/o unexplained deaths in the neonatal period± consanguinity
• If prenatal diagnosis is suggestive (see sections 1.2.4, 1.2.8)
• Suspect IEM- in the presence of unexplained encephalopathy,
seizures, persistent vomiting and unexplained neonatal deaths. (see
section 33.3)

34.5 APPROACH TO SUSPECTED GENETIC/ SYNDROMIC


ILLNESS:
To approach systematically, incorporate the following 5 essential tools in
the evaluation of a neonate with suspected genetic/ syndromic illness.
• History (antenatal & perinatal)
• A pedigree analysis and family history
• A detailed dysmorphology examination
• Comprehensive literature search
• Focused genetic analysis including cytogenctic studies
321
34.5.1 History:
• Antenatal- take h/o maternal teratogen exposure during pregnancy;
maternal diabetes. seizure disorder, oligo/polyhydramnios; results of
triple screening, amniocentesis. chorionic villus sampling studies, if
done.
• Construct a 3-generation pedigree chart, take detailed family history,
and procure photographs if available.
34.5.2 Physical examination:' (consult Judith G Hall's Handbook of
Physical Measurements for normative data)
Specifically examine the following
• Head shape, sutures.
• Eye slant, inter- inner canthal distance, inter-outer canthal distance,
interpupillary distance, iris, fundus
• Ear size, position
• US/LS ratio
• Anterior & posterior hairlines
• Mouth- philtrum, cleft lip/ palate
• Chin- micro/ retrognathia
• Neck- webbing, short/long neck
• Chest- sternum, intemipple distance
• Hands: clinodactyly, poly/syndactyly, simian crease
• LL: Congenital talipes equino varus (CTEV) & other anomalies,
sandal gap, great toe abnormalities.
• Examine the other family members- because the suspected
dysmorphic feature can be normal family variant.
Note:
UL length- is to be measured from the tip of acromion to tip of middle
finger.
LL length- from greater trochanter to lateral malleolus.
Lower segment- from the upper border of pubic bone to sole of foot
Upper segment- deduct lower segment length from the total length.
Penile length: measure from the base of the penis to tip of glans (not until
tip of prepuce) with the penis slightly stretched.
Dermatoglyphics: Shown in Table 3,.1

T a bl e 341 D ermato21vn h"1cs 10 vartous svn dromes


Dermatoglyphic Associated distrders
pattern
Excess arches Trisomy 13, trisomy 18, Kleinfelter syndrome
(47, XXY)
Excess ulnar loops Trisomy 21
Excess whorls Smith-Lemli-Opitz syndrome, Turner
syndrome (45, XO)
322

Abnormalities in Down syndrome: Shown in Figure 34.2

Figure 34.2 Findings in hand in Down syndrome

I . Excess ulnar loops


2. Radial loops of 4th digit
3. Distal triradius: 'triradii'
are the points at which
three sets of converging
ridges patterns meet.
Usually there is a triradii
just above the wrist flexion
crease (proximal). In
Downs the distal triradius
is present with increased
'atd' angle.

34.5.3 Expert consultations:


• Take consultation of Dr. AK Bhalla for detailed description of
dysmorphology, by sending the baby to Growth lab if stable enough.
(APC-5D at 9 am on Mon, Tues, Fri and Saturday and 2 pm on
Wednesday !Tom the follow-up clinic)
• Take the consultation of Pediatric Geneticists, Dr. lnusha Panigrahi.
or Dr Sheela] Sharda
34.5.4 Clinical photographs:
• Take clinical photographs in case of all dysmorphic babies, after
taking parental consent. Contact clinical photography dept.
Otherwise get the digital photographs using the digital camera of the
unit (contact Dr Venkataseshan).
Guidelines for obtaining a digital photograph 1
• Take consent from either parent
• In addition to the photograph of the area of interest, take one
photograph of whole body profile in anatomical position i.e. head
end towards the top of the photograph.
• Light- preferably day light or fluorescent light, light should be
coming from above downwards.
• Background- white sheet or light blue and should be tidy.
323

• The person holding/restraining the baby should preferably wear


gloves.
• Use optical zoom, but avoid digital zoom as it tends to blur the
image.
• Store the images in the departmental computer.
34.5.5 Literature review: Comprehensive database search will be
helpful to reach a syndromic diagnosis. Use 'well defined' and
'uncommon' features as search words rather than using soft pointers.
Some resources are
• Smith's Recognizable Patterns of Human Malformation
• OMIM (Online Mendelian Inheritance in Man)- accessible via
http://ncbi.nlm.nih.gov/
• http://www.kumc.edu/gec/prof/genecomp.html -this provides link to
many web sites which provide information about genetic syndromes
34.5.6 Investigations
Tests should be directed toward identifying the associated anomalies and
confirming the suspected syndrome.
Karyotyping:
Karyotyping with banding (done in PG!) can detect numerical
abnormalities and large deletions. The laboratory should be told what is
being clinically suspected, rather than nonspecifically asking for a
karyotype result. Karyotyping may also be done when there is a disorder
of sex development. The appointment is to be obtained from cytogenetics
lab (Research block- A, 5th floor, Room no: H-9). If karyotyping is
required early, discuss the case with Dr. Reena Das. During non-office
hours, ifthe baby's survival is in doubt, collect I mL of sterile blood in a
heparinized vial and refrigerate at 4°C. This sample must be transported
to the lab as early as possible, not beyond 16-18 h of collection.
If karyotyping does not yield the diagnosis, further cytogenetic studies
(E.g. FISH, DNA analysis) are needed to confirm the diagnosis.
Preferably both karyotyping & FISH need to be done for diagnosis. For
that the following labs need to be provided information about the
suspected cytogenetic abnormality.
Labs where FISH i.< done:
• Genetic lab, GMCH, Sector-32, Chandigarh- Discuss with Dr. Gurjit
Kaur 0172 -2665253, 2665545-49 (Ext. 1013). FISH facilities arc
available for Trisomy 13, 18, 21, X, Y and Sex-determining region
Y (SRY).
• Dr Lal's Path Lab (private)- t(l5;17) t(8;21) t(l2;21), CATCH 22
(Cardiac, Abnormal facics, Thymic aplasia, Cleft palate,
Hypocalcemia), Prader-Willi syndrome
Adjunct studies:
• Send buccal smear for Barr bodies to 'A' Block, IV"' floor, R No 5
for cases of suspected Turner syndrome.
324

• Do infantogram for all cases of suspected skeletal dysplasias.


• USG abdomen- to rule out any internal malformations m the
abdomen
• Echo- if clinical findings suggest CHD.
• CT head: in case of craniosynostosis syndromes and if any
congenital abnormalities of the brain are suspected.
• Ophthalmic evaluation, EEG, BERA as needed.

34.5.7 Approach to genetic/syndromic illnesses: Shown in Figure 34.3

Figure 34.3 Approach to genetic/syndromic illnesses


History & Examination

Congenital anomaly detected

Isolated Multiple anomalies

Major like Minor ~ultiple


\foltiple including
maJor malformation
cardiac, GIT
I mmor
I
I No recurrence risk,
reassure
Look for occult
Likely polygenic nlllj<Jr malfonnation
Tl)· to categonze mlo
inheritance, recurrence
a_ Association b. Svndrome
risk 1% c. Sequence d. 'complexes

ls it recognizable syndrome/ entity?

Yes


Lab confirmation if possible
(Karyotypc, DNA analysis or en7ymalic
testing)
No

Database search & expert


opmrun

Recognized

+ No
Treat as per organ involvement.

34.6 FOLLOW UP:


I. Attach the baby to Genetics Clinic (held in APC-3D, Monday 2 pm)
2. Many syndromes evolve over time and diagnosis can still be
obtained during follow up.

34.7 COUNSELING:
For general issues refer to chapter on 'counseling'. The risk of recurrence
will depend on the diagnosis.
325

• Most isolated CMFs have a risk of recurrence varying !Tom 2-5% .


• Associations, complexes, sequences, de nova chromosomal
abnormalities will have low risk of recurrence of< I%.
• The single gene disorders will vary according to the mode of
Mendelian inheritance (autosomal recessive-25o/o, autosomal
dominant-50%, X-linked recessive- 50% of males, X-linked
dominant- 50% of all children if mother affected & all daughters and
no sons if father affected, mitochondrial inheritance- 4-11% if
mother is a carrier of the deletion).

34.7.1 Recurrence risk in Down syndrome: Shown in Figure 34.4

Figure 34.4 Recurrence risk in Down syndrome

Karyotyping of the baby with Down phenotype

Trisomv 21 Translocation
I I
Recurrence risk I% Do karyotyping of parents

t(21; 13)ort(21;14) t (21 ;21)


ort(21; 15)
I
Recurrence risk
If mother is the If the father IOOo/o
carrier is carrier

Recurrence risk 15°/o Recurrence risk 5%

34.8 PROCEDURE IN CASE OF DEATH


In case of death of neonate with suspected inheritable disorder, counsel
the parents for autopsy (see section 40.8). If autopsy is refused by the
parents a consultant must talk to the family. Take the post-mortem
infantogram for any infant with suspected skeletal anomalies.

34.9 PRENATAL DIAGNOSIS


All prenatal and pre-symptomatic testing requires written consent.
Enclose a duly signed consent form with all samples reaching the lab.
Prenatal diagnosis is now available for a large number of conditions in
India.
326

REFERENCES:
I. Judith G Hall. Handbook of physical measurements. 2"0 Ed, 2007,
Oxford University Press US.
2. Nayler JR. J. orPostgrad Medicine 2003; 49: 256
327

35. SURGICAL PROBLEMS

35.1 GENERAL GUIDELINES FOR RESIDENTS WHO MANAGE


SURGICAL PROBLEMS IN NICli/NNN
• Notify Pediatric Surgery SR as soon as you are aware of a pending
admission or birth of a neonate with a surgical problem.
• Neonates admitted to NICU/NNN with surgical problems should be
discussed at least once daily with the Pediatric surgical team.
• Before transport of baby to the OT ensure reliable IV access; obtain
consent for surgery and anesthesia.
• Ensure baby is NPO prior to surgery:
o If formula fed, last feed 6 h prior to surgery
o If breast fed, last feed 4 h prior to surgery
• Transport the baby to OT in Nehru hospital in the transport
incubator. Transport to OT in APC must be done in a transport
incubator only if an ambulance is available that can accommodate
such an incubator. Otherwise, transport on the bed of the ambulance.
A resident must accompany the baby to the OT.
• At the end of the operation, discuss with surgical and anesthesia
resident regarding blood loss; anesthesia and other drugs and fluids
that the patient received and any significant events during operative
procedure. Also discuss regarding postoperative care of the patient.
• Notify Pediatric surgery immediately if there are any major changes
in the condition of the patient.
• Do not begin feedings on any surgical patient without first
discussing it with the pediatric surgeons.

35.2 SURGICAL PROBLEMS PRESENTING AS RESPIRATORY


DISTRESS
35.2.1 CDH
Patient presents with respiratory distress, scaphoid abdomen and
apparent dextrocardia. Pulmonary hypoplasia may occur both on
ipsilateral and contralateral side. It may be difficult to distinguish
hypoplasia from lung collapse pre-operatively. PPHN supervenes both
pre-operatively and post-operatively. A CXR with feeding tube in situ
must be done to diagnose CDH.
Preoperative Management
• Planned resuscitation: The patient should not be ventilated by mask.
Prepare for inunediate intubation if respiratory assistance is required.
The patient should be kept warm to prevent hypothermia. An OG
tube should be placed to avoid bowel distension.
• Gentle ventilation: With conventional mechanical ventilation, limit
PIP up to 24 mm Hg and PEEP up to 5 mm Hg and MAP between
12 and 18. Maintain preductal saturation 90-95% and tolerate pH up
328

to 7.25 and PaC0 2 up to 60 mm Hg. Sedation and paralysis should


only be employed if hypoxia persists.
• HFOV: HFOV is used as a rescue strategy in case the above
parameters are not achieved with maximal acceptable pressure limits
(see section 14.13).
• Surfactant: Observational data do not suggest any benefit with the
use of surfactant in preterrn or term infants with CDH. or in those
receiving surfactant while on Extra Corporeal Membrane
Oxygenation (ECM0)1.
• Nitric oxide: The largest RCT of early iNO treatment in patients with
CDH found no difference in the combined endpoint of death/ ECMO
utilization between iNO-treated and control infants and ECMO
utilization was higher in the iNO treated group. Available evidence
suggests that iNO therapy in patients with CDH should not be
routinely used. Its use should be limited to patients with
suprasystemic PVR after establishing optimal lung inflation and
demonstrating adequate LV performance 2.
Both iNO and surfactant may be used only after discussion with
consultant in-charge (see chapter 15 and section 14.9).
Operative Management
Surgical repair of CDH should be performed on an elective basis, when
the patient has been stabilized medically (pulmonary hypertension has
resolved as evidenced by resolution of preductal and postductal
saturation differential and weaning to minimal support care)
Postoperative Management
• Continue gentle ventilation strategy
• The chest tube should be kept at underwater seal and at <5 ems H 20
suction. It can usually be removed by the fifth post surgical day, if
the patient is off ventilatory support. Consult Pediatric Surgery SR
before removal.
35.2.2 Esophageal atresia with or without TEF
Diagnosis:
• Esophageal atresia may often be suspected prior to the first feeding
by a h/o polyhydramnios or observation of copious oral secretions
than require very frequent suctioning.
• Attempt to pass 10 Fr feeding tube into the stomach. lfthe tube does
not pass beyond 10 cm from the alveolar ridge, leave it in place and
obtain a CXR.
• If the tube curls up in blind esophageal pouch and there is no air in
bowel, assume a diagnosis of pure esophageal atresia. If it curls up
in blind esophageal pouch and there is air in the distal bowel, assume
a diagnosis of esophageal atresia with distal TEF.
329

Preoperative management
• Keep baby in a prone positio11 or lateral head end up to prevent
aspiration.
• Place replogle sump tube on continuous suction (<5 cm H20) to drain
the blind pouch.
• Avoid bag and mask ventilation and nasal CPAP/IMV to prevent
over-distension of the stomach. If the baby needs respiratory
assistance, intubate the infant.
• If the baby has severe lung disease and a distal TEF, ventilation of
the lungs may be extremely difficult because of the low resistance
through the fistula into the stomach and bowel. Notify Pediatric
Surgery immediately as the baby may need immediate closure of the
fistula or an emergency gastrostomy with placement of a distal
esophageal balloon to facilitate adequate ventilation.
• Examine infant carefully for other anomalies associated with
VACTERL or CHARGE or evidence of Down syndrome.
Postoperative management
• If a chest tube is in place draining the area of the anastomosis, do not
connect negative suction without consulting with the attending
surgeon. The chest tube is usually in place for 7-10 d until x-ray
studies show no leak at the anastomosis.
• Do not extubate until the baby is extremely stable on very low
ventilatory settings, because positive pressure mask ventilation must
be avoided to prevent transmission of pressure to the esophagus,
which may rupture the anastomotic suture line.
• If the baby needs to be reintubated, the most experienced person
should do this. Faulty (i.e., esophageal) intubation could result in
injury to the anastomosis.
• Leave the OG or NG tube in place until x-ray studies show no leak
at the anastomotic site, and attending surgeon agrees to removal of
the tube. If the tube accidentally comes out, do not reinsert tube
without consulting with the attending surgeon, as you may damage
the anastomosis.
• X-ray contrast study should be done at approximately I 0 d
postoperatively to assess for leakage at the anastomotic site prior to
starting oral feedings.
• Gastrostomy tube feedings and NG tube feedings may be started
earlier.
330

35.3 NEONATAL INTESTINAL OBSTRUCTION: Approach is


shown in Figure 35.1

Figure 35.1: Approach to intestinal obstruction


Polyhydrarnnios, antenatal
diagnosis and family history

i
Vomiting, abdominal distension
and failure to pass meconium
I

Complicated Distension Progressive


mcconium....,__ at birth abdominal

!
ileus,
Duplication Absent distelnsion
cyst anus

DoAXR
ARM
More vomiting
Less abdominal dist
j
Prominent abd
distension

AXR diagnostic Non specific AXR

i
Surgery
i ;=r·
Upper GI series Calcification
Do contrast

i enema

Meconium
peritonitis
l
Therapeutic for SCLS,
meconium plug and
simple meconium ileus;
Surgery in other cases

Suspect intestinal obstruction in the following scenarios


• Antenatally diagnosed intestinal obstruction (antenatal USG
showing double bubble appearance or dilated bowel loops > 15 mm
331

in length and 7 mm in diameter with increased echogenicity.


Whirlpool appearance to the bowel and bowel mesentery may
indicate malrotation with vol vu us.)
• Antenatal h/o polyhydramnios.
• Family history- Hirschsprung disease andjejunal atresia
• Delayed passage of meconium in a term/near term baby-
Hirschsprung disease, meconium ileus, meconium plug syndrome
and small left colon syndrome (SLCS). In these conditions,
meconium usually appears as small grayish plugs of mucus. Note:
Among premature infants, up to 32 percent have "delayed" passage
of the first stool beyond 48 h. In 99 percent of preterm infants, the
first stool is passed by the 9'" dafter birth3.
• Vomiting: See Table 35.l

Table 35.1: Nature ofvomitinl! and differential dia2nos1s


Non bile stained with Pyloric atresia/stenosis, preduodenal variety
abdominal distension of duodenal atresia
Non bile stained GER, diaphragmatic hernia, nonsurgical
without abdominal disorders like prematurity and sepsis
distension
Bilious vomiting - Malrotation, duodenal stenosis, duodenal
surgical causes atresia or proximal jejunal atresia.
Bilious vomiting - Intestinal ileus secondary to electrolyte
other causes imbalance and sepsis.

Neonates with bile stained vomitus are supposed to have intestinal


obstruction unless proved otherwise. Onset after birth is delayed the
more distal the obstruction is and is preceded by progressive
abdominal distension. Gastric aspirate volume at birth > 20 mL also
mandates ruling out intestinal obstruction.
• Mass abdomen - cystic meconium peritonitis, duplication cysts,
pouch colon
• Suspected Downs syndrome and anorectal malformations
35.3.I Radiological diagnosis of obstruction
• Obtain an AXR - anteroposterior and cross-table lateral view. An
erect abdominal view is done in case of non-sick babies; in other
cases, supine films suffice. A prone cross table lateral view should
be done at >24 h after birth for suspected anorectal malformations
(see Table 35.2). The radiological findings in plain AXR are shown
in Table 35.3
332

Table 35 2: Th e normal proe:ress1on o f air . the intestine


. 10 . after birth
Stomach First breath
Duodenum Second and third breath
Proximal small bowel I hour
Distal small bowel 3h
Cecum 6h
Rectum 18-24 h

. tic s12ns on 011.


T a bl e 353 : Ch aract eris a1n AXR
Double bubble sign- represents air or fluid
filled distended stomach and duodenal
Duodenal atresia
bulb. Rest of abdomen is otherwise
gasless.
Triple bubble siQ'Tl Proximal iei unal atresia
Distal obstruction.
In meconium plug
Uniformly dilated bowel loops with syndrome
multiple air fluid levels with paucity of (most common form of
pelvic air. functional distal obstruction
in the newborn)
no fluid levels are seen
Fewer air fluid levels with disparity in
Meconium ileus
size of dilated bowel loops
Ground glass or soap bubble annearance NEC, meconium ileus
Speckled calcification in abdomen and
Meconium ileus
scrotal sac
Mild double bubble with distal gas ±
bowel wall thickening, with orientation of Malrotation
2"' part of duodenum to the left of spine

Contrast enema: If clinical scenario and AXR suggests distal bowel


obstruction do contrast enema (Table 35.4)
Upper G.l. series
Jt is the procedure of choice in diagnosing malrotation of the intestines.
The most important signs of malrotation on upper GIT contrast study are
(i) an abnormally sited duodeno-jejunal flexure (normally 2"' part of
duodenum is situated on the right of spine) (ii) the proximal jejunum
located in the right side of the abdomen and (iii) a spiral, "corkscrew" or
Z-shaped course of the distal duodenum and proximal jejunum.
USG
Normally, the superior mesenteric artery is on the left of the superior
mesenteric vein. This relation is reversed in malrotation. USG can also
diagnose intussusception and we can see free fluid in peritoneal cavity.
333

T a ble 35 4 : s·Il!ns on contrast enema


Meconium ileus (associated with
small filling defects in microcolon
and the terminal ileum)
Microcolon
SLCS: microcolon IS associated
with an abrupt cone of transition at
or just distal to solenic flexure
Abnonnal cecal position Malrotation
Right sided colonic beaking Volvulus
Abnormal rectosigmoid index Hirschsprung disease (transitional
(Defined as the ratio between the zone is not visible in newborns)
widest diameter of the rectum and The presence of barium in the 24-
the widest diameter of the sigmoid. hour delayed film IS also
In normal neonates it should be 2: 1. suggestive of Hirschsprung's
In Hirschsprung"s disease, the ratio disease.
is < 1. It is not a sensitive test.)

35.3.2 Pre operative management


• NPO and head end elevation
• Insert a size 7-9 Fr OG tube and ensure continuous aspiration. If
drainage is more than 10 ml/kg per 12 h shift, replace volume loss
with an equal volume of0.45% NaCL
35.3.3 Post operative management
• IVF replacement at maintenance levels with parenteral nutrition
starting within 2 d of operation. If there has been extensive bowel
manipulation, the baby may reqmre more baseline fluid
administration because of capillary leak. Titrate fluids based on
SERFT, Wt and urine specific gravity.
• Maintain Replogle tube to continuous suction and measure output.
Replogle tube may be removed when drainage is minimal and non-
bilious.
• After the baby has passed stool, start feedings with small volumes
and advance slowly to ensure that baby is not developing abdominal
distension secondary to postoperative ileus or to stricture at the
anastomotic site.

35.4 ABDOMINAL WALL DEFECTS


(OMPHALOCELE AND GASTROSCHISIS)
Diagnosis is obvious at birth and in some cases prenatal USG diagnosis
is available. Look for other associated anomalies, especially in case of
omphalocele.
334

35.4. I Pre-operative management:


• Bowel stabilization: Twisting of the mesentery or constriction at the
edge of the defect may compromise blood supply to the eviscerated
intestine. The baby should be placed on his/her side to help support
the externalized intestine and ensure adequate blood flow. Observe
continuously to ensure adequate perfusion of the gut.
• Thermoregulation: Heat is lost rapidly through the eviscerated
organs so particular attention should be paid to thermoregulation.
The bowel should be wrapped in plastic wrap to minimize heat loss
and so prevent hypothermia. Wet gauze wraps should be avoided
since evaporation and cooling of the swabs can exacerbate heat loss.
• Gastric decompression: Insert a IO Fr feeding tube and aspirate
regularly.
• Fluid and electrolyte balance: Large fluid and protein losses occur
from the exposed bowel and NG aspirates are often in excess of
30 mL/kg/d. It is important to continually assess perfusion and
titrate fluid requirements.
35.4.2 Post-operative management
Considerations similar to post-operative management of intestinal
obstruction

35.5 OPEN NTD


35.5.t Diagnosis
Detected either antenatally or postnatally. Myelomeningocele appears as
a red, raw neural plate structure devoid of dura and skin with seepage of
CSF. A meningocele, in contrast, usually has a nearly complete skin
covering.
35.5.2 Management (shown in Table 35.5)
35.5.3 Indications for surgery: Shown in Table 35.6

35.6 NEONATAL HYDRONEPHROSIS: Evaluation is shown in


Figure 35.2
35.6.1 Diagnosis
Majority of neonates are antenatally detected. Other presentations are
palpable abdominal mass, hypertension and features of urinary tract
obstruction or urosepsis.
35.6.2 Postnatal Evaluation of Hydronephrosis
Note: MCU is performed under antibiotic cover and without sedation.
Amoxicillin is administered orally in a dose of 50 mg/kg, 1 h before the
procedure and 25 mg/kg 6 h later. Alternatively, gentamicin (2-3 mg/kg
IM) may be given 30 min before the MCU
335

Table 35.5 Clm1cal assessment and mana2ement of open NTD


• Avoid latex Jroducts
General Care
(use latex-free gloves for all handling).
•Place the infant prone and evaluate the size,
position, and appearance of the lesion.
•Palpate the fontanel and sutures for evidence of
raised ICP.
• Measure the OFC.
• Evaluate spontaneous movements
Clinical •Evaluate the level of sensation. This can be
Assessment determined using an open nappy pin (not a
hypodermic needle).
• Assess anal tone.
• Assess urine output, urinary stream and bladder
palpability
• Look for presence of associated orthopedic
defonnity
•Cranial USG scan to evaluate ventricular size and
to assess other malformations.
• MRI should be obtained peri-operatively on the
Investigations
instruction of the neuro/pediatric surgeon.
•Renal USG should be performed in the pre
oocrative oeriod.
•Administer antibiotics based on suspicion of
Infection Risk
sepsis.
•The baby should be nursed in the prone position or
left lateral position.
•Under aseptic precaution cover the defect
Dressings immediately with saline-moistened gauze. Insert
butterfly tubing without needle between multiple
layers of gauze and seal entire dressing with
Tegaderm. Irrigate periodically with warmed NS

35.6.3 Antibiotic prophylaxis


Prophylactic antibiotics should be administered, once daily, to all
neonates with hydronephrosis (also see section 24.8.4 for UTI) until
VUR is excluded. Cephalexin or amoxicillin (10-15 mg/kg once daily)
should be used for the initial 3 mths, and cotrimoxazole ( 1-2 mg/kg/d of
trimethoprim) can be rotated thereafter. In the absence of VUR,
prophylactic antibiotics should be discontinued after 1 yr of age. This is a
controversial area and should be gwded by the Pediatric surgeon.
336

.
T a bl e 35 6 In d"1cat1ons of sur2erv 1n NTD
•Open defects with no/minimal neurological
Immediate deficit
surgery • With impending rupture
• Recent leak (onerate after 24 h of antibiotics)
• Good skin cover
Delayed surgery • Infected defects or defects leaking for > 24 h
with no neurological deficit
• Infected or leaking defects with neurological
Contraindications deficit
• Neurogenic bladder or gross hvdroceohalus

Figure 35.2: Evaluation of hydronephrosis


Antenatal Hydronephrosis

Antenatal USG shows


solitary kidney or bilateral
hydronephrosis; clinical
suspicion of posterior urethral +---
1
Do detailed clinical
exam at birth
valves; palpable abdominal
mass, features of urinary tract
obstruction or urosepsis
AN USG shows U/L hydronephrosis;
normal clinical exam and diagnosis
of posterior urethral valves unlikely
Do immediate USG KUB,
SERFT, urine culture and
MCU
USG by 4-6 d

USG shows no USG shows hydronephrosis


hydronephrosis
i
i
USG at 3-4 mths
Start antibiotic prophylaxis, Do SERFT,
urine culture at 1-2 wks, DTPA
(Diethylene triamine pentaacetic acid)
i
No further evaluation
with diuretic renography and MCU at 4-
6 wks. Consult Pediatric Surgery SR.
337

35.6.4 Indications for Surgery in J\ eonatal Hydronephrosis


• PUJ obstruction
o At initial diagnosis
• Presence of symptoms
• Solitary kidney with hydronephrosis
• B/L hydronephrosis
• Differential renal function of obstructed kidney <30%
o On follow-up
• Increasing renal pelvic dilatation
• > 10% decline in differential renal function
• Posterior urethral valve, ureterocele
• VUR
• Grade IV-V reflux persisting beyond infancy
• New renal scars or recurrent UT! despite antibiotic
prophylaxis

35.7 OTHER COMMON SURGICAL PROBLEMS: Shown in Table


35.7

Table 35.7 Other common surgical problems

Problem Intervention Remarks


Needs repair as and when Can get obstructed if
Indirect
diagnosed left alone
inguinal
Operate before discharge in
hernia
case of preterms
Surgical indications are Occurs in 20% of

Umbilical • Large hernias, newborns; closes


hernia • One which has not closed spontaneously in 12
for 3 yrs mths but may take up
• Incarceration to 3 yrs.
Analgesics, cold fomentation Manifests as sudden
Incarcerated and gentle pressure to reduce size increase,
hernia contents. tenderness and
vomiting.
Apply a very small pinch of Silver nitrate
table/ cooking salt over the application not
umbilical granuloma advisable as there is a
Cover the area with a gauze risk of bums to the
Umbilical
dressing and hold it in place surrounding skin.
granuloma
for 10-30 mins. In case of continuous
Clean the site using a clean discharge ftom
gauze soaked in "\\arm water umbilicus rule out
Repeat the procedure twice a infection and patent
338

day for at least 3 d vitello-intestinal duct.


Correct mild cases before In severe cases rule
school going age. Do not out intersex disorders
Hypospadias
circumcise as prepuce is and urological
needed for repair. abnormalities

REFERENCES
I. Moya F R. Semin Perinatol 2005; 29: 112
2. Neonatal Inhaled Nitric Oxide Study Group. Pediatrics 1997; 99:838
3. Weaver LT. Arch Dis Child 1993; 68: 317
339

36. EXTREMELY LOW BIRTH WEIGHT IELBW) BABIES

Only those issues unique to ELBW babies are mentioned. For more
details. refer to the respective protocols.

36.1 RESPIRATORY ISSUES


• Resuscitation:
o Ensure presence of SR during delivery of an ELBW infant.
o Keep all the equipments including ET size 2.5 ready.
Occasionally size 2.0 may be required for babies between 500-
750 g.
o After initial stabilization in the delivery room, administer
prophylactic surfactant to infants with GA <28 wks.
o Start early therapeutic NIPPY or nCPAP if signs of respiratory
distress are present in babies, especially <28 wks, irrespective of
availability of surfactant. The need for surfactant should be
discussed with the parents during antenatal counseling and
arranged beforehand.
• Early rescue surfactant may follow the INSURE approach which
consists of "CP AP--INtubation-SURfactant-Extubation--CP AP" (see
sections 14.9, Dl20), however INSURE must be used with caution
in ELBW babies. This approach has definite short-term benefits
(decreased need for mechanical ventilation) but effects on long-term
outcomes are not clear'. A BW of<750 g, Pa0,1Fi0 2 <218 and a/A
ratio <0.44 are independent risk factors of INSURE failure 2.
• ELBW infants are prone to develop BPD (see chapter 16). Even a
single assisted breath has been shown to increase the risk of BPD.
Similarly, hypocarbia (PaC0 2 <30 mmHg) is associated with
increased risk PVL 3. Hence a strategy using lower driving pressures,
faster rates and lower Ti are preferred in ELBW infants (see section
14.12).

36.2 HYPOTENSION
Up to 45% of ELBW infants have hypotension. Risk of hypotension is
high due to
• High JWL
• Loss of auto regulation & vasodilatation, low systemic blood flow
• Fluid shift (due to capillary leak), PDA
• Low adrenal reserves & poor adrenal response to stress
36.2.1 Management
• Administer 0.9% saline I 0 mL/kg over 30 min period (once)
• If there is inadequate response within 30 min or response not
sustained for at least 30 min, start inotropes
340

• Stress dose hydrocortisone (5 mg/kg IV followed by 2.5 mg/kg q 6


hourly), when dopamine 0".10 µglkg/min, should be considered (see
section D65). VLBW infants have an immature hypothalamic-
pituitary-adrenal axis leading to inadequate cortisol release
following stress during the first 7 d of life. In ELBW babies, this
extends into the 3'' wk oflife4 .
• Get an Echo to rule out PDA. In the presence of PDA, avoid further
fluid boluses.
• Check for hypothermia, hypoxia & inadvertent high PEEP/CPAP
• Invasive BP recording fiom U A or a peripheral artery is preferred.

36.3 THERMOREGULATION
• ELBW infants lose heat through all avenues especially by
evaporation. This high evaporative loss may be up to 6 times higher
per unit surface area in comparison to a term baby. Additional losses
occur due to adhesive trauma to the skin.
• Methods to reduce heat loss:
• Increase ambient relative humidity up to 70-80%.
• Use double walled incubator or a Perspex heat shield in a single
walled incubator (see section 7.8)
• Use caps and clothing, even in an incubator
• Use portholes instead of opening the incubator door for
handling or procedures
• Use an extra heat source like a mobile heating lamp during
procedures.
• Waterproof the baby: This can be done in various ways:
o Food grade plastic film wrapped around the baby
o Clean plastic film stuck edge to edge above the infant in a
open care system
o Application of vegetable oils (e.g. sunflower seed oil). Use
oil sparingly as evidence in hospital settings is lacking.

36.4 SKIN CARE


• The stratum comeum in adults is l0-20 layers thick whereas in a <30
wks baby, there are only 1-2 layers and in a 24 wk infant there is no
stratum corneum. It becomes functionally mature only by 32 wks
gestation. Acceleration of maturation occurs postnatally, with a
mature epidermal barrier by about 2 wks of age (longer in more
premature babies). Until that time, full thickness skin injury can
occur if proper precaution is not taken.
• Common situations causing skin injury:
o Adhesive tape removal
o Local pressure from body positioning
o Prolonged exposure to products containing alcohol / iodine
341

• Risks associated with skin injur::


o Increased IWL
o Risk of infection
o Percutaneous absorption of [OXins
36.4.1 Prevention of skin injury: Shown in Table 36.1

Table 36.1 Prevention of skin injury in ELBW neonates

• Apply always to a dry. clean surface of skin


• Use smallest length I amount of tape as possible
Adhesive • Use Tegaderm or Dermafilm (transparent semi-
application occlusive dressings) as a base before applying an
adhesive tape like Dynaplast, Durapore etc.
• Avoid adhesive over areas of skin breakdown
• Avoid direct peeling off the adhesive. Peel along
the longitudinal axis of the adhesive
Adhesive
• Apply warm, wet. cotton ball over the adhesive
removal
• Facilitate removal with oil if reapplication is not
necess::irv

36.4.2 Adhesives to be used


• Fixing ET tube: Stick a layer of Tegaderm (width of frenulum)
which forms a skin-friendly base. Fix the ET with stretchable
sticking plaster (e.g. Durapore or Dynaplast) on top of the
Tegaderm. Avoid direct contact of adhesive to the skin. Similarly,
place a layer of T egaderm base on the forehead and secure the ET tie
with Dynaplast.
• OG tube: Fix by the angle of mouth. Use Durapore silk (cut V-
shaped to fix). Do not use paper adhesives (e.g. Micropore) as they
may cause skin irritation.
• Chest tube: Secure the tube with purse string sutures by avoiding
skin puckering. Fix transparent dressing around the incision site and
further secure it with an adhesive like Durapore or Dynaplast.
• Vascular lines: Use transparent dressings to secure the venous lines.
They are thin, polyurethane films that are water and bacteria proof
but allow air & water vapor to permeate. Transparent dressings
allow easy site assessment. Do not apply any other adhesive over it.
• ECG electrodes & temperature probe covers: Has hydrogel base,
which reduces IWL. But cannot be used for longer durations as they
lose their adhesive capacity
36.4.3 Preparations available
• Transparent dressing: Tegaderm (3M), Dermafilm, IV3000 frame
delivery (Smith-Nephew)
342

• Wound I abrasion dressing: OpSite, Flexigrid moisture vapor


permeable adhesive dressing (Healthcare Common Procedure
Coding System (HCPCS) code: A6257). Replicare thin & ultra
hydrocolloid dressing (Smith-Nephew; HCPCS code-A6234),
Tegaderm hydrocolloid (3M) - meant for dressing of sores, bums &
open wounds
• Skin preparatWn before dressing: Skin-prep, No sting skin-prep-
liquid film forming dressing, reduces friction while adhesive
removal
36.4.4 Role of oil
Applying sunflower oil, thrice daily for first 2 wks and then twice daily
till discharge has shown to reduce nosocomial infection and improve skin
condition in premature infants (<33 wks) in two recent RCT's. It can be
recommended in a non-NICU setting. It's efficacy in NICU setting is
untested.

36.5 PDA OF EXTREME PREMATURITY (see section 30.2):


• PDA in an ELBW infant can manifest within hours due to a
premature fall in the PVR especially in a ventilated ELBW infant
• The "silent dangerous ductus" (Echo proven significant ductus
without any clinical signs) is very common in extremely premature
infants.
• Echo signs of shunt can precede clinical signs by 3 d to a wk.
Reliable early diagnosis of PDA in an ELBW infant in the first 4 d
of life depends solely on Echo. Clinical findings alone are
misleading'. Hence, echocardiography is recommended in all
ventilated ELBW infants in the first 24 h of life irrespective of the
symptoms.
• Prophylactic medical therapy for PDA with Ibuprofen is not
recommended as per current available evidence'. Prophylactic
indomethacin has shown various short-term benefits (reduction in
PDA, IVH) but is not recommended because it does not improve
long-term neurodevelopment.

36.6ANEMIA
Low iron stores, multiple blood tests & associated blood loss and rapid
growth make anemia an unavoidable complication in these infants.
36.6.J Measures to reduce the severity of anemia
• Plan investigations: Group the investigations for the next 12 h [by
the SR] including the volume of blood required and the timing of
sampling. Morning's elective sampling has to be planned by the SR
on the previous evening. This has to be clubbed with the emergency
sampling decision taken by the on-duty SR. The amount sampled has
to be duly recorded in the nursing observation chart.
343

• Preferably use arterial lines for •ampling. Do not use central venous
lines for drawing blood.
• Venous sampling: l n babies without an arterial line, a fresh
peripheral vein can be used for drawing blood after thorough aseptic
preparation of the skin. Approximate volume of blood by drop
method should be calculated and specified in the nursing chart.
Roughly 16 drops correspond to 1 mL.
• Use noninvasive monitoring wherever possible (pulse-oximeter,
transcutaneous devices) especially after initial 7 d of life or after the
acute disease process has settled.
36.6.2 Measures to reduce transfusion-acquired infections (see
section 17.6)
An ELBW infant, on an average requires 6 PRBC transfusions during a
hospital stay of 6 wks. The requirement for transfusion usually starts
from 2"' wk onwards.
• Send a blood sample 3 working days prior to the first BT for blood
grouping & cross matching. The blood bank will reserve a dedicated
unit for that baby. Satellite bags of the request volume will be
prepared using sterile connecting device (see section 17.7.1 ).
• Irradiation of blood: Currently there is no data to support mandatory
irradiation of simple PRBC transfusions in neonates. Irradiation may
be considered in ELBW infants undergoing DVET & transfusion of
blood from biologic relatives (see section 17.7.3).
• Leukoreduction: ELBW infants are in an immunocornpromised
state. Hence, CMV negative blood products are preferred. Routine
CMV antibody screening is not done in PGIMER. Hence,
leukoreduction using 3"' generation fiber mesh filters (to which
leukocytes adhere) can be used (PAL filter-SQ40 costing - ~ 1000),
depending on affordability. The filtered product should have less
than 5 x!0 6 residual WBC's (3-log reduction~ 99.9 % reduction).

36.7 FLUID & ELECTROLYTES (Also see chapter 8)


ELBW infants are vulnerable to dehydration, hypernatremia & resultant
hypertonicity (risk of!VH)
• Send electrolytes (Na+ and K+) and RFTs (Urea & creatinine) in the
first sample (base line). Repeat electrolytes once in every 12 h or
more frequently (based on the clinical requirement) & RFTs as and
when required.
• Renal threshold for glucose absorption is immature leading to
glycosuria and resultant polyuria and dehydration. This occurs even
with normal BS. Hence, always check for glycosuria in case of
polyuria.
344

• Hyperkalemia frequently complicates the management of ELBW


infants during the I" wk of life (see section 8.8.5). This is due to a
low GFR as well poor distal tubular excretion of K -

36.8 NUTRITION
Due to excessive catabolism postnatally, enteral nutrition alone can never
provide the Calories required (I 00-120 Cal/kg/d) for growth in these
infants. Parenteral nutrition (starting at 80-85 Cal/kg/d) is essential for
growth (see chapter 32).
• Start parenteral nutrition on day I of life in all ELBW infants who
are NPO.
• Start trophic feeds (I 0 - 20 mL/kg/d) once stable and transition to
nutritional feeds depending on the tolerance.
• To facilitate uninterrupted PN, place a dedicated PICC. Under
aseptic precautions, PICC does not increase risk of infection.

36.9 INITIAL MANAGEMENT: Shown in Figure 36.1


345

Figure 36.1: Flow chart for initial management of ELBW infants

Resuscitation comer:
1) Personnel: at least 2; one of them SR
2) Additional equipments: Pulse-oximeter, infusion pump,
polythene wrap, surfactant
LR ___.,. Precautions:
1) LR temperature: 28-30°C
2) Wrap (plastic) may be considered
3) Gentle PPV; avoid excessive pressure on head
4) Maintain Sp02 : 87-93% (not>95%)
5) If transfer expected :S30 min to NICU - do not start IV lines;
If delay anticipated - start dextrose infusion at 6 mg/kg/min
6) Consider prophylactic surfactant & start early CPAP (as
indicated)
7) Always wash hands and use alcohol hand rub

Pre-transport:
1) Check STABLE* & vitals
Transport ~ 2) ET intubation if mechanical ventilation anticipated
3) Ensure adequate communication with NICU
During transport:
I) Avoid jerks (risk of IVH)
2) Care of airway (obstruction, accidental extubation)

Expose to ambient environment minimally


I)
2)
Place in a double walled incubator
3) Humidify the incubator (70-80%); avoid condensation
4) Check Wt (inline); sugar and temperature (axillary)
5) Attach various probes (saturation & temperature)
6) Start ventilation (as indicated); strategy- refer to text
NICU-7) Place peripheral IV line (if not placed) & start dextrose infusion
through a preloaded infusion pump
8) Place central lines (UAC & Umbilical venous catheter) preferably.
Send ABG, baseline investigations (SERFT, CBC, sepsis screen)
9) Administer surfactant (if not given early)
10) Start antibiotics (as indicated)
11) Perform USG head (for IVH) and Echo (for PDA) on day one

*S-Sugar, T-temperature, A-airway, B-breathing, L-lincs, E-empathy


346

REFERENCES
1. Stevens TP, Blennow M, Myers EH, Soll R. Cochrane Database of
Systematic Reviews 2007; 4.
2. Dani C. J Maternal Fetal Neonatal Med 2010; (epub)
3. Ikonen RS, Janas M 0, Koivikko M J, Laippala P, Kuusinen E J.
Acta Pediatr 2008; 81: 802.
4. Pak C Ng. Pediatrics 2008; 122: 873.
5. Skelton R, Evans N, Smythe J. J Pediatr Child Health 1994; 30: 406.
6. Ohlsson A, Walia R, Shah S S. Cochrane Database of Systematic
Reviews 2008; Issue 1.
347

37. RETINOPATHY OF PREMATURITY

ROP is a vasoproliferative retinal disorder that increases in incidence


with decreasing GA.

37.1 RISK FACTORS:


The most consistent association is with low GA, low BW, oxygen
exposure (see sections 14.1.2, 14.8) and duration of mechanical
ventilation. Other putative risk factors include multiple transfusions,
hypolhypercarbia, sepsis, Candida sepsis, BPD, PDA and NEC, IVH.
There is no relation between ROP and bright-light exposure, maternal
smoking and maternal PIH.

37.2 CLASSIFICATION AND DEFINITIONS OF ROP:'


The classification of ROP is based on location, extent, stage and 'plus'
disease.
37.2.1 Location ofROP: Shown in Figure 37.1
Figure 37.1 Location of ROP according to different zones
a. Zone 1: innermost zone,
the radius of which is
....
twice the distance from ?'
the centre of optic disc to
macula.
b. Zone 2: extends from
zone I to ora serrata of
nasal side and about hall
of the distance from ora
serrata on temporal side.
c. Zone 3: residual crescent
of retina on temporal
side.
37.2,2 Stage: It is divided into 5 stages.
• Stage 1: Demarcation line that separates avascular retina anteriorly
from the vascular retina posteriorly.
• Stage 2: Ridge of scar tissue between the avascular retina and
vascular retina.
• Stage 3: Ridge with extraretinal fibrovascular proliferation or
neovascularization. Abnormal blood vessels extend into vitreous.
• Stage 4: Partial renal detachment due to pull of scar tissue. 4A- if
detachment involves outside the fovea. 48- if detachment involves
fovea.
• Stage 5: Total retinal detachment.
348

37.2.3 Extent: It refers to the circumferential location of the disease and


is reported as clock hours in the appropriate zone.
37.2.4 Plus disease: It implies venous dilatation and arterial tortuosity of
posterior retinal vessels. And later may include iris engorgement. rigid
pupil and vitreous haze.
37.2.5 Pre-plus disease: Intermediate level of vascular dilatation and
tortuosity between normal appearing posterior pole vasculature and frank
plus disease.

37.3 AP-ROP (AGGRESSIVE POSTERIOR ROP):


This is an uncommon. rapidly progressive and severe form of ROP. The
characteristic features are its posterior location, prominence of plus
disease, its ill-defined nature and rapid progression to stage 5.

37.4 SCREENING OF ROP: 2


37.4.1 Whom to screen?
I. Gestation <34 wks and/ or <1750 g at birth.
2. Preterm (34-36 617 wks) neonates with invasive ventilation and 0 2
requirement for '?:7 d: ROP screening should be done irrespective of
gestation and BW.
37.4.2 When to screen?
First ROP screening should be done at 4 wks of post-natal age. Repeat
examinations should be done as advised by ophthalmologist based on the
findings of first examination.
37.4.3 How to get the babies screened for ROP?
For the babies admitted in NICU and NNN, ROP bedside screening is
done on Saturdays. To get the babies screened for ROP, inform the
concerned Ophthalmology JR or SR a day before.
For the babies who are discharged, counsel the parents regarding the
need for ROP screening and mention the date of appointment in the
discharge summary and the booklet. For outpatients the ROP screening is
done on Wednesday/Friday in Advanced Eye Center, Room No: 229/231
from 9 am- I pm.
37.4.4 How to dilate the pupils for examination?
Drosyn drops (phenylcphrine) come as 10% solution (see section DlOO).
Add 3 drops of NS to I drop of Drosyn. Apply one drop each of Drosyn
(2.5%) and Cyclomid (Cyclopentolate) 1% to each eye and wipe away
the excess drug with cotton (see section 037). Repeat the same every 20
min for 3 times.

37.5 TREATMENT OF ROP


37.5.1 Who to treat?'
• Zone I, any stage ROP with plus disease or
• Zone I, stage 3, with or without plus disease or
349

• Zone II, stage 2 or 3 ROP, with Jius disease or


• APROP
37.5.2 The following groups require frequent serial examinations:
• Zone I, stage 1 or 2 with no plus disease or
• Zone II, stage 3 with no plus disease

37.6 LASER THERAPY


Laser therapy is done on outpatient basis and there is no need for
admission. The stomach should be decompressed before the procedure.
The resident of NNN should examine the baby before the starting the
procedure. For pain relief, see section 44.6. During the procedure baby
should be preferably monitored by pulse-oximeter. Resuscitation set
should be ready. Baby should be re-examined by the NNN resident at the
end of the procedure. Observe the baby and monitor the vital signs for a
minimum of 3 h after the procedure. Follow the instructions of the
Ophthalmologists. Administer 0.3% Tobramycin eye drops thrice daily
for 7 d and 0.1 % bctamethasonc eye drops 0.1 % thrice daily for 7 dafter
the laser procedure.

REFERENCES:
I. The !CROP revisited. Arch Ophthalmol. 2005; 123:991.
2. Jalali S. Indian J Ophthalmol. 2003 Mar;5 l :89-99.
3. Good WV. Trans Am Ophthalmol Soc. 2004;102:233.
350

38. OSTEOPENIA OF PREMATURITY

38.1 INTROOUCTIO"I
OOP 1s a metabolic bone disease associated with decreased bone mineral
content in preterm infants. Preterm babies are prone for OOP as two
thirds of skelernnmneralization occurs in the last trimester of pregnancy.
~itiorus accret on 1s ffie pnnc1pal et10log1cal factor m the
development of OOP. Rou I half of ELBW and one-fourth of VLBW
babies develop radiological sign ofosteopenia if untreated.

38.2 RISK FACTORS


• <30 wks gestation. ""\
ti' f"3'""0----
• < I 500 g birth weight. )
• Delayed establishment of full enteral feeds/prolonged parenteral
nutrition. ~
• Enteral feeds with low mineral content or bioavailability (unfortified
EBM, standard tellTl formula) (see section 9.13.1 ). .....-----
• Chronic use of medications that increase mmeral excretion
(diuretics, dexamethasone, sodium bicarbonat~
• Cholestatic jaundice.

38.3 DIAGNOSIS
Diagnosis 1s suggested b~rnical4 radiolog!sal a~hnic~feature~
38.3.1 Biochemical - - -

j i
• Scrum lllorganic phosphate < 4.5 mg/dLl
• Scrum ALP > 450 IU/dL __.l
38.3.2 Other helpful markers in cases of ambiguity
• Urinary calcium/ creatinine ratio (spot sample) >0.5
• Tubular reabsorpt1on of phosphate (TRP)=
I- Urine PO~ x plasma creatinine x I 00 (>95% 1s abnormal) I ~O
Plasma P04 x urine creatinine - l
38.3.3 X ray
Osteopenic infants may manifest after 2-4 wks of postnatal life.
Diagnostic findlllg include fraying and widenin of mctaphyses; s -
.£i!riosteal bone~. a_ ~s. he rad1ograph1c mdmgs
may not be visible until bone mineralization is reduced bif4@ Get X-
ray \\-TISt'chest done if clinical or b1ochenucal signs of osteopcnia arc
present. X ray should be repeated after 4 wks of therapy to document
resolution.
38.3.4 Dual x-ray absorptiometry (DEXA)- used to measure bone
density. It can diagnose early demineralization accurately and 1s the gold
standard diagnostic modality. DEXA is available in PGIMER but cannot
be used in pretcrm babies as the appropriate software for prctcrms is
currently not available and there is lack of normati vc data.
351

38.3.S T ibial b one sou nd cot1d uction by q ua ntita tive USG:


Attenuation of the speed of s~ conduction is a measure o~e
density. This is currently not availab le m PGIMER.
38.3.6 C linical features: -
Rachitic rosary, compliant rib ca~ soft skull bones, rib fractures,
widenmg of wrists, faiTurc to weaii from mechanical ventilation are"llle
clinical signs suggestive of OOP The clinical features are evident
usually between 3-6 mths of postnatal life.

38.4 MONITORI NG:


38.4.1 Who and when to screen: S 1own in Table 38. 1

T able 38.1 Scrceninl! for OOP I


Babies I, Time of screening
jl
VLB WI gestation < 32 wks After day 14 of life
Receiving TPN After 2 wks ofTPN /
Y'
Receiving diuretics or steroid therapy After 2 wlcs of therapy """
Having conjugated jaundice After 2 wks ofonset . /
I

38.S PREVENTION
• Babies on pretcnn fonnuJa feeds (e.g. Lactodex-LBW) at the rate of
180 mL/kg/d do not need suppl ~mentatton.
• Babies on EBM require supp emcntation as pretenn milk cannot
fulfill Ca, P04 requirements \ ithout supplementation. From EBM
babies get 45-50 mg/kg/d of calcium and 20-22 mg/kg/d of P04 (see
section 9.11.3, 9.12).
o Calcium ( 148-232 mg/kg/11) and phosphorus (75-120 mg/kg/d)
must be given to all premature breast-fed babies (<34 wks of
gestation) in a ratio of 1.8: to 2: I .
o Supplement vit 0 in a dose of 400 500 IU/d (see section 047).
• Requirements in babies on TP1' are-
a Calcium 60-75 mg/kgtd
o Phosphorus 35-50 mgikg1cl. Parenteral phosphorus preparations
arc not yet available in India. Hence OOP 1s almost universal in
Indian preterm mfants on long-term TPN

38.6 TREATMENT
• Calcium I phosphorus supplementation- should be started m the
same doses as above and esca ated to maximum perrrussible. Syrup
Ostocalcium provides 82 mg elemental Ca, 41 mg of elemental
phosphorus and 200 IU Vit 0 'er 5 mL. A sachet of Lactodex-HMF
has 50 mg of calcium, 25 mg C'f phosphorus and 250 JU Vit 0 3• (see
section 9. 12)
352

• Vit D 400 U/d-1600 U/d is required in all babies. Starting doses can
be hiked to 1600 U/d if there is no response to small doses (as
assessed by weekly ALP levels). There is no evidence that higher
doses are beneficial. Vit D deficiency states require doses up to 5000
U/d.
• Physiotherapy- There is weak evidence from a metanalysis 1 that
physical activity programs might promote moderate short-term Wt
gain and bone mineralization in pretenn infants. Gentle
physiotherapy should be done.
38.6.1 Duration of therapy
Continue until there is radiological healing of rickets or biochemical
parameters return to normal. Usually it takes 2-3 mths.

38.7 MONITORING, WHILE ON TREATMENT


• Wt and length weekly.
• Evaluation of biochemical markers weekly. Rise in P0 4 and fall of
ALP is associated with resolution. The therapy can be stopped if
ALP falls below <450 U/L with normal P0 4 level. Radiological
changes are reviewed with a follow up X-ray after 4 wks.

38.8 PROGNOSIS
Prognosis is good in most cases with the resolution of osteopenia by 6-9
mths. The long-term effects of OOP, including the effects on bone
mineralization and stature during adolescence as well as the effects on
the risks of osteoporosis in adult life, remain unknown. Peak ALP level
of >1200 lU has been shown to be associated with reduced Ht at 12
years 2 .

REFERENCES
1. Schulzke S. Cochrane Database of Systematic Reviews2009; Issue
4.
2. Mary SF. J Pediatr 2000; 137: 668.
353

39. COUNSELING IN \ARIOUS SITUATIONS

Good counseling alleviates parenta anxiety. removes uncertainties and


helps the family take informed deci,ions about further management. The
JR should always be present when counseling is done by the SR and both
should be present when counseling is done by the consultant.

39.1 GENERAL PRINCIPLES OF COUNSELING:


• Know the family resources. edocation & knowledge level.
• Talk to everybody but try to identify the dominant members and
decision makers of the family.
• Focus on a few important points. Individuals under stress cannot
absorb too many issues. Don't go into minute details.
• Provide factual information. Do not speculate. For survival and
morbidity figures of the unit, refer to the previous year's annual
statistics. This is available from the NSR computer.
• Talk like a friend and discuss rather dictate. Speak in the local
language as far as possible. Use non-technical terms. Illustrate with
simple diagrams, when necessary.
• Talk while sitting; not in a hurry. Keep the atmosphere relaxed by
appreciating useful views of family members.
• Encourage questions from the family.
• Encourage active involvement of JRs and nursing staff.

39.2 ANTENATAL COUNSELING:


• It should be done by the neonatology SR of the particular area
(maternity I gynecology ward I LR). He/she should explain the
anticipated problems (short & long-term morbidities). expected
duration of stay in the hospital, expected survival and expected
costs.
• The family must be advised to arrange a certain amount of money
for initial ICU care (including surfactant), ifthat is anticipated.
• Parents can be brought to the unit antenatally and introduced to the
team.
• In case of antenatally diagnosed malformations, the parents should
be counseled about the prognosis prior to delivery and should be told
that certain conditions may require postnatal confirmation. If the
malformation is surgically correctable, involve the Pediatric Surgeon
antenatally and let him/her counsel the family. The SR must be
present during the counseling by the Pediatric Surgeon.

39.3 POSTNATAL COUNSELING:


• It is very important that all members of the team must convey the
same thing to the family. If different people (SR, JR, nurse,
354

consultant) give contradictory messages, the unit loses credibility.


The SR is the nodal person. He/she must keep the in-charge JR and
nurse informed about what must be conveyed (and what must not be
conveyed) to the parents. ln case the JR or nurse is in any kind of
doubt, he/she must crosscheck with the SR before blurting out
something.
• Explain to the family about the nature of the disease, immediate
problems anticipated, expected short & long term outcome, the
treatment required, expected response and inherent risks of treatment
process.
• The mother should see the baby before transfer to any area and the
reason for transfer must be conveyed to her. She must be encouraged
to visit the baby as soon as possible. Give a realistic picture but do
not say anything that would make the mother lose hope.
• Cost for NICU care per patient per day for the family is
approximately ~ 1350 per day and nursery care (non-intensive) ~
100 per day. These figures were calculated in the year 2005 and may
change with time. 1 (See Table 39.1)

Table 39.1 Cost and duration according to birth weight category

Ventilated Non- Ventilated


BW(g) Median Median Cost to
Cost to
length of length of family
family (f)
stav (d) stav Id) (fl
500-999 g 68 54,300 36 34,850
1000-1249 g 48 41,050 21 14,600
1250-1499 g 30 23,000 15 7,750
1500-1749 g 20 18,250 11 4,850

• In case of severe birth asphyxia, initially give a guarded prognosis


for long term outcome, then reassess after 24-48 h and prognosticate
according to stage of HIE and other organ dysfunction.
• ln case of antenatally diagnosed CMFs, reassess the baby
postnatally, in detail, for confirmation of diagnosis, severity of
illness, any new findings & related management issues. Explain
about the malformations to the parents (after showing the baby to
them) and counsel accordingly. If one is not sure of the outcome of
the malformation, continue supportive treatment until diagnosis is
established.
• Talk regularly to the mother; relieve her anxiety and give advice
regarding effective lactation (diet, expression of milk). Encourage
355

handling of the baby by mother and encourage her to provide skin-


to-skin contact (Kangaroo mothe ·care)
• If the baby is very sick, discuss \lith the parents frequently and keep
them well informed about the nature of illness and the reason for the
acute worsening. The SR of the area should act as the leader of the
team and discussion with the parents should be uniformly carried out
by him/her. SR on duty may update the condition if any fresh
problem arises.
• All counseling sessions- antenatal as well as postnatal- should be
documented in the patient's file by the SR.

39.4 GROUP COUNSELING:


Group counseling should be done daily by SR in-charge of NJCU/NNN
at a specific time of day and parents should be informed of the general
status of their babies and any new development in last 24 h. Avoid
personal and sensitive issues during group counseling. Reserve such
issues for one-on-one counseling.

REFERENCES:
I. Narang A. Indian Pediatr. 2005;42:989.
356

40. WITHDRAWAL OF SUPPORT AND PROCEDURE


FOLLOWING DEATH

There are situations in which continuing intensive care may be futile as


far as short term and long-term prognosis and outcome is concerned. In
such situations, the intensive care being offered to baby may be
withdrawn and only basic humane care continued. The issue is
complicated by the fact that Indian laws are ambiguous about the legality
of withdrawal of life support.

40.1 INDICATIONS WHERE WITHDRAWAL OF INTENSIVE


CARE MAY BE CONSIDERED
• Severe birth asphyxia with HIE stage Ill
• Preterm baby with B/L grade 4 IVH and neurologically obtunded
• Major CMFs not compatible with survival without life support or
where severe neuro-morbidity is certain
• Conditions where brain death is diagnosed

40.2 DIAGNOSIS OF "BRAIN DEATH"


Criteria for diagnosing brain death in neonates arc not very clear; more
so in preterm babies. Establishing brain death status requires various
parameters to be tested on multiple occasions over a prolonged period of
time and by at least 2 experienced physicians.
40.2.1 Tools for assessing brain death:
• Continuous cardio respiratory monitoring
• EEG monitoring·
• Blood gas estimation (for PaC0 2)
• Serum barbiturate levels (if baby was on barbiturates). Send 2 mL of
whole blood in a plain vial to the microtech laboratory in APC 3C. It
is mandatory to send the trough levels. Hence take sample just prior
to the next dosing.
• Rectal thermometer (low reading)
40.2.2 Criteria
The following criteria are proposed pending further concrete evidence:
Clinical criteria (all are required):
• Coma (lack of response to pain, light or auditory stimulation)
• Apnea - confirmed by documentation of failure to breathe when
partial pressure of C0 2 is higher than 60 mm Hg (tested by keeping
for 3 min without ventilator support while continuing 1OOo/o 0 2
supplementation by a cannula; or tbr shorter periods if hypotension
or bradycardia intervene)
• Absent bulbar movements (gag and cough) and brain stem reflexes
(including midposition or fully dilated pupils with no response to
light or pain and with absent oculocephalic, caloric, corneal, gag,
357

cough, rooting and sucking n flexes) all of which are normally


elicitable by 33 wks gestation.
• Flaccid tone and absence of ~ pontaneous or induced movements
(excluding activity mediated at >pinal cord level)
Period of observation for brain death:
Based on clinical criteria alone, a period of observation of 48 h for term
and 72 h for preterm infants is required for diagnosing brain death.
Confirmatory neuro-diagnostic studies (EEG for electrocerebral silence)
are of value in potentially shortening the period of observation to 24 h.
If the above-mentioned clinical findings remain unchanged in the
absence of a barbiturate level over 25 mg/L, hypothermia (<24 °C), or
cerebral malformations (e.g. hydranencephaly, hydrocephalus), it is
confirmatory of brain death.
Note: In isolation, EEG alone is not sufficiently sensitive to diagnose
brain death. It has always to be combined with a clinical diagnosis to
shorten the period of observation. On the contrary, persistent EEG
activity is known to occur in newborn infants' in spite of brain death and
hence does not preclude the diagnosis of brain death in them.

40.3 PROCEDURE OF WITHDRAWING INTENSIVE CARE


• The decision has to be made after a detailed discussion involving at
least two consultants, who should have examined the baby
independently.
• Counsel the parents by explaining them about the brain death status,
the expected grim outcome, and discuss the management options
available at that point of time. End of life decisions are made
collaboratively with parents through a series of meetings with the
treating team, headed by the area consultant. Do not enforce a
deadline within which they have to take the decision. Never make it
appear that the "bed" is required for another "more deserving"
patient.
• The written consent of the parents must be obtained before
withdrawing intensive care, preferably in the parent's own
handwriting. Consent should be obtained in the presence of at least
two witnesses who are unrelated to both the parties and also not a
part of the treating team. Names and addresses of the witnesses
should be written in the file in their own handwriting. The staff nurse
looking after that baby should be involved in the whole process of
counseling and withdrawal of care. Withdrawal of intensive care
must be done only during daytime when everybody is around, except
for exceptional circumstances in the labor room.
• Meet in a quiet, private area- like the NSR- and allow ample time for
the family to understand the information presented. Ask the parents
how they feel and perceive the situation. Preferably both the parents
358

should be present while discussing about the decision for withdrawal


of intensive care.
• Decision to redirect care away from intensive care measures to
comfort measures must be accompanied by a discussion on how
intensive care will be withdrawn and involve the parents in the plan,
describing extubation and pain relief. Let them know that death will
not always occur immediately.
• A detailed plan must be documented and conveyed by the SR to the
staff and JR's managing the baby. Ventilation, TPN, monitoring or
pressor therapy should be withdrawn and "do not resuscitate" orders
should be passed.
• Baby must be provided warmth, pain relief, !VF or tube feeds and
oxygen. Cleaning routines should be maintained, and a kind and
gentle approach to the supportive care of the dying baby is
important.
• Allow parents to hold their infant for as long as they desire after
withdrawing intensive care.
• Autopsy should be discussed before or after death at the discretion of
the attending physician.
• It should always be remembered that such decisions are a great stress
to both the managing physicians as well as parents. A calm,
sympathetic approach is of utmost importance. The integrity as an
individual of the dying baby should never be disrupted in any
manner.

40.4 PROCEDURE AFTER DEATH: Shown in Figure 40. l


Death of a neonate is very significant event and it is absolutely necessary
to follow the specified procedure and necessary formalities should be
completed as soon as possible.
• Convey the information of death in a gentle and non-technical
manner.
• Parents should be offered that the hospital has the facility to dispose
the body if they so wish.
• Parents should be given an opportunity to see their baby after death.
The infant should be presented to the parents clothed or wrapped in a
dignified manner. Do not leave tubes and lines hanging or blood
stains without cleaning.
• Health care professionals should be aware that, in keeping with
certain religious practices or cultural beliefs, the parents might
decline to see the baby.
• Plan for a follow-up visit in the follow up clinic with the family at a
time when the autopsy report is available. The SR in-charge of the
Autopsy Meeting will be responsible for sending a covering letter
with summary and autopsy report to the parents. When greeting
359

them in the clinic for the first t', me after the death, express feelings
such as you are saddened and di> appointed.

40.5 ROLE OF THE RESIDENT DOCTOR


• To prepare the family gradually iJR and SR)
• To inform the family about the death (JR or SR)
• To prepare the death certificates (JR or SR). Cause of death has to be
discussed with SR before filling the death certificate.
• To fill up the autopsy request (JR or SR; but SR's countersign is
necessary).
• To write in the file, a note about events preceding death (both JR and
SR)
• Pathological samples should be taken wherever indicated, after
parental consent.
• Postmortem x-rays can be done in the radiology department if
required, after parental consent. The JR has to accompany for
postmortem x-ray.

40.6 ROLE OF THE STAFF NURSE


• To ensure that the body is sent to the mortuary along with 2 death
certificates within 60 min after death. The body must be sent only
after the decision to perfonn/not to perform an autopsy has been
taken. The body must be sent to the mortuary even if autopsy is not
to be done. Under no circumstances should the body be directly
handed over to the family in the newborn unit. The ward attendant
should take the body to mortual)
• To ensure that the hospital bill is cleared by the family.

40.7 DEATH CERTIFICATES


• There are 4 certificates: I original (filled in with a ballpoint pen) and
3 carbon copies.
• The original is given to the family only after dues have been cleared.
• Carbon copy no. I (also called 'file copy') is filed in the patient's
file.
• Carbon copy no. 2 (also called 'CRD copy') must be kept in the unit
under the custody of the sister-in-charge and it is sent to the central
records department (CRD) next morning along with daily census
report.
• Carbon copy no. 3 (also called 'mortuary copy') is made only if
autopsy has to be done. It is sent to mortuary with the statement
"Release body only after autopsy" written behind it.
• All three certificates should have respective label mentioned on the
top of the form.
360

40.8 PROCEDURE FOR AUTOPSY


• Counseling about autopsy should be done by the SR. 1f the family
refuses autopsy. a consultant must counsel the family. If the family
refuses to give consent for a complete autopsy, every effort must be
made to convince them about the need for a limited autopsy.
• Consent for autopsy should be taken in both the patient file and the
autopsy request form. In case the family docs not agree for autopsy,
a statement stating the refusal for autopsy should also be recorded in
the file and the head of the family/available family member should
sign it. For autopsy requisition use the neonatal autopsy form only.
Specifically take consent for shaving scalp hair as some families
may object to it on religious grounds.
• The autopsy requisition form should be sent to the mortuary with the
body. The resident in-charge autopsy should be contacted and
briefed about the case.
• If death occurs during the stay back duty hours, the detailed
information about the death should be given to the day duty JR and
SR by the stay back duty JR and SR respectively, the next day.
361

Figure 40.1: Procedure to be followed after death


Death

Dues cleared within 1 h Dues not cleared within I h

{'
No autopsy Autopsy to be done No autopsy Autopsy to be done

t i t t
• ~urse will send body to • Nurse wi II send body to • Nurse \Vil! send body to • Nurse \\'iii c>-.:n..! !;.,..!J ·~
mortuary with no certificate. mortuary with I carbon copy mortuary with no certificate. mortuary with carbon
• Will simultaneously give certificate with "Release body • Will give original certificate copy certificate with
original certificate to parents only atler autopsy" written to parents with "Dues cleared. "Release body only after
with "Dues cleared. Release behind. Relea'}e body" written behind autopsy'' written behind.
body" written behind. • Will give original certificate once dues is cleared. • Will give original certificate
• Parents will collect body from to parents with "Dues cleared. • Parents will collect body from to parents with "Dues
mortuary after showing Release body after autopsy" mortuary after showing cleared. Release body after
original certificate. written behind. original certificate. autopsy" written behind
• Parents will collect body from once dues are cleared.
mortuary after showing • Parents will collect body
original certificate after from mortuary after
autopsy is done. showing original certificate
after autopsy is done.
362

41. VISUAL AND AUDITORY MORBIDITIES

This chapter deals with problems other than ROP. For ROP see chapter
37.
41.1 VISUAL PROBLEMS:
41.1.1 Whom to screen?
• All preterm neonates, especially those who received therapy for
ROP (see section 37.5)
• Symptomatic neonatal hypoglycemia
• Any infant found to be neuro-developmentally abnormal (see section
43.4.3) or suspected to have abnormality of vision due to any cause
on follow-up.
41.1.2 What problems can occur?
• Significant refractory errors
o Hypermetropia of> +3 D (diopters) is regarded as significant.
o High myopia defined as <-3 D) and slight myopia as >--3 D and
<OD.
o Astigmatism of>! D and of>2 D regarded as "significant" and
"high", respectively.
o Anisometropia defined as the difference in the spherical
equivalent between the eyes of at least 1 diopter. "Moderate" is
defined as"> I D and <2 D" and "high" is defined as ">2 D".
• Strabismus
• Decreased visual acuity
• Cortical blindness
41.1.3 When to evaluate?
• <34 wks and/or <1750 g BW: at 6, 12, 24 & 36 mths of corrected
age and as per the abnormality thereafter.
• Late preterm babies (34-36 wks) should have at least one
ophthalmological examination including retinoscopy between 6-12
mths and one after 24 mths.

41.2 AUDITORY PROBLEMS


41.2.1 Whom to screen?'
• Family h/o hereditary childhood sensori-neural hearing loss
• In utero infection (see chapter 26)
• Craniofacial anomalies
• BW '.01500 g
• Hyperbilirubinemia requiring DVET (see section 20.10)
• Ototoxic medications (administered for more than 5 d or used in
combination with loop diuretics or other ototoxic medications)
• Bacterial meningitis
363

• Perinatal asphyxia with eviden, e of HIE (Apgar scores of 0-4 at 1


min or 0-6 at 5 min) (see sectiO'I 12.3)
• Mechanical ventilation 2:5 d
• IVH or PVL (see chapter 21 )
• Stigmata or other findings associated with a syndrome known to
include sensorineural and/ or conductive hearing loss
41.2.2 What problems can occur?
Hearing loss (2:45 dB)
41.23 When to screen?
Before discharge, 3 mths, 6 mths & thereafter as per the abnormality
found. Post discharge hearing screening is done in ENT OPD, Room no
441, level 4, New OPD. BERA examination at the neurophysiology unit
in APC 5A can also be done, and will require referral of the baby to the
Pediatric Neurology OPD for permission and counter-signature on the
form from a consultant.
41.2.4 What method to use as a screening tool?
• Screening BERA: this is done before discharge and/or 3 mths. A
click stimulus at a single intensity (generally 40 dB) is provided and
the auditory response is determined.
• Detailed frequency-specific BERA: this is done at 6 mths and
beyond.
• BOA can be used beyond 3-6 mths.
• Oto-acoustic emission (OAE) is currently not available in the unit.
41.2.SBERA
• There are 5 waves clearly visible in BERA. These (in sequence) are
attributed to the auditory nerve, cochlear nucleus, superior olive,
nucleus oflateral lemniscus and inferior colliculus respectively.
• Bilirubin encephalopathy is characterized by prolonged latencies and
inter-wave conduction times (wave 1, 1-111 and I-V); decreased
amplitudes (I, III and V). Normally, the latencies of the waves
decrease as gestation increases. There is an increase in amplitude
and decrease in threshold with increasing gestation. The normal
values of latencies in BERA from Indian babies are (at 75 decibels,
20 clicksis)' shown in Table 41.1:

Table 41.1: Latencies of waves I, III and Vin Indian neonates

Latency (msec) Birth 12 mths


Wave I 1.86 ± 0.11 1.64 ± 0.17
Wave Ill 5.11 ± 0.31 4.4 ± 0.27
WaveV 7.10 ± 0.3 6.15 ± 0.21
364

• Inter-wave conduction times (I-Ill, 111-V, I-V) can be estimated by


calculating the difference in the nonnal latencies of the respective
waves.
• If the infant fails BERA at 3 mths, it must be repeated at 6 mths.

41.3 CLASSIFICATION OF DEGREE OF HEARING LOSS:


Shown in Table 41.2
Table 41 2 Cl asst'Ii1cat1on ofd e2;ree ofh ear1n2 oss
Nonna! hearing 25 dBHL
Mild >25 dBHL <40 dBHL
Moderate >40 dBHL :S65 dBHL
Severe >65 dBHL :S95 dBHL
Profound >95 dBHL

41.4 PREVENTION:
• Ideally, as proposed by the US Environmental Protection Agency, a
noise level exceeding 45 dB must be avoided in the neonatal unit.
• Maintain silence. Avoid discussions at bedside.
• Give ototoxic drugs like aminoglycosides always by slow IV
infusion.
• Avoid combination of ototoxic medications like aminoglycosides
with Vancomycin and loop diuretics as they have synergistic
ototoxic effects.
• No tapping or writing on the tops of incubators and hoods.
• Careful closing of incubator doors
• Set desired and individualized alarm limits.
• Careful maintenance of equipments to avoid false alanns.

REFERENCES:
I. AAP, Joint Committee on Infant Hearing. Pediatrics. 2007;120:898.
2. Deorari AK et al. Ind Pediatr. ! 989;26:981-6
365

42. FOLLOW-UP

Appropriate follow up is an integral ! >art of neonatal intensive care.

42.1 NFC
• All discharges for which NFC follow up is required are to be entered
in a diary, which is kept in the NICU office. JR's must ring up the
Newborn Unit office to get an appointment date for the Wednesday
NFC. At the time of discharge the JR must consult the SR and write
"To make NFC file" on top of the discharge booklet if a file has to
be made during follow up. The JR must ask the parents to bring
along a photocopy of the discharge summary during the first follow-
up visit.
• NFC's are held on Wednesday and Friday from 2 pm to 4.30 pm in
the Pediatrics OPD, level 3, D Block, APC.
• Wednesday NFC is meant for routine follow up, nutrition and
growth monitoring of high-risk babies. Friday NFC is meant for
detailed evaluation of babies with neurodevelopment abnormalities
detected during follow up and also for high risk babies at 36 wks and
40 wks postmenstrual age for neurological assessment; and at 3, 6, 9
and 12 mth corrected age for neurological and development
evaluation. Babies should be called strictly on prior appointment on
both days. Appointments will be given by SR-in-charge of NFC
(Room no. 3413, APC). For the next appointment, ring up the SR-in-
charge on his/her PGJ mobile. Just mention approximately when the
next appointment is required- e.g. "after 2 mths". The SR-in-charge
will provide the date and will make an entry in the appointment
diary. The SR-in-charge is also responsible for allocating patients to
various doctors in the NFC. Given these additional administrative
responsibilities, the SR-in-charge must allocate fewer patients to
himself/herself.
• Parents who are unable to come on the scheduled date have to ring
the Newborn Unit office (0172-2755318) to get a fresh date.

42.2 WHO TO FOLLOW UP


42.2.1 Long Term Follow up
High risk group (includes but not limited to)
o Babies <1800 g BW
o <33 wks
o Asphyxiated babies with HIE or seizures
o Neonatal jaundice needing DVET
o All ventilated babies
o Babies with sepsis/meningitis/NEC
o BPD
366

0 Symptomatic hypoglycemia or polycythemia


0 Major malformations
0 SFD<2 SD
42.2.2 Short term Follow up
• Babies with birth wt > 1800 g, gestation >34 wks and others
requiring short term follow up should be called in the morning
OPD's on Wednesday or Friday for neonatology consultation.
• Uncomplicated term and near term babies should be followed up by
local pediatrician or in the Pediatric OPD (any day, at 6 wks) or
postnatal clinic at 6 wks. Postnatal clinic is held on Wednesdays at 9
am in New OPD Block (Gynecology OPD, level 2, room no 2036).
See section 20.5 for follow-up of jaundice in neonates discharged
early.
• At the time of discharge. the JR must consult the SR and then
mention clearly in the discharge booklet where the baby has to be
followed up. Note: Some babies may need specific follow up as per
the research protocol and should be called after discussing with the
investigator.

42.3 FOLLOW UP SCHEDULE


• Babies should be followed up weekly until they reach the Wt of 2
kg. Those coming from far off places may be called fortnightly.
• Monitor fortnightly between 2-3 kg Wt.
• If normal until 3 kg Wt, the babies are called at 3, 6, 9 and 12 mths
corrected age on Friday by appointment for Denver-II/Neurological
examination.

42.4 RESPONSIBILITIES OF RESIDENTS DURING FOLLOW


UP CLINICS
• All SR's (except NICU and labor room SR) must attend both NFC
clinics. The consultant should be informed if any SR is busy and
unable to come. All JR's should also attend both NFC clinics, except
one JR posted in NICU, one posted in the intensive area ofNNN and
one in labor room.
• Everyone is supposed to carry the Denver-II kit to the NFC clinic
(available with NJCU Store-keeper, on payment of~ 300 to the New
Heart Trust)
• On first visit read the discharge summary carefully and complete the
NFC file. Attach a photocopy of the discharge summary in NFC file.
• On each visit the following parameters are entered in NFC file: Date,
chronological and corrected age, Wt with gain/loss, OFC with gain
(cm/wk), feeding methods and nature of feed, supplements and full
signature (with legible name)
367

• Plot Wt and OFC at all visits ac, ording to corrected age in the charts
provided.
• Important issues during folio" -up are feeding issues (chapter 9),
weaning, vitamin and mineral s11pplementation, Wt gain, OFC gain,
neurological problems (chapter 43), development, hearing deficits
(chapter 41), visual deficits, ROP (chapter 37), OOP (chapter 38),
hyponatremia of prematurity, anemia of prematurity (chapter 17).
• Sampling for PCV is done in room no. 2406.
• For getting appointments for BERA & EEG send to APC-5A. For
CT and MRI send to Radiology reception.
• Discourage visits without appointment.
42.4.1 Specific responsibilities during Friday NFC
• Do complete neurological and developmental evaluation as per pro
forma in the file (see sections 43.1, 43.2)
• Physiotherapy, occupational therapy and play therapy services are
available in APC ground floor, room no 2416
• Consider referral to PRAYAS. Parents should be counseled
regarding simultaneous follow up in NFC.

42.5 DURATION OF FOLLOW UP


All high-risk babies (as listed above) should be followed up until 18 mths
of age and if normal can be discharged ftom NFC after consultation with
consultant and followed up in general Pediatrics OPD.

42.6 SCHEDULE OF SPECIAL CLINICS OF RELEVANCE TO


NEONATOLOGY: Shown in Table 42.1

Table 42.1 Schedule of special clinics

Name of the clinic Davis> Time Site


PCC Thur 2.00 pm ACC, IC
Genetic clinic --do-· 2.00 pm APC-4D
NDC Mon, Thur 9.00 am APC-3D
Growth clinic Wed 2.00om APC-4D
PGC Wed, Sat 9.00 am APC-4D
PEC Wed 2.00 pm APC-4D
NDC Thur 2.00 om APC-3D
PIC-H clinic Fri 9.00 am APC-4D
Nutrition clinic Sat 9.00 am APC-4D
Child psycholoav Mon, Wed, Fri 9.00 am APC-2D
Retina clinic Wed, Fri 9.00 am AEC/level 2, 229
Speech & hearin~ unit Daih 9.00 am New OPD, level 4
Ped Surgery Dail} 9.00 am APC-5D
368

Name of the clinic Day(sl Time Site


Ped Ortho Clinic Wed, Sat 9.00 am APC-50
Allernv & Immunology Tue 2.00 om APC-30
PRC Tue 9.00am APC-40
PHC Tue 9.00 am APC-40
Pulmonology clinic Fri 9.00 am APC-40
POC Fri 9.00 am APC-40
ACC= Advanced cardrnc centre, NOC= neuro-development chmc, PEC=
Pediatric endocrinology clinic, PGC= Pediatric Gastroenterology Clinic,
PHC= Pediatric hematology clinic, PIC-H= Pediatric immunodeficiency
diseases and HIV clinic, POC= Pediatric oncology clinic, PRC= Pediatric
rheumatology clinic,
369

43. DEVELOPMENTAL DEL<\Y AND CEREBRAL PALSY

Subjects who satisfy the criteria for high-risk follow up (see chapter 42)
are all candidates for neurodevelopnjental assessment.

43.1 NEUROLOGICAL EXAMINATION (by Amiel-Tison


method)'"
• The detailed chart is available in the NFC file.
• The 7 components includes:
o Craniofacial exam
o Neuro-sensory exam
o Neurobehavioral assessment
o Passive tone
o Active tone
o Postural reaction
o Automatic movements & primitive reflexes.
• In each of the 7 components, a score of 'O • indicates the typical
result for that age within the normal range. Scores of 'I' and '2'
respectively indicate moderately and definitely abnormal result for
that age.
• The final interpretation is reported as normal/minor deficit, moderate
deficit and severe deficit.

43.2 DEVELOPMENTAL ASSESSMENT TOOLS


• Denver II • Griffith's scale
• PEDS • BSID 1-11
• Developmental profile (DP) III • ASQ
• VSMS • DASII
ASQ= Affective social quotient, DASII= Developmental Assessment Scale for Indian
Infants, PEDS= Parents' evaluation of developmental status, VSMS= Vineland social
maturity scale

Select the test according to what aspect of development needs to be


tested (based on the history and age of the child). For developmental
assessment, take an appointment from Dr. Prabhjot Malhi (APC 2D,
room no. 2414) during 9-11 am.
370

43.2.l Characteristics of common developmental tests: Shown in


Table 43.1

Table 43.l Characteristics of common develoomental tests


Time taken
Name Age range Domains
(min\

Denver-II 0-6 yr -do- 35

DP-Ill 0-12 yr -do- 40

CAT/CLAMS 0-3 yr Visual-motor, Language 20

ELM 0-3 yr Language 15

BSID 0-42m Mental, motor, behavioral 30-60


BSID- Bayley Scale of Infant Development, CAT/CLAMS- Cognitive Adaptive
Test/Clinical Linguistic and Auditory Milestone Scale, ELM= Early language milestone

43.2.2 Denver-II
There are 4 sectors- personal-social, fine motor-adaptive, language, and
gross motor. Testing begins with items that fall completely to the left of
the child's age line and continues to the more difficult tasks to the right,
irrespective of the age of the child. At least three items in each sector to
the left of the child's age line should be tested. All items intersected by
the age line should also be administered. Testing continues with items to
the right until three failures are obtained in each sector. The child may be
given up to three trials to perform each item. Items are scored as "pass,"
"fail," "no opportunity," or "refusal." The four "test behavior" ratings are
scored after the completion of the test. The test behaviors rated are
compliance, interest in surroundings, fearfulness, and attention span.
Denver II determines child's relative "advances" and "delays" in
development. A child who passes one or more items that have
distribution bars to the right of his/her age line is relatively advanced on
that item. Scoring a "pass," "fail," or "refuse" on items having the age
line intersect between the 25th and 75th percentile is considered to be
well within the normal range. Failing or refusing items having the age
line intersect the bar between the 75th and 90th percentile is cause for
concern and is classified "caution." A child failing one or more items that
have distribution bars to the left of the age line is relatively slow in that
area of development. The more items a child fails that are totally to the
let1 of the child's age line, the greater the likelihood that the child is slow
in development.
43.2.3 Assessment of passive tone on follow-up
371

The normal ranges of angles used in the assessment of passive tone are
shown in Table 43.2

Table 43.2 Passive tone at various al!es in infancv


12
Sign 36 wks 40wks 3 mths 6mths 9 mths
mths
Popliteal 110- 150-
100 <90 80-100 90-120
angle 160 170
120- 140-
Heel to ear 100 <90 80-100 90-130
150 170
Adductor 100- 130-
40-80 40-70 40-80 70-110
angle 140 150
0-10
Dorsiflexion
20-30 (preterm 60-70 60-70 60-70 60-70
of foot
40)
Elbow Does Does
Slightly
slightly not not Passes Passes
Scarf sign passes
passes reach reach midline midline
midline
midline midline midline

43.3 COMMON TERMINOLOGY


43.3.1 Developmental delay
It is frequently used to identify children with delay in meeting
developmental milestones in one or more streams of development.
Developmental delay is best viewed as a chief complaint rather than a
diagnosis.
43.3.2 Global developmental delay
It is defined as significant delay in two or more developmental domains:
gross motor, fine motor, cognition, speech/language, personal/social, or
activities of daily living skills. Significant delay is defined as
performance 2 or more SD below the mean on developmental screening
or assessment tests. The term global developmental delay is usually
reserved for younger children (< 5 yrs of age), whereas MR is usually
applied to older children when IQ testing is more valid and reliable.
The term motor delay implies delay in the motor sector prominently and
it can be due to CP, neuromuscular disorders and progressive,
degenerative brain disorders
43.3.3 CP
CP is a disorder of movement and posture and is defined as a group of
non-progressive, but often changing, motor impairment syndromes
secondat'y to lesions or anomalies of the brain arising in the early stages
of its development.
372

43.4 CP
43.4.t Classification
Two major categories are spastic (pyramidal) and extrapyramidal. The
spastic group is further subdivided based on the pattern of body
involvement: quadriplegic, diplegic, and hemiplegic. The subdivisions of
extrapyramidal group are based on the type of movement disorder which
predominates: rigidity, dystonia, choreoathetosis and ataxia. Around IOo/o
are classified as mixed, displaying prominent spastic and extrapyramidal
features.
The critical feature characterizing spasticity is velocity dependent
increase of tone. The faster the attempt to passively move the joint, the
greater the resistance. Rigidity is characterized by consistent increased
tone unrelated to speed of movement or joint position.
43.4.2 Diagnosis of CP
• The diagnosis of CP is made largely through clinical observations.
The major signs that collectively suggest a diagnosis of CP are
delayed motor milestones, abnormal neurologic examination,
persistence of primitive reflexes, and abnormal postural reactions. It
is important to remember that although no single abnormal physical
sign is diagnostic, clusters of symptoms or evolving abnormal
movement patterns may be indications of CP.
• When calculating any developmental quotient in the first 24 mths of
age, correction up to 40 wks should be given for prematurity. A
motor quotient of :S70 is classified as motor delay.
• Significant in the neurologic examination are abnormali6es in
muscle tone, weakness, brisk deep tendon reflexes, clonus persisting
beyond 12 mths of age, and asymmetries in muscle tone or
functional abillties.
• The persistent of primitive reflexes is often the earliest clue to the
diagnosis of CP. Primitive reflexes should gradually disappear over
the first 6 mths. Prominent fisting, obligate positive support reflex,
and obligate asymmetric tonic neck reflex are suggestive of spastic
CP. Prominent Moro and tonic labyrinthine reflexes, especially
when they persist past 6 mths, are early markers for extrapyramidal
forms.
• Failure to develop protective reflexes such as the parachute response
also may be seen.
• Serial examinations are important to monitor progress when there is
suspicion ofCP. The diagnosis Often is easier if there is known brain
damage documented by cranial USG, CT scan, or MRI.
373

43.4.3 Evaluation of the child with CP: Shown in Figure 43.1


Figure 43.l Evaluation of the child with CP
History and examinatior findings suggest diagnosis ofCP
(Non-progressive disorder of motor control)

1.
i
Confirm that the history and examination does not suggest a progressive or
degenerative CNS disorder
2. Classify the type ofCP (quadriplegia, ataxic, etc)
3. Screen for associated conditions including:
a. MR (52o/o)
b. Ophthalmologic (28o/o)/hcaring impairments (12%)
c. Speech and language delay (38o/o)
d. Epilepsy (45°/o), obtain EEG ifh/o suspected seizure
e. Feeding/swallowing dysfunction

Did the child have previous neuroimaging or other laboratory studies?


(e.g. in neonatal period) that determined the etiology ofCP?

1~ l~
No need for further Obtain neuroimaging study
diagnostic testing (MRI preferred over CT)

!
Nonual MRI

Consider metabolic or genetic testing if


upon follow up the child has:
lAbnonnal
MRI

I. Determine ifneuroimaging
abnonualities in combination with
A. Evidence of deterioration or evidence history and examination establishes a
of metabolic decompensation specific etiology of CP
B. No etiology detenuined by medical 2. If developmental malformation is
evaluation present, consider genetic evaluation.
C. Family hlo childhood neurologic 3. If previous stroke, consider evaluation
disorder associated with CP for coagulopathy or other etiology

43.4.4 Management aspects of CP


The goals for management of the child with CP include the following: to
promote optimal function; to maintain general health; to foster
acquisition of new skills; to assist and educate parents and caregivers;
and to anticipate, prevent, and treat the complications of this disorder.
Spacticity
Physical therapy and occupational therapy are the cornerstones of
treatment
Provided by physiotherapists in PG! (Room No. 2416, APC 20. daily 9
am) as well as in Prayas.
• Daily range of motion/stretching exercise
374

• Positioning techniques
• Use of splints to maintain stretch/position properly. Contact
physiotherapy.
• Oral medications (Diazepam, Baclofen and others) (see section D41)
o Improvement in mobility and reduction of spasm related pain
o Results in drooling or drowsiness but may improve fine motor
skills
• Botulin um toxin (contact Prof. Dr. Prabhakar, the Head, Dept of
Neurology)
o Muscle relaxation by blocking the release of acetylcholine
esterase
o Decreases focal muscle spasticity, increasing mobility or motor
function without the systemic effects of oral muscle relaxants
o Remember: effects lasts from 2 to 6 mths only
o Physical therapy, serial casting, or use of splints can maximize
the benefits of Botulinum toxin
o Botulinum toxin can be used in children > 1 yr age with spastic
CP
o Requires repeated treatments. May result in muscle weakness.
• Baclofen pump (contact Dr. Prabhakar, Neurology; pump available
with Medtronics company, cost - ~ 2,50,000)
o Baclofen delivered into the spinal cord via a pump implanted
surgically
o Less medication is required which results in fewer adverse
effects
o Risk for infection and mechanical failure
• Surgery options
Selective dorsal rhizotomy permanently decreases spasticity. Dorsal
or sensory nerve roots of the lumbar spinal cord are cut with the
reduction in spasticity often leading to improved motor function. For
children without potential for ambulation, this treatment option may
facilitate ease of care and decrease the risk of contractures. Long-
term benefits versus risks of surgery need to be considered for each
patient. Procedure is done in PGIMER, AIIMS, and NIMHANS-
more often in the latter two institutions.

43.4.5 Other problems in spastic children: Shown in Table 43.3


375

Table 43.3 Problems in spastic children and their management

Possible
Problems Management
mechanisms
• Poor oral motor • Accurate Wt, Ht, OFC,
skills skin fold thickness
• ineffective measurement at each visit
swallowing • Determine the possible
patterns mechanism in each case
• pain due to • Calculate intake (protein,
esophagi tis Calories)
(Gastro- • Calorie dense food
esophageal reflux • Gastrostomy tube feeding
disease (GERD) in difficult cases
• dental issues
Malnutrition &
Inadequate • chronic
constipation
growth
• lack of
independence in
feeding
• need for extra
Calories
(spasticity or
choreoathetoid
movements)
• inability to
request food or to
indicate hunger
• Inability of • Nursing care
Pressure sores
posture change • Proper fitting splints
Friction
• Tight feting • Gloves
erosions
splints/casts
Thickening of
skin • Commando
crawling
Nystagmus, Yearly eye examination by
strabismus, a pediatric ophthalmologist
Visual refractory errors,
abnormality hemianopsia,
dyskinetic eye
movements
Hearing • Sensorineural • Audiological evaluation
problems hearing loss • Adenoidectomy
Sleep apnea • Large tonsils, • Check tvmoanic
376

Possible
Problems Management
mechanisms
Otitis media adenoids membrane at each visit
• Inability to tell
about ear pain
• Increased • Oro-motor therapy to
secretion of saliva close lips & swallow
• Poor lip closure effectively (done in PG!
• Inadequate jaw physiotherapy and Prayas)
Drooling
closure • Glycopyrrolate (currently
• Postural problems not available in India)
• Scopolamine patch (not
yet available in India)
Dental evaluation
(Pedodentistry, room no
202, 1" floor, Dept of oral
Dental caries Poor oral hygiene
health sciences, Monday,
Wednesday and Saturday 9
am)
Recurrent Ineffective cough, • Thickening of feed
pneumonia weak respiratory • Maneuvers (chin tuck)
Chronic muscles, recurrent • Pneumococcal/influenza
bronchitis aspiration, spasticity vaccines
asthma of chest wall
Motility Slow gastric • Erythromycin
problems emptying • Formula with fibers
Constipation
Voiding Timed toileting
dysfunction
Scoliosis Splints & braces
Progressive hip
adduction and
Orthopaedic consultation
flexion leading to
Hip disorders (contact Dr. P. Sudesh,
deformity of
Wed, APC SD, 9 am)
femoral head,
dislocation
Osteoporosis No Wt bearing Phvsiotherapy, walking
Anti-convulsants
Epilepsy
Sedatives: Melatonin,
Sleep problems
clonidine, diphenhvdramine
Behavior/ Consult Dr P Malhi (APC
emotional 2D, room no. 2414)
problems
377

REFERENCES
1. Amiel-Tison C, Gosselin J. Neurological development from birth to
six years- guide for examination and evaluation. The John Hopkins
University press, London.
2. Amie!-Tison C. Curr Prob! Pediatr 1976; 7: 1.
378

44. PAIN

Both preterm and term neonates experience pain. Repeated exposure to


pain and stress during neonatal period affects later perception of painful
stimuli during childhood and neurodevelopment.

44.l MANIFESTATIONS OF PAIN


Manifestations can be either autonomic, behavioral or biochemical.
Autonomic/physiologic changes Behavioral changes
Tachycardia or bradycardia Facial grimacing
i RR or apnea Crying
Hypertension Excessive body movements
Desaturation Fussiness
tHR variability Sleeplessness
Palmar sweating
Skin color changes

44.2 RECOMMENDED TOOLS FOR ASSESSMENT OF PAIN


• Assessment of prolonged pain & degree of sedation: For babies on
ventilation and for those having chronic pain use N-PASS (Neonatal
Pain Agitation and Sedation Scale) (Table 44.1). This should be
scored once at the end of each nursing shift. Monitor trends.
• For procedural pain, routine use of a pain assessment tool is not
required.

Table 44.l: N-PASS for assessment of prolonged pain

Assessment Sedation Normal Pain/ A2itation


Criterion -2 -1 0 I 2
Crying No cry with Moans or Little Irritable or High pitched
Irritability painful cries crying crying at or silent
stimuli Briefly with Not intervals continuous
painful irritable Consolable cry.
stimuli Inconsolable.
Behavior No arousal to Arouses Appropriate Restless Constantly
State any stimuli. minimally for GA sleep. awake or
No to stimuli. Awakens arouses
spontaneous Little frequently minimally.
movement spontaneous
\movement.
~acial Mouth is lax Minimal Relaxed Any pain Any pain
Expression No expression expression expression
expression !with stimuli intermittent continual
Extremities No grasp Weak eraso Relaxed Intermittent Continual
379

Assessment Sedation Normal Pain/ A2itation


Criterion 2 ~i 0 1 2
fone eflex. ~eflex. hands & clenched clenched
Flaccid tone. Decreased feet. .oes/fists or oes/fists or
~one. Normal finger finger splay.
tone. splay. Body is
Body is not ense.
ense.
Vital signs No variability I< 10% Within ncrease Increase>
HR, RR, with stimuli. wariability baseline or 10-20% 120% from
BP, Sao, Hypoventilati ~ith stimuli normal for from baseline,
change on or apnea from GA Jase line, Sa0 2
with baseline Sao, decrease to <
stimulation decrease to 75 % with
76-85% stimulation,
with slow rise.
stimulation,
~uick rise 'I
Note: To the above score, add +3 if< 28 wks corrected age, add +2 1f
28-31 wks corrected age, add+ I if32-35 wks corrected age

Interpretation: -10 to -5: Deep sedation, -4 to -2: Light sedation, 24-4:


requires intervention for pain

44.3 PAINFUL PROCEDURES IN NEONATES: Shown in Table


44.2
Table 44.2 Painful procedures in ntonates

Mild painful Moderate Severe pain Chronic pain


Drocedures 'ainful procedures
Heel prick ~P Surgeries IVentilation
V enepuncture Elective intubation NEC
Arterial ET suction Meningitis
puncture !CD insertion
SC/IM ROP screening
injection Ventricular tap
l!mbilical PICC lines
catheterization Suprapubic urinary tap
Adhesive tape
removal
380

44.4 MEASURES TO ALLEVIATE PAIN:


• Co-opt non-pharmacological measures during procedures that cause
pain.
• Use non-pharmacologic measures before using pharmacological
interventions whenever feasible.
44.4.1 Non-pharmacological:
• Breast feeding during the procedure
• Kangaroo mother care: Start 15 min. prior to the procedure, continue
during the procedure and recovery phase.
• Non-nutritive sucking: On empty breast (or) gloved finger
• Facilitated tucking: Holding the arms & legs in a flexed position.
• Swaddling: wrapping the neonate in a warm sheet or blanket.
• Individualized developmental care:
o Nest and position the extremities in midline
o Respect circadian rhythms by darkening the room
o Cluster the nursing care activities and sampling to avoid
repeated interruption of sleep
o Reduce the light/noise by covering the incubator canopy,
reducing the volume of alarms and avoiding loud bedside
discussions
44.4.2 Pharmacological:
Oral glucose: Use 25% glucose as it readily available and sterile.
Administer 2 min before the procedure. Put on anterior portion of tongue
with a sterile syringe (or) drop on a sterile gloved finger and place in
mouth. Dose can be repeated after 5-10 min. Do not give> 4 doses/d if
the gestation is '.'.30 wks, because of concern of NEC. Dose for
• Infants requiring intensive care, not on full feeds: 0.5 mL
• Premature neonates (32 to 36 wks) on full oral feeds: I mL
• Term neonates: 2 mL
Oral sucrose: 12-24% can be used. Most effective is 24% solution. Dose
is as mentioned for glucose. Difficulties in obtaining sterile sucrose
preclude its use in the unit currently.
Oral Paracetamol:
• 28-32 wks gestation: 10 mg/kg single dose. Max. dose: 20 mg/kg/d.
• >32 wks: 10-15 mg/kg single dose. Then 10-15 mg/kg q 6-8 h if
necessary.
lignocaine: This is used as a local anesthetic prior to invasive
procedures e.g. insertion of chest drains. Dose: up to 3 mg/kg SC inj.
Prilox cream: This is a eutectic mixture of 2.5o/o lidocaine & 2.5%
prilocaine (substitute of EMLA).
• Dose is I g/I 0 cm' area (approx. 3x3 cm). This should be applied
over the skin 60 min prior the procedure and should be removed
within 2 h of application.
381

• In neonates with :S32 wl s of gestation it may cause


methemoglobinemia and hence lo not use more than once/din them.
It should not be used ifthe bab) is on iNO.
Opioid analgesics (Morphine & Fmtanyl): Fentanyl is faster acting,
shorter-lasting, less hypotensive, more prone to chest rigidity and
dependence than morphine.
• Morphine: bolus 0.1 mg/kg followed by 5-20 µg/kg/h in preterm and
10-20 µg/kg/b in term infants.
• Fentanyl: bolus 2 µg/kg over 2 min followed by 1 µg/kg/b. Do not
infuse bolus fentanyl more rapidly than 1 µg/kg/min, as it increases
the chances of chest wall rigidity.
Weaning off opioids: Gradual weaning recommended when used for >3
d.
• < 1 wk : Reduce by 20% every 6 h
• > 1 wk : reduce by 20% every 12 h
Midazolam, lorazepam; These sedative agents should not be used in the
NICU for sedation. Midazolam infusion has shown to increase the
incidence of lVH, PVL and duration of NICU stay according to a meta-
analysis.

44.5 MEASURES TO BE IMPLEMENTED FOR SPECIFIC


SITUATIONS
44.5.1 Ventilated neonates:
• The routine use of opioids in ventilated neonates is not
recommended. This is because use of opioids in ventilated neonates
reduces the pain scores, but there is no effect on mortality, duration
of ventilation, lVH, PVL and long term neurological outcomes. 1
• Before considering opioids, objectively assess pain using N-PASS.
First institute non-pharmacological measures (swaddling, facilitated
tucking and developmental supportive care).
• Use opioids in the following situations: (i) the score is ;>4 despite
non-pharmacological measures, and there is no other reversible
cause of pain, (ii) PPHN (iii) invasive ventilation on high pressures
(in SIMV PIP>22 & in HFV MAP >12) (iv) if there is asynchrony
with ventilator2 • If indicated, give continuous infusion rather than
intermittent doses.
• Use with caution in neonates of ::;28 wks gestation as opioids
increase the risk of hypotension.
44.5,2 Postoperative pain: Use N-PASS for objective assessment of
pain. Use non-pharmacological measures in all cases. Use opioids
infusion if the score is ;>4. (Note: Though N-PASS has not been
validated for post-operative pain, this has been proposed for the ease of
the staff in the unit as most of the components are similar with PIPP, a
scale validated for post-operative pain).
382

44.6 RECOMMENDED INTERVENTIONS FOR PROCEDURAL


PAIN'·'' Shown in Table 44.3

Table 44.3 Recommended interventions for procedural pain

Procedure Mana!!ement
Heel lance •Consider use ofvenepuncture, ifftequent
sampling is not anticipated.
•Breast feeding and/or KMC, swaddling, do
not squeeze
•Oral olucose
V enepuncture •Breast feeding and/or KMC, swaddling,
facilitated tucking
•Oral glucose
•If sampling is not urgent, apply Prilox
cream 60 min. before venepuncture
Arterial puncture & arterial •Facilitated tucking, swaddling
line •Oral olucose
IM/SC injection •Preferably avoid IM/SC injection, use IV
route
•Breast feeding
•Oral olucose
PICC line •Swaddling, facilitated tucking
•Oral glucose
• Prilox cream 60 min. before the nrocedure
Nonemergent intubation •Atropine 20 µg/kg over I min+ fentanyl 2
(Excluding INSURE) "o/k" over 2 min.
LP •Oral glucose
•Prilox cream at the site 60 min. before the
nrocedure
Chest tube •SC lignocaine 0.3 mL/kg of 1% solution+
IV morphine 0.1 mg/kg
•Oral paracetamol 6-8 hourly while the tube
is in situ
!umbilical catheter •Facilitated tucking. Avoid sutures or
hemostat clamps on the skin around the
umbilicus
•Oral !!]ucose
ET suction •Swaddling, facilitated tucking
Suprapubic urinary tap •Oral glucose
• Prilox cream at the site 60 min. before the
orocedure
383

Procedure IM anae•ment
Adhesive tape removal •We the edges with NS swab and keep
wettmg the taoe while removing
ROP screening •Facilitated tucking, swaddling
•Screen l -2 h post feed
•Oral glucose
LASER for ROP •KMC, Facilitated tucking, swaddling
before the procedure
•Local anesthetic drops (0.5% Proparacaine
eye drops- I drop administered once about I
min before the orocedure)
In intubated & sick neonates: depend more on individualized developmental
care, reduce light & noise and use momhine boluses selectivelv.

REFERENCES:
1. Ng E. Intravenous midazolam infusion for sedation of infants in the
neonatal intensive care unit. Cochrane review 2003: CD002052.
2. Bellu R. Opioids for neonates receiving mechanical ventilation.
ADC F&N 2009; doi: 10.1136/adc.2008.150318
3. Menon G. How should we manage pain in ventilated neonates?
Neonatology 2008;93:316.
4. Lago P. Guidelines for procedural pain in the newborn. Acta Pediatr
2009;98:932.
5. AAP policy statement. Prevention and management of pain in the
neonate: An update. Pediatrics 2006;118:2231
384

45. FIRE AND OTHER EMERGENCIES

45.t FIRE
45.1.1 Information regarding fire
• In case of fire, immediately give infonnation to fire control room
(6101, 6110, 85-8905, 85-9101). Also, give infonnation to the
central complaint office ( 6341 ), nearby security guard, security
control room (6100), and to electricity department (6343, 85-9343).
Give exact location of fire and identify yourself.
• Also, infonn the PG! central oxygen plant (5889), central air
conditioning (AC) plant (5867), in-charge AC manifold room 85-
8887. In case of major fire inform main fire station, sector 17 (tel no
IOI, 2702333) or fire brigade sector 11 (no 2747820) or chief fire
officer (2703236).
45. 1.2 Switching off electricity
• In case of electrical fire, immediately switch off the main switch
(panel) that supplies that area. In case of any type of fire in any area,
remember to switch off all electrical appliances in the area.
• SEE MAP OF PGIMER NEWBORN UNIT AND FAMILIARIZE
YOURSELF BEFOREHAND WITH ALL THE MAIN SWITCHES
(figure 45.1 ). Take a walk around the unit and see the locations.
o The UPS is designated "A". Panels from B through E are
located in the NICU complex and panels from F through L are
located in the NNN complex. See Table 45. I for panels to be
switched off according to area of fire.

Table 45.t Electric panels (i.e. main switches) to be switched off


according to the area of fire (areas listed alphabetically)

Area Of Fire Switch off these panels


BERA room H
Comouter room c
Faculty offices c
KMCroom c
KMC staff room c
Lab G
Mothers' Room F
NICU -A SIDE UPS, Bl, B2, E
NICU -B SIDE UPS, B2, DI, D2, E
NICU nurses' room DI, D2
NICU sister-in-charge room DI, D2
NICU SR duty room F
NICU store room F
385

Area Of Fire Switch off these panels


NICU store-keeper's room c
NNN-1 1
NNNlCU B2,K
NNN isolation L
NNN nurses' room H
NNN SR's duty room H
NNN store K,J
NNN-2 J
NSR (Seminar Room) H
Phototherapy room H
Servants' room L
Sluice Room L
Unit Head (Dr Praveen)'s room D!,BI
USG room F

• In case the panels themselves catch fire, switch off the controlling
panels as shown in Table 45.2

Table 45.2 Electric panels to be switched off according to the panel


that catches fire
Panel that
Switch off these panels
catches fire
UPS Call for help as per section 45.1.l
Panel opposite Endoscopy Room, GE block, Ground
Bl
floor, Nehru Hospital
B2 Panel in CLR-OT area (near bathroom)
c Bl
DI Bl, B2 and UPS
D2 Bl, B2 and UPS
E Bl, B2 and UPS
F G
Panel near Lab No. 7, near Dr SV Rana's office, GE
G
block, Ground floor, Nehru Hospital
Panel near Dr Kochhar's office, GE block, Ground
H
floor, Nehru Hospital
1 G
Panel near Dr Kochhar's office, GE block, Ground
J
floor, Nehru Hospital
B2 and Panel near Dr Kochhar's office, GE block,
K
Ground floor, Nehru Hospital
Panel near Dr Kochhar's office, GE block, Ground
L
floor, Nehru Hospit1l
386

Figure 45.1 Map of PGIMER Newborn Unit

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_,_
:rl!JJO~J _,_,
.
-.a1t1111S
~-
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~

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~....,.il:XN
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~-
~~
t
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gu
.! ~ ~
~ H j
•:\•
rl ffi

:!!"'~..
<
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o:
.. 0

z.~
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"ii: """""' ........ • •
~

.
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11~ •• •• ............... •
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~ ~
IE •
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~ I l!
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~NNN

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~

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l
!
!
'~ ~
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--
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• <
387

45.1.3 Fire extinguishers


• Try to control the fire with fir' extinguishers. In the NlCU, the
extinguisher is located to the left of the entrance near the wash area;
and in the nursery, it is located in the corridor near the NSR
entrance. They contain carbon dt0xide for extinguishing fire. They
are periodically checked by fire control staff. For ordinary fires use
water or C0 2 fire extinguishers, for electrical fires use C0 2 fire
extinguishers or sand bags, for fires of inflanunable liquids use foam
type fire extinguishers but never use water.
• If you cannot control the fire, trv to isolate the area by closing the
doors & windows. Do not lock doors.
• Do not use elevator in case of fire.
• If smoke is present in the ward or room, open all windows and doors
if possible or break the window /door.
45.1.4 Fire escape routes
• The nearest fire escape doors are marked.
• Fire escape route should be used for evacuation of patients and
attendants. There are 3 fire escape routes from the unit:
o Staircase to GE ward
o Corridor to maternity ward
o Fire escape staircase located at the far end of NNN (beyond
isolation room). Keys to the lock of the door to this staircase are
located in a glass-covered box on the wall of the corridor. Break
the glass to get the key.
• From the NICU, one may escape either through the front door or
through the NICU SR Duty Room or through the USG Room into
the NSR.
• From the NSR, one may escape either through the front door
towards maternity ward or through the USG Room to NlCU and
thence to the staircase leading to the GE ward.
45.1.5 Steps of evacuation
• Use wet cloth to cover your nose and mouth in presence of smoke.
Go along the wall but avoid touching any electric wire. Use wet
sheet or blanket for pushing hot or burning obstacles from your path.
• If there is lot of smoke one can crawl as near floor as exposure to hot
gases is less.
• All inflammable material like oxygen cylinders and spirit should be
segregated from the place of fire.
• Evacuation of babies: Stable babies should be shifted by staff nurse
after properly wrapping them to nearest possible safe area/ward
where the temperature is best suitable for the baby and oxygen is
available. Ventilated babies have to be shifted on resuscitation bag
along with resident and staff nurse after wrapping them properly. If
suction is necessary, rubber mucus sucker can be used. Resuscitation
388

medications with syringes should also be taken along. Parents


should be informed regarding the incident & shifting of the babies
only after they are transferred to safe area. SRs, JRs and nursing
staff from safer areas should help in evacuation of patients from the
area of fire. Potential areas for shifting are maternity ward and
Gastroenterology ward. Shift first and take permissions later.

45.2 IF THERE IS POTENTIALLY EXPLOSIVE ARTICLE IN


THEAREA
• All attendants, patients and staff should vacate the area if possible
• Open all exits to facilitate movement.
• Inform security guard, police and security control room (No 6100-
Available 24 h, No 6000-Available 9 am to 5 pm)
• Inform adjacent wards/offices.
• People should be guided to prevent stampede, which can be more
damaging.

45.3 EARTHQUAKE
• Do not panic. Open all exits to facilitate evacuation. Reassure
people, to prevent stampede. Tell them intensity of earthquake is
maximum at the onset and reduces thereafter.
• If possible leave the building; otherwise take cover under tables or
beds and protect head, face and torso.
• !vlove away from large objects, which may fall.
• After the shaking stops, assess your immediate surroundings fire.
Put out small fires if possible.
• Do not light match or turn on electrical switch. Use torch light.
• Assist others and initiate rescue efforts if necessary. Do not re-enter
a severely damaged building.
• Check utilities (power, gas supplies) and shut off if necessary. Never
touch hanging power lines. Only shut off gas ifthere is leak.
389

46. EQl IPMENTS

46.1 EQUIPMENTS COVERED l NDER


Equipments in the Newborn Unit are covered under one of the following
4 conditions:
46.1.1 Warranty
Warranty period extends for a period of 24 mths starting from the date of
satisfactory installation. During the warranty period, the replacement of
any part of the equipment is done free of cost. There are no labor
charges.
46.1.2 CMC
This contract is generally done for a period of 5 yrs for maintaining the
equipment after the period of warranty. During CMC the firm provides
preventive maintenance, attends to all emergency breakdown calls and
replaces most parts at no extra cost. There are no labor charges.
46.1.3 Annual Maintenance Contract (AMC)
The only difference between AMC and CMC is that the company would
not replace parts free of cost.
46.1.4 None of the above
If a piece of equipment were under none of the above, the company
would charge for each visit. Spare parts for replacement would have to
be bought.
The area SR should know about the state of contract of the equipments.
This information can be obtained frorn the equipment registers in various
areas that are maintained by the sisters-in-charge of the respective areas.

46.2 IDENTIFYING DEFECTIVE EQUIPMENTS


• Routine morning equipment rounds.
• Accidental failure of equipment during the day.
• Monthly equipment rounds.
46.2.1 Routine morning equipment rounds
Every morning the area sister-in-charge and SR have following
responsibilities:
• Sister in charge- must take morning equipment round and note down
the working state of equipments in the equipment register and show
it to the area's SR. The working state of equipments is defined as
o W - Fully working without any fault.
o PW- Partly working, but in a manner that would not jeopardize
the patient.
o NW- Not working (includes working in a manner that is risky).
o No other words or phrases or ticks etc are allowed for use in
register.
• SR of the area- He/she must check the equipment register daily.
46.2.2 Accidental failure of equipment during the day
390

• Area SR: He/ she must immediately


o Inform the local engineer of the company (lists are available in
NICU, NNN, Neonatology office, N!CU Lab).
o Inform the SR-in-charge of equipments/consultant-in-charge of
equipments so that he/she can follow up the case.
o Inform the SR-in-charge of equipments/consultant-in-charge of
equipments once it is rectified.
• SR-in-charge of equipments
o Inquire from the area SR about the exact fault in the equipment.
o Follow the complaint with the company concerned in the
subsequent days.
o Keep the consultant in-charge of equipments informed about the
PW/NW equipment and what has been done for the complaint.
o Direct store-keeper to send letter/fax to the concerned company
by day 3.
o Sign the report once the equipment has been rectified.
46.2.3 Monthly equipment rounds
The consultant-in-charge of equipments and the SR-in-charge of
equipments take a round of all the equipments in the unit on 4th or 5th of
every month in the presence of outgoing and incoming SR.
Details of equipments are entered in an Access-based program called
NICU Equipment Manager.
391

INVESTIGATIONS

1-1 SAMPLING METHODS


Blood samples can be arterial, venou; or capillary. Preferably use arterial
lines for sampling. Do not use central venous lines for drawing of blood.
Most investigations can be performed satisfactorily with arterial blood,
the exceptions being coagulation studies, PCV estimation and blood
cultures.
1-1. l Sampling from an indwelling arterial catheter
Choose an appropriate syringe (depending upon the amount of blood
sample required - use only I mL syringes when < I mL of sample is
required). Heparinize the syringe, if required.
1-1.2 Venous sampling
In babies without an arterial line, a fresh peripheral vein can be used for
drawing blood after thorough aseptic preparation of the skin using the
triple swab techoique. Squeezing of the limb during collection of sample
should be avoided.
1-1.3 Capillary sampling by bee! prick
This method is suited for very small blood volumes, such as for BS, TSB,
micro ESR, CRP, !EM screening by filter paper, peripheral smear
preparation etc.
Warm the site with warm, moist wrapping (water temperature 39°C-
440C, 3-10 min) to increase the rate of arterial blood flow to the area (for
collecting samples for blood gas measurement). This also increases
volume of blood available for collection. Choose a site medial to an
imaginary line drawn posteriorly from the middle of the great toe to the
heel or lateral to an imaginary line drawn posteriorly from between toes
four and five to the heel. Puncture done lateral and medial to these lines
avoids the area of calcaneus bone.

Clean the site by triple swab technique .. Wipe dry with sterile gauze.
Dryness is essential to avoid hemolysis by alcohol or water. Make
puncture with lancet with tip shorter than 2.0 mm. Wipe off first small
drop of blood with a sterile gauze .Avoid "milking" or massaging as this
causes hemolysis and admixture of interstitial/intracellular fluid with
blood. Hold the collecting tube in a nearly horizontal position and allow
it to be filled. Seal the capillary tubes with clay sealant (plasticene) at one
end after col1ection.
392

1-2 PRACTICAL ISSUES REGARDING SENDING BLOOD


SAMPLES
1-2.1 Type of container for collection
There are mainly four types of containers for collecting blood samples -
Plain, Oxalate & fluoride, EDTA and Na citrate. Some investigations
require special containers that have to be procured from the laboratory by
sending the requisition in advance. Type of container to be used for each
investigation is given in the tables belo\v.
1-2.2 Labeling of samples
The container should be labeled properly with details of baby's name,
sex, CR no, nature of sample, whether heparinized, name of the ward,
collection date and time.
1-2.3 Storage and transport
As a rule, the sample should be transported immediately to the concerned
Jab. All planned tests should be carried out by the JR on night duty so
that the samples reach the concerned labs before I0 am on all working
days.
Blood for serum ammonia, serum lactate, serum potassium estimation
and blood gas; and body fluids for cell count estimations cannot be stored
and need to be transported immediately to the lab. Hematological
parameter estimations, enzyme assays (like G6PD) and antigenic assays
tend to vary with storage time and fresh samples (at least Jess than 6 h
old) are preferred. Until the time of transfer, the sample has to be stored
in a refrigerator at 2-8 °C.
Samples for serum ammonia should be transported on ice to the Jab
immediately after collection. If ABG samples cannot be immediately
analyzed they should be chilled in a plastic packet with crushed ice to
slow metabolic processes, and it has to be warmed back to body
temperature before processing.
Investigations for which require serum is required and which perchance
cannot be transported immediately, should be stored in room temperature
until the serum gets separated (to prevent hemolysis) and then should be
stored at 2-8 °C in a refrigerator till time of transfer.
All the samples should be transported only by the ward or laboratory
attendant to the corresponding laboratory. Samples should not be sent
through patient's relatives.
1-2.4 Collection of reports
Processing time required for various tests are given in the tables below.
For routine investigations results are dispatched from corresponding labs
at 6 hourly intervals through hospital anendants. JR in charge of the
patient should ensure the availability of results on time and, if delayed,
contact the concerned lab by phone to verify the status. These processes
might change once the hospital computerization project is completed.
393

1-3 TESTS TO BE DONE AT BED~IDE I NICU LAB


Facilities for doing the following te>ts are available at the bedside or in
the NICU side-lab in PGIMER. The>e tests should never be sent to other
labs unless the NICU lab machines ai e out of order.

ABG analysis The minimum an1ount of blood required for the


current machine is 0.3 mL. Only SR's are permitted to
use the ABG machine.
Apt test Mix specimen (gastric aspirate or stool) with distilled
water, dissolve blood clots and filter the specimen.
Fill 2 test tubes with equal amounts. Add I mL of I%
NaOH to I test tube and I mL of distilled water to the
other. Shake both and compare the colors. Pink color
stays: fetal blood present
Pink color changes to yellow brown: maternal blood
present
CRP Semi-quantitative latex agglutination slide method of
CRP estimation is done using CRP reagent kit. Follow
the instructions in the kit. Remember to use +ve and -
ve controls.
CSF and body Using NC
fluids cell • Mix 10 drops ofCSF + I drop of methylene blue
count • Wait for 10 min and then mount the preparation
• Place cover slip over NC, put a drop of CSF on the
comer of cover slip and let it spread by capillary
action. Place the NC chamber on the platform and
use !Ox objective lens for focusing on the lines. Use
both eyes to have clear focus
• You will find stained fluid with lines at background
• Switch over to 45x and use fine focus knob while
using high power objective lens
• Start counting fi-om the upper left square of the
chamber and move systematically to cover 16 small
squares.
•When you have counted 16 small squares (1 big
square) the comer of the NC area covered is 0.1
mm3 (i.e. 0.1 µL)
• In a similar fashion, count the cells in the 4 big
squares in the comers of NC- that gives cells in 0.4
µI
• Multiply this to 2.5 to get total cells I mm 3
• Neutrophil count is calculated by the total
leucocvtes x neutrophil o/o.
Micro ESR Heel prick /venous blood to be collected in a standard
394

75 mm heparinized microhematocrit tube with


internal diameter of I. I mm. Ends of capillary tube to
be sealed with clay sealant. Keep the capillary vertical
for one hour by fixing it to a firm surface with
transparent adhesive. The Ht of the plasma column to
be measured after the first hour, and reported in
mm/h.
PCV Method:
• Fill two plain capillary tubes approximately 'h to %
full of well mixed blood
• Seal the ends of the tubes with clay sealant. Hold
the filled tube horizontally and seal by placing the
dry end into the clay at a 90° angle. The plug should
be at least 4 mm long.
• Balance the tubes in the micro-hematocrit centrifuge
with the clay ends facing the outside, away from the
centre, and touching the rubber lining
• Tighten the cover of the centrifuge and close the
top.
• Spin for 3 min at 12000 rpm (or 5 min at 11000)
• Place the capillary tubes in the micro hematocrit
reader and adjust so the top of the clay seal is level
with the bottom zero (0) line and the top of the
plasma is in line with the I 00 line
• Move the slider until the slanting line is level with
the top of the packed red cells Read the PCV result.
• The values of the two tubes should agree within 1%
(0.01).
Shake test Absolute alcohol 0.5 mL is added to 0.5 mL of gastric
aspirate in a 4 mL glass test tube. The test tube capped
by the thumb is vigorously shaken for 15 s and
allowed to stand for 15 min.
• Negative= no bubbles
• I + = Very small bubbles in meniscus extending one
third or less of distance around test tube
• 2 + = Single rim of bubbles extending one-third to
all around the test tube
• 3 + = a rim of bubbles all the way around the test
tube with a double row in some areas
• 4 + = A double row or more of bubbles all the way
around the test tube.
TSB Capillaries containing venous blood samples sealed at
one end with clay sealant should be soun in the
395

centrifuge at 12000 revolutions per min for 3 min.


Make sure the specimen is not hemolyzed and a clear
separation of plasma is visible. Check the calibration
of bilirubinometer by inserting a capillary filled with
distilled water and taking the measurement. The
reading should be zero with distilled water. Then
insert the spun capillary tube into the slot provided in
the machine and make sure the portion of capillary
tube that contains plasma occupies the slit in the
handle. TSB reading is displayed. Promptly switch
off the machine after use and dispose off the capillary.
Urine - pH, protein, blood, ketones, specific gravity, sugar etc
dipsticks

Glucose stix • Prewarm the heel before puncture.


(Method for • Take the reagent strip out of the foil and insert in
optium the glucometer port.
glucometer) • The sign for application of blood will appear on
g1ucometer screen as it starts automatically with
insertion of strip.
• Give a bold prick and wipe the first ooze of blood.
• Let the further drop of blood fall from top in sample
area/fill the area from side.
• If sample is inadequate to fill the sample area, fill it
with another drop within 30 s.
• Do not squeeze the heel with excess pressure.
• Do not rub the strip against the skin as it may
damage the electrode.
• Sample required - 2.5 µL/test.
• Test time - 20sec.
396

l-4 BIOCHEMICAL INVESTIGATIONS

l-4 I B.toe hem1srry


. t Lab ora tor1es
. 1n. PGIMER
NAME OF LAB SAMPLE ACCEPTANCE
Pediatric biochemistry 8 am to 8 pm on all days including holidays
lab (popularly called (samples accepted till 6 pm)
"Microtech lab")
Emergency 24 h daily (preferably send from 6 pm to 8
biochemistry lab am)
Adult biochemistry 8 am to 5 pm Mon to Friday
lab 8 am to 2 pm Saturdays. Closed on holidays.
Values may differ slightly between different labs due to difference m
calibrations of machines. Hence all routine biochemistry investigations
from the Newborn Unit should be sent to Microtech lab to facilitate
uniformity and comparison of results.
In Microtech Lab, samples received up to 3.30 pm are processed by auto-
analyzers. Only selected important investigations are done on samples
received between 3.30 pm and 6 pm and they are processed only by
manual methods. No samples are received after 6 pm. Manual methods
require a larger quantity of blood compared to auto-analyzers, which
must be kept in mind when sending a sample after 3.30pm.
Emergency Biochemistry Lab works round the clock and utilizes auto-
analyzers. Only selected tests are done here and the JR must send
samples to this lab only if immediate results are required for management
of the baby and between 6 pm and 8 am.
Biochemical labs require estimated quantities of serum for most of their
tests. In cases of high PCVs the amount of serum available from whole
blood samples will be less. In the tabulation given below the amount of
whole blood sample required is calculated taking into account the high
PCV values of the neonate.
397

I -4 2 B"IOC h em1ca 1nvesti1~ af ions


Investigation Sample& Container Lab Reporting Units Normal Special instructions
volume values for
(before neonates
3.30 pm/ (Microtech
after 3.30) lab std)
Glucose Whole Oxalate Microtech lab After 3 h mg/ 40-120 mg/dL Routine glucose
blood (0.5 vial Emergency Biochemistry lab dL estimations to be done
mU0.5 with glucometer. Sample
mL) to be sent to lab to
confinn abnormal
glucose values. Amount
of oxalate meant for 2
ml blood. Excess oxalate
causes hemolysis
Electrolytes Whole Plain vial M1crotcch lab All.er 3 h mEq1 Na: 136-145 Sa1npl..::> h<vjJct1;11;"'._....; .,;,:,
alone blood Emergency Biochemistry lab L Ko 3.0-7.0 Na heparin can give
(sodium, (I mUJ Clo 96-106 falsely high Na values.
potassiutn & mL) Delay in transport and
chloride) squeezing during
samolin2 leads to hi!!h K.
BUN& Whole Plain vial Microtech lab After 3 h mg/ Preterm: 3-25 Remember: BUN x 2.14
Enicrgency Biochemistry lab Tenn: 3-12
- - - ----------- blood (1 dL
--------------- = Blood urea in m/dL
Creatinine mUl.5 mg/ 0.3 1.0
mL) dL
Electrolytes + Whole Plain vial Microtcch lab After 3 h See above
BUN& blood (2 Emergency Biochemistry lab
creatinine mU2mL)
398

Investigation Sample& Container Lab Reporting Units Normal Special instructions


volume values for
(before neonates
3.30 pm/ (Microtech
after 3.30) lab std)
TSB alone Venous Capillary Microtech lab After 3 h Use AAP Send to lab only if NICU
sample tube nomograms lab bilirubinometer is out
of order

Bilirubin total Whole Plain vial Microtech lab. After 3 h Conjugated


& conjugated blood (0.5 Emergency Biochemistry lab. bilirubin > l
mUlmL) mg/dL ifTSB
'.S 5 mg/dL or
>20%ofTSB
ifTSB >5
m•idL
METABOLIC Whole Plain vial Microtcch lab. Same day Plan on previous day.
PROFILE blood 2 mL Not done on holidays. 4pm Sample to be taken and
Bilirubin total mg/ sent by night duty JR by
& direct dL See above -- 8am
-Asf ___ - ----- ------- ------------
U/L AST 0-5 d:
35-140
>5 d: 15-55
------------- ---- - -- -Ar::t:o:s·d:·---
ALT U/L
6-50
- - -
>5 d: 5-45
- ---------- - -ALP 145420-
ALP U/ L
------------- - - - - ---- --- ----------
Serum total g/ dL Total proteins
proteins Preterm: 4.3-
7.6
--- - - - - ------- ---- - ------- -------
399

Investigation Sample & Container Lab Reporting Units Normal Special instructions
volume values for
(before neonates
3.30 pm/ (Microtech
after 3.30l lab stdl
Tenn: 4.6-7.4

Serum g/ dL
Albumin Preterm: 1.8-
3.0
Tenn: 2.5-3.4
Serum g/ dL -TOtaf P~Ot~i~ ---
Globulin minus
albumin
BUN, mg/ ·see·ai;~.;e -----
crealmine & dl
- ~~t:C-~ly_t~~ - - - -
Calcium mg/ · 3:24 ·11:9 a:· ---
(total) dL 10.6
24-48 h: 7.0-
12
4-7 d: 9.0-10.9
>7 d: .8-10.8
Inorganic mg/ · a=s Cf:-4.s=s.2· -
phosphorus dL >5 d: 3.8-6.5

Magnesium Whole Plain vial Microtech lab. Same day mg/ 0-6 d: 1.2-2.6 Plan on previous day.
blood (0.5 Not done on holidays. 4pm dL >6 d: l.6-2.6 Sample to be taken and
mL) sent by night duty JR by
8 am
CRP (Hioh Whole Plain vial Microtcch lab. Same day ml!/ 0.50-3.00 Cut-off for bacterial
400

Investigation Sample& Container Lah Reporting Units Normal Special instructions


\'olume ,. alues for
(before neonates
3.30 pm/ (Microtech
after 3.30) lab std)
sensitivity blood 0.5 Not done on holidays. 4pm dL sepsis: IO mg/L
method) mL
Lactate 2 ml whole Oxalate Microtech lab. Same day 1nmol 1-12 mth: 1.1- Ensure sample reaches
Blood.IC SF blood/ vial Not done on holidays. 4pm IL 2.3 the lab within 15 niin of
I mLCSF collection. Delay leads to
abnormally high values.
Ammonia Whole Special vial Microtcch lab. Saine day µmol/ <30d: 21-95 Sample should reach lab
blood 2 from lab Not done on holidays. 4pm L 1-12 mth: 18- immediately without any
ml EDTA 74 delay. Sample to be
vaccutaincr transported on ice. Make
sure no water enters the
tube durine: transport.
LIPID Whole Plain vial M icrotcch lab. Processing
PROFILE blood 2 mL Not done on holidays. done in
~ ----- - - - - ---- batches. mg/ ----- - - - ----- -
Choleslcrol Reporting 45-182
dL
after 3-4 J. Plan on previous day.
------ - - - - - - --- --- - - - ------ - Sample to be taken and
TG 32-99
sent by night duty JR by
-------- ---- --- - ------- s,m
Very low 6-40
density
lipoproteins
_(V_LDL) _____
- - ----- - ------
Low density 60-140
lipoproteins
-- -------- ------ -------
401

Investigation Sample& Container Lab Reporting Units Normal Special instructions


volume values for
(before neonates
3.30 pm/ (Microtech
after 3.30) lab std)
(LDl)

·- - ----- - -35:48- ---


High density
lipoprotcins
(HDl)
Uric acid \Vhole Plain vial Microtech lab. Same day mg/ 1.7-5.8
blood 2 n1L Not done on holidays. 4pm dl

Amylase Whole Plain vial Microtech lab. After 3 h U/l 30-100


blood I ml Emerj!;ency Bioche1nistry lab.
Copper Whole Plain vial Microtech lab. After 2 wks µg/ 0-5d: 9-46 Processing done once in
blood 2.5 Not done on holidays. dl 1-2 wks only. Samples
ml will be accepted daily.
Zinc Whole Plain via! Microtech lab. After 2 wks µg/ 64-118
blood 2.5 Not done on holidays. dl
ml
CPKMB Whole Not done in Microtech lab. Done After 3 h U/l 0-25
levels blood I mL 24 h-only in Emergency Biochcm
lab.
CSF protein CSF 0.5 Plain vial Microtech lab. After 3 h mg/ < 150: Term
ml Emcrgencv Biochemistrv lab. dL <180: nrcterm
CSF glucose CSF 0.5 Oxalate Microtech lab. Atlcr 3 h mg/ >60o/o of BS Delay in transport will
ml vial Emergency Biochemistry lab. dl lead to falsely low sugar
values.
Stool for Pea sized Plain vial Microtech lab. Same day Reported as
402

Investigation Sample & Container Lab Reporting Units Normal Special instructions
volume values for
(before neonates
3.30 pm/ (Micro tech
atrer 3.30) lab std)
occult blood stool Not done on holidays. 4pm positive/negati
(Hemospot sample ve.
card method)
Urine Urine 0.5 Plain vial Microtech lab. Same day mEq/ FENa (o/o)
electrolytes mL Not done on holidays. 4pm L Pre term
1001-1500 g Plan on previous day.
1-2 d 2.0±3 Sample to be taken and
8-9 d 1.3±0.2 sent by night duty JR by
15-16d: 8am
0.7±0.1
1501-2000 g
1-2 d 2.2±0.5
8-9 d 0.9±0.2
15-16d
0.3±0.1
2001-2500 g
1-2 d 1.1±0.2
8-9 d 0.6±0.2
15-16 d
0.15±0.1
Term
1-2 d 0.3±0.l
8-9 d 0.5±0. l
15-16 d
0.25±0.1
403

Investigation Sample & Container Lab Reporting Units Normal Spe<:ial instructions
volume values for
(before neonates
3.30 pm/ (Microtech
after 3.30) Jab std)
Urine spot Urine I ml Plain vial Microtech lab. Same day mg/ Preterm (5-30
Protein Not done on holidays. 4pm dL d): 88-845
Tenn: 94-455

Calcium Urine Calcium


Creatinine :creatinine
ratio (mg/mg)
~ 0.86
Urine"MR" Fresh urine Special vial Microtech lab. Same day Reported as
screen 15ml from lab Not done on holidays. 4pm +ve or -ve
(FeCI,, 2,4 Di-
nitro phenyl
hydrazine
(DNPH),
Mucopolysacc
harides screen,
homocysteine
& reducing
SU""N\
ABG analysis Whole Heparinize ABG Lab. 24 h daily Within 15 Sample should not contain any air bubble.
(ABG) blood 0.3 d syringe min To be stored on ice in case of any unexpected delay
mL in transport. ABG analysis to be sent to room no 21
onlv when NICU lab's ABG machine is not in order.
404

1-5 HEMATOLOGICAL INVESTIGATIONS

1-5.I Hematology laboratories in PGIMER

LAB SAMPLE ACCEPTANCE


Central hematology lab 9-11 am Mon-Fri and 9-10 am on Saturday. Not on holidays. Uses auto analyzers for
(with its various subdivisions) most investigations and hence quantity of sample required will be less.
Emergency hematology lab Accepts samples round the clock daily. Only manual methods used/ no autoanalyzers.
Quantity of sample required will be more. Does only basic investigations.
.
Blood Bank (for DCT) 9 am to 5 pm on working days

1-5.2 Hematological investigations

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required
CBC I mL whole EDT A vial Hcmogram Same day
(RBC. WBC, Platelet counts, PCV, blood (sysmax lab 4pm
Mean corpuscular volume (Mean autoanalyzcr)
corpuscular volume (MCV),
Mean corpuscular hemoglobin (MCH),
Mean corpuscular hemoglobin
concentration (MCHC) &
Peripheral blood film examination
CBC (as above) plus reticulocytc count 3.0 mL whole EDTA vial Hemogram Same day
blood- for lab 4pm
autoanalyzcr
405

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required
Hb ·manual l mL whole EDTA vial Emergency After 3 h
TLC & peripheral blood film blood hematology
examination lab
• manual
Differential leukocyte count - manual Only on Saturdays and Sundays. Only
between 8 am and 2 om.
Platelet count in Emergency I mLwhole EDTA vial Emergency Not routinely done. SR to discuss with
blood hematology Hematology Lab SR.
lab
Reticulocyte count 1.5 ml whole EDTA vial Hemogram Same day Fresh sample required (not more than 6 h
blood-for lab 4pm old)
autoanalyzer
0.5 mL -

manual

PT, 1.8 ml whole Special Coagulation Same day Timings: Coagulation lab (Mon to Sat. 9
APTT(aPTn& blood- to be 3.2% lab 4pm am -12 noon. Not done on holiday)
PTI added to 0.2 Sodiwn Emergency Emergency hematology lab (Mon to Sat -
ml Sodium citrate test hematology 12 noon to 9 am next day. 24 hon Sunday
citrate. Ratio tube lab after 3 h & holiday)
9:1 (procure
from lab\
406

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required
d-dimer assay, l.8 mL whole Special Coagulation Only on prior appointment. Concerned SR
Fibrinogen levels blood- to be Sodium lab to discuss the case with consultant and to
added to 0.2 citrate test get an appointment for the test.
mLsodium tube Consultant-in-charge Dr. Jasmina
citrate RATIO (procure Ahluwalia.
9: I. from lab)
2 such
samples are
required
Individual clotting factor assays 4 mL whole Sodium Coagulation
blood (2 citrate I lab
samples of2 plain vials
mL each)
Thrombotic workup 4mLwhole Sodium Coagulation
Protein C blood (2 citrate I lab
Protein S Antithrombin Ill Factor V samples of 2 plain vials
Leiden Lupus antibodies mL each)
Anticardiolioin antibodv levels etc
Plasma Hb 2 mLwhole EDTA vial Hemolytic Same day
blood workun lab 4om
Urine Hb 2mL Plain Hemolytic Same day
workun lab 4om
G6PD levels I mLwhole EDTAvial Hemolytic Same day
(methemoglobin reductase method) blood workup lab 4pm
Plasma hemosiderin 2 mLwhole Special iron Hemolytic Next day
blood free tubes workup lab
(procure
from lab)
407

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Reouired
Urine hemosiderin 2 mL first Special iron Hemolytic Next day
morning free tubes workup lab
sample x 3 (procure
consecutive from lab)
days
Hb F levels 2 mL whole EDTA vial Hemolytic After I wk
blood workup lab
Hb electrophoresis 2 mL whole EDTA vial Hemolytic After 1 wk ONLY ON PRIOR APPOINTMENT.
blood workuo lab Concerned SR to discuss the case with
Osmotic fragility test 2 mLwhole EDTA vial Hemolytic consultant and to get an appointment for
blood workuo lab the test. Consultant-in-charge Dr. Reena
Sickling test I mL fresh EDTA vial Hemolytic Das. Along with detailed summary of
whole blood workuo lab index patient, family members to be sent
~- --
Serum iron TJBC 6-8 mL whole Special iron Hemolytic to coagulation lab tu get appu1nuuc1n 1u1
Serum ferritin blood free tubes workup lab screening.
(procure
from lab)
Screening other family members for Sample will be taken at the Hemolytic
underlying hemolytic disease lab workup lab
Bone marrow examination Bone marrow sample to be Bone marrow Contact SR bone marrow lab after 11 am
taken only by pathology lab on working days for appointment.
resident Reporting will be done on the next day of
sampling.
MICROSCOPY 0.5 mL in Plain vial Emergency Microscopy should always be done by the
Urine hematology resident himselffllerself in NICU lab·. To
CSF lab be sent to lab only if unit's microscope is
Body fluids not working.
408

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Reauired
DCT I mLwhole EDTA vial Blood bank Contact SR transfusion medicine in special
blood situations - can get OCT done round the
clock after discussion
Hemolytic Only on prior appointment.
work-up Lab Concerned SR to discuss the case with
consultant and to get an appointment for
the test. Consultant-in-charge: Dr. Reena
Das
409

1-6 MICROBIOLOGICAL INVESTIGATIONS

1-6.1 Microbiology laboratories in PGIMER

NAME OF LAB SAMPLE ACCEPTANCE


Bacteriology, Mycology, 9 am to 3 pm Mon to Fri.
Mycobacteriology, Sexually transmitted 9 am to 12 noon Sat.
disease (STD) labs Closed on Sundays & holidays.
Emergency microbiology lab Mon to Fri 3pm to 9 am the next day. Sat 12 noon onwards. Sundays &
holidays - 24 h. (Apart from doing gram staining on body fluids this lab mainly
acts as a collection centre for samples. All culture samples received here are
incubated overnight and transported to the concerned main labs for plating)
Virology labs 9 am to 12 noon Mon to Fri; 9 am to IO.JO am on Sat.
CMV pp65: Done only twice weekly- Tuesdays and Fridays. Sample to reach
before 9.30 am.
Closed on Sundays & holidavs.
Parasitology lab 9 am to I pm Mon to Fri. 9 am to 11 am on Sat.
Closed on Sundavs & holidays.
VCTC 9 am to 11 am Mon to Friday
9 am to I0 am on Saturdays.
Closed on Sundays & holidays.
410

1-6.2 Microbiological investigations

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required

Blood bacterial 1-3 mL 40mL Clinical Plating is Indwelling arterial catheters not to be
culture & whole blood BACTEC bacteriology done only used for sampling. Skin over sampling site
sensitivity. culture lab. after to be cleaned with triple swab technique
bottle Emergency overnight before sampling.
CSF and other body fluids ---<:ulture & I mL CSF/ Sterile test micro lab. incubation. Sterile syringe to be used for collecting
sensitivity Body fluid tube I vial Overnight blood. Blood to be pushed into culture
culture bottle without opening its cap by poking it
Urine culture & 2 mL urine Sterile test reports - with needle of the syringe.
sensitivity collected by tube I vial 2 pm on the Separate requisition forms to be sent along
suprapubic day after with samples if sensitivity pattern for
puncture platting. se<:ond line drugs is required.
Pus 1-2 mL Sterile swab Final Ask for plating on anaerobic media if
ET aspirates /sterile report- after anaerobic infections are suspected
Broncho-alveolar lavage (BAL) container 5 d of
ConjunctivaVbuccal/ plating.
wound swabs Any growth
gram stain, in mean
culture & time will be
sensitivity informed
immediatel
v by !ah.
411

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required

Blood for fungal culture & sensitivity I mL in each 2 Fungal Mycology lab. Culture In case of fungal gro'Nth sensitivity results
pediatric culture Emergency results: will be available in another 3 d against
fungal culture bottles- to micro lab First report Fluconazole,
bottle be procured after I wk. Kctoconazole,
from lab. Final report Amphotericin B
KOH Smear, gram stain & culture for I mL sample In sterile after 4 wks. 5 Flucytocine &
fungus in I swab container I Smear Nericonazole
Urine swab results:
CSF Same day
BAL 3pm
ET aspirates
Conjunctival/buccal'
wound swabs
Fungal serology against 1 ml whole Plain vial Mycology lab After I wk
Candida, Aspecgillus niger, flavus & blood - serology
fumigatus section
AFB staining for mycobacterium. Depending on Mycobacteriol Routine
Mycobacteria site ogylab cultures -
-Routine culture after 6 wks.
-BACTEC culture (on all samples except BACTEC
blood & urine) after 2 wks.
VDRL titers in 3mL Plain vial STD lab Processing VDRL titers< I :8 reported as negative.
Blood I CSF Blood I CSF done only Quantitative titers will be given for values
twice >1:8
weekly on
Mondays &
- ----- - ------ --------- ---- -- --------- --------------
412

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required

Treponema pallidwn particle Done only Thursdays


agglutination (TPPA)/Treponema when VDRL Reporting
pallidum hemagglutination (TPHA) in is positive at 12 noon
Blood I CSF (with same day of
samo\e) orocessin_e
Gram stain & culture for gonococci Conjunctival Sterile swab Gram
swab stain- 3 pm
same day/
Cultures
after 48h
HIV screening by ELISA 2 mLwhole Plain vial VCTC Next day
blood 10 am
CD4 counts 2mLwholc EDTA vial Done only on appointment & when
blood referred bv ART clinic
HSY antigen detection by Fluid from Special Viral serology 2-3 d
immunofluorescence- for HSVI & herpctic slide - to be Jab
HSV2 lesions procured
from lab.
Sample to
be added to
premarked
well on the
slide
Serology for HSY - by IF lmL Plain vial IF cannot
Blood /CSF Blood I CSF differentiate
HSVI & HSV2
413

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required

CMV pp65 antigen detection by IF l ml Fresh EDTA vial Viral serology Same day 4
whole blood lab pm
(<6 hold)
Urine for CMV inclusion bodies Equal volume Special vial Viral serology Next day
of urine as with lab
that of alcohol- to
preservative be procured
from lab.
CMV IgM Serology - ELISA 2 mLwhole Plain vial Viral hepatitis ELISA.o; Contact the lab for probable date of
blood lab done only reporting.
when 6-10
samples
Rubella lgM -by ELISA 2mLwhole Plain vial Viral hepatitis accumulate.
blood lab But are
done at
least once
in I wk.
Serology for varicella zoster lmL Plain vial Viral serology Only when
Blood I CSF - Blood/CSF lab kit is
By ELISA available.
Serology for parvo B 19 Check
Blood I CSF- availability
By ELISA before
sampling.
414

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required

RSV antigen by IF Maximum Special vial Viral serology Next day


available containing lab
nasopharyngc 2mL
al secretions MEM-to
to be added to be procured
media in.vial. from lab
Adenovirus Conjunctiva! I Special Next day
antigen by IF co meal slide- to be
secretions procured
from lab.
Sample to
be added to
premarked
well on the
slide
Hepatitis A lgM 2mLwhole Plain vial Viral serology HbsAg: 2-3
/HbsAg/ Hepatitis C IgM blood lab d. Others: I
/Hepatitis E lgM wk
All ELISA
415

Investigation Sample & Container Lab Reporting Special instructions


Quantity
Required

Hepatitis B complete profile (HbsAg, 2mLwhole Plain vial Hepatology Done only
anti HbsAg, HbeAg, antiHBeAg, HBc blood lab on selected
Ag) days
depending
on number
of samples.
Contact the
lab for
probable
reporting
date.
Ioxoplasma I mL whole Plain vial Pardsitology Done once
IgM I IgG / lgA levels by blood I CSF lab in I wk on
ELISA Wednesday
Blood/ CSF sonly.
Reporting
on
Thursdays
Animal inoculation for toxoplasma Placental Tissue in Parasitology 1·2 wks
tissues sterile NS lab
Malarial parasite I mLwhole EDTA vial Parasitology Same day 3
Peripheral smear blood lab pm
Antigen by spot
QBC
416

1-7 ENDOCRINOLOGICAL INVESTIGATIONS

1-7.1 Labs for endocrinological investigations in PGIMER

NAME OF LAB SAMPLE ACCEPTANCE


9 am to 12.30 pm Mon to Fri. 9 am to 10.30 am on Satordays.
Endocrinology lab
Not done on Sundays & holidays.
9 am to 12.30 pm Mon to Fri. 9 am to I 0.30 am on Saturdays.
Nuclear Medicine lab
Not done on Sundays & holidays.
9 am to 12.30 pm Mon to Fri. 9 am to 10.30 am on Saturdays.
Immunopathology lab
Not done on Sundays & holidays.

1-7.2 Endocrinological investigations

In\·estigation Sample & Container Lab Reporting Special instructions


Quantity
Required

Thyroid profile 2mLwhole Plain vial Nuclear After 3-4 d


Total TSH (Thyroid stimulating blood medicine lab
hormone), T3 (Tri-io<lo-thyronine) &T4
-------------- --------------
(Thyroxine) 2 ml whole Endo- After 2 wks
blood crinology lab
Hormone Estimations {Radio immuno 2 ml whole Heparinized Endocrinology After 2 wks Case to be discussed with SR
assay) blood for vial lab endocrinology or consultant before
FSH each test sending samples
Lii
417

GH
Insulin
ACTH
Cortisol
Testosterone
Estradiol
AFP levels 2 mL whole plain vial Immuno After I wk
blood
--------- ---------- -- --- -------------- pathology lab
------- - - -
6 Human chorionic gonadotropin (HCG) 2 mL whole
levels blood
FSH~ folltcle sttmulatmg hormone, LH~ lutem1zmg hormone
418

1-8 GENETIC & PATHOLOGICAL INVESTIGATIONS

Investigation Sample & Container Lab Sample acceptance timings Reporting Special instructions
Quantity
Required

Karyotyping I mLwhole Hcparinized Pediatric Only on appointment After 2-4


(G banding) blood syringe Cytogenetics Contact Dr lnusha Panigrahi/ wks
lab Dr Sheetal Sharda for
annointment
Adult Done only on prior Sample to be collected under
cytogenetics appointment. Contact Dr. aseptic precautions. If cannot
lab Neclam Verma. be transported to lab
Chromosomal 3-5 mL Heparinize Adult Done only on prior immediately to be stored at
breakage study - (for whole d syringe cytogenetics appointment. Contact Dr. After 2-4 4 C in refrigerator.
Fanconi's anemia) blood lab Neelam Verma. wks
CD4 markers for 2 mLwhole EDTA vial Molecular Mon to Saturday Consult with SR hematology before sending
leukemia blood studies lab 9 am to 11 am. samples.
Not done on
Sundays &
holidays
Renal biopsy Renal Special vial Immuno 9 am to 12.30 pm Mon to Fri After l wk
·light microscopy, biopsy for biopsy- pathology 9 am to 10.30 am on Saturdays
IF microscopy material procure lab Not done on Sundays &
from lab holidays
419

1-9 RADIOLOGICAL AND MISCELLANEOUS INVESTIGATIONS


INVESTIGATION LOCATION WORKING HOURS
Xravs Emere:encv x-rav room Round the clock
USG Ultrasound (APC) Weekdays 9 am to 4 pm. Saturday 9 am to 2 pm.
Closed on holidays.

---------
·uf~OUlld (Em;rg-eO-cY)- ------ -w~;k~ys s·pm-10· 9·a-m: saturdays-2 pm ·1~-9 am· -
Level II emergency block Sundays - round the clock.
Nehru hosoital
Doppler sn.idies (on prior Requisition to be sent to APC Ultrasound. Weekdays 9 am to 4 pm
appointment ) Procedure done at main USG room. Saturday 9 am to 2 pm
Closed on holidays
MCU Radiology, APC Weekdays 9 am to 4 pm
GIT contrast studies (only on Saturday 9 am to 2 pm
orior "nnnintment ) Closed on holidavs
ECG ECG Room (call for portable) Round the clock

Holter ECG (only on prior Holter ECG Room Weekdays 9 am to 4 pm


appointment) Saturday 9 am to 2 pm
Closed on holidays
EEG (only on prior BERA lab, APC Weekdays 9 am to 4 pm
appointment ) Saturday 9 am to 2 pm
Closed on holidavs
BERA (only after 3 mths of BERA lab, APC Weekdays 9 am to 4 pm
age - on prior appointment ) Saturday 9 am to 2 pm
Closed on holidays
--BERA,
------ ----------
ENT OPD
-- - --- ---- --- - -- - -- -- - ------------ --- -- - -- ------- - ---- - --- - - --
Week days 9 am to 4 pm
Saturday 9 am to 2 pm
Closed on holidays
420

INVESTIGATION LOCATION WORKING HOURS


Visual evoked potential BERA lab, APC Weekdays 9 am to 4 pm
(YEP) (only after 3 mths of Saturday 9 am to 2 pm
aP"e - on nrior a...""ointment ) Closed on holidavs
Radionuclcar studies (only Department of nuclear medicine Weekdays 9 am to 4 pm
on prior appointment ) Saturday 9 am to 2 pm
• Bone scan Closed on holidays
• Joint" scan
• Thyroid scan
• GE Reflux scan
• DMSA
• DTPA
• DRCG (VUR study
OAE ENTOPD Weekdays 9 am to 4 pm
BOA Saturday 9 am to 2 pm
Closed on holidavs
CT SCAN (only on prior CT Scan, Radiology Dept Round the clock
appointment)

MRI (only on prior MRI scan, Radiology Dept Weekdays 9 am to 4 pm


appointment) Saturday 9 am to 2 pm
Closed on holidavs
421

I-10 UNCOMMON INVESTIGATIONS AVAILABLE WITH PRIVATE LABORATORIES IN CHANDIGARH

Note that situations keep changing. Many investigations that are currently not done in PGIMER may become available in due
course. Investigations that are available in PGIMER must not be done from private laboratories, unless there are exceptional
circumstances, in which case the consultant Neonatology must write down the justification in the file. Under no circumstances
must any representative of a private lab be allowed to come into the hospital premises. The sample must be handed over to the
parents for transportation to the lab.

I-10.1 Laboratories that provide special investigations in Chandigarh (list is not exhaustive)

NAME OF LAB LOCATION CONTACT NOS WORKING ONLINE SUPPORT


HOURS
Fortis Hospital (Met 0172-5021222, 24 hours
Sector-62. Phasc-8, Mohali-62
llbJ 4692222
0172-2665253, 9am--5pm
Dr. Gurjit Kaur,
Genetic Lab, GMCH, Sector-32 2665545-49 (Ext.
GMCH-32
!Oil)
Dr Lal Path Labs SC0-24, Sec 11-D 0172-2748216-18 8 am to 8pm- Mon Availability of a particular test &
To Sat Reports - available online at
8 am to 12.30 pin- www.lalpathlabs.com I
Sun & Holidays For collection of reports user ID= Lab
no Password = Patients Surname
Medicos Centre SC0-822, sector 22A 0172 270R255 7.30 am to 7.30 pm-
SC0-839-40, sector 22A 0172 2715284 MonToSat7.30am
SC0-65, sector 20-C 0172 2708382 to 2 pm-Sun &
Holidavs
422

NAME OF LAB LOCATION CONTACT NOS WORKING ONLll'E SUPPORT


HOURS
Metropolis Collection centre 9814102655 8 am to 8 pm- Mon Email
Laboratories City Metro diagnostic centre To Sat rajeshpkl I(4/redi ffmai I.com
House no 17 8 am to 12.30 pm-
Sector 11 Sun & Holidavs
Ranbaxy Super Collection centers 0172-5025093, 8 am to 8 pm- Mon srl.chandigarhsco@religarewellness.co
Religare Laboratories Specialty Path Lab, SCF 154, sector 09888043030 To Sat m,
(SRL) diagnostics 24-D------------- -- - ---- --- - ----
----- --- 8 am to 12.30 pm- srl_pkl@yahoo.com
Religare wellness, sco 423-424. -9838458390_____ -
Sun & Holidays
Ground floor, sector 35-C
--- --- -- -- - --- - ---- --- --- - - ------- ------ - ------ ------
Cure Well Pathology Centre, SCF 0172-5025093,
154, sector 24-D 09888043030,
09815462178,
09988351098
Khandelwal SC0-108-109, sector 8-C 0172-2772052 8 am to 8 pm- Mon
Diagnostics 0172-2540731 To Sat
8 am to 12.30 pm-
Sun & Holidays
• All the above labs prefer sample collectton using their own containers.
• Amount of sample required varies from lab to lab and hence to be decided after contacting the lab.

1-10.2 Selected specialized tests available in private labs in Chandigarh

INVESTIGATION LAB REPORTING 01'


17 Hydroxyprogesterone Levels Serum Medicos Centre Fri, Wed
Dr. Lal Path Labs Wed
Metropolis Lab next day
SRL Ranbaxv next dav
423

INVESTIGATION LAB REPORTING ON


AA profile Serum Dr Lal Path Labs Sample Mon/Thu & Report Thu/Mon
SRL RanbaxvlHPLC) 4"d
AA profile Urine Dr Lal Path labs Sample Mon/Thu & Report Thu/Mon
Metropolis Lab 3d
SRL RanbaxvlHPLCl 4"d
Antiplatelet antibodies for immune Medicos Centre 2-3 wks
thrombocvtooenias Metronolis Lab next dav
Barr body assay - in buccal smear Medicos Centre same day
Metropolis Labs JOd
SRL Ranbaxy 7• d
CMV PCR Medicos Centre 5d
Dr. Lal Path Labs Sample Tue report Friday
Metropolis Labs next day
SRL Ranbaxv next dav
-
Cortisol Serum Medicos Centre same day
Dr. Lal Path Labs third day
Metropolis Lab next day
SRLRanbaxv next dav
CSF glycine Dr Lal Path Labs 4• d
Metronolis Lab next dav
Cystic Fibrosis screen by TMS Dr Lal Path Labs Sample by sat/Wed: Report on Thu/Mon
Metronolis Lab 7d
Dehydroepiandrosterone (DHEA) levels Medicos Centre Tue, Fri
Dr. Lal Path Labs Sample by Mon, report on Thursday
Metropolis Lab next day
SRL Ranbaxv next dav
424

INVESTIGATION LAB REPORTING ON


FISH for
t(l5;! 7) Dr Lal Path Labs after 7 d

1(8;2 I) Dr Lal Path Labs after 7 d

t(12;2 I) Dr Lal Path Labs after 7 d

22 q deletion Dr Lal Path Lab~ after 7 d


Di George (Peripheral Blood only)

Prader-Willi Syndrome SNRPN (Small nuclear Dr Lal Path Labs after 7 d


ribonuclconrotein nol'""'entide N)
G6PD mutation studies Dr Lal Path Labs I wk
GALT enzyme assay Metropolis Lab next day
SRL Ranbaxv next dav
HCV-RNA PCR qualitative/quantitative Dr Lal Path Labs 2d
SRL Ranbaxy next day
HCV-RNA PCR nualitative Metronolis Lab next dav
HEV-RNA PCR Medicos Centre 5d
HIV DNA PCR Medicos Centre 5d
SRLRanbaxv next dav
HIV P24 assay Medicos Centre 2d
Dr. Lal Path Labs next day
Metronolis Lab next dav
HIV RNA PCR (quantitative titres) Medicos Centre 5d
Dr. Lal Path Labs Sample Moru'Thu. Report on Frirrue
Metropolis Lab 5d
SRL Ranbaxv next dav
425

INVESTIGATION LAB REPORTING ON


HIV western blot Dr Lal Path Labs Sample by Thursday report on Sat
Metropolis Lab next day
SRL Ranbaxy next day
HSV l &2 PCR aualitative Dr Lal Path Labs 3d
lg assays Dr Lal Path Labs next day
Total and individual in serum SRL Ranbaxy next day
Insulin Serum Medicos Centre same day
Dr. Lal Path Labs third day
Metropolis Lab next day
SRL Ranbaxy next day
Karyotyping Medicos Centre 17 d
Dr. Lal Path Labs 3 wks
Metropolis Labs 3 wks
SRL Ranbaxv 2 wks
Organic Acid Quantitative Dr Lal Path Labs 2-3 wks
random Urine
Phenobarbitone levels serum Medicos Centre same day
Dr. Lal Path Labs next day
Metropolis Labs next day
SRL Ranbaxy next day
Phenvtoin levels serum SRL Ranbaxv next dav
Pyruvate CSF Medicos Centre 4"'d
Metropolis Lab next day
SRLRanbaxy 3rdd

Pyruvate serum Medicos Centre 4•d


Metropolis Lab next day
SRLRanbaxv 3rd d

RBC en7Vme assavs Medicos Centre same dav


426

INVESTIGATION LAB REPORTING ON


Rubella lgG Medicos Centre same day
Dr. Lal Path Labs nest day
Metropolis Labs next day
Rubella PCR Medicos Centre 5d
Metronolis Labs 5d
Serum osmolality Medicos Centre same day
Dr. Lal Path Labs next day
Metropolis Lab next day
Serum total bicarbonate levels Medicos Centre same dav
TBPCR Dr Lal Path Labs 3d
Toxonlasmosis lvM & lgG western blot Metronolis Labs next day
Toxoplasmosis ll!M ISAGA Medicos Centre same day
Toxoplasmosis PCR Medicos Centre 4d
Metropolis Labs 5• d
Urine osmolality Medicos Centre 2d
Dr. Lal Path Labs next day
Metrooolis Lab next dav
a 1 Antirrvnsin Levels serum Metrooolis Lab 3rd d
427

1-11 SELECTED LABORATORIES OUTSIDE CHANDIGARH

LAB, contact oerson TESTS ADDRESS CONTACT NOS ONLINE SUPPORT


Genetic & Mental Retardation OII-26561123, mkabra_aiims@yahoo.co.in,
AllMS, Tests for genetic/metabolic
Clinic, Dept. of Pediatrics, 26588500 rnadhulikakabra@hotmail.com
Dr. Madhulika Kabra diseases
AIIMS, New Delhi-29.
0172-5021222,
Fortis Hospital Methemoglobin level Sector-62, Phase-8, Mohali-62
4692222
0172-2665253,
GMCH-32, Tests for genetic/metabolic Genetic Lab, GMCH, Sector-
2665545-49 (Ext.
Dr. Gurjit Kaur diseases 32
1013)
Manipal Acunova Ltd., Mobius 9814610892 Email:
HIV DNA PCR, HIV RNA PCR,
Medicose Diagnostics Towers, SJR i-Park, EPIP, 080-66915700 bd.asia(d]ecronacunova.com
p24 Antigen
Whitefield, Bangalore 560066
NIMHANS, Neonatal screening for IEM - TMS Dept ofncurochemistry, 080-26995163/62 (0) Email
Dr Rna Christopher NIMHANS, Bangalore- rita(gln1mhans.kar.nic.in
560029, India
Navi Mumbai Institute Neonatal screening for IEM - NIRMAN Tei/Fax- Website -
of Research in Mental TMS, HPLC for AA and organic 312, Nirman VyaparKendra, 789 1410 http://jalananiI.tripod.com/N IR
and Neurological acids etc Sector 17,Vashi, Navi Mumbai MAN
handicap (NIRMAN), India 400 705
Dr Anil Jalan
Sir Ganga Ram Molecular Diagnoslic Tests, Sir Ganga Ram Hospital, Dept Tel; gangaram@sgrh.com
Hospital, Chromosomal I Cytogenetics of Genetic Medicine, Rajinder Ol I-25735205,
Dr IC Venna Prenatal Diagnostic Facilities Nagar, New Delhi 110060, 25861463 Fax:
INDIA 25861002
Sri Ramchandra Solomon FD Paul, Dept. Fax-044-24767008 wise_soly@yahoo.com
Tests for genetic/metabolic
Medical college, Human Genetics, SRMC,
diseases
Chennai; Genetics Cell Porur, Chcnnai-600116
428
429

DI. ACETAZOLAMIDE
Indications: Hydrocephalus. Not recommended for PHH.
Presentation: 250 mg tablets, to be made into sachets. Store at room
temperature.
Dosage: Start with I0 mg/kg/dose q 6-8 hourly. Increase to 25
mg/kg/dose
Duration: As indicated by underlying condition
Administration: Oral
Comments: Causes G.I irritation, drowsiness, hypokalemia & acidosis

D2. ACYCLOVIR
Indications: HSV and severe Varicella zoster infections (CNS &
pulmonary) & herpes simplex encephalitis
Presentation: IV: 250 mg vial of I0 mL. Store below 25°C.
Oral syrup: 200 mg/5 mL concentration. Store at room temperature
Dosage: 20 mg/kg/dose q 8h
Duration: Localized Herpes Simplex infections - 14 d
CNS or disseminated infections - 21 d
Reconstitution: Add IO mL of WFI or N/S to the vial to make a 250-
mg/l 0 mL solution. Discard after use. Reconstituted solution is stable in
room temperature for 12 h. Do not refrigerate.
Dilution: Dilute the contents of the reconstituted vial to 50 mL with N/S
or N/4 saline to make a 250 mg/50 mL solution (5 mg/I mL dilution). 2
mL/kg ~ I 0 mg/kg
Administration: Syringe driver infusion over l hour.
Comments: The drug is metabolized in liver & excreted by the kidney
and the dose interval may need to be adjusted if there is renal impairment
or hepatic failure. Normal hydratioo to avoid crystalluria and renal
tubular damage.

D3. ADENOSINE
Indications: SVT involving the A-V node (re-entrant type)
Presentation: 6 mg/2 mL vial. Store below 25°C. Do not refrigerate.
Dosage : 50 µglkg/dose, increasing by 50 µg/kg with each dose until
there is reversion to sinus rhythm or the maximum dose of 250 µg/kg is
reached. I - 2 min between doses.
Dilution: Dilute 0.33 mL (I mg)/kg from the vial to 20 mL with N/S to
make a 1000 µg/kg/20 mL solution. I mL ~ 50 µg/kg. Solution
compatibility: 5% D, NS
Administration: Rapid injection at proximal cannula site. Flush IV with
saline immediately
Comments: Higher doses required for patients on theophylline. May
430

cause dyspnea and flushing (transient- resolves within 1 min). Observe


for transient complete A-V block, sinus bradycardia and ventricular
extrasystoles. Short half-life precludes administration via an UA catheter.

D4. ADRENALINE
Indications: Hypotension and circulatory failure not responding to other
drugs. Acute cardiocirculatory arrest.
Presentation: I: 1000 ampoule (1000 µg/mL). Store below 25°C. Protect
from light. Always use as a 1:10000 concentration (100 µglmL) (class
III)
Dosage : Low dosage 0.05 - 0.1 µg/kglmin. High dosage 0.2 -
µglkglmin
Dilution: First dilute 1 mL of the adrenaline in 9 mL N/S to make
1:10,000 solution. For low dose infusion dilute 1.5 mL (150 µg)/kg from
the ampoule to 50 mL with 5% D or N/S to make a 3 µg/kglmL solution.
I mL/h ~ 0.05 µg/kglmin. For high dose infusion dilute 6 mL (600
µg)/kg from the ampoule to 50 mL with 5% D or N/S to make a 12
µg/kglmL solution. 1 mL/h ~ 0.2 µg/kg/min. Solution compatibility: 5%
D, 10%0, NS
Administration: Syringe pump infusion.
Comments: Ensure adequate circulating blood volume. Concurrent
vasodilator therapy is usually necessary if a high dose is used.

D5. AMIKACIN
Indications : Gram-negative bacillary infection resistant to other
aminoglycosides
Presentation: I 00 mgl2 mL vial. Store below 25°C. 1
Dosage : S l 500 g babies in the first 7 d oflife: 7. 5 mglkgldose q 241'.J
All others: 15 mg/kgld~h
Dilution: Dilute 0.6 mL (30 mg) from the vial to 10 mL of N/S or 5% D
to make a 30 mgllO mL
solution. 2.5 mL/kg ~ 7.5 mglkg.
Solution compatibility: 5% D, 10% D, NS
Incompatibility: Cloxacillin, amphotericin B, phenytoin, ampicillin
Administration: Syringe driver infusion over 1 hour.
Serum levels: Peak 20 - 30 mglL; Trough 2 - 5 mglL.
Storage: Store at 2-30 °C.
Comments: Ototoxic and nephrotoxic; avoid concurrent use of
frusemide, vancomycin. Excreted by the kidney and the dose interval
may need to be increased if there is renal impairment, significant
asphyxia, PDA, lndomcthacin therapy. May prolong the action of
neuromuscular blocking agents.
431

D6. AMILORIDE
Indication: Chronic lung disease
Preparation: See hydrochlorothiazide
Dose: See hydrochlorothiazide
Comments: Potassium sparing, hence can cause hyperkalemia

D7. AMINOPHYLLINE
Indications : Apnoea of prematurity, Weaning preterm infants from
intermittent mandatory ventilation, BPD, PGE 1 induced apnea
Presentation: 250 mg/2 mL ampoule (IO mL). Store below 25°C.
Protect from light.
Dosage: Loading 6-8 mg/kg. Mamtenance 1- 2 mg/kg/dose q Sh
Dilution: Dilute 0.4 mL (I 0 mg) from the ampoule to I 0 mL with 5% D
to make a I0 mg/lO mL
solution. I mL/kg ~ I mg/kg
Administration: The loading dose is given by syringe driver infusion
over I hour. The maintenance dose is given by syringe driver infusion
over 20 - 30 min. Rapid infusion has been associated with marked
hypotension, syncope and death.
Plasma levels: Blood is collected 1 hour pre-dose. Therapeutic levels are
7-12 µg/mL
Comments: Reduce the doses in liver disease and heart failure. Adverse
effects- tachycardia, GIT irritation, hyperglycemia, CNS irritability.
Toxicity: failure to gain Wt, vomiting, and seizures. Treatment:
Activated charcoal Jg/kg as slurry by gavage tube q2-4 h.

D8. AMIODARONE
Indication: Supra-ventricular & ventricular tachyarrhythmias
Presentation: Supplied: Injection 50 mg I mL ampoules. Ampoules
usually 150mg. Tablet 200 mg
Dosage:
IV (only in emergencies): 5 mg/kg JV over I min, followed by infusion
of 5 µg/kg/min; infusion may be increased up to I 0-20 µg/kg /min. IV
continuous infusion concentration for peripheral administration should
not exceed 2 mg/mL and must be diluted with 05 W.
2
Oral: Loading dose of JO mg/kg/d, or 800 mg/J.72m Id for JO d,
thereafter tapering to maintenance of 2.5 mg/kg/d.
Administration: PO, JV
Comments: Amiodarone reduces clearance of Digoxin, Flecainide,
Procainamide, Quinidine, Sildenafil, Theophylline and Warfarin.
Monitor ECG, electrolytes, liver enzymes, thyroid functions, Chest X-
ray. May cause worsening of preexisting arrhythmia with bradycardia
and A-V block. Protect patient from sunlight for up to 3 mths after
stopping treatment using a Zn or Ti based sun block.
432

09. AMOXICILLIN
Indications: L1steriosis, Prophylaxis for UTI, Otit1s media
Preparation : Suspension 125 mg;5 ml. After reconstitution the
suspension should be refngeratcd but that is not essential. It can be used
for 14 d at room temperature.
Dosage
50 mg,kg;dose q 12 hourly in first 7 d PO.
50 mg,ikg/dose q 8 hourly in 2nd to 3rd wk PO.
50 mg/kg/dose q 6 hourly in 4lh wk PO.
Comments: In case of hypersensitivity to penicillin 1t should be 8\01ded.
lt is more completely absorbed than ampicillin. Can cause diarrhea.

010. AMOXICILLIN-CLAVULANATE
Indications: Acute bacterial LRI (pneumonia), UTI, Skin & Soft tissue
infections.
Presentation: (7: I formulation)
lnJ Vial 250 mg. (Amox1c1lhn 200 mg ... Clarnlamc acid 50 mg)
Syrup (Amox1c11lin 200mg + Clavulamc acid 28.5 mg/5 mL}
Dosage: 30 mg; kg of Amoxicillin. (<3 mths of age)
Interval: 12 hourly.
Storage of injection: Unconstituted: Store at less than 30°C.
Reconstituted'. 24 hat room temp .. 5 d at 4°C
Comments: Causes Diarrhea, skin rash, Urticaria Must not come in
contact with an aminoglycoside. Each 3 1.25 mg of Potassium clavulanate
has 0.16 mFq ofK.

);/ 011. AMPHOTERICIN B


1 Indications : Systemic fungal infections such as moniliasis (Candida
a/h1cans) and aspergillos1s (Aspergillus fumigatus) etc.
Presentation : Plain amphotencm B: 50 mg vial. Store below 8°C. Do
not freeze. Protect from light.
L1p1d complex: I0, 50, I00 mg vial. Store below 8°C. Do not freeze.
Protect from light.
Liposomal. 50 mg vial. Store below 8°C. Do not freeze. Protect from
light
Dosage
Day I 0.5 mg/kg/dose
Day 2+ 1.0 mglkgldose q 24 h. A total dose of25 30 mgikg is usually
given
Lipid complex ... 5-7 mg/kg/dose q 24 h
Liposomal ....... 5-7 mg/kg/dose q 24 h
Reconstitution: Add 10 mL of WFI to the vial to make a 50-mg/10 mL
solution. Stable for 7 d in the refrigerator. Lipids complex and liposomal
433

are srable for 48 h and 24 h 'fter reconstitution respectively in


refrigerator.
Dilution: Dilute mL (5 mg) of tLe reconstituted vial to 50 mL with
'amphotericin' labelled 5% D (pH >4.2) to make a 5-mg/50 mL solution.
10 mL/kg ~ 1.0 mg/kg
Do not flush IV or dilute in NS as the precipiration will occur.
Lipid complex comes in ready to use admixture. To be diluted in the 5%
D to make final concentration as l-2mg/mL.
Liposomal is 50 mg powder, which is to be reconstituted in 12 mL sterile
water to make 4 mg/mL concentration. Shake vigorously immediately &
check for complete dispersion. Before infusion final concentration should
be2 mg/mL
Administration: By syringe driver infusion over 4 h.
Storage: Unconstituted product: 4 °C. Protect from light.
Reconstituted: 24 h at room temp, 7 d at 4 °C. Do not freeze. Protection
from light not required.
Comments: Neonates generally tolerate well. Monitor renal functions,
K' levels, Mg- levels, CBC, and liver functions. Na' intake of >4
meg/kg/d may prevent or decrease renal toxicity. Other side effects are
anemia, thrombocytopenia, hypokalemia, nausea, vomiting, and
fever/chills.

D12. AMPJCILLIN ·.
Indications: Ampicillin together with an aminoglycoside (genramicin)
may be used for the treatment of suspected community-acquired early-
onset bacterial sepsis. Ampicillin has a broader spectrum of activity than
penicillin. It is useful against GBS, Listeria, susceptible E coli.
Ampicillin is preferred to penicillin for the treatment of listeria
monocytogenes sepsis.
Presentation: 250 mg, 500 mg vial. Store below 25°C. Suspension 125
mg/5 mL
Dosa e: m d
,;7 d >7 d
100-200 200-400
The higher dose is recommended for meningitis.
Route: PO, IM, IV
Interval
j,;7d
I 12 h
1;:d
Reconstitution: Add 1.7 mL ofWFI to the vial to make a 250 mg/I mL
solution. 0.5 mL/kg ~ 125 mg/kg. 5% D, 10% D, NS are compatible.
Administration: Slow injection at proximal cannula site.
Storage of injection: Unconstitutcd: Keep at less than 30°C.
Reconstituted: 24 h at room temp, 5 d at 4 °C.
434

Comments: Sodium content of IV preparation: 3 mEq/g. Must not come


in contact with an aminoglycoside. Hypersensitivity reactions
(maculopapular rash, urticaria! rash, or fever) are rare.

Dl3. AMRINONE
Indications: Post-cardiac surgery, cardiogenic shock
Presentation: Injection: 5 mg/mL in 20 mL vial .
Dosage: Loading dose~ 1-3 mg/kg IV over 30 min. Continuous infusion
~ 5-10 µg/kg/min
Reconstitution: Do not dilute with Dextrose containing solutions.
Comments: Onset of action 2-5 min with peak effect in 10 min. Not to
be infused with frusemide. Monitor for thrombocytopenia,
hepatotoxicity, GIT effects, fluid and electrolytes.

D14. ATROPINE SULPHATE


Indications: Prevention of vagally induced bradycardia during tracheal
intubation. Prevention of the muscarinic effects of neostigmine.
Presentation: 600 µg/mL ampoule. Store below 25°C. Protect from
light.
Dosage: 20 µg/kg/dose (10-30 µg/kg/dose IV over 1 min, or IM). Can be
repeated q 10-15 min to achieve desired effect. 5% D, 10% D, NS are
compatible.
Dilution: Dilute one ampoule (600 µg) to 10 mL with N/S to make a 600
µg/10 mL solution. 0.3 mL/kg ~ 20 µg/kg
Administration: Rapid injection at proximal cannula site.
Comments: Adverse effects include cardiac arrhythmias, fever,
abdominal distension with decreased bowel activity, esophageal reflex,
mydriasis and cycloplegia.

DIS. AZITHROMYCIN
Indication: Active against a broad spectrum of organisms, including
most g +ve organisms, Hemophilus, atypical organisms, such as
Ureaplasma. Mycoplasma, Chlamydia and S typhi
Preparation: Syrup I 00 mL/5 mL
Dose: 6 mg/kg/dose
Interval: 24 h •
Duration: 3 d
Comments: Can cause diarrhea. Less gastric irritation and hepatic
adverse effects than erythromycin.

D16. AZTREONAM
Indication: Sepsis due to major gram negative pathogens like £. coli,
Klebsiella species, H. influenzae, Serratia species and Pseudomonas
aeruginosa. Ineffective against gram positive.
435

Presentation: Available as 0.5 g anc 1.0 g vials. Once reconstituted it


must be used within 48 h if kept at nom temperature or within 7 d if
refrigerated.
Route: IV, IM
Dosal!e & interval:
Postnatal Wt(g) Dose Interval
a"e (d) lmnllm/dosel
<7 <2000 60 12 h
<7 >2000 90 8h
>7 <2000 90 8h
>7 >2000 120 6h
Reconstitution: Stable m 5% D, NS. I 0% D, should be used quickly if
not prepared with NS or SWFI. The recommended final concentration for
infusion should not exceed >20 mg/mL. The rate of infusion 6mg /kg/
min.
Administration: IV infusion over 15-30 min by syringe driver.
Comments: Aztreonam penetrates inflamed meninges, and reach
therapeutic levels in the CNS. Adverse reactions: Thrombocytopenia,
Neutropenia, leucopenia, elevated liver enzymes, seizures.

DI7. BUDESONIDE
Indications : BPD
Presentation: Respules containing nebulising suspension 250, 500 µg, I
mg /2 mL. Store below 25°C.
Dosage: 100 µg/kg/dose. Maximum dose~ 400 µg/d
Interval: 12 h
Dilution: Dilute the prescribed dose with N/S to give a total fill volume
of4 mL.
Administration: Nebulise for I 0 min and discard the remainder.
Comments: The effect on growth and adrenal function has not been
studied in newborn infants, though there is a favourable topical to
systemic effect ratio. The drug can also be administered using a metered
dose inhaler, spacer or face mask. May cause pharyngitis, cough, and
epistaxis.

DIS. CAFFEINE CITRATE


Indication: AOP
Preparation: 60 mg in 3 mL bottle: both IV & PO
Route: IV, (not IM), oral
Dosage
Loading I 0 mg/kg of caffeine base
Maintenance 2 .5-5 .0 mg/kg/dose of caffeine base, to begin 24 h after
loading dose
Interval: 24 h
436

Comments: Desired plasma concentration: 5-20 mg/L. Can cause


tachycardia, seizures; but safer than aminophylline. Avoid use in
symptomatic cardiac arrhythmias

D19. CALCITRIOL (I, 25 dihydroxyvitamin D3) [for Vit D, see


ergocalci feral]
Indications: Hypocalcaemia secondary to hypoparathyroidism.
Presentation: 0.25 µg capsule. Store below 25°C.
Dosage : 0.025 - 0.05 µg/kg/dose
Interval: 24 h
Administration: Aspirate the desired dose from the capsule using a
needle and I mL syringe.
Give the required amount orally.
Comments: Calcitriol has a more rapid onset of action and a shorter
half-life than ergocalciferol but it is more expensive. Monitor plasma
calcium, phosphorus, magnesium and ALP levels.

D20. CALCIUM INJ.


Indications: Hypocalcaemia.
Presentation: 10% Calcium Gluconate: I 0 mL ampoule containing 9 mg
Ca/mL. Store below 25°C. Calculated osmolarity is 700 mOsm/L
Route: For IV use only. SC or IM may cause severe tissue necrosis
and/or sloughing. Use hyaluronidase for calcium extravasation
Dosage : I - 2 ml/kg/dose. Use higher end of dose range for treatment
of hypocalcemia, lower for maintenance
Dilution: For IV injection dilute I: I with WFI.
Administration: Slow injection at proximal cannula site over 10 - 15
min. Don't use scalp vein.
Comments : Electrocardiographic monitoring is mandatory during IV
injection. Inject slowly into a large vein because of the possibility of
tissue necrosis. Plasma calcium levels should be monitored closely.

D21.CAPTOPRIL
Indications: Congestive cardiac failure. Neonatal hypertension including
that associated with coarctation of the aorta.
Presentation: Tablets of 12.5 mg. To be reconstituted into sachets. Store
below 25°C.
Dosage : Test 0.05 - 0.1 mg/kg. Use the smaller test dose when the
infant is receiving other vasoactive drugs or diuretics.
Maintenance 0.1--0.3 mg/kg/dose. Commence maintenance at 0.1
mg/kg/dose and increase each day by 0.1 mg/kg/dose to 0.3 mg/kg/dose
depending upon the desired hemodynamic effects.
437

Interval: 8 h
Administration: Orally before feeds
Comments: Use with caution in patients with low renal perfusion
pressure. Reduce dose with renal in1pairment and in sodium and water
depleted patients. May cause prott"inuria, neutropenia, hyponatremia.
May cause hyperkalemia as it spares potassium at renal level.

D22. CARNITINE
Indication: Fatty acid oxidation defects, camitine deficiency, dilated
cardiomyopathies
Presentation: 330 mg per tablet. Make sachets.
Dosage: Carnitine deficiency: initial 50 mg/kg/d, mcrease to I 00
mg/kg/d. Max dose 3 g/d
Cardiomyopathy: initial 100 mg/kg/d, increase to 200 mg/kg/d
Interval: 24 h
Administration: Oral
Comments: Causes transient diarrhea

D23. CEFOPERAZONE
Indication: Systemic infections based on sensitivity report. Covers
Pseudomonas.
Presentation: 250 mg per mL vials
Dosage: 30 - 40 mg/kg/dose. IV bolus: Over 3-5 min. IV infusion: Dilute
to 20 mL, infuse over 20-60 min
Interval: 8 hourly
Reconstitution: I g diluted to 5 mL and subsequently to 15-20 mL with
any diluent except RL. For injection the final concentration should be
maximum of I 00 mg/mL. Wait till foaming subsides before injection.
Straw yellow colour does not indicate loss of potency.
Storage: Unconstituted: Store at less than 25 'C. Reconstituted: 24 h at
room temp., 5 d at 4°C.
Comments: Extensively excreted in bile, use with caution in patients
with hepatic failure. Does not penetrate well into CSF. Sodium contenF
1.5 mEq/g

D24.CEFOT AXIME
Indications: Active against many Gram negative organisms but not
Pseudomonas species. Good CSF penetration and therefore the drug of
choice for Gram negative meningitis.
Presentation: 125, 250, 500 mg vial. Store below 25°C. Protect from
light.
438
~\ 1 . tGY"'·
Dosa /k Id
>7 d
~1 ~°'! \A.
:£7 d
100-150 l 50-200
The higher dose is recommended for meningitis.
Interval
Gestation $7 d >7 d
Preterm 12 h 8h
Term 8h 6h
Reconstitution: Add 4.8 mL of WFI to the vial to make a 500 mg/5 mL
solution. Stable for 24 h in the refrigerator. l mL/kg = l 00 mg/kg.
Colour can become yellow without loss of potency; however dark brown
colour implies loss of potency.
Storage: Unconstituted: Store at less than 30°C. Protect unconstituted
product from light. Reconstituted: 24 h at room temp, l 0 d at 4 °C.
Administration: Slow injection at proximal cannula site.
Comments: Blunting of peak aminoglycoside concentration if
administered< 2 h before/after cefotaxime. Sodium content: 2.2 mEq/g

D25.CEFTAZIDIME
Indications: Active against many Gram-negative organisms including
Pseudomonas species. Good CSF penetration and therefore the drug of
choice for Pseudomonas meningitis.
Presentation: lg vial. Store below 25°C.
Dose And Interval (mg/kg/dose)
Wt <:1200 g 1200-2000 g >2000 g
Age Any <: 7 d >7 d <: 7 d >7 d
Dose 50 50 50 50 50
Interval 12 h 12 h Sh 12 h Sh

Reconstitution
Add 10 mL of WFI to the vial to make a 90 mg/mL solution. Shake to
dissolve and wait until the solution is clear (l - 2 min). Stable for 7 d in
the refrigerator. l.l mL/kg = 100 mg/kg. Yellow, amber or dark colours
do not indicate loss in potency.
Storage: Unconstituted: Store at 15 - 30°C. Reconstituted: 24 hat room
temp., 7 d at 4 °C, 3 mths frozen. Carbon dioxide is released as
ceftazidime dissolves, generating pressure within the container. A vent
needle should be inserted after the drug has dissolved.
Administration: Slow injection over 3-5 min. at proximal cannula site.
Comments: Sodium content: 2.3 mEq/g. Must not come in contact with
aminoglycosides, vancomycin or bicarbonate.
439

D26. CEFTRIAXONE
Indications: Broad spectrum antibio ic.
Presentation: 1 vial with dry substa 1ce equivalent to 0.25 g or 0.5g or 1
g ceftriaxone. (contains 3.5 mEq Na;•)
Dosage:
Wt :01200 g 1200-2000 g >2000 g
Age Any :s 7 d >7 d <7d >7 d
Dose 50 50 50-75 50 50-75
Interval 24h 24 h 24 h 24 h 24 h
Severe mfechons: 80-100 mgikg/d m 2 d1v1ded doses
Reconstitution:
IV injection: For IV injection, ceftriaxone 0.$ ~dissolved in 5 mL, and
ceftriaxone 1 g in 10 mL, of SWFI. The IV administration should be
given over two to four min.
IV infusion: The infusion should last at least 30 min. For IV infusion,
0.5 g ceftriaxone are dissolved in 10 mL (I0-40 g/mL) of one of the
following calcium-free infusion solutions: sodium chloride 0.9%, sodium
chloride 0.45o/o + dextrose 2.5%, dextrose 5%, dextrose 1Oo/o infusions,
sterile WFI.
Storage: Reconstituted solutions retain their physical and chemical
stability for 6 h at room temperature (or 24 h at 2-8°C). Store below
25°C.
Comments: Coombs' test may rarely become false-positive. False
positive tests for galactosemia. Incompatible with vancomycin,
fluconazole and aminoglycosides. Ceftriaxone can displace bilirubin
from serum albumin. Should not be used in neonates at risk of
developing bilirubin encephalopathy. Can cause biliary sludging

D27.CHLORAL HYDRA TE
Indications : Sedation.
Presentation: 100 mg/mL syrup. Store below 25'C.
Dosage
Hypnotic 50 mg/kg/dose
Sedative 5 - I 0 mg/kg/dose
Sedation for medical imaging 50 mg/kg
I ntervaI: 6 - 8 h
Administration: Oral. 1

1
Comments: Use with caution in the~resence of hepatic dysfunction
since use has been associated 'th both indirect and direct
hyperbilirubinemia. Repeated dosing at frequent intervals causes
accumulation of toxic metabolites. Causes irritation of skin and mucous
membranes because of its high osmolarity. \Contraindicated in renal and
hepatic impairment. \~
440

D28. CHLOROQUINE
Indication: Acute malaria- congenital or transfusion related.
Presentation: Suspension 50 mg/5 mL. Inj 40 mg/mL ampoule.
Dosage: 10 mg/kg stat followed by 5 mg/kg 6 h later, and OD for 2 d.
Comments: Avoid in severe liver disease. Parenteral injection can cause
hypotension, respiratory depression.

D29. CIMETIDINE
Indications: Reflux esophagitis. Treatment of gastric ulceration and
gastritis secondary to stress or indomethacin.
Presentation: 200 mg tablet. To be reconstituted into sachets. Store
below 25°C.
Dosage : 5 - I 0 mg/kg/dose. Commence treatment with the lower dose.
Interval: 6 h
Dilution: For oral administration dissolve one tablet (200 mg) in I 0 mL
of sterile water to make a 200 mg/10 mL solution. 0.5 mL/kg ~ 10 mg/kg
Administration: Orally with feeds.
Comments: Use with caution when hepatic or renal function is impaired.
Reduce the dose of theophylline by 50 % if used concurrently. Routine
use has been associated with increased respiratory infections.
Neutropenia, cholestasis and elevated transaminases are the side effects.

D30. CIPROFLOXACIN
Indication: Active against gram-negative bacteria including
Pseudomonas. Also active against gram-positive bacteria like Staph
aureus, Staph epidermidis.
Presentation: IV 200 mg/100 mL bottle. Tablets- 100 mg, 250 mg, 500
mg.
Dosage: 10 mg/kg/dose. No difference in meningitis.
Interval: 12 h
Administration: Infuse over 30-60 min
Storage: Store IV preparation at less than 30 °C
Comments: Several reports are now available showing safety in
neonates. There are reports confirming successful use of Ciprofloxacin in
neonatal meningitis. Use with caution along with Aminophylline, as
serum levels of Aminophyllinc may rise and cause toxicity.

D31. CLINDAMYCIN
Indications : Gram-positive coccal and anaerobic sepsis. First-line drug
combined with an aminoglycoside (gentamicin) in the treatment of
proven anaerobic sepsis.
Presentation: 300 mg/2 mL vial. Store below 25°C.
Dosage & interval
(mg/kg/ dose)
441
Wt <1200 g 1200-2000 g >2000 e
Age Any <7d >7 d <7d >7 d
Dose 5 5 5 5 5-7.5
Interval 12 h 12 h 8h 8h 6h

Dilution: Dilute 0.5 mL from the vial to 25 mL with N/S or 5% D to


make a 75 mg/25 mL solution. 1.67 mL/kg = 5 mg/kg
Administration: Syringe driver infusion over I hour.
Comments: There is little information regarding pharmacokinetics in
newborn infants. Does not cross blood brain barrier, do not use to treat
meningitis.

D32. CLONAZEPAM
Indications: Seizures not controlled with phenobarbitone and phenytoin.
Presentation: I mg/mL ampoule (with diluent). After reconstitution I
mg/2mL. Tablets: 0.5 mg and 2 mg.
Dosage: Intermittent: 0.05 - 0.1 mg/dose; Maintenance: 0.05 - 0.1
mg/kg/d
Interval: 8 h
Storage: Store below 25°C.
Administration: IV & Oral; If IV, give as slow injection at proximal
cannula site.
Comments: The therapeutic plasma levels: 60 - 150 nmol/L; May cause
respiratory depression; May cause hypotonia.

D33. CLOTRIMAZOLE LOCAL APPLICANT


Indication: Candidiasis, fungal nappy rash, intertrigo, ringworms.
Presentations: Candid cream for skin application, Candid lotion for
scalp application, Candid mouth paint for oral application
Dose: Apply thinly and evenly to affected areas, 2-3 times per day and
rub it gently and continue for 14 d after healing of lesion. Oral: apply
after every feed.
Comments: can cause local irritation, itching, burning sensation, contact
dermatitis

D34. CLOXACILLIN
Indication: Septicaemia caused by gram-positive bacteria including
MSSA
Presentation: 250-mg/ vials; 125 mg/5 mL Syrup.
Dosage: 25- 30 mg/kg/dose
Interval: 6- 8 h.
Storage of injection: Unconstituted: Store at less than 30°C;
Reconstituted: 24 h at room temp. & 7 d at 4 °C
Comments: Sodium content of IV preparation: 2.5 mEq/g. Can cause
442

drug fever, skin rash, thrombophlebitis.

D35.COLISTIN
Indication: MDR bacterial infections. No data on efficacy & safety in
neonates.
Presentation: Colistimethate sodium in vials containing 150 mg colistin
base.
Dosage: 5 mg/kg/d
Interval: 8 hourly
Reconstitution: With 2 mL WFI to yield 75 mg/mL base. Gently swirl
to avoid frothing
Storage: Reconstituted solution at 2-8 'C for 24 h
Administration: IV slowly over 3-5 min
Comments: Nephrotoxic

D36. COTRJMOXAZOLE (TRIMETHOPRIM-


SULPHAMETHOXAZOLE)
Indications: Pneumocystis carinii pneumonia, prophylaxis against
Pneumocystis carinii in HIV infected neonates, useful when there is
resistance to all commonly used antibiotics, prophylaxis against urinary
tract infection (UT!).
Presentation: TMP/SMX 80/400 mg/5 mL ampoule; TMP/SMX 40/200
mg/5 mL syrup.
Dosage
Loading ................ TMP/SMX 2/10 mg/kg
Maintenance ........ TMP/SMX 1.2-2.4/6--12 mg/kg/d
UTI Prophylaxis .... TMP/SMX 2/10 mg/kg/d
High dose ............. TMP/SMX, 10-15/50-75 mg/kg/d, has been used in
neonatal meningitis.
Interval
Maintenance ............. 12 h
UT! Prophylaxis ....... 24 h
Reconstitution: Dilute JV 2 mL (TMP/SMX 32/160 mg) to 50 mL with
5% Dor N/S to make a TMP/SMX 32/160 mg/50 mL solution.
3 mL/kg ~ TMP/SMX 2/10 mg/kg
I mL/kg ~ TMP/SMX 0.6/3 mg/kg
Storage: Store below 25°C. Protect from light.
Administration: If IV Syringe driver infusion over not less than I hour;
Oral.
Comments: Good CSF penetration, Oral absorption is unpredictable.
Although sulphamethoxazole has not been shown to displace bilirubin
from albumin binding sites, it should be use with caution in preterm
infants with jaundice.
443

D37. CYCLOPENTOLATE EYE DROPS


Indication: For pupillary dilatation for ROP screening, to look for
chorioretinitis.
Presentation: 0.5%, 1% eye drops.
Dose: 1-2 drops on both eyes 15 -20 min apart.
Comments: Can cause tachycardia increase intraocular pressure, hence
avoid in buphthalmos. Action may last for about 24 h.

D38. DESMOPRESSIN (DDA VP)


Indications: Diabetes insipidus.
Presentation: 1 µg/mL bottle plus a measuring device capable of
delivering 0.05 mL and 0.1 mL intranasal doses. Store below 8°C. Do
not freeze. Protect from light.
Dosage: 0.5 µg
Interval: 8 - 24 h
Administration: Intranasal
Comments: The recommended dosage varies from 0.14 µg/kg/d to 30
µg/d. The dose and frequency of administration are altered according
to the infant's state of hydration.

D39. DEXAMETHASONE
Indications: The use of post-natal dexamethasone {irrespective of
indication & dose regime) is controversial, because of major concerns
regarding poor neuro-developmemal outcome. It should be sparingly
used, after seeking i'1formed parental consent.
Preterm infants with BPD.
ET intubation injury with upper airway oedema and obstruction resulting
in repeated extubation failures.
Presentation: 4 mg/mL ampoule; Tablets: 0.5 mg tablets to be
reconstituted in sachets
Dosage: BPD: 0.89 mg/kg of cumulative dose over IO d
Peri-extubation: 0.25mg/kg/dose q 8 hourly for 3 doses, I" dose at least
4 h prior to extubation
Reconstitution: Dilute 1 mL (4 mg) from the ampoule to 4 mL with N/S
to make a 1 mg/mL solution. 0.5 mL/kg ~ 0.5 mg/kg
Storage: Store below 25°C.
Administration: Slow injection at proximal cannula site. The IV route is
preferred but the oral route may be used after the first 3 - 6 d.
Comments: Hypertension, hyperglycemia, GIT bleeding or perforation
and hypertrophic obstructive cardiomyopathy may occur. May cause
adrenal suppression, lowered immunity.

D40. DIAZOXIDE
Indications: Hypoglycemia secondary to hyperinsulinism, Hypertension
444

Dosage: Hyperglycemia: 8-15 mglkg/d. Hyperinsulinism: 5-20 mg/kg/d


in 3 divided doses according to the dose response.
Interval: q 8 - 12 hourly
Administration: Oral
Comments: Can cause hypotension, tachycardia, arrhythmia, extra
pyramidal signs. Edema from sodium and water retention is a common
occurrence. Potentiate effect of diuretic and hypotensive agents,
increases phenytoin metabolism and displaces bilirubin from albumin.

D41. DIAZEPAM
Indication: Status epilepticus/continuous refractory seizures,
sedation/muscle relaxation, hyperglycinemia
Presentation: 1Omg/2 mL ampoules
Dosage: 0.1-0.3 mg/kg/dose.
Comments: To be injected slowly, not to be mixed with other solutions.
The vehicle of diazepam contains sodium benzoate, and it displaces
bilirubin from albumin binding site.

D42. DIGOXIN
Indications: Congestive cardiac failure, SVT, congenital atrial flutter
and fibrillation.
Presentation: 50 µg/2 mL ampoule for IV injection. 50 µg/mL elixir for
oral use.
Dosa e
Term
Di italisation 30
Maintenance d
Interval: For Digitalisation: Give one-half of the digitalising dose stat
and the other one-half in three divided doses at 6 - 8 h intervals. For
Maintenance: 12 h
Reconstitution: Dilute 1 mL from the ampoule to 5 mL with WFI or N/S
to make a 25 µg/5 mL solution. 1 mL/kg ~ 5 µg/kg
Storage: Store below 25°C.
Administration: lflV- Slow injection at proximal cannula site; Oral.
Comments: The therapeutic plasma concentration is 1 - 2 ng/mL
Digoxin toxicity is rare when the plasma level is <3.5 ng/mL. Cross
reactivity may result in spuriously high levels in newborn infants.
Toxicity causes arrhythmias (usually supra-ventricular), sinus
bradycardia, heart block, vomiting.

D43. DOBUT AMINE


Indications: Cardio circulatory failure
Presentation: 250 mg vial. Store below 25°C.
Dosage: 1 - 20 µglkg/min. Max: 40 µg/kg/min
445

Reconstitution: Add I 0 mL of WFI :o a 250 mg vial to make a 250


mg/1 0 mL solution.
Dilution: Dilute 1.2 mL (30 mg)/kg from a vial to 50 mL with D5% or
N/S to make a 30 mg/kg/50 mL solution. (Max 5 mg/mL); 1 mL/h ~ 10
µg/kg/min
Administration: Use syringe pump infusion. Stable in parenteral
solution for 24 h. Incompatible with alkaline solution. Don't give through
same line as heparin, NaHC0 3• Penicillin.
Comments: Ensure adequate circulating blood volume. Tachycardia
occurs less commonly than with dopamine. May cause hypotension. Pink
discoloration indicates oxidation but no loss of potency. May cause
ectopic heart beats, VT and arrhythmia in high dose. phlebitis, skin
necrosis on extravasation.

044. DOMPERIDONE
Indications: Upper GIT motility disorders
Presentation: I mg/mL syrup
Dose: 0.3 mg/kg/dose
Interval: q 8 - 12 hourly
Administration: Oral
Comments: Anticholinergic agents reduce its effect

045. DOPAMINE
Indications: Circulatory failure. Oliguric prerenal failure- this is
controversial, as it has no effect on mortality. PPHN- controversial, as it
is likely to increase pulmonary artery pressures as well.
Presentation: 200 mg/5 mL ampoule. Store below 25°C.
Dosage: Always by IV infusion. low: I - 5µg/kg/min, increases RBF
and urine output; Intermediate: 5-15µg/kg/min, increases RBF, CO, HR,
BP; High: >15µg/kg/min adrenergic effects. In neonates (particularly
preterrns) cut-offs may not be as clear-cut.
Reconstitution: Dilute 0. 75 mL (30 mg)/kg from an ampoule to 50 mL
with 5% D or N/S to make a 30 mg/kg/50 mL solution. 1 mL/h ~ IO
µg/kg/min; Max concentration 3200 µg/mL
Storage: protect from light, solution slightly darker than yellow should
not be used.
Administration: Administration in UA catheter not recommended.
Stable in D 5%, NS
Comments: Ensure adequate circulating blood volume. Inactivated by
sodium bicarbonate. Extravasation 1nay cause tissue necrosis. Peripheral
tissue ischemia can be treated with 2% glyceryl trinitrate ointment 4
mg/kg. Adverse effects similar to dobutamine, except that tachycardia &
tachyarrhythmias commoner with dopamine. Cardiac effect antagonized
by p - blockers.
446

D46. ENALAPRIL
Indications: Treatment of moderate to severe hypertension, after load
reduction in newborns with CCF, asymptomatic LV dysfunction.
Presentation: Tablets 2.5 mg, IV: 1.25 mg/mL (1 mL & 2 mL vials)
Dosage: Oral: 0.05-0.1 mg/kg/dose OD, Max 0.5mg/kg (i over 2 wks);
IV: 5-10 µg/kg/dose 8-24hrly
Reconstitution: Crush 2.5 mg tablets and dissolve in 12.5 mL of sterile
water to yield final concentration of 0.2 mg/mL. IV infusion mixed with
NS, D 5%, and DNS
Storage: Store vials below 30°C
Comments: May cause renal failure in preterm infants. Use within 6 h of
use of ~ blocker not recommended. Displaces bilirubin from albumin.
May cause hyperkalemia- monitor electrolytes. Can cause angioedema,
neutropcnia, and hypotension.

D47. ERGOCALCIFEROL
Indications: Hypocalcaemia secondary to hypoparathyroidism. Difficult
to treat OOP.
Presentation: 60,000 JU per sachet & 5000 IU/mL
Dosage: Adequate intake - 400 JU/ d
Nutritional rickets, OOP-1000 -5000 lU/d
Hypoparathyroidism: 1.25 - 5 mg/d (50,000-200000 JU)
Interval: 24 hourly
Administration: Oral (any time). Slow onset of action and long half-life.
Comments: Use with caution in patients with renal impairment, renal
calculi. Ensure adequate calcium intake. Plasma calcium, phosphorus and
ALP should be monitored closely. Each µg ~ 40 JU.

D48. ERYTHROMYCJN
Indications: Infections with Chlamydia trachomatis, Bordete/la
pertussis, Ureaplasma urea/yticum and Mycopla':lrna pneumonia; as a
pro-kinetic drug in preterm babies with GER.
Presentation: 200-mg/5 mL (ethyl succinate) and I 00 mg/mL as drops
(ethyl succinate): for oral use
D osage:
Postnatal <7d >7d
Age < 1200 g 1200- > 2000 g
2000 g
Dose 20 20 30 30-40
(mg/kg/d)
Interval 12 hrlv 12 hrlv 8 hourly 6-8 hourly
447

Neonatal gonococcal ophthalmia - 0 5 - 1 cm ribbon of ointment in each


eye (prophylaxis)
Prokinetic - 3 mg/kg/dose 6 hourly, i" neonates > 32 wks gestation
Administration: Oral: avoid milk I I before and after each dose.
Comments: Monitor ECG during IV injection. Can cause hepatic
impairment, ventricular arrhythmia, long QT interval, eosinophilia,
cholestatic hepatitis. Decreased clearance of -protease inhibitors,
midazolam, theophylline, warfarin, and digoxin.

D49. ERYTHROPOEITIN
Indications: Anemia of prematurity, Anemia of chronic disease.
Presentation: Without preservative: 2000, 3000, 4000, 10000, 40000
U/mL (1 mL)
Dosage regimens: (i) 25-100 U/kg/dose- 3 times/wk (ii) 100 U/kg/dose-
5 times/wk (iii) 200 U/kg/dose every alternate day for IO doses. Decrease
dose when target range reached or Hb increase > 1 g/dL in any 2 wk
period. Increase dose when Hb doesn't rise by 2 g/dL after 8 wks of
treatment and Hb is below target range. Stop therapy when Hb > 13 g/dL.
Re-initiate therapy with 25% lower dose after Hb decreases to target or
12 g/dL
Stability: Refrigerate. Single dose vial doesn't contain any preservative.
Multidose vials - stable for 2 wks at room temperature, for 2ld
refrigerated.
Administration: Do not shake. SC preferred. IV dilution I: I with NS
and infuse over 1-3 mins
Comments: Iron 3-6 mg/kg should be given during EPO therapy. Can
cause hypertension, edema, seizures, rash, neutropenia, hypersensitivity
reaction. Potentiates effect of diuretic and hypotensive agents.

DSO. ETHAMBUTOL
Indication: Bacteriostatic anti-tubercular drug used in treatment of TB in
conjunction with other antitubercular drugs.
Presentation: 200mg/400mg/800mg tablets
Dosage & Interval: 15-20 mg/kg 24 hourly
Administration: Orally on empty stomach
Comments: Can cause optic neuritis, use with caution in neonates.
448

D51. FENTANYL CITRATE


Indications: Narcotic analgesic agent used during mechanical
ventilation, particularly when PPHN is present, and following operative
surgery.
Presentation: [Note: available only through hospital supply] 100 µg/2
mL ampoule. Store below 25°C.
Dosa e

Maintenance

Reconstitution: Dilute 5 mL (250 µg)/kg from an ampoule to 50 mL


with 5% D or N/S to make a 250 µg/kg/50 mL solution. I mL/h = 5
µg/kg/h
Administration: Syringe pump infusion
Comments: Hypotension occurs less often than with morphine. May
cause respiratory depression, urinary retention, chest wall rigidity. Very
high doses (30 - 50 µg/kg/h) have been used, particularly in infants with
PPHN. Tolerance may develop. Dependence may develop after
5-7 d.

D52.FLUCONAZOLE
Indication: Mucosal and systemic candidiasis, Cryptococcal meningitis
and as prophylaxis during Candida! epidemics
Presentation: 200 mg per 100 mL reconstituted vial, 50,100,150 mg
capsules and 50, 100, 150 mg tablets
Dosage: 6 mg/kg/dose
Interval
GA < 29 wks 30-36 wks > 37 wks
Postnatal age <14d[>l4d < 14 d I > 14 d <7d I >7d
Dosing interval n h I 48 h 48 h I 24 h 48 h I 24 h
Administration: Oral (absorpt10n ts excellent). IV slow bolus over 30
mm
Comments: Inhibits fungal cytochrome P450 enzyme lanosterol 14
demethylase and thus impairs ergosterol synthesis. Side effects include
vomiting, rashes. Avoid giving to a patient getting Cisapride.

D53. 5-FLUOROCYTOSINE
Indications: May be used together with amphotericin in the treatment of
systemic Candida sepsis, particularly when there is CNS infection or
persistent candidemia.
Presentation: Capsule: Not easi/v available. IV: Currently not available
in India
Dosage:
Preterm ..................... 100 mg/kg/d
449

Tenn ......................... 200 mg/kg/d


Interval: 6 - 12 h
Administration: Syringe driver infcsion over I hour IV and orally.
Comments: Deaminated to 5-fluorouracil by sensitive pathogens and
thereby interferes with nucleic acid synthesis. Oral administration is
preferred. The therapeutic range of drug serum level is 25 - 50 mg/L.
The drug should not be used alone because of the development of
resistance. Renal, hepatic and haematological function should be
monitored.

D54. FLUDROCORTISONE
Indication: Maintenance therapy for adrenocortical deficiency states,
e.g. salt-losing CAH
Presentation: Tablets: 0.1 mg. To be reconstituted into sachets.
Dosage & Interval: 0.05 -0.1 mgik:g/dose 24 hourly
Administration: Oral
Comments: A synthetic corticosteroid with predominant
mineralocorticoid action. Monitor BP, serum electrolytes. Contra-
indicated in the presence of CHF

DSS. FRUSEMIDE
Indications: Congestive cardiac failure (CCF), Prerenal failure (RF),
BPD (not routinely recommended).
Presentation: 20 mg/ mL ampoule. Store below 25°C. Protect from
light. Tablets 40 mg. Store below 8°C. Do not freeze.
Dosage
CCFandRF
Single 0.5 - 2 mg/kg
Maintenance 1 - 2 mg/kg/dose
BPD
I - 2 mg/kg/dose
Interval
CCF and RF 8 - 12 h
BPD 48 h
Reconstitution: Reconstitute with NS or sterile water
Administration: Slow injection at proximal cannula site.
Comments: May cause osteopenia, nephrolithiasis, cholelithiasis,
hypercalciuria (chronic use), hypokalemia, volume depletion, contraction
alkalosis, hyponatremia, and ototoxicity. May open the ductus arteriosus
in infants with HMD.

D56. GANCJCLOVIR
Indication: Life-threatening or sight-threatening congenital CMV
infection
450

Presentation: 500 mg vial, lyophilized powder for injection and 250 &
500 mg capsules
Dosage & Interval: 6 mg/kg/dose, JV 12 hourly (reduce dose by half for
significant neutropenia (<500/mm)
Duration: Minimum of 6 wks
Reconstitution & Storage: Add 10 mL WFJ to 1 vial (500 mg) of
ganciclovir to make 50 mg/mL. Shake to dissolve and use promptly;
discard if particulate matter is visible; after reconstitution stable for 12 h
in room temperature; do not refrigerate. Dilute I mL (50 mg) of
reconstituted vial to 10 mL to make 5 mg/l mL; can refrigerate for 24 h.
Solution is compatible also with NS and 5%D.
Administration: Infuse over I h through infusion pump.
Comments: Do CBC every 2-3 d for first 3 wks, weekly thereafter if
stable. Keep the patient well hydrated. As undiluted product of
ganciclovir is very caustic (pH 11) use gloves and goggles during
reconstitution. Use soap and water to wash accidental contact with skin.

D57. GENTAMICIN
Indications: Gram-negative sepsis with susceptible organism.
Presentation: 20 mg/2 mL vial.
Dosage & Interval: 4 mg/kg/dose 24 hourly
Reconstitution: Dilute 1 mL from the vial to I 0 mL with N/S or 5% D
to make a 10 mg/ I0 mL solution. 1 ml/kg~ I mg/kg
Storage: Store at 2 - 30 °C
Administration: Syringe driver infusion over 30 min.
Comments: Serum levels should be measured on the fourth dose, if the
drug is to be given for longer than 48 h. Peak serum level is 6 - 8 mg/L
and trough level is <2 mg/L. Ototoxic and nephrotoxic, particularly
when used in conjunction with frusemide. Must not come in contact with
P-lactam antibiotics. heparin, frusemide.

D58. G-CSF
Indication: Severe neutropenia due to sepsis (ANC<lOOO/mm'l, severe
neutropenia due to maternal PIH
Presentation: 30- MU/0.5 mL in a prefilled syringe. Store between 2-8°
C. Do not freeze.
Dosage: 5-10 MU/kg SC/IV OD for 5 d
Administration: SC
Comments: When used for sepsis, there is a rise in ANC noticed within
48 h of administration. There is no convincing impact on mortality.

D59. GM-CSF
Indication: Severe neutropenia due to sepsis (ANC<I 000/mm\ aplastic
anemia, severe neutropenia due to maternal hypertension
451

Presentation: 150 µg/ 300µg/450µg


Dosage: 5- I Oµg/kg/d OD for 5 d
Administration: SC
Comments: Same as for G-CSF

D60. GLUCAGON
Indications: Refractory hypoglycaemia
Presentation: Lyophilised powder 1 mg vial + syringe prefilled with
WFI. l IU= 1mg. Store below 25°C.
Dosage: 200 µg/kg/dose IV push or SC (max. 1mg). Infusion: 5 - 20
µg/kg/h (rise in BS should occur within I hour of starting the infusion)
Reconstitution: Add the accompanying diluent to the vial of freeze-
dried glucagon. Dilute the contents of the reconstituted vial to 50 mL
with 10% D to make a 1000 µg/50 mL solution. 0.5 mL/kg/h = IO
µg/kg/h.
Administration: Syringe pump infusion.
Comments: Can cause nausea, vomiting, tachycardia, hyponatremia and
thrombocytopenia.

D61. GLYCERYL TRINITRATE


Indications: Pulmonary hypertension following cardiac surgery
Presentation: 50 mg/10 mL ampoule. Store below 25°C. Protect from
light.
Dosage: 1 -4 µg/kg/min (range 0.5 - 12 µg/kg/min)
Reconstitution: Dilute 0.6 mL (3 mg)/kg from an ampoule to 50 mL
with 5% D or N/S to make a 3000 µg/kg/50 mL solution. 1 mL/h = 1
µg/kg/min
Administration: Use Becton Dickinson (BO) syringes. Change the
infusion set every 12 h if minimum \•olume extension tubing is used or
every 24 h if manometer tubing is used.
Comments: Ensure adequate circulating blood volume. Concurrent use
of an inotropic agent is recommended. Drug interaction may occur with
non-depolarising muscle relaxants and narcotics.
D62. HEPARIN
Indications: Thrombotic disseminated intravascular coagulopathy. renal
vein thrombosis, prophylaxis & treatment of peripheral arterial
embolism. maintaining patency of the arterial cannula.
Presentation: Heparin: 1000 IU/mL ampoule. Store below 25°C. Protect
from light. LMWH: 25 mg/0.2 mL.
Dosa11:e:
Dose(JU/kg/h) CheckAPTT
Loading 75 After 4 h
Maintenance 2~ After 4 h
452

Adjustment of maintenance by APTT 1


APTT<50 s tby20% After 4 h
APTT 50-59 s t by 10% After 4 h
APTT 60-85 s No Change 24 h
APTT 86-120 s .j, by 10% After 4 h
APTT >120 s Stop for l h & then.), by 15% After 4 h

Enoxaprin:
1.5 mg/kg/dose twice daily
Monitor for anti factor Xa level after 4-6 h of first dose
Theraoeutic level- 0.5-1.0 umts/mL anti"factor Xa
Adjustment of maintenance by Anti factor Xa
<0.35 U/mL t bv 25% After 4 h
0.35-0.49 U/mL t by 10% After 4 h
1.1-2 U/mL .j, by 20-30% 24 h

With-hold until factor is <0.5 U/mL, Stop for I


>2 U/mL
h & then restart at 40% of original dose

Thrombolvsis accordin to Gestat1on


Heparin Loading Maintenance
<28 Wks 25 IU/kg 15 IU/kg/h
28-36 Wks 50 IU/kg 20 IU/kg/h
>36 Wks 75 JU/kg 25 IU/kg/h

Reconstitution: Dilute 1.25 mL (1250 lU)/kg to 50 mL with 5% D or


N/S to make a 1250 IU/kg/50 mL solution. l mL/h ~ 25 JU/kg/h.
Solution is compatible with 5% D, 10% D and NS.
Administration: Syringe pump infusion. Give the loading dose (4 mL)
over I 0 min, that is 24 mL/h for 10 min.
Comments: Maintain PTT at 1.5 - 2.5 times normal. Heparin assays for
plasma levels arc of uncertain value. LMWH is safer, and requires less
frequent monitoring. Keep protarnine sulphate on hand to manage
hemorrhage. I mg for each I 00 units of heparin given in last 4 h.

D63. HEPATITIS B IMMUNOGLOBULIN


Indication: lmmunoprophylaxis of babies born to HbsAg positive
mother
Do•age: 0.5 mL ( 100 IU) IM
453

Administration: IM in antero-latcr 11 aspect of thigh, preferably within


12 h of birth
Comments: Does not interfere with Hep 8 vaccine. HBIG should never
be administered IV. When given with the vaccine, use separate syringe
and separate site. Local pain and tenderness may occur.

064. HYDROCHLOROTHIAZIDE
Indication: Maintenance diuretic therapy for BPD. Can be used in mild
to moderate edema and hypertension.
Presentation: 12.5mg and 25 mg tablets. To be reconstituted into
sachets.
Dosage & Interval: 1-2 mg/kg/dose 12 hourly
Administration: Oral
Comments: Electrolyte imbalance hyponatremia, hypokalemia,
hypomagnesemia, hyperglycemia, hyperuricemia. Contra-indicated in
renal failure and hyperkalemia.

D65. HYDROCORTISONE
Indications: preterm neonate with refractory shock, neonatal
hypoglycaemia, hypoadrenocorticism, adrenal crisis.
Presentation: I 00 mg vial. Protect from light. Tablets: 20 mg. To be
reconstituted into sachets.
Store below 25"C.
Dosaee:
Hypoglycaemia JO mg/kg/d
Physiological 7-9 mg! m2/d
Adrenal crisis 25 - 50 mg/m2/d
Maintenance for CAH 20 mg/m2/d
Preterm with refractory shock 25 - 30 mg/m2/d

Wt (ko1 0.6 I 1.4 2 3 4


Body
surface area 0.08 0.1 0.12 0.15 0.2 0.25
(BSA) (m2)
BSA (m' ) -- (0.05X kg) +0.05 (Also see sectton N9)
Interval:
Hypoglycaemia q 12 h
Physiological q6h
Adrenal crisis Continuous IV infusion
Maintenance for CAH q8h

Reconstitution: Add 2 mL of WFI to the vial to make a 50 mg/ml


454

solution. 0.1 mL/kg ~ 5 mg/kg


Administration: Slow injection at proximal cannula site. Oral
suspension is used for physiological maintenance treatment.
Comments: Can cause hyperglycemia, hypertension, salt and water
retention, GIT perforations if used with indomethacin, Candida
infections. Must be combined with Fludrocortisone for salt-losing CAH.

066, IBUPROFEN
Indications: Treatment of PDA, treatment of fever/ inflammation
Presentation: Oral suspension 100 mg/5 mL.
Dosa2e:
I 0 mg/kg stat, followed by 5 mg/kg q 24 h for 2
PDA
doses
Fever/inflammation 5 mg/kg q 6 h
Comments: Used with caution m mfants with thrombocytopema,
receiving anticoagulants or decreased renal, hepatic functions.
Contraindicated in NEC, evolving IVH, duct dependent lesions.

067. IMIPENEM-CILASTATIN
Indications: Serious infections resistant to other antibiotics.
Presentation: 250 mg vial. Store below 25°C.
Dosage & Interval: 25 mg/kg/dose 12 hourly
Reconstitution: Add 5 mL of N/S from a 25 mL syringe to a 250 mg
vial to make 250 mg/5 mL. Light to deep yellow colour does not indicate
loss of potency. Brown colour indicates loss of potency. Add the contents
of the reconstituted vial to the remaining 20 mL of N/S in the 25 mL
syringe to make a 250 mg/25 mL solution. 2.5 mL/kg ~ 25 mg/kg.
Storage: Unconstituted: Store at less than 30 °C. Reconstituted: 10 h at
room temp., 48 h at 4 °C, do not freeze.
Administration: Syringe driver infusion over 30 min
Comments: May cause convulsions. CSF penetration is poor and
therefore best avoided in the treatment of meningitis. Sodium content:
3.2 mEq/g Induces B-lactamase production by Gram-negative organisms
thereby leading to resistance to B-lactam antibiotics. Physically
incompatible with Amikacin, Gentamicin, Fluconazole, sodium
bicarbonate, lorazepam.

068. IMMUNOGLOBULIN
Indications: Early in the course of Rh isoimmunisation. Alla-immune
thrombocytopenia. Life threatening bacterial sepsis not responding to
specific antimicrobial therapy (benefit is marginal, the cost-benefit ratio
is high and utility against Indian strains of bacteria is unproven).
Presentation: Gamma IV: 0.5 g, 2.5 g & 5 g per vial. Do not freeze.
Protect from light. I mL ~ 60 mg IgG. Pentaglobin: 10 mL, 50 mL, 100
455

mL ampoules. Store at 2-8 C°


Dosage: Gamma IV: 400 mg/kg 'may be up to I g in cases of
alloimmune thrombocytopenia). Pentaglobin: 5 mL/kg
Interval: Gamma IV: Single dose for Rh iso-immunization; OD for 3 d
for sepsis. Pentaglobin: OD for 3 d
Administration: Syringe driver infusion at 1 mL/min.
Comments: Rarely hypoglycemia, tachycardia, hypotension- usually
resolved after stopping drug.

D69. INDOMETHACIN
Indications: Symptomatic PDA in preterm infants.
Presentation: Oral: 25 mg capsule. IV: l mg vial. Store below 25°C.
Protect from light.
Dosa e:
Short course 0.2 mg/kg/dose for 3 doses
Prolonged course 0.1 mg/kg/dose for 6 doses
Interval:
rl~~-S_h_o_rt~co-ur~se~~~~~~~-q-1_2_h~~~~

Reconstitution: For IV: Add I mL of WFI or N/S to a vial. 0.2 mL/kg =


0.2 mg/kg
Administration: Oral: Reconstitute into sachets. Not a standard route.
IV: infusion over 20 to 30 min.
Comments: Contraindications include thrombocytopenia, bleeding
diathesis, NEC, renal failure and ductus dependent CHD. The concurrent
use of frusemide may prevent or attenuate indomethacin induced renal
insufficiency. May cause GIT hemorrhage and/or perforation.
Indomethacin prophylaxis for IVH in ELBW babies should no longer be
used because of evidence of poor long·term neurological outcome.

D70. INSULIN, REGULAR


Indications: Hyperglycaemia with glycosuria and osmotic diuresis,
hyperkalemia
Presentation: IO mL vial. 40 units/mL, 100 unit/mL. Store below 8°C.
Do not freeze.
Dosa e:
Intermittent 0.05 - 0.1 unit/kg/dose
Infusion 0.05 - 0.2 unit/kg/h
Interval: 6 - 12 h
Reconstitution: Dilute 0.2 mL (20 units) from a vial to 10 mL with WFI
to make a 2 unit/ml solution. For intermittent injection use the 2 unit/ml
solution. 0.1 mL/kg = 0.2 unit/kg. For continuous infusion: Dilute 2.5
456

rnL (5 units)/kg of the 2 unit/rnL solution to 50 mL with N/S or 5% D to


make a 5 unit kg/50 mL solution. 1 mL/h = 0.1 unit/kg/h
Administration: Intermittent SC injection. Syringe pump infusion.
Comments: The BS should be monitored closely. Before start of
infusion, purge IV tubing with a minimum of 25 mL of the infusion
solution to saturate plastic binding site.

D7l. IPRATROPIUM BROMIDE


Indications: BPD (BPD) with reversible bronchospasm.
Presentation: Solution for inhalation 0.025% (250 µg/mL). Store below
25°C.
Dosage: 125 µg/dose
Interval: 4 - 6 h
Reconstitution: Dilute the prescribed dose with N/S to give a total fill
volume of 4 mL.
Administration: Nebulise for 10 min and discard the remainder.
Comments: Usually used in conjunction with salbutamol. Limited data
regarding use in BPD.

D72. ISONIAZID
Indications: Prophylaxis against TB. Treatment of TB
Presentation: Syrup ( 100 mg/5 mL), Dispersible tablet (1 OOmg)
Dosage & Interval: 5 mg/kg/dose OD
Administration: Oral
Comments: For prophylaxis always combine with Rifampicin. Duration
of prophylaxis 6 mths Pyridoxine supplementation is not needed in
infancy.

D73. ISOPRENALINE
Indication: PPHN. Congenital heart block. Cardio-circulatory failure.
Bradycardia not responsive to atropine.
Presentation: 2000 µg/mL ampoule. Store below 8°C. Do not freeze.
Protect from light.
Dosage: 0.05 - I µg/kg/min
Reconstitution:
6 x desired dose (ug/kg/mL) x Wt (kg)= mg drug
desired rate (mL/h) I 00 mL fluid
Administration: Syringe pump infusion.
Comments: Efficacy limited by its propensity to cause tachycardia.
Ensure adequate circulating blood volume.

D74. ITRACONAZOLE
Indication: Systemic fungemia, which is resistant to fluconazole, and
where oral therapy possible
457

Presentation: I 00 mg capsule. To be' 'constituted.


Dosage: 6-10 mg/kg/dose for 4-6 wks
Interval: Once daily
Administration: Oral

D75. LIGNOCAINE
Indication: Local infiltrative anat•sthesia, pre-procedural surface
anesthesia (EMLA), ventricular armythmias (premature ventricular
complexes, VT, VF), resistant status epilepticus
Pre•entation: Injection: Xylocaine: 1% solution (50 mL vial), Xylocard
2% solution (50 mL vial)
EMLA cream: I g cream containing 25 mg lignocaine and 25 mg
prilocaine
Dosage:
Local infiltrative anesthesia: 0.3 mL/kg of 1% solution.
EMLA: 0.5 g applied to skin 45-60 min before procedure.
Arrhythmia & seizure: Stat dose: 1-2 mg/kg (0.1 - 0.2 mL/kg of
adrenaline free I% solution) IV slow bolus over 5 min. Can be given
through ET tube if no IV access. May be repeated after 5-IO min as
needed. Maximum total dose 5 mg/kg. 5 mg/kg IM injection will give
effective blood concentration in 15 min. Infusion: I 0-50 mcg/kg/min.
Taper after 12-36 h of starting infusion.
Reconstitution:
Bolus dose: N/S or 5% D
Infusion: 5% D
Administration: SC, IV, IM, ET
Comments: Toxicity includes hypertension, seizures (treatment with
diazepam, DVET) respiratory arrest, and arrhythmias (usually
bradycardia). Warning: use with caution in hepatic and renal disease,
because of potential of accumulation. Contraindicated in WPW
syndrome, severe sino-atrial, AV or intraventricular block EMLA may
raise methemoglobin levels.

D76. LINEZOLID
Indications
Activity against S. Aureus, S. Epidermidis, Clostridium difficile and C.
Perfringens is equivalent to vancomycin. Linezolid is highly effective for
resistant streptococcus pneurnoniae. Active against all enterococcal
isolates and other gram-positive. Ineffective against most gram negative
pathogens.
Presentation: Tablets containing 600 mg. Injections of 100 mL and 300
mL containing 2mg/mL (linospan, linox IV). Oral suspension (20
mg/mL).
Dosage & Interval: I 0 mg/kg every 8- 12 h.
458

Reconstitution & Storage: Compatible IV Solutions: 5% D, NS and RL.


Store at 25°C (77°F); excursions permitted to 15-30°C (59-86°F) Protect
from light. Keep bottles tightly closed to protect from moisture. Protect
infusion bags from freezing. Use suspension within 21 d after
reconstitution.
Administration: IV administration of drug should be done over 30-120
min. No dose adjustment is necessary when switching from IV to oral
administration.
Comments: Physical incompatibility with amphotericin B, diazepam,
erythromycin, phenytoin and ceftriaxone. Thrombocytopenia,
myelosuppression. Weekly monitoring of CBC if linezolid received for
longer than 2 wks.

D77. LISINOPRIL
Indications: Maintenance therapy of congestive cardiac failure which
has been treated with Captopril.
Presentation: 2.5, 5 and 10 mg tablets.
Dosage & Interval: 0.1 mg/kg/dose q 24 h
Reconstitution: Dissolve a 5 mg tablet in 5 mL of water to make a 5
mg/5 mL solution. 0.3 mL/kg = 0.3 mg/kg. Discard reconstituted solution
after each dose.
Administration: Oral
Comments: BP should be monitored when commencing treatment.
Hyperkalemia may occur. Plasma potassium should be monitored when
commencing treatment, particularly in infants receiving potassium
supplements or spironolactone. Azotemia may occur.

D78. LORAZEPAM
Indications: Treatment of seizures, after phenobarbitone and phenytoin
have been used
Presentation: 2 mL ampoule, 2 mg/mL; tablets- 0.5mg, 1mg, 2mg.
Dosage: 0.05-0. l mg/kg slow bolus over 2-5 min
Interval: May be repeated twice at 15-20 min interval for acute
management
Administration: For IV use dilute with equal volume of NS or 5%D
and give as slow bolus. Do not exceed 2 mg/ min. Can be given IM.
Comments: Do not use if injection is discoloured or contains precipitate.
Protect from light. Refrigerate injectable form and oral solution. Injection
is stable at room temperature for 8 wks. Three times more potent than
diazepam. Onset of action is within 2-3 min. of infusion, and action lasts
for 24 h.

D79. MAGNESIUM SULPHATE


Indications: Hypomagnesemia which persists despite correction of
459

associated hypocalcaemia. PPHN.


Presentation: 50% (500 mg/mL) so ution in a 5 mL ampoule.
Dosage:
Hypomagnesemia ....
0.1 mL (50 mg)-0.3 mL (150 mg)/kg/dose q 12 - 24 h
PPHN
Loading .............. 200 mg/kg
Maintenance ....... 20 - 50 mg/kgih
Dilution:
Hypomagnesaemia: Dilute 0.1 mL (50 mg)- 0.3 mL (150 mg)/kg of the
ampoule to 2 mL with 5% D.
PPHN: Loading - Dilute 0.4 mL (200 mg)/kg of the ampoule to 10 mL
with 5% D. 10 mL = 200 mg/kg. Maintenance - Dilute 2 mL (1000
mg)/kg ftom an ampoule to 50 mL with 5% D or N/S to make a 1000
mg/kg/50 mL solution. 1 mL/h = 20 mgikg/h
Storage: Store below 25°C. Protect ftom light.
Administration: Loading dose - Syringe driver infusion over 20 - 30
min. Maintenance - syringe pump infusion.
Comments: Plasma levels - Hypomagnesemia: 0. 71 - 0.96 mmol/L.
PPHN: 3.5 - 5.5 mmol/L. The HR and BP should be monitored during
treatment. Muscle relaxation should be discontinued in infants with
PPHN.

D80. MANNITOL
Indications: Raised symptomatic ICP
Presentation: 20% Mannitol in I 00 mL, 250 mL, 500 mL bottles
Dosage: I gikg (5 mL/kg). Subsequent doses may be lower.
Interval: May be repeated once or twice at intervals of 4-8 h
Administration: Over 10-20 min as IV infusion through filter to trap
small crystals
Comments: Co-existence of congestive cardiac failure is a contra-
indication. Babies with HIE often have associated cardiac dysfunction.
Impact on survival and long-term outcome is not established.
460

D81. MEROPENEM
Indication: Serious infections resistant to other antibiotics, but not
effective against MRSA and enterococci.
Presentation: 500 g/l 000 g vial.
Dose And Interval (/kg/dose)
Wt :01200 1200-2000 g >2000 g
Age ,; 4 wk ,; 7 d >7 d ,; 7 d >7 d
Dose 20mg 20mg 20mg 20 mg 20
mg
Interval 24 h 12 h 12 h 12 h 8
mg

Administration: Meropenem can be given as IV bolus dose over 5 min.


or as infusion over 15- 30 min. If given as bolus dose it should be
reconstituted with sterile water and if given as infusion it can be
reconstituted with saline or dextrose.
Storage: Drug reconstituted with sterile water maintains its potency at
room temperature (up to 25°c) up to 8 h and under refrigeration (4"c) for
48 h.
Comments: Each gram of reconstituted meropenem contains 3. 9 mmol
of sodium. Seizures have been reported less often with Meropcnem
compared to Imipenem. Dose should be modified in renal failure, need
not be modified in hepatic dysfunction.

D82. METOCLOPRAMIDE
Indications: Reduces symptoms of gastro-esophageal reflux. Facilitates
nasojejunal intubation. Useful for insufficient maternal lactation.
Presentation: I 0 mg/2 mL ampoule. 1 mg/mL syrup. 5 mg dispersible
tablet.
Dosage:
Infants 0.1 - 0.2 mg/kg/dose
(Lower end of dose range for preterms, higher for term infants)
Lactating women I 0 mg/dose
Interval:
Preterm infants 8h
Term infants 6h
Lactating women 8h
Dilution: For IV administration dilute 0.8 mL (4 mg) from the ampoule
to 20 ml with 5% D or N/S to make a 0.2 mg/ml solution. 0.5 ml/kg~
0.1 mg/kg
Storage: Store below 25"C. Protect from light.
Administration: Slow injection at proximal cannula site. Orally 15 - 30
min before feeds.
Comments: Extra-pyramidal side-effects caused by metoclopramide can
461

usually be reversed by diphenhydiamine. Contraindications include


bowel obstruction, perforation, pheoJchromocytoma, seizure disorder,
extrapyramidal risk.

D83. METRONIDAWLE
Indications: Anaerobic sepsis owing to sensitive Bacteroides and
C/ostridia species.
Presentation: 100 mg/mL in 100 mL bottle.
Dosage:
Loading: 15 mg/kg
Maintenance·
Postnatal age <7d ,, 7 d
Birth wt (k~) < 1.2-2 >2 < 1.2-2 >2
Dose (mg/kg/dose) 7.5 7.5 7.5 15
Dosing interval 24h 12 h 12 h 12 h
Commence 24 h after the loadmg dose m term infants and 48 h after the
loading dose in preterm infants. Higher doses have been used for
meningitis.
Storage: Store below 25°C. Protect ftom light.
Administration: Syringe driver infus10n over 10- 15 min.
Comments: Apparently well tolerated by newborn infants. Effectively
penetrates into the CSF. Newborns demonstrate a diminished capacity to
eliminate metronidazole. The elimination half-life inversely relates to
GA.

D84. MIDAWLAM
Indications: Sedation during mechanical ventilation. Status epilepticus.
Presentation: 5 mg/ml ampoule.
Dosage:
Bolus 150 - 200 µg/kg
Infusion 1 - 5 µg/kg/min
Dilution: For bolus injection dilute 0.4 ml (2 mg)/kg from an ampoule
to 20 mL with 5% D or N/S to make a 2000 µg/kg/20 ml solution. 1 mL
~ 100 µg/kg. For infusion dilute 0.6 mL (3 mg)/kg ftom an ampoule to
50 mL with 5% D or N/S to make a 3 mg/kg/50 mL solution, 1 mL/h ~ 1
µg/kg/min.
Storage: Store below 25°C.
Administration: Slow injection at proximal cannula site. Syringe pump
infusion.
Comments: May cause respiratory depression and hypotension. Use may
be associated with dependence.
462

D85. MILRINONE
Indications: Reversing the low cardiac output frequently observed in
infants and children after cardiac surgery:
Vu in Septic Shock: No data available in neonates In addition to its use
after cardiac surgery. milrinone may also be beneficial in the
management of low cardiac output resulting from septic shock.
Presentation: Milrinone is available in a I mg/ml concentration in 10,
20. and 50 mL single-dose vials, 5 mg/5mL sterile cartridges, and in 200
mcg/mL premixed 100 and 200 mL bags.
Dosage: Recommended loading dose of milrinone is 50 mcg/kg given IV
over 15 to 30 min. The loading dose may be reduced to 25 mcg/kg or
omitted in patients at risk for hypotension. Immediately after the load, a
continuous infusion of 0.375 to 0.75 mcg/kg/min may be started.
Administration of milrinone within this range should produce serum
concentrations above the minimum desired concentration of 100 ng/mL.
The maintenance infusion rate should be titrated to patient response.
Reconstitution: The loading dose of milrinone may be given undiluted
or diluted to 10 to 20 mL. For infusion, milrinone should be diluted to a
concentration of 200 to 400 mcg/mL with 5% D, 0.9% sodium chloride,
0.45% sodium chloride, or lactated Ringer's solution.
Comments: Milrinone is considered 10-30 times more potent than it's
parent drug Amrinone . After IV injection half life is 0.8 h.

D86. MORPHINE SULPHATE


Action: Narcotic analgaesic agent.
Indications: Analgaesia-sedation during assisted ventilation and after
operative surgery. Neonatal abstinence syndrome.
Presentation: 15 mg/mL ampoule, I 0 mg/2 mL oral solution
Dosage
Intermittent... ..................... 50 - I 00 µg/kg
Infusion ............................. I 0 - 40 µg/kg/h
Oral ................................... Oral: IV ratio~ 4: I
Dilution
IV: For intermittent dose dilute 1.0 mL ( 15,000 µg) from an ampoule to
10 mL N/S to make a 1,500 µg/I mL solution. 0.65 mL/kg ~ 1000 µg/kg.
For infusion dilute 0.65 mL (IOOO µg)/kg of the 1,500 µg/mL solution
prepared as above to 50 mL with 5% D or N/S to make a I 000 µg/kg/50
mL solution. I mL/h ~·20 µg/kg/h
Oral: Dilute the oral solution with WFI or water for irrigation for the
desired dose-volume.
Storage: Store below 25°C.
Administration: Rapid injection at proximal cannula site for intermittent
bolus. Syringe pump for infusion.
Comments: May cause respiratory depression, urinary retention, ileus.
463

Prolonged use (>5 - 7 d) may be associated with dependence.


Intermittent doses increase IVH.

D87. MUPIROCIN
Indication: Bacterial infection of skin (furunculosis, impetigo,
folliculitis etc)
Presentation: 2o/o ointment
Dose: Apply to affected areas 3 times per day. For JO d (maximum)
Comments: It can cause burning sensation, itching, stinging and dryness.

D88. NALOXONE
Indications: Reversal of narcotic depression.
Presentation: 400 µg/ I mL ampoule.
Dosage: 100 µglkg/dose
Storage: Store below 25°C. Protect from light.
Administration: Rapid injection at proximal cannula site.
Comments: The dose may need to be repeated because the duration of
action of naloxone may be shorter than that of the narcotic.
Cardiorespiratory monitoring should be continued for at least 6 - 8 h
after the administration of naloxone.

D89. NEOSTIGMINE
Indications: Reverse non-depolarising muscle relaxant. Diagnostic test
for neonatal myasthenia gravis.
Presentation: 0.5 mg/mL ampoule.
Dosage: 50 µg/kg
Dilution: Dilute 1 mL (0.5 mg) from an ampoule to 5 mL with N/S to
make a 500 µg/5 mL solution. 0.5 mL!kg ~ 50 µg/kg
Storage: Store below 25°C. Protect from light.
Administration: Slow injection at proximal cannula site.
Comments: Atropine is usually required to reverse muscarinic effects.

D90. NETILMICIN
Indication: Susceptible gram-negative infections
Presentation: Ampoules I 0 mg/mL and 25 mg/mL
Dosa e:

Interval: 24 hourly
Reconstitution: To 2 mg/mL by diluting with NS/5% D/10% D
Storage: Stability of reconstituted product - 72 h in the refiigerator
Administration: Over 30-60 min by syringe driver
Comments: Ototoxicity at serum peak cone. > 12 µg/mL, nephrotoxicity
at serum peak cone. > 4 µg/mL. Ideally, draw serum levels around 4'"
464

maintenance dose and adjust dose. Monitor renal functions before and
during therapy and BERA after completion. Avoid simultaneous
treatment with Frusemide. Must not come in contact with 13-Iactam
antibiotics, heparin and frusemide.

D91. NEVIRAPINE
Indications: Mother-to-child transmission of HIV during labor and at
birth (prevention)
Presentation: 200 mg tablets. Oral Suspension: 50mg/5mL
Dosage: If the mother received NVP IP, then give the infant a single
dose of oral NVP (2 mg/kg) within 48 to 72 h after birth. If the mother
did not receive NVP IP, then give the infant a single dose of oral NVP (2
mg/kg) as soon as possible after birth.
Storage: Tablets and Oral Suspension should be stored at 15°-30°C
Comments: Adverse reactions arc hepatitis/hepatic failure, Stevens
Johnson syndrome, toxic epidermal necrolysis, and hypersensitivity
reactions, eosinophilia, granulocytopenia. Co-administration of
clarithromycin, rifampicin, fluconazole, ketoconazole may result in
decreased plasma concentrations of these drugs and attenuate their
therapeutic effects.

D92. NITRIC OXIDE (INHALED)


Indication Persistent pulmonary hypertension of newborn. Best for near-
term baby with echo-proven PPHN and Oxygenation Index> 25.
Presentation: 10 L pale green and yellow cylinder containing 1000 ppm
of nitric oxide in nitrogen.
Dosage: Start with 20 ppm on nitric oxide. Taper to doses as low as 1-5
ppm.
Administration: Through special ventilator circuits
Comments: Can cause methemoglobinemia, platelet dysfunction.
Environmental levels of nitrogen-dioxide must be monitored
465

D93. NITROPRUSSIDE
Indications: Systemic arterial hype1tension. Congestive cardiac failure.
Presentation: 50 mg/mL vial.
Dosage: 0.5 - 8 µg/kg/min. Commence treatment at 0.5 µg/kg/min and
increase by 0.5 µg/kg/min every 15 - 20 min until there is a satisfactory
response, complications occur or the maximum dose of 8 µg/kg/rnin is
reached.
Reconstitution: Dissolve the powder with 3 mL of 5% D to make a 50
mg/3 mL solution. Dilute 0.18 mL (3 mg)/kg from the reconstituted vial
to 50 mL with 5% D to make a 3 mg/kg/50 mL solution. 1 mL/h ~ I
µg/kg/min
Storage: Store below 25°C. Protect from light.
Administration: Syringe pump infusion using black opaque infusion
tubing.
Comments: Measure thiocyanate levels if use is prolonged (>3 d).
Symptoms of toxicity (seizures, muscle spasms and vomiting) appear at
5-10 mg/dL. Treatment should be discontinued iflevels are >12 mg/dL.
Cover solution with aluminium foil to protect it from light. Discard after
24 h. May cause tachycardia. Ensure adequate circulating blood volume.
Concurrent use of an inotropic drug is recommended.

D94. NORADRENALINE
Indications: Cardiogenic shock following cardiac surgery.
Presentation: 1 mg/mL solution in 2 mL ampoule.
Dosage: 0.05 - 1 µg/kg/min
Reconstitution: Dilute 0.15 mL ( 150 µg)/kg from an ampoule to 50 mL
with 5% D to make a 150 µg/kg/50 mL solution. 1 mL/h ~ 0.05
µg/kg/min.
Administration: Syringe pump infusion.
Comments: No published data are available regarding use in newborn
infants. Ensure an adequate circulating blood volume. Concurrent use of
a vasodilator drug is usually necessary. Incompatible with sodium
bicarbonate.

D95. OCTREOTIDE
Indications: PHH!, Insulinoma, GVHD induced diarrhea, post- operative
chylothorax.
Presentation: IV: I mL ampoules in 3 strengths- 50 µg, 100 µg, 500 µg
Dosage:
PHH!: 1 - IO µg/kg/dose 12 to 24 hourly (IV/SC). Individualize dose
depending upon patient response with decreasing time interval (4-6
hourly). Maximum dose: 40 µg/kg/d.
466

GIT Bleed: I µg/kg bolus followed l µg/kg /hour infusion. Taper dose to
50% every 12 hour when no active bleeding for 24 hour. Discontinue
when dose is 25% of initial dose.
Chylothorax: 1 - 4 µg/kg /hour continuous IV infusion.
Storage: store in refrigerator, protect from light. Stable in NS for 4 d and
5% D for 24 hat room temperature. Not compatible with TPN solutions.
Comments: Can cause hypertension, CHF, bradycardia, arrhythmia,
seizures, hyperglycemia, hypothyroidism, fat malabsorption, elevated
liver enzymes, j CPK, biliary obstruction, cholecystitis, cholelithiasis.
Chronic use associated with ! vit B 12 levels and GH suppression.

D96. PANCURONIUM
Indications: Muscle relaxation for extremely difficult controlled
mechanical ventilation.
Presentation: 4 mg/2 mL ampoule.
Dosage:
Bolus ........................ 50 - 100 µg/kg
Infusion .................... 25 µg/kg/h
Reconstitution: For bolus injection dilute one ampoule (4 mg) to 8 mL
with WFI to make a 4 mg/8 mL solution. 0.1 mL/kg ~ 50 µg/kg. For
constant infusion dilute 0.625 mL ( l.25 mg)/kg from an ampoule to 50
mL with 5% D or N/S to make a 1.25 mg/kg/50 mL solution. I mL/h ~
25 µg/kg/h
Storage: Stable at 25°C for six wks. If stored in refrigerator may be kept
until the designated expiry date.
Administration: Slow injection at proximal cannula site. Syringe pump
infusion.
Comments: Monitor HR and BP. Infant may require increased Fi0 2
and/or ventilation. Fluid balance requires careful attention.

D97. PARACETAMOL
Indications: Postoperative analgesia in term and preterm infants. May be
used alone or combined with a narcotic analgesic
Presentation: 125-mg/5 mL oral syrup. 150 mg/mL oral drops. Rectal
suppository: 80 mg, 170 mg
Dosage;
467

Gestation 28-32 wks 32 36wks and Term >lOd


ter,n <10 d
Oral (mg/kg/dose) 10-12: 6- 10-15: 6hourly 10-15: 4-6
8 hourly (m.1x 60mg/kg/d) hourly
(max 40 (max - 90
mg/kg/d) mg/kg/d
Rectal(mg/kg!dose) 20: 12 30 followed by 30 followed by
hourly 15: 8 hourly (max 20: 8hrly (max
(max 40 60 mg!kg/d) 60 mg!kg/d)
mg/kgld)
- -
Comments: Hepatotox1c1ty has not been descnbed m the newborn
infant.

098. PENICILLIN G
Indications: Many Gram positive organisms including Group 8 13-
haemolytic streptococcus, Streptococcus pneumoniae, Clostridium
welchii and non-j3-lactamase producing Staphylococcus aureus.
Penicillin (or ampicillin) and an aminoglycoside (gentamicin) is
recommended for the treatment of suspected EOS.
Presentation: 500,000 and 10,00,000 units per vial. Store below 25°C.
D osa2e:
Age <'. 7d

Category <:2000 >2000 Meningitis Meningitis Cong OBS


g g <2000 g >2000 g svohilis meninaitis
Dosage 50000 75000 100000 150000 100000 250000-
unitlkg/d 12h Sh 12h 8h 12h 450000
Sh

Age > 7d

Category <1200 g 1200- Meningitis Meningitis Cong OBS


2000 g <1200 g 1200- syphilis meningitis
2000.
Dosage 50000 75000 100000 200000 150000 450000 6
unit/kg/d 12 h 12 h Sh 6h Sh
Reconstitution: Add I 0 mL of WFI to the vial to make a 50,000-unit/mL
solution. Stable for 7 d in the refrigerator
Administration: Slow injection at proximal cannula site over 15-30
mins Incompatible with amino glycosides. Inactivated in acid/alkaline
solution
Comments Hypersensitivity reactions not reported in neonates. Rarely
blood dyscrasias and convulsions can occur. Antibacterial effect
synergistic with aminoglycosides. Penicillin G contains Potassium~ K+
1.7 mEq/l MU; Sodium-Na 2 mEq/I MU.
468

D99. PH E1'0BARBITONE
Indications: Neonatal seizures, treatment of prolonged jaundice.
Presentation: 200 mg mL ampoule, 20 mg/0.5 mL ampoule. 20mgi5
~oral suspension. - - -
Dosage:
Anti conrnlsant· Loading - 20 mg leg for seizures, single dose. If seizures
are not controlled give additional 5mg/kg at 15-30 mm intervals till
seizures are controlled or max dose of 40 mg· kg achieved. Maintenance -
3-5 mg. kgti;l OD.J 2 h after loading dose.
Jaundice: Loading - I 0 mg/kg; Maintenance - 5 mg/kg/d OD for 4 d
Administration: Compatible with D5°10 and NS. The loading dose is
given by syrmge driver infusion over 20 - 30 min. Don't inject fas ter
than I mg/kg min with a maximum of 30mg/min. The maintenance dose
is given by slow injection at the proximal cannula site.
Storage: Store below 25°C. Protect from light. Not stable in aqueous
solution. Use only clear solution.
Comments: Plasma levels: 40 - 80 µmol/L Effect. Oral Onset of
action- 20-60mins. Durauon 6-10 h; IV Onset of action- 5 mins.
Duration - 4 -10 h
Comments: Adverse Effects - Hypotens1on. drowsiness. skin rash,
megaloblastic anemia. hepat1t1s, respiratory depression Decreases
concentration of lamotrigine. warfann, chloramphenicol, P-blocker,
theophylhne, conicosteroids. Levels increased by valpro1c acid and
chloramphemcol. CNS depression synergistic with bcnzodia7cpincs.

DIOO. PH EN YLEPHRINE EYE DROPS


Indication: Pupillary dilatation for ROP screening
Presentation: Drosyn eye drops 10%
Dose: 1-2 drops of 2.5% Drosyn on both eyes. repeat afler 15-20 mi n if
pup1l 1s not fully dilated
Reconstitution: dilute 10% Drosyn to NS at I: 4 to get 2.5%.
Comments. It causes local irritation. blurring of \lsion. hypcncns1on.
Avo id in babies with paralytic ileus, NEC.

DJOt. PHENYTOIN
Indications: Sci?Ures not controlled with phenobarb1tone.
Pre entation: 100-mg:2 mL ampoule. 25 mg mL oral suspension.
Dosage: Loading dose. 15-20mg/k:g;dose single m dtvf<1Cd: Maintenance
dose: 12 hour aficr loadin'l_S mg kg/din 2 divided doses (max 8mg/kg/c!l
Dilution: Dilute 1 mL (50 mg) from an ampoule to, 0 mL with N S to
make a 50 mg/10 mL solution. 4 mL/kg = 20 mg/kg
Administration:
The loading dose 1s given by syringe driver infusion over 20 30 min.
The maintenance dose is given by slow injection at the prox imal cannula
469
site. IV infusion rate max 0.5mg/kg/m in IV injection to be followed by
NS flush.
Storage: Store below 25°C. Stability Use parenteral solution till not
hazy. Do not mix with other medicin<:s. Compatible with NS and RL.
Infusion should start within I hour of preparation. Diluted solution
should not be refrigerated. Discard 4 h after preparation.
Comments: Plasma levels: 40 - 80 µmol/L. Adverse Effects: Lethargy,
nystagmus. Arrhythmia, hypotension, bradycardia with IV route,
hirsuitism, coarse facial features, S-J syndrome, megaloblastic anemia,
blood dyscrasia. Hold feed 2 h prior and 2 h after drug. Avoid giving Ca
and Mg supplements with phenytoin, spacing by :0:2 h. The HR should be
monitored during IV administration.

0102. PIPERACILLIN AND TAZOBACTAM


Indication: Broad spectrum antibiotic for use against ESBL producing
organisms
Dosa,,e:
Wt Postnatal age Dose ( ml!lkiddose) Interval
< 2000" > 1 wk 225 8h
< 1 wk 150 12 h
> 2000 g >I wk 300 6h
< 1 wk 225 8h -
Reconstitution: To 400 mg/mL with WFI. Pale yellow to slightly dark
colour does not indicate loss of potency.
Storage: Unconstituted: Store at less than 30 °C. Reconstituted: Up to 24
hat room temp., 7 d at 4 °C, and I m frozen.
Administration: Infuse over 30 min with syringe driver with
concentration go mg/mL (piperacillin). Separate amino glycoside
infusion by at least 30-60 ruins. I g piperacillin = 2.35 mEq Na.
Comments: Adverse Effects: Fluctuation in BP, blood dyscrasia,
convulsion, increased liver enzymes, skin rash, deranged RFT, decreased
K+, diarrhea, false +ve DCT.

0103. PREDNISOLONE
Indications: Chronic lung disease presenting like asthma, immune
thrombocytopenia
Presentation: Tablets: strength 5 mg, lO mg, 20 mg. Syrup 5 mg/5 mL
Dosage: 0.5-2 mg/kg/d
Interval: 6-8 hourly
Administration: Oral
Comments: Adverse effects are hyperglycemia, hypertension, gastritis.

DI04. PROPRANOLOL
Indications: Hypertension, PSVT, cyanotic spells
470

Presentation: Tablets: I 0 mg, 40 mg


Dosage: 0.5-2 mg kg d
Inter val: 6-12 hourly
Administration: Oral
Comments: Can prec1p1tate heart failure, heart blocks, bronchospasm

DIOS. PROSTAG LANDIN El


Indication: PDA dependent CHO.
Presentation: 500 µg/mL ampoule.
Dosage
Nonna I dosage .................. SQ - 100 nJY'kg/min
Low dosage ....................... 5 - 20 ng/kg/min
Reconstitution
For the nonna l dose infusion dilute 0.3 mL ( 150 µg)/kg from an ampoule
to 50 mL with N/S to make a 150 µg/kg/50 ml solution. I mLJh - 50
ngkg,min
For the low dose infusion dilute 0.06 mL (30 µg) kg from an ampoule to
50 ml with N S to make a 30 µg/kg/50 mL solution. I mL h - 10
ng,kg.min
Stor age: Store below 8°C. Do not freeze.
Administration: Syringe pump infusion.
Comments: May cause apnoea and mechanical ventilation should be
ava1lable. Bradycardia, hypotensio°' c~us flushing, fever~e!?Urcs,
irritability and lethargy may occur. Do not use in suspected ~C.
Prolonged administration can cause oedema, cortical hXJ>erostqsis (bone-
withm-bone) of the long bones and ~stric outlet obstruction from antral
hrpcrpl~sia. - - --- - --....

Dl06. PROTAMINE SULFATE


Indications: Heparin overdose. To neutralize heparin activity during
surgery
Presentations: 10 mg/mL (5 mL, 25 ml)
Dosage: I mg of protamme neutralizes 90 USP umt of heparin (lung),
115 USP unit of hepann (intestinal), and I mg ( 1OOunit) of LMWH.
Maximum dose: 50mg m any 10 min interval

Time since last heparin dose Dose of Protamine (mg) to


(min) neutralize IOO unit of heparin
<30 I
30 60 0.5 0.75
60 120 0.375 0.5
> 120 0.25 - 0.375
471

If heparin given by SC injection, use I - 1.5 mg protamine per I 00 unit


heparin. Administer l/3 - 1/2 dose IV slowly and rest 2/3 - Y, by
continuous IV infusion over 8 - 16 h.
LMWH: if last dose within 4 hour - <tse I mg protamine per 100 unit
LMHW. 2"' dose of 0.5 mg protamine per 100 unit LMWH given if
APTT remains prolonged 2-4 h after first dose.
Administration: reconstitute vial with 5 mL WFI (preservative free) to
make IO mg/mL. Inject without further dilution over IO min not to
exceed 5mg/min. Heparin neutralization begins within 5 min of
administration.
Storage: Keep refrigerated. Stable at room temperature for 2 wks.
Comments: Heparin rebound with anticoagulation & bleeding can occur
8 - 9 h after protamine administration. Can be as late as 18 h. Can cause
thrombocytopenia

D107. PYRAZINAMIDE
Indications: Congenital/ neonatal TB
Presentation: Tablets 250 and 300 mg
Dosage: 30 mg/kg/dose
Interval: 24 h
Administration: Oral. During l" 2 mths of ATT
Comments: Monitor hepatotoxicity

Dl08. PYRIDOXINE
Indications: Therapeutic trial in neonatal seizures, which may be the
result of pyridoxine dependency.
Presentation: Tablets of 100 mg, 50 mg/mL ampoule.
Dosage: 50 - I 00 mg once daily
Storage: Store below 25°C. Protect from light.
Administration: Rapid injection at proximal cannula site, oral
Comments: The effect on seizures should be evaluated using EEG
monitoring. Seizures cease and the EEG becomes normal within minutes.

D109. PYRIMETHAMINE
Indications: Congenital toxoplasma infection
Presentation: 25 mg tablets
Dosa e
/dose) Interval
<6 mths 24 h
6-12 mths 48 h
Administration: Oral
Comments: Combine with Suphadiazine 100 mg/kg/d .. Give Folinic
Acid (Leucovorin) 5-10 mg three times a wk. Adverse effects include
leukopenia, thrombocytopenia, megaloblastic anemia, anorexia,
472

vomiting, atrophic glossitis, rash, seizures, shock. Administer with feeds


if vomiting persists. CBC twice a wk in first 6 mths and twice a month
between 6 and 12 mths. If ANC < 1000, increase dose ofLeucovorin and
if ANC < 500 withhold the drug temporarily.

Dl 10.RANITIDINE
Indication: GERD, Upper GIT bleeding, Hypersecretory conditions
Presentation: Ampoules 25 mg/mL, Tablets 150 mg
Reconstitution: IV 2.5 mg/mL with NS/5% D/10% D. Stability at room
temp 48 h
Dose and Interval
IV : 1 mg/kg/dose q 6 h
PO: 1-2 mg/kg/dose q 12 h
Administration: Over 5 min
Comments: Increased colonization with pathogenic bacteria and yeast,
Constipation, sedation, tachycardia.

Dlll. RIFAMPICIN
Indications: Congenital/ neonatal TB
Presentation: Suspension I 00 mg/5 mL
Dosage: 10 mg/kg/dose
Interval: 24 h
Administration: Oral
Comments: Orange discoloration of body fluids. Hepatotoxicity,
vomiting, blood dyscrasias, eosinophilia, elevated BUN. renal failure.
Induces hepatic drug metabolising enzymes and reduces activity of
steroids, digoxin, opioid, phenytoin, Phenobarbital, theophylline.

D112. RESONIUM A
Indications: Hyperkalemia (plasma potassium >7.0 mmol/L).
Presentation: Powder. Store below 25°C.
Dosage: 1.0 g/kg
Interval: 4 - 6 h
Dilution: Dissolve the powder in 4 mL/kg of 10% D.
Administration: Retention enema.
Comments: May cause constipation. Nonselective cation DVET.
Therefore monitor plasma calcium and magnesium as well as potassium
and sodium.

Dll3. SALBUTAMOL
Indications: BPD (BPD) with reversible bronchospasm.
Presentation: Respirator solution 0.5% (5 mg/mL). Store below 25°C.
Dosage: 0.1 mg (0.02 mL)/kg/dose
Interval: 6 h
473

Dilution: Dilute the prescribed dose Hith N/S to give a total fill volume
of4 mL.
Administration: Nebulise for IO min ind discard the remainder.
Comments: There are limited data r"garding use in infants with BPD.
Can cause hypokalemia, tachycardia

Dll4. SILDENAFIL
Indications:
PPHN
Presentation: Tablets 25 mg 50 mg I 00 mg
Dosage: Initial dose should be 0.25-0.5 mg/kg/dose q 4-8 h. Increase by
0.25 mg per dose. Doses are titrated on response. Maximum dose is 2
mg/kg/dose every 4 h.
Storage: Store at l 5-30°C
Comments: May lead to a fall in systemic pressure. Medications, which
inhibit cytochrome 3A4, will enhance activity of sildenafil
(erythromycin, clarithromycin, ketoconazole and protease inhibitors)
Medications which induce the cytochromes 3A4 enzymes will or may
decrease activity of sildenafil. Rifampin, carbamazepine, fosphenytoin,
phenytoin, Phenobarbital.

DllS. SODIUM BENWATE


Indication: Treatment of hyperammonemia in neonates with urea cycle
defects.
Presentation: 20 g packet of Sodium Benzoate powder
200 mg/mL as )1iiI ampoules [currently not available in India]
I 00 mg/mL syrup [currently not available in India]
Dosage: Oral: Start at 500 mg per day. Can go up to 3000 mg per day in
divided doses. '
Comments: 500 mg of sodium benzoate contains 3.5 mmol of sodium,
so take care of sodium overload. Drug doses and diet should be adjusted
to keep the plasma ammonia concentration below 60 umol/L, and the
plasma glutamine concentration below ~ µmol/L while maintaining a
normal essential AA profile. Nausea and vomiting are the commonest
side effects and ge3nerally avoided by giving smaller doses and more
frequently.

Dll6. SOMATROPIN
Indications
Long term treatment of GH for lack or inadequate endogenous GH,
Prader Willi syndrome, SGA babies with failure to catch up growth by 2
yrs of age, Turner syndrome
Dosage: Check instruction leaflet provided with drug.
474

Humatrope: 0.18 mg/kg (0.54 IU/kg) weekly divided in equal doses on


alternate day or 6 times/wk
Genotropin: 0.16 - 0.24 mg/kg weekly divided into daily does (6-7
doses)
Administration: IM/SC (not for IV use)
Storage: Store in refrigerator. Don't freeze. If diluted without
preservative, stable for 24h if refrigerated. If diluted with preservative -
check instruction leaflet for stability.
Comments: Intracranial HT, j growth of preexisting nevi, local
lipoatrophy or lipodystrophy, hyperlipidemia, gynecomastia, pancreatitis.
Rotate injection site.

D117. SOTALOL
Indications: Refractory supraventricular tachyarrhythmia's (SVT, Atrial
flutter & fibrillation)
Presentation: Tablets of 40 and 80 mg. 80 mg/8 mL ampoule (currently
not available in India)
Dosage : Oral 2 - 4 mg/kg/d (gradually increase every 3-5 d if
needed; max.dose
4mg/kg/dose)
Infusion 0. 1 - 0.2 mg/kg/h
Commence treatment with the lower dosage.
Dilution: Dilute 0.5 mL (5 mg)/kg from an ampoule to 50 mL with 5%
Dor N/S to make a 5 mg/kg/50 mL solution (I mL/h ~ 0.1 mg/kg/h)
Interval: Oral 12 h
Administration: Orally before feeds; milk reduces absorption by 20-
30%
IV by syringe pump infusion.
Comments
Use with caution in the presence of heart failure; avoid in the presence of
hypokalemia and hypomagnesemia (due to the risk of torsades de
pointes)

Dl 18. SPIRONOLACTONE
Indications: Congestive cardiac failure & BPD
Presentation: Tablet: 25 mg and I 00 mg. Reconstitute into sachets.
Store below 25°C.
Dosage : I - 3 mg/kg/dose
Interval: 8 - 24 h
Administration: Oral.
Comments: Used with frusemide to facilitate diuresis and conserve
potassium. May prolong the half-life of digoxin. May cause
hyponatremia and hyperkalemia.
475

Dll9. SULPHADIAZINE
Indication: Congenital toxoplasmo&is
Presentation: Tablet 500 mg
Dosage: l 00 mg/kg/d
Interval: 6-l 2 hourly
Administration: Oral
Comments: Can cause rash, hepatitis, cytopenias, SJ syndrome

Dl20. SURFACTANT
Indications: Prophylaxis and therapy ofHMD, Acute respiratory
distress syndrome (ARDS) due to any cause, MAS, PPHN (still
experimental), Surfactant protein B deficiency (use Survanta)
Presentation:
Survanta: Vial containing 4 mL or 8 mL of suspension. Store below
s0 c.
Curosurf: Vial containing 1.5 mL of white creamy suspension.
Neosurf: Vial containing 3 mL or 5 mL of suspension. Store below 8 oc.
Dose
Survanta: 4 mL/kg
Curosurf: First dose 2.5 mL/kg; subsequent 1.25 mL/kg
Neosurf: 5 mL/kg
Reconstitution: Allow to warm to room temperature. Using an 18-G
needle and a I0 mL Luer-Lock syringe withdraw the required dose from
the vial.
Administration: Attach a 6-FG end-hole catheter cut to the same length
as the infant's ET tube to the surfactant syringe. Insert the catheter into
the ET tube and inject in two aliquots. Vials are for single use.
Comments: Adverse effects of surfactant include acute ET tube block,
pulmonary hemorrhage, opening of PDA.

Dl21. TEICOPLANIN
Indication: Serious infections caused by aerobic and anaerobic gram-
positive bacteria (esp. Staph aureus)
Presentation: 200mg/400 mg per vial. Wait till foaming subsides after
reconstitution.
Dosage: 16 mg/kg stat followed by 8 mg!kg/d
Administration: IV or IM
Interval: 12- 24 h
Storage: Unconstituted: Store at less than 30 °C. Reconstituted: Up to 24
hat 4 °C.
Comments: Can cause pain, phlebitis at site of injection. Slowly
eliminated in kidney with serum half-life of70-100 h.
476

0122. TETANUS IMMUNOGLOBULIN


Indications: Prevention and/or treatment of tetanus neonatorum
Presentation: 250 I.U/500 I.U/JOOO l.U in 1 mL vial.
Dosage: 500- JOOOU therapeutic, or 250 U intrathecal, 250-500 I. U
(prophylaxis)
Administration: IM
Adverse reactions: Local pain, fever, flushing, headache and chills.

Dl23. THEOPHYLLINE
Indications: Apnoea of prematurity, Weaning from mechanical
ventilation, BPD.
Presentation: 50 mg/5 mL syrup. Store below 25°C.
Dosage
Loading (optional) 5 mg/kg
Maintenance 2 mg/kg/dose
Interval: 6-8 h
Plasma levels: should be monitored
Therapeutic range: apnoea of prematurity 7-12 µg/mL
Bronchospasm 10-20 µg/mL
Tachycardia at 15-20 µg/mL, seizures >40 µg/mL
Comments: Side effects include vomiting, sinus tachycardia and SVT.

Dl24. THIAMINE
Indication: Thiamine-responsive Maple Syrup Urine Disease
Presentation: 100 mg/tablets, Inj. JOO mg/mL
Dosage: 10-25 mg/dose IV, 10-50 mg/dose PO

Dl25. THYROXINE
Indications: Hypothyroidism.
Presentation: 25, 50, 100 µg tablet. Store below 25°C. Make sachets.
Dosage : JOO µg!m2/d or 8 µg/kg/dose
The usual starting dose is 25 µg/d in a term infant and 12.5 µg/d in a
preterm infant.
If rapid correction is desired, one may start with 50 µg/d.
Interval: 24 h
Administration: Dissolve desired fraction of a tablet in a small amount
of WFI, water for irrigation or milk and give orally. Administer oral
doses on an empty stomach.
Comments: Monitor T4, T3 and TSH levels and clinical status at regular
intervals
477

Dl26. Ticarcillin-clavulAnic acid


Presentation: 3. lg vials contain l.O g of ticarcillin and 100 mg of
clavulanic acid.
Reconstitution: The 3.1 g vial should be reconstituted by adding 13 mL
of sterile WFI or NS and shake well. The concentration of ticarcillin in
dissolve solution is 200 mg/mL .md corresponding concentration of
clavulanic acid is 6. 7 mg/mL. The reconstituted drug is stable for about
6 h in room temperature or up to 72 h under refrigeration.
Dose: (mg /Im/dose)
Wt :Sl200 g 1200-2000 a >2000
Age Any :S 7 d >7 d :S 7 d >7 d
Dose 75 75 75 75 75
Interval 12 h 12 h Sh Sh 6h
Administration: Syrmge driven mfus10n over 30 mm
Comments: Sodium content: 4.75 mEq/L. Must not come in contact with
an aminoglycoside. Can cause bleeding diathesis, hypematremia,
hypocalcemia and rash.

Dl27. TROPICAMIDE EYE DROPS


Indication: Pupillary dilatation for ROP screening
Presentation: 1%, 2.5% eye drops
Dose: 1-2 drops on both eyes, repeat after 15-20 min if pupil is not fully
dilated

Dl28. URSODEOXYCHOLIC ACID


Indications: Preparation for hepatobiliary scintigraphy, Long-term
treatment of cholestatic liver diseases and postoperative management of
extrahepatic biliary atresia.
Presentation: Only tablets available 75 mg, 150 mg, and 300 mg.
Dosage:
For scintigraphy: 20 mg/kg/din 2 divided doses (12 h apart) for 4S~72 h
before the second scan and continued till the second scan is over.
For cholestasis: 13-20 mg/kg Id in two or single dose.
Administration: Oral
Comments: Can cause diarrhea
478

D129. VANCOMYCIN
Indications: Sepsis from S. epidermidis and methicillin-resistant S.
aureus (MRSA).
Presentation: 500 mg vial. Store below 25°C.
Dosa2e and interval: lm!!lk!!ld)
Wt < 1500 g " >1500 g
Aqe ' <7d >7 d <7d >7 d
Dose 20 30 30 45
Interval 24h Sh 12 h Sh
Reconstitntion: Add 10 mL ofWFI to the vial to make a 500 mg/10 mL
solution.
Dilution: Dilute 2 mL ( 100 mg) of the reconstituted vial to I 0 mL with
5% D to make a 100 mg/10 mL solution. 1 mL/kg ~ 10 mg/kg
Administration: Syringe driver infusion over 1 hour.
Serum levels
Peak .......................... 25 - 40 mg/L.
Trough ...................... <12 mg/L.
Storage: Unconstituted: Store at less than 30 °C. Reconstituted: Up to 14
d at room temp., 3 m at 4 °C
Comments: Precipitation occurs if mixed with other drugs (particularly
ceftazidime, heparin, bicarbonate, steroids) or TPN. Rapid infusion can
cause an erythematous rash ('red man' syndrome). Potentially
nephrotoxic and ototoxic.

D130. VECURONIUM
Indications: Skeletal muscle paralysis in case of difficult ventilation &
PPHN. Adjunct to facilitate ET intubation.
Presentation: 4 mg/2 mL ampoule
Dosage: 0.03- O.OS mg/kg/dose
Comments: Can cause transient fall in BP, slight increase in HR,
reduction in GIT motility. Can cause malignant hyperthermia

D131. VIT K
Indications: Prophylaxis or therapy for Hemorrhagic disease of newborn
Presentation: 1.0 mg/0.5 mL ampoule. Store below 25°C. Protect from
light.
Dosage: 1.0 mg
Administration: Intra-muscular to all at birth

D132. ZIDOVUDINE
Indications: Infants born to HN positive mothers, Symptomatic and
asymptomatic HIV infected infants
Dosage
Term: 2 mg/kg/dose PO q 8 hourly
479

Pretenn: 32-36 wks- 2 mg/kg/dose, I 8 hourly


<32 wks- 2-mg/kg/dose q 12 hourly
Presentation: JOO mL bottle contarning 50 mg/5 mL of AZT syrup
Comments: Start AZT within 12 h of birth. Anemia and
granulocytopenia are common and reverse to nonnal within 6 wks after
completion of therapy

D133. WSTER IMMUNE GLOBULIN


Indications: Infants born to mothers who have had the onset of chicken
pox within 5 d before or 2 d after delivery. Postnatally exposed
premature infants <I kg or< 28 wks.
Presentation: 5 mL ampoules
Dosage: Baby: 125 U
Administration: Injected JM as single dose at one site.
Comments: V-ZIG does not reduce the incidence but does decrease tbe
complications associated with varicella. Pain, erythema, swelling and
rash at the site of injection and rarely anaphylaxis.
480
481

RF. DRUG REQUIRING DOSE ADJUSTMENT IN RENAL FAILURE


Adapted with modifications from The Harriet Lane Handbook
RF.I Antimicrobials requiring dose adjustment in renal failure
(Q=every, Qd=every day, QOD=every other day, D=dose, I=interval)

Pharma co kinetics Adjustments in Renal Failure


Creatinine in Renal
Drug Normal
Route of Failure(mL/min)
Dose Method
Excretion Mild Moderate
Interval Severe(<10)
(>50) (10-50)
Acyclovir(IV) Renal Q8hr rn I Q8hr Ql2-24hr
50%and
Q24hr
Amikacin Renal Q8-12hr I / Q8-l2hr Q12-l8hr Q24-48hr
Amoxicillin Renal Q8-12hr I Q8-l2hr Ql2hr Q24hr
Amoxicillin- clavulanate Renal Q8-12hr I Q8-12hr 0 12hr Q24hr
Dosage adjustments are unnecessary
with preexisting renal impairment; if
Renal 40% decreased renal function is due to
Amphotericin 8 QD I
up to 7d amphotericin B. the daily dose can be
decreased by 50% or the dose given
QOD
482

Amphotericin B choleteryl
? QD I No guidelines established
sulfate (Amphotec)
Amphotcricin B liquid
Renal 1% QD I No guidelines established
complex (Abelect)
Amphotericin B liposomal Renal
QD I No guidelines established
(AmBisome) '.010%
QI2-
Ampicillin Renal Q6hr I Q6hr Q6-l2hr
16hr
Renal 75%-
Aztreonam Q6-12hr D 50% 25%
(heoatic) 100%
Cefaclor Renal Q8-12hr D 100% 100% 50%
Q24-
Cefadroxil Renal Q12hr I QJ2hr QJ2-24hr
48hr
Ql2 h regimens:
Est Cr Cl
Dose
(mL/min)
Cefepime 50mg/kg/dose
Renal Q8-12hr DI 30-60
Q24hr
25mg/kg/dose
11-29
Q24hr
<JO 12.5mg/kg/dose
Q24hr
483

Q8hr regiments:

CrCl(mL/min)
Dose
30-50 50mg/kg/dosc
Ql2hr
10-30 50mg/kg/dose
Q24hr
<IO 50mg/kg/dose Q24-
48hr
Renal 75% (CrCI 50%(CrC
Cefiximc QI2-24hr D 100%
(hcoatic) 21-60) 1<20)
Ccfotaxime Renal Q6-12hr D 100% CrCI <20 ~ t dose by 50%
CrCI 30-50
Normal ~Q8-12hr Q24-
Cefoxitin Renal Q4-8hr I
Interval CrCI 10-30 48hr
~QI2-24hr
CrCl<30~Q2
Cefpodoxime proxctil Renal QJ2hr I Q12hr Q24hr
4hr
CrCI30-50 Q24-
~QI2hr 48hr
Ceftazidime Renal Q8-l 2hr I Q8-12hr
CrCI 10-30
~Q24hr
484

Q48-
Ceftizoxime Renal Q6-12hr I Q8-12hr Q36-48hr
72hr
CrCl 10-20=
Cefuroxime Renal Q8-12hr I Q8-12hr Q24hr
Ql2hr
Q\2-
Cephalexin Renal Q6hr I Q6hr Q8-12hr
24hr
50% (or
50-75%(or Ql8-
Renal
Ciprofloxacin Q8-12hr D,I 100% QI 8-24hr for 24hr for
(hepatic)
CrCI <30) CrCI
<30)

Cr Cl<30= t
dose by 50%
Renal/ No
C!arithromycin Ql2hr DI and ?
hepatic Change
administer
BID-QD

Sulfametho Cr CI
Ql2hr
Co-trimoxazole (sulfa- xazole: D No CrCI 15-30 <15=
methoxazole/trimethoprim) Hepatic Change =50% Not
(Renal) Recomm
485

Trimethopr -ended
im:
Renal
(hepatic)
Hepatic 50%-
Erythromycin Q6-8hr D 100% 100%
(renal) 75%
Renal Q48hr±L
Ethambutol 24hr I Q24hr Q24-36hr
(heoatic) dose
Fluconazole Renal Q24hr D 100% 25-50% 25%
Flucytosine Renal Q6h [ Q6h Q 12 h Q24H
!V:Dl IV: 50%-
25°10-50°!0
100% 25% and
IV: Ql2hr and Q24hr
and Q24hr
Ql2hr
Ganciclovir Renal
P0:50%
-100% 50%and 50%and
PO:T!D PO:DI
and-TID B!D-QD QD

Q24-
Gentamicin Renal Q8-12hr 1 Q8-12hr Ql2-18hr
48hr
50-100% 25%-50% 25% and
Imipcncm/cilastatin Renal Q6-8hr DI
and Q6- and Q8hr Ql2hr
486

8hr
Hepatic
Isoniazid Q24hr D 100% 100% 50%
(renal)

f. Mcropcncm

Methicillin
Renal

Renal
Q8hr

Q4-6hr
DI

1
JQQ:lli..
and Q8hr
Q4-6hr
50%-100%
and Ql2hr
Q6-8hr
50% and
24hr
Q8-12hr
Renal .
Metronidazole Q6-12hr D 100% 100% 50%
(hepatic)
Hepatic
Nortloxacin BID 1 BID QD-BID QD
(renal)
Ofloxacin Renal BID 1 BID QD QOD
Use
lower
Renal
Oxacillin Q4-12hr D 100% 100% range of
(liver)
normal
dose
Penicillin G-potassium/Na Renal 20%-
Q4-6hr D 100% 75%
+(IV) (hepatic) 50%
Renal CrCI 20- CrCl <20
Pipcracillin Q4-6hr 1 Q4-6hr
(hepatic) 40~Q8hr ~Ql2h

Piperacillin/ Renal DI DI 100% 70% and 70% and


487

Tazobactam and Q 6- Q6hr(CrCI Q8hr


8hr 20-40) (CrCI
<20)
Hepatic
Rifampin Ql2-24hr D 100% 50%-100% 50%
(renal)
50% (CrCI
Sulfamethoxazole Renal Q12hr D 100% 25%
I 0-30)
Q8hr(CrCl
Ticarcillin Renal Q4-6hr 1 Q4-6hr Q12hr
I 0-30)
Q12hr
(Q24hr if
Q8hr(CrCl comorbid
Ti...:.<lh-illin- clavulanate Renal Q4-6hr I Q4-6hr
I 0-30) hepatic
impair-
ment)
Renal Q24-
Tobramycin 1.5-3 1 Q8-12hr Q12-18hr
(hepatic) 48hr
Q48-
Vancomycin Renal Q6-12hr I Q6-12hr/ Q18-48hr /
96hr

I /
488

RF.2 Nonantimicrobials which require dose modification in renal failure

Pharmacokinetics Adjustments in Renal Failure


Creatinine in Renal
Drug Normal
Route of Failure(mL/minl
Dose Method
Excretion Mild Moderate
Interval Severe(< IO)
(>50) (10-50)
Acetaminophen Hepatic Q4hr I Q4hr Q6hr Q8hr
Acetazolamide Renal Q6-24hr I Q6-8hr Ql2hr AVOID
100% or 50o/o or 25o/o or
Atenolol Renal (GIT) QD D,I
Q24hr Q48hr 096hr
100% Q8- 75% or 50% or
Captopril Renal(hepatic) Q6-24hr D,I
12hr Ql2-18hr Q24hr
75% (monitor
Carbamazepine Hepatic(renal) Q6-24hr D 100% 100%
sermn levels)
Chloroquine Renal(hepatic) Q6hr-7d D 100% 100% 50%
100% or 75%or
Cimetidine Renal( hepatic) Q6hr-12hr D,I 50%orQI2hr
Q6hr Q8hr
(
I 489

Digoxin l00%or 25%-75% 10%-25% or


Renal Ql2-24hr D,l
Q24hr orQ3 6hr Q48hr
Enalapril (JV:
Renal (hepatic) Q8-24hr D 100% 75%-100% 50%
Enalaprilat)
100% or 50% or 25% or Q 36-
Famotidinc Renal (hepatic) Q8-12hr D,I
Q8-12hr Q24hr 48hr
Q30min-
Fentanyl Renal (hepatic) D 100% 75% 50%
lhr
Insulin (regular) Hepatic (renal) Variable D 100% 75% 25%-50%
Metoclopramide Renal Variable D 100% 50%-75% 25%-50%
Midazolam Hepatic (renal) Variable D 100% 100% 5M~

Morphine Hepatic(renal) Single dose D 100% 75% 50%


Phenobarbital Hepatic (renal) Q6-12 I Ql8-12hr Q8-12hr Q12-16hr
Spironolactone Renal (hepatic) Q6-12hr I Q6-12hr Q12-24hr AVOID
Terbutaline(IV/PO) Renal (hepatic) Variable D 100% 50% AVOID
One-time
Thiopental Hepatic(renal) D 100% 100% 75%
dose
Verapamil Renal (hepatic) Variable D 100% 100% 50-75%
490

_
491

NOMOC RA\.1S

NJ. PGIMER L'ffRA-UTERINE G ROWTH C HART


(Unpublished)

s I·rth we1e:
· h t ·m e:rams
Gestation -2 SD - 1 so \1can + I SO +2 SD
27 185 473 861 1149 • 1407
28 666 914 1162 1410 1608
29 861 1088 1315 1542 1769
30 837 1139 1441 1743 2045
31 549 1058 1567 2076 2585
32 844 12.95 1746 2197 2648
3) 1210 1517 1824 2131 2438
34 1229 1670 2111 2552 2993
35 1438 1879 2320 2761 3200
36 1674 2117 2560 3003 3+t6
37 1918 23.39 2760 3181 3602
38 2020 2440 [2864 3286 3708
39 2095 25 17 [2939 ! 336J 3783
40 2178 2593 3008 3424 3838
41 2205 2678 3151 3624 4097
42 2130 2555 2980 3405 3856
>42 2079 2505 [2931 3367 3783
.
l

- \ -1 I
-
I \ -:rt
492

N2. LUBCHENCO'S INTRAUTERINE GROWTH CHAR~


(Reproduced with p.:mu~1on from Pediatrics, Vol 37, Page~ 403-408. Copynght ~
bytheAAPl
-;
----tftt.,UU

I I I I
.. .. .......
I
· - - - - _ , .,, .... Jll

..,..,.0 ... i...Pr"QWto#! ....


.. ........ I

I
I
,, ,, ·~
- .--
. I
,
,.,
,.,
.....
., v v
IJ
IJ
IJ
,,
. IJ
IJ
- ...
1-l~" v
IJ

....
~-
-....
'

--
v
~-i-
I ~---~
--· fil ,
,., v v
....
~-
y
f) (,

:;I I~
,, , '·' -..
lo-
L..
... r.;.
~ .....
-
"'

---
,, "l
' ' .......... '

/
493

N3. FENTON'S CHARTS FOR Th TRAUTERINE GROWTH AND


INITIAL 10 WKS OF J:'Q[fNA TAL AGE (Reproduced rrom the open
access article: Fenton et al, BM~: 13. I,iccnsee BioMed Central Ltd.)
65 ! F .. tal-l"l""' G<"<>Wth Cho•rt for Pr~term ,,.,_(WHO a..,... .. """;"'"""• Y...... 1<1•1 65
'
··. : i. . .~ ->··+ .' i-- t· ___.;,
• . · · • -~" .· I ·:.;_1:1".r.• • '
i ' • • •... 60

h-+'--'.-1,f-+++-;-J+,..::::,.+c,:±-H'CT-b.
. . I. I •'i
":1 ·-1~i----~i -·!:·
V1 i ~ •• ' j'
·'-r-1 ' L i .'
l
t • j
1 ••
'°J
••
•M•• .-l<L-t-""1.L-T..f il
494

l'li4. EHRE'JKRANZ'S POSTNATAL GROWTH CHARTS FOR

14 28 42 56 70 84 98
Postnatal Age (Days)

~4.2 Avera~e length versus postnatal age (Wks) for \'LBW infants
stratified by I 00-g BW intervals
495

N4.3 Average weekly OFC versus postnatal age (Wks) for VLBW
infants stratified by 100-g BW intervals

35

'
f 'j'
···'··· t .
30 j

i
i······-+-·-···~----;
. . !

i--··---L--.t----L-.
. j -+---.--~--·
. . i.. ___l_'
l..

20 - ·--·1
2 3 4 5 8 7 8 9 10 11 12 13 14 15 16 17
Postnatal Age (Weeks)

N4.4 Average weekly mid-arm circumference versus postnatal age


(Wks) for VLBW infants stratified by 100-g BW intervals

I
i i
8 ;
i .---------·!
. '
7
r:·:~~==~~f~~= :·--~:~::1
7'·r">' I ••• • ··1 ,.___ -
1
-+·---~~::~=_:._ __ . f. .--.=~
r-·-~···71°······,· .- T.:::~_.J _____ ~ ----~-----_:
6 "" i.

'
---· ..... t---- ._.,.. ___ .., __ _
$
·!· . .
r=r,1 , "*"'
.>.. • - · · · · · · - , · - · - -- •

4 ·-· ~--· -.l . . · j·- ·:.:l:: ___:_~


···1
;--t---ic-c--r i ;---,---,-~,--~~

2 3 4 5 6 7 8 9 10 ti 12 13 14 15 16 17
Postnatal Age (Weeks)
496

N4.5 Growth curves of VLBW infants with major morbidities and


(dashed lines) and without major morbidities (solid lines). Infants
are stratified by 200-g BW intervals.

2000

1750

I
.!!! 1250
i
~ 1000

750

14 28 42 56 70 84 98
Postnatal Age (Days)

N4.6 Growth curves of SGA infants (Solid lines) and AGA (AGA)
infants (dashed lines). Infants are stratified by 200-g BW intervals.

I 1250
i
;;! 1000

.... •· -~-- .. ~ ·~- --··.,---~--··+··•·


500 .._·._t·"'._.-'-·-··--···,..,+,.,.._.-·i_.·_.!_.:·t:

14 26 42 56 70 98
Postnatal Age (Days)
497

NS. KELLY WRIGHT'S POSTNATAL GROWTH CHARTS FOR


VLBW NEONATES (Reproduced with permission from Pediatrics, Vol 91, Pages
922-926, Copyright© 1993 by the AAP)
NS.I Average body Wt (g) Vs. postnatal age (d) for infants with BW
ranges 500-7SOg, 751-lOOOg, 1001-1250 g, J2Sl-ISOO

·~~~~~~~~~~~~'fl"''~
.....
Borth
Weigh!

u ]-~-
·' !_.~,,._,_
3
>111-HCI

1 ' •...
,_·· ... --:i.;.·~+--
....................
O.>~~=F:f::+--!--+-J-1--1--~-J---!--+-J-l--l--k+-i

~'w~w"~"~~~"~~~n~u~~~~
POSTNATAL AGE (days)

NS.2 Average crown-heel length and occipital-frontal circumference


vs. postnatal age (d) for infants wit6 BW ranges S00-7S0g, 751-
lOOOg, IOOI-12SO g, 12Sl-1500g - -

~ lHl-1$00

t -1--1--Hriri-+-+-+~++++-t-cbf-"-H:-:i'--11001-tuo
501- l'l-1000.

501·7'0

200 !! 10 u 20 25 10 3!! 40 45 JO 55 60 65 70 75 80 8!! 90 9!! 10010!!


498

N6. WHO GROWTH CHARTS (Reproduced from the open access site
http://www.who.int/childgrov.rth/standards/en/)
N6.I Wt for age (Girls) - Birth to 2 yrs (percentiles)

---(
'

~ ~~...:-"']
_-.
·a--··--~ .
~~

,......,.,.,,- ------

'i

N6.2 Length for age (Girls) - Birth to 2 yrs (Percentiles)

w~ocn.1:1 Grewlti >wiclord•


499
500

N6.5 Wt for age (Boys) - Birth to 2 yrs

WHOO.kl(;,_.,,.,~
501
N6.7 Wt for length (Boys) - Birth to 2 yrs
502

N7. GROWTH CHARTS FOR TWINS (Reproduced \\ilh permis~ion from


Pcd1atncs. Vol 37. Pages 409-416. Copynght C 1966 by the AAP)
~7.1 Dicborionic twins
6~

- ..
l

, 1......-
i-
2 ••

///........._
2 .- I

,., /]::
~

,.,v' .. / •• ....
, /-.!'-.
/
.--
2 4- I /
V)/ A ;.,. ......
I
... I/ / ,, ,..
2000
/ ,/
,_..-
,.v
/
/
I/
/1,... /
•'
,,.·
'°"

V' v,./ (.... ..


00
I .. v
_
12 00

- - v v.
;_,...-'
........ I
24 6 2' n 3'I 36 31f «>-42

N7.2 Monochorionic ""ins


W1wt•li•w.llfltt O.rt
MaMd•lue• Jwlnl
,-
l 200
//
~,,..

--
-t::-
.......... .........
2a·- / /
'"
.. vv v/
/
/
/ --... """'""

-
~

2 4~
v
-
i/

00
/
.. v l/
/v
I/
/
/
/ / ~.,,,...""'
/ / /
00
v _,.,,,. ..-
OA
_.... /
,..... /
!/-'
800
y""'
~

24 <:ti 30 2 34 ~6 38 4()- 2
2'
Weft of 0.lutluei
503

NS. JiVENE'i NOMOGRAM J'OR VENTRICULAR WIDTH


AND ACTION LINE (Reprinted fr >m Archives of Disease in Childhood,
Measurement of the growth of the lateral "' ntricles in preterm infants with real-time
ultrasound, Levene Ml, volume 56, pages 9())-4, copyright 1981, with pennission from
BMJ Publishing Group Ltd.) ------- -

Venlrfculm'
Index (mm}
20.

11'
'
16 - ; '

14. -~.!.·
•..•.~ ..
'

• ;
12 -
' l '

10 ~ --"
-
8
21 28 30 32 34 38 31 40
Gettallon(-)

-
N9. BODY SURFACE AREA
_.,.,,
lg)
4000 ·-
S..rl~

fcmi)
2500 Crown-hetl

'""''
(cm)
55
3000 2000
50
45

1600 40

35

30
1000
,.
1000 20

500
"
10
so4 f I {(
""110. MANROE'S CHART FOR TERM § A~OF
NEONA TES (Rcpnnted from Journal of Pediatrics, \'Olum~ BL, Weinberg
AG, Rosenfeld CR. Browne R, The neonatal blood count m health and disease. I. Reference
values for neutroph1lic cells, pages 89-98, copynghl 1979. with pemuss1on from Elsevier)

TIAIE (hon!

1:- .~·~..;..
:l · .. - .

.· :
1: ·:~·:! .::·t·....:
i ,:··:I • •
r.

.
••
5- :!!·.... ·.. ... . ::. ..... --··
1 ,··:, • :_ ·. '. ~.~.-- ·:
i - ~:.:-·.. ·:. ·-
- -:=::-::. ..·. .. s•• ••
00 • • • ~ '° ~ ......... 60
TIM(-
505

Nll. MOUZJNHO'S CHART FOR \NC OF VLBW NEONATES


(Reproduced with pennission from Pediatrics, /ol 94, Pages 76-82, Copyright© 1994 by

·-·--
the AAP)

·-·--....
n oo
"/
/

".
......
~ ...... Birth to
60 h of
life

.
i ....
l·- ·=·
. . ••...... ._,- .. .. .. ..
,_;,....
•• •
,.

I--.-~~~-~-~~~-~~
~
_.,........ ·····- 61 h to
28 dof
.. life

120 19D MO IGO MO 411 4H IMO - MO 120


TIME "-•1
506

N12. CHRISTENSEN'S NOMOGRAMS FOR ANC OF


NEONATES BORN AT HIGH ALTITUDES (Reprinted from Seminars in
Perinatology, volume 33, Christensen RD, Henry E, Jopling J, Wiedmeier SE, The CBC:
reference ranges for neonates, pages 3-11, copyright 2009, with permission from Elsevier)
N12.1 5th and 95th centile values of neutrophils in I" 72 h (>36 wks
gestation)
JO

!',:
---- ,,
.. ·-. -- .
...... . -····- ····-

''0 ' " " " " .. n

N12.2 5th and 95th centile values of neutrophils in I" 72 h (28-36 wks
gestation)
"'
507

Nl3. SCHELONKA'S NEUTkOPHIL VALUES IN TERM


NEONATES AT 4 HAGE (Reprirted from Journal of Pediatrics, volume 125,
Schelonka RL, Yoder BA, desJardins SE, H Iii RB, Butler TJ, Peripheral leukocyte count
and leukocyte indexes in healthy newborn tc m Infants, pages 603-6, copyright 1994, with
pennission from Elsevier)
Mean±SD Range (10% to 90%)
IIT ratio 0.16±0.10 0.05 to 0.27
ANC (x 10 9/L) 15.6±4.7 9.5 to 21.5
TLC(x 109/L) 24.1 ±6.I 16.2 to 31.5

N14
Macmi
Nt4.1
~
~UBROW'S) CHARTS
Zubrow's
FOR BP (Reprinted by pennission from
pubhshers Ltd: Journal of Perinatology; volume 15: pages 470479, © 1995)
charts for BP according to GA

90 Upper 95% C.l.


01 80
I
E
70
--
E 60
0. 50
-- -- a--
"'
~ 40
-- -- lower 950,

l ~~1· ---
10
o 'r'...,.....,....,...,........,~...,......,...,-,-...,........,...,........,...,...

22 24 26 28 JO 32 34 J6 JS 40 42
Gestational age (weeks)

70
60
°'EE
I
50
Upper 95°t C.L.
-___ ... ---
c.. 40 ---
-- -- ---
Ill
.!::' JO
E 20
'
.~
• ---
---
Lower 95% C.L

0 10
0
22 24 26 28 JO J2 34 36 38 40 42
Gestational age (weeks)
508

NI4.2 Zubrow's charts for BP according to BW


Upper 95% C.L.
90
--- -
~

Ol 80

-- ---- ---
I
E 70
E 60 ---- -- -
~

a. 50
--- -
• - -- -
a:i
Lower 95 %C. L.
-~ 40 --
Ci 30
~

"'>-
\fl 20
---
10
0 ' I I • . . I II I
I I . I
750 . 1.250 . 1.750 . 2.250 2.750 I 1250 ' 3750 I
1.000 1.500 2.000 2.500 3.000 3.100 4.000
Birth weight (kg)

Upper 95 % CL.
~ --- --- ---
t
E
SC·
~ -- ---- --- --- •
a. 40
r •
L
' --
al
v 30 - i I i • ---
0
VI 20
• --- --- ---
re
0 10 -- --- - - - Lower 95% C.L.

:;~o I1.iso
0
1.lSO I2J.so I2.iso I12so I3.i5o I
r

1.000 1.500 2.000 2.500 3.000 3.500 4.000


Birth weight (kg)
509

N14.3 Zubrow's chart for Bl' by post conceptional age

110 Upper 95 %C. L.


~ 100
- -- - -
:F
r
t
90
80
-- --
-
r
t
Cl.
70
60 - -
Q'.)
u 50
-- - Lower 95 % C. L.
.,0 40
"'>. 30
V\
- -- -
20
10
,,
0 ' ' ' i I

24 26 28 30 32 34 36 38 40 42 44 46
Post conceptional age (weeks)

100
Oi 90
I 80
E Upper 95% CL
E 70
--- --- -·
--- ---
~

c. 60
m
u 50
40
--- ---
0
.,
--- ---
0
"'
l'J
30
20 ___ - - - - - -
--- Lower 95% C.L.
10
0 '' I l

24 26 28 30 32 34 36 38 40· 42 44 46
Post conceptional age (weeks)
510

N15. AGE SPECIFIC BP UP TO 1 YR (Reproduced with permission from


Pediatrics, Volume 79, Pages 1-25, Copyright© 1987 by the AAP)

111[

;1~1r--5llT>
;tt----------=:
70
65
0 1 d 5 6 7 10 11 12
MONTHS

7'
-----95TH
-----90TH

-----
-----5CTH

012345S789101112
MONTHS
5:
Nlti. MEAN BP IN NEONATES \\'JTH GA 23-43 WKs (Reprinted &o
Clinic, in Perinatology, Volume 26, Nuntna Umit P, Yang W, Bada-Ellzey HS, Bloo
&om Elsevier)
pressure measurements in the newborn, pag,, 981-96, copyr;ght 1999, with P<miissio,

"[~-=-==-~. . . . . .: .:. . .. . .:.:.: . .: ; . ;:;:;~ ~ ~J .< 37 wk ~,,-

E~
gJ. 50
l!!
~- w .r------·-----
. . 33-36 Wk
----· -------------
- ------- 27-32""'
30
l
r·---- ---- ............. .. ------··.::~-:.::;.;..·.;.:.;. ..... -- ....... ~,:":'..
23-26 Wk
20
0 12
48
60 72
512

----
Nl 7. HEY'S CHARTS FOR._NTZ (Reprinted from Archives of Disease in Childhood, The optimum thennal env1rorunent for naked babies, Hey EN ,
Katz G, ~olume 45, pages 328-34, copYtighr1970, with pcm1iss ion from BMJ Publishing Group Ltd.)

Naked

24

0 10 20 30 0 10 20 30
jy 513

18. NEW BALfkRD SCORING FOR GA ASSESSMENT CRepnnted


from Journal of Pediatrics, volume 119, Bal ud JL, Khoury JC, Wedig K, Wang L, Eilers-
Walsman BL, Lipp R, New Ballard Score. <:. ;panded to include extremely premature
infants, pages 417-23, copyright 1991, with 1cnnission from Elsevier)
_,.._•....cllfu Wa1 .. 11

I
• '
I • I • • • I
....
,.. ~ c¢:::: 1~ etc: a;['.
> ·-· ... .. r ..
~ I ~
s_..
C• mJJ r.to. r. . f' ...
1<. Ana R<K. .
I ~. . {} {} 1}
140"-IW 11...... t> tO·llO•
'fr'<to'

......... ~ ~ . ct>
~-·'
2) ~
f ,~
(f:)
''°' ••. 1 ... ;~ 100' •••
5 ....... -ir -~ -& -~ _g -~
H "..r1111r..
ea l oS 1d9 , &9 I crl3 a:9'

••-.,, ••••ll"Ollf ....tltt.


...""1l
~
..... . ., I ..... ••ft•
.......
,,,••,, ,,. pt•octlh ..,, orad.ed
lrait•••t•l'll t1a utvc:e e1 •lt..,_ ve-.1 IJarf'I# w rifiil~•
-·· ••
. . . - 1- ....
..... -· ..
..
p .......
••60-·t .........
(.40-- · P
-- I ... ,.....u -..- 1 ......
-
..........
CftUt ~
<-· •~
... 11J:

-·- •• ••
/J •.... -........ ·~
.. j
--· ...,,.,..I),,...... . ,. •,. ,,... .,....
..._., •I

""°''
KJ• .._ ".. . I ......
.... 1-·-
J -
Gc.._tt. ....-Uf'lll ...U ..... ,......, ...........

....
t ---
I ......

-.... ,- -··-
I

.......
Clit9"I
--· 1.......
·-· .....
i -·
.....
~· _._....I .... I ' ....
514 CO;/)~'R )
N19. BHUTA~l'S PREDICTION NOMOGRAM FOR J-
HYPERBILTRUBI EMIA FOR WELL NE01'ATES OF~ 36 WKS
& ~ 2000 G. (Reproduced with pcnmss1onr om Pediatncs. vo110J. Page' 6-14.
Copyright 1999 by the AAP) rj C t) TS'[S

20 ~-+---+---+---+---+--+----lf---.+--.-+-
....--1-----1-~' ~ .( ~ I,_
)

i f ~~z- ~-+---t---1---.1.-1 "1 /


!. '5 -+--+--+--+--+-J.~~6.-~::t=:::::t=:±::===*=l 257 '1 ....,

I.E 10 -
~r
2

~+
~~ h~Y) ,,kQw~v-.J ·).~\,"7 ~
~ o -~-
N20 AAP GUIDELINES FOR J Al ' NOICE AGEMENT
(Rcpr~"ith pennisston from PedJatncs \ ol 114. Pages '.!97-316. Copynght C 2004
by the
'120 PT or neonates ~ 35 w_!<s g~ tation
-':;:::>'
'28

,.
. -· -·
--
3'2

. .
-·, ,_
.- ,

~ 257
.•

... ,,
,,
., ,
171
p

.....
·~ ~
5
,__ ~• • • • lnlanla a1 tow.r nsl( (l 38 wlc ndwel)
,.: :::: - - 1n1an1a 111 mlOQT\ ns« (l 38 flt + ns1111c101S"' 35-37 en on and .... -
-
0
'-- L _ _ - "'*'15 at h9llf r1lk (JS.37 " ' wlc ~ ,,. llelo<sJ ::+= 0
llinh 24 t({uj~ h 72h j 96h 5Dlys eo.ys 7 Daya
~

·u.--. DonoclLC!nel-'-*'Vor~lilfAOr\.

· ""*"'-
--·--1....i,tit-Ga'O~
.. l ..,,.,....__.~.-"'**"
- .-.i~(ll~
TSB-10tt--......., .. ,,_.,,,..,.
.....
•l'otwol-~el7""Cllt ..... l•M-11
....
---1111 -
--·-rsa-lbr..--•3SwlllMd•~~-..,--.,:11111

N20.2 Guidelines
_..~_,~.,r-··-·Till-2-3,...,.la-~
. . ,_. ...._
r~( DVET:Jlr neonate( > JS}Vks gestation
30 513
._,___ "T I I I I ~I I I I I I-'--
'-- ,___ •• - • lnlarits Ill lowef llsl< ~ 38 Wk lr1d - '--
,__ L - - - lnlanta 111....o..m ,,... p 31 v.lt • faaors cw 35-~7111 wl< ~ wel _._
lntlntsath4ghelnsk(35-3711/7W' +nsU1elots) _ ,_

..
'--L- -
I
'28

T .• -··
.... . - .. - -· - ... -
l

. .·., ,
- - I-

,, . _. I "
, ., .--. .
--
.. ,, -
:-11"
,, I I
257
7 i
. I
i

.
,_ l I I

. ..
i I I I I I
I I i
'" i

10 171
24h 48h 72h I 96h 5 Days

• Tht ~ _1"',,..,. "°'"" ...............


24 ~Wt Ill ..... roogodclncll........,,..
-•r-.d--IO~
• ..,..... ~ trll'Wf\dlO"l• ...
- - ,....
..,...
,_
. . . . . . lhowl,9Ql'tlol eo.Mt*\bn•1CA1pt r ~
=:::9.....,.-......,_,1Mr. ~CIJl0tlTS8io»"'!>'IL (~~111»\.I

- -- · -~-. Gel'OOllciio<, _,,_19"b.. _ _ _ •


----~
·----lnd--BIA,_ CSM~
·--·.- 0onac..--~-~­
_ _, ..
• 11-..--~tnwt1 ,~rsa-111r~- ... -...

516

N21. ACID- BASE NOMOGRAM


Reproduced with permission. JAMA 1973, Vol 223, Pages 269-275, 1973, Copyright©
1973, American Medical Association. All rights reserved.

ACID - BASE IMP

Pco 2 mm Ha

The sloping lines going across the chart represent HC0 3 values
517

N22. UMBILICAL ARTERY AND VEIN CATHETER LENGTH (Reprinted from Archives of Disease in ChHdhood, Localiza6on of the
umbilical catheter by post-mortem measurement, Dunn PM, volume 41, pages 69, copyright 1966, with pennission from BMJ Publishing Group Ltd.) The
shoulder to umbilicus distance is the perpendicular distance between parallel horizontal lines at the umbilicus and through the distal ends of the clavicles.
Umbilical Vein Umbilical Artery
10 11 12 13 14 1~ 16 17 18
"' ' "
" "
" "
,.,"' "
" 2S

" "
"
l&ttAtn1X11
"'2
"
"
~ "'
19
5 18
~ 17

~ ~:
"
"
"
"1D
'8

,' '
1'J 11 12 rn u 1s ,~ 11 1s
Length 1r001 Shrulderto Umbik:us \cm.1 Shouldar-Umbilicus Distance \cm}
518

N23. WTS OF DISPOSABLES


Please deduct the following (as applicable) from the baby's Wt
Small splint 10.0 g
Big splint 13.0 g
Neoflon 2.0 g
3-way stopcock 3.5 g
Umbilical clamp 3.0 g
ET tube 2.0 g
liT tube adaptor 4.0 g
Feeding tube 3. 5 g
Sanitary napkin 8.5 g
519

INllEX

a/A ratio triple test ............................... 12


assessment of gas exchange.121 Amiel-Tison method ........... 369
prediction of INSURE failure 339 Aminophylline
A-aD02 ...................•••••.•.•••• 120 apnea .................................. 112
ABG extubation ........................... 142
capillary blood gas ................. 86 Amniocentesis ....................... 14
effect of delayed analysis ...... 85 Amniotic fluid index (AFI) ... 11
excess heparin ....................... 85 Anemia .163-70, See also Blood
reference ranges .................... 85 transfusion
room air contamination ......... 85 causes .................................. 163
venous blood gas ...................86 clinical presentation ............ 165
Absent/reversed end diastolic definition ............................ 163
flow erythropoietin (EPO) ........... 170
feeding policy ........................ 79 evaluation ........................... 165
NEC ...................................... 298 of prematurity ..................... 164
Absolute neutrophil count prevention ................... 170, 342
(ANC) Anion gap ...................... 87, 312
sepsis screen ........................ 228 A-no ...................................... 25
TPN monitoring .................... 308 Antepartum hemorrhage (APH)
Acetyl cholinesterase (AChE) cause of anemia .................. 164
amniotic fluid ................... 12, 14 shock ................................... 288
botulinum toxin ................... 374 Antibiotics ......... See also Sepsis
Acute bilirubin encephalopathy neural tube defect ............... 335
(ABE) ............ See also Jaundice policy ............................. 232-35
indication for DVET .............. 188 post asphyxia ...................... 107
indication for MRI ................ 194 post DVET ............................ 192
risk factors ................... 188, 309 prophylaxis for PICC ............ 221
Acute fatty liver, maternal .... I 0 prophylaxis for VUR ............ 335
Admission vit K deficiency .................... 176
criteria ................................... 19 Anti-phospholipid antibody
record sheet. ..................... 25, 28 (APLA) .................................... 9
Air mode ............................... 49 Apnea ............................ 109-14
Alcohol causes .................................. 111
based hand rub ............ 217, 219 classification ........................ 109
in pregnancy .......................... 10 evaluation ........................... 109
Alkaline phosphatase (ALP) immediate management ..... 109
definition of OOP ................. 350 periodic breathing ............... 112
monitoring ............... 24, 77, 352 recurrent
prognosis of OOP ................. 352 aminophylline ................ 112
TPN-induced cholestasis ...... 309 caffeine .......................... 112
Vit D for OOP ....................... 352 definition ....................... 112
Allen's test ............................. 84 management .................. 113
Alpha fetoprotein (AFP) seizures ............................... 112
neural tube defect ................. 14 Apt test ........................ 177, 393
520

Arrhythmia Bilirubinometer ................... 394


bradyarrhythmias . ...... ........ 281 Biochemical investigations . 397
DC cardioversion .................. 281 Biochemistry labs ................ 396
ECG changes ........................ 279 Biomedical waste disposal .. 225
tachyarrhythmias Biophysical profile (BPP) ..... 11
narrow complex ............. 279 Birth trauma ............................ 9
SVT ................................ 282 Bleeding neonate ... 176--82, See
wide complex ......... 280, 284
also Thrambocytopenia; and
Asphyxia ...... I 00-108, See also Disseminated intravascular
Hypoxic ischemic coagulation (DIC)
encephalopathy (HIE) approach to ......................... 176
apnea in term infants .......... 112 differential diagnosis ........... 178
counselling ........................... 354 investigations ...................... 176
definition ............................. 101 treatment ............................ 178
monitoring asphyxiated infant Blood culture ....................... 229
....................................... 101
Blood glucose ...................... See
monitoring cakium ................ 66
Hypoglycemia
PIH ........................................... 9
measurement ........................ 92
SIADH and ADH deficiency ..... 62
monitoring ............................ 93
withdrawal of care ............... 356
Assist control (NC) mode .134, Blood pressure ... See alsa Shock
measurement ...................... 287
138
Blood samples ..................... 392
Auditory problems
prevention ........................... 364 Blood transfusion ......... See also
screening ............................. 362 Anemia
Autopsy ....... See Withdrawal of blood group choice ............. 166
GVHD .......................... 169, 343
intensive care
hemolytic reaction .............. 168
Barlow, test for dislocation ... 31
indications for transfusion .. 166
Bathing leukoreduction filters .......... 343
frequency at home ................ 38
satellite bags ....................... 169
HIV exposed baby ................ 260
volume ................................ 167
policy in PGIMER .................... 36
Breast milk ...................See also
use of soap ............................ 38
Breastfeeding
BCG
composition, preterm mothers
before discharge .................... 22
birth dose .............................. 39 ········································· 72
perinatal TB ......................... 254 composition, term mothers .. 69
Below poverty line (BPL)20, 27 Breastfeeding .... 32-34, See also
Bilirubin ........ See also Jaundice Feeding regimen, stable
amniotic fluid ......................... 14 preterm
direct fraction ...................... 188 exclusive ................................ 37
displacement by lipids ......... 304 for pain relief .............. 380, 382
evaluation of jaundice ... 183-87 maternal HIV ....................... 257
investigation for seizure ...... 212 maternal varicel1a ............... 248
pre-discharge ....................... 187 problems related to ........ 34-36
Hoffman technique .......... 34
521
Kesaree method ............... 34 congenital syphilis ......... 254-56
regimen .................................. 70 congenital toxoplasmosis .... 245
Broncho-pulmonary dysplasia examination in EOS ..... 227, 228
(BPD) ............................ 157--{)2 examination in LOS ............. 229
bronchodilators ................... 160 fungal sepsis ........................ 237
chest physiotherapy ............ 142 Herpes simplex PCR ............. 249
dexamethasone ................... 160 open NTD ............................ 334
diuretics ............................... 159 perinatal TB ......................... 253
feeding policy ........................ 79 sub-arachnoid hemorrhage. 202
follow-up ............................. 162 tests in IEM .................. 212, 316
home oxygen therapy .......... 161 therapeutic LP ..................... 205
NICHD definition .................. 157 traumatic ..................... 201, 230
nutrition ............................... 159 VP shunt .............................. 205
physiologic test .................... 15 7 Chest physiotherapy ............ 143
use of PSV ............................ 135 Chest Xray (CXR)
ventilator strategy ............... 158 before iN0 ........................... 150
Vit A .......................................80 chest inflation with HFOV ... 141
Buffalo's milk ....................... 69 CPAP ............................ 126, 130
C reactive protein (CRP) ..... See diagnosis of CDH ................. 327
also Sepsis diagnosis of TEF ................... 328
fungal sepsis ........................ 237 ET tube position .................. 134
quantitative ......................... 229 in cardiac diseases ............... 270
semi-quantitative ................. 393 in respiratory diseases ........ 121
sepsis screen ........................ 228 perinatal TB ......................... 253
stoppage of antibiotics ........ 233 post-extubation ................... 143
TPN investigations ............... 308 pre-extubation .................... 158
Calcium surfactant ............................ 126
in TPN .................. 305, 307, 351 Cholestasis of pregnancy ....... I 0
maintenance requirements ... 55 Chorioamnionitis ................... I 0
metabolic screen ................... 24 Chromosomal analysis .......... 14
osteopenia prevention ........ 351 Clean labor room (CLR)
osteopenia treatment .......... 351 care of neonate in ................. 30
requirements in preterms ...... 73 near term infants .................. 36
Cardiopulmonary resuscitation transportation from .............. 49
(CPR) ............................ 23, 284 Clothing, of neonate .............. 32
Cardiotocography .................. 14 Coagulogram ....................... 177
decelerations of fetal heart ... 14 Colony stimulating factor .... 236
Cerebral palsy (CP) Computer records .................. 26
approach and management Congenital diaphragmatic
.................................. 371-76 hernia (CDH) ....................... 327
BPD follow-up ...................... 162 clues to diagnosis ................ 116
PVL ....................................... 208 iNO ...................... 149, 155, 328
Cerebro-spinal fluid (CSF) . See surfactant ............................ 328
also Meningitis Congenital heart disease (CHO)
cell count procedure ............ 393 ......... 268-86, See also Cyanotic
CMV PCR .............................. 250 congenital heart disease
522

chest Xray ........................... 269 post·extubation .................. 142


contra-indication to iNO ...... 149 precautions ......................... 131
feta I echo ............................... 10 titration ............................... 130
presenting with CHF ............ 276 variable flow ....................... 128
presenting with collapse ...... 275 weaning ............................... 131
presenting with cyanosis ..... 273 with INSURE ........................ 339
recurrence risk ..................... 285 CT scan
when to suspect .................. 268 cerebral palsy ..................... 372
Congenital heart disease congenital herpes ............... 249
(CHO), maternal ..................... 9 congenital toxoplasmosis .... 246
Congenital malformation craniosynostosis ................. 324
(CMF) ..................................... 9 for HIE ................................. 107
maternal USG ........................ 10 for intra·cranial bleed ......... 202
Congestive heart failure (CHF) for IVH ................................. 204
clues to diagnosis ............... 277 for suspected IUI ................. 244
in CHD .................................. 276 Cyanotic congenital heart
management.......... ....... 277 disease
PDA .............................. 293, 297 hyperoxia test ..................... 273
PET for severe anemia ......... 167 PGEl .................................... 275
pulmonary edema ............... 278 Cytomegalovirus (CMV) ... 250-
Cordocentesis ........................ 14 51
Cost ofNICU care .............. 354 leukoreduction of blood ..... 343
Counseling .................... 353-55 Danger signs, after discharge 3 7
antenatal ............................. 353 Death ............................. 357--01
before admission ................... 19 brain death .......................... 356
by Pediatric Surgeon ............ 353 certificates .......................... 360
genetic /syndromic illnesses324 investigation of IEM ............ 312
HIV status of mother ........... 258 notes in file ........................... 26
in groups ............................. 355 Dehydration
postnatal.. ............. 353 contraction alkalosis ............. 88
cost of NICU care ............ 354 ELBW infants ....................... 343
withdrawal of care ............... 357 hypernatremic ...................... 62
Cow's milk management ................... 62
composition ........................... 69 rate of correction ............. 62
protein allergy ....................... 81 hyponatremic ........................ 59
CPAP 3% saline .......................... 60
administration ............... 130-31 approach to ............... 59, 61
avoidance with TEF .............. 329 management ................... 59
bubble .................................. 128 isonatremic ........................... 57
definition of failure ............. 119 management ................... 59
devices ................................. 128 near term infants .................. 36
for apnea ............................. 113 Developmental assessment..369
indications ........................... 128 Diabetes mellitus, maternal ..... 9
indigenous ........................... 128 Diaper
judging adequacy ................. 130 care at home ......................... 39
nasa I prong sizes .................. 129 care of diaper area ................ 36
523

Diarrhea irradiation of blood ............. 343


cause of vtt Kdeficiency ....... 180 transfer from emergency ...... 20
feature of NEC ..................... 298 Down syndrome
GVHD ................................... 169 dermatoglyphics .................. 322
Diarrhea, maternal ................ l 0 recurrence risk .................... 325
Discharge triple test ............................... 12
advice to parents ................... 37 Downe'sscore ............... 44, 117
early ................................. 22, 37 Drugs, in pregnancy .............. 15
guidelines and procedure .... 21- DTP vaccine .......................... 39
24, 28 Early onset sepsis (EOS) ..... See
hearing screen ..................... 363 also Sepsis
high risk neonate ............. 23-24 antibiotic duration .............. 233
home oxygen therapy .......... 161 approach to management. 226-
immunization ......................... 39 28
jaundice assessment .............. 36 meningitis ............................ 230
local physician ........................ 22 presentation ........................ 226
monitoring lab parameters .... 77 risk factor.s ............................. 10
neonatal examination ............ 32
EEG
NFC file ......................... 365, 366 brain death .......................... 356
on theophylline .................... 113 herpes encephalitis ............. 249
summary ................................ 21 relation to clinical seizures .. 213
umbilical ..............................337 Sarnat staging ...................... 105
vaginal .................................... 31 ELBW babies ................ 339--46
vaginal, maternal ................. 227
fluid electrolyte management
Disseminated intravascular
······································· 343
coagulation (DIC) ........ See also hypotension ........................ 339
Bleeding neonate nutrition .............................. 344
d-dimer ................................ 177 skin care .............................. 340
NEC ...................................... 299 Electrocardiogram (ECG)
peripheral smear findings .... 177 arrhythmias ......................... 279
sepsis ................................... 226 chamber hypertrophy .......... 271
treatment ............................ 181 hyperkalemia ........................ 64
Double volume exchange hypocalcemia ........................ 66
transfusion (DVET) 190-92, See hypokalemia .......................... 63
also Jaundice normal findings ................... 271
admission ............................... 19 PPHN ................................... 145
for ABE ................................. 188 Electrolyte requirements
for DIC .................................. 181 maintenance ......................... SS
for hyperbilirubinemia ......... 187 Emergency
for IEM ................................. 317 admissions ............................. 19
for sepsis .............................. 236 gastrostomy ....................... 329
hearing screen ..................... 362 transfer from ......................... 20
hyperkalemia ....................... 169 transport from ...................... 49
hypocalcemia ......................... 66 Endocrinological investigations
in preterms .................. 188, 189 .................................•........... 416
indications ........................... 190 Epidemic
524

definition ............................ 240 escape route ....................... 387


investigating ........................ 240 extinguishers ....................... 387
source determination .......... 241 switching off electricity ....... 384
Equipment Fixing tubes and lines .......... 341
AMC ..................................... 389 Fluid and electrolyte disorders
CMC ..................................... 389 ......................................... 59-67
decontamination ................. 222 Fluid requirements
warranty .............................. 389 additional allowances ........... 55
Esophageal atresia ......... 30, 328 calculation ............................. 54
Estriol, maternal.. .................. 12 deficit replacement ............... 55
Extubation maintenance ......................... 54
aminophylline ...................... 142 Fluorescent in situ
BPD ...................................... 158 hybridization (FlSH) ..... 14, 323
dexamethasone ................... 142 Follow-up ..... See also Neonatal
planning ............................... 141 follow-up clinic {NFC}
to CPAP ................................ 142 indications ........................... 365
to NIPPV ............................... 142 schedule .............................. 366
Family special clinics ....................... 367
congenital rubella ................ 251 Fresh frozen plasma ............ I 79
counseling ............................ 353 Fungal sepsis ....................... 236
handing dead body .............. 359 cerebra-spinal fluid (CSF) .... 237
history in genetic disorders .320 treatment ........ ................... 238
home oxygen therapy .......... 161 urine .................................... 237
screening HIV ....................... 262
G6PD deficiency
withdrawal of care ............... 357 clues in history .................... 186
Feeding regimen, stable preterm donor blood ........................ 191
advancement ......................... 70
drugs to be avoided ............ 197
interval .................................. 70 repeat test .......................... 197
volume ................................... 70 sample storage .................... 392
with-holding feeds ................. 71 screen before PCPP ............. 261
Fetal alcohol syndrome ......... I 0 Toxoplasma treatment ........ 245
Fetal Doppler ........................ 12 Gastro-esophageal reflux
Fetal echo .............................. JO (GER)
File feeding policy ........................ 80
admlssion ............................... 20 nature of vomiting .............. 331
contents of ............................ 25 pharmacological measures ... 81
copy of death certificate ...... 359 relation with apnea ............. 110
cover page ............................. 25 with BPD ............................. 158
daily notes ............................. 26 Gastroschisis ....................... 333
inpatient ................................ 25 Genetic and syndromic illnesses
investigation folder ................ 26 approach to ................. 320, 324
investigations ......................... 21 counseling ........................... 324
NFC .............................. 365, 366 Down syndrome ............ 325
no dues clearance .................. 29 investigations ...................... 323
poor free ................................ 27
Glucometer .................... 92, 395
Fire Growth, postnatal
525

desired goals .......................... 77 prevention of MTCT ............ 258


with TPN .............................. 303 screening blood products ... 167,
Hand washing ..................... 21 7 191
HBIG status code of exposure source
with Hepatitis B vacdne.39, 252 ....................................... 266
hCG, maternal.. ..................... 12 Housekeeping routines ........ 222
Heart block .............................. 9 Human milk fortifier (HMF)
Heel prick ............................ 391 ......................................... 74-75
HELLP .................................... 9 BPD ................................ 79, 159
Hematological investigations composition .......................... 75
............................................ 404 monitoring lab parameters ... 77
Hematology labs ................. 404 osteopenia of prematurity .. 351
Hemoglobin, normal values J63 Humidification, inspired gas 124
Hepatitis 8 Hydration status .................... 55
management of infant ......... 252 Hydronephrosis
perinatal transmission ........... 10 management ....................... 335
Hepatitis B vaccine postnatal evaluation ........... 334
birth dose ......................... 22, 39 Hydrops fetalis .................. 9, 11
HBsAg positive mother ........ 252 Hyperbilirubinemia ............. See
Hepatitis C .......................... 253 Jaundice
Hepatitis E .......................... 253 Hypercalcemia ....................... 67
Herpes simplex Hyperglycemia .................... 100
diagnosis ..............................249 Hyperkalemia
treatment ............................ 249 causes .................................... 63
Hib vaccine ..................... 39, 40 ECG changes .......................... 64
High frequency oscillatory in ELBW infants ................... 344
ventilation (HFOV) management ......................... 65
for CDH ................................ 328 stored blood ........................ 169
settings ................................ 140 Hyperthyroidism, maternal.. .... 9
weaning ............................... 141 Hypocalcemia
HIV ............................... 257-67 causes .................................... 66
clinical manifestations ......... 262 definition ............................... 66
counseling mothers ............. 258 seizure ................................. 210
disinfection practices ........... 260 treatment ...................... 66, 236
ELISA test ............................. 258 Hypoglycemia ............... 92-100
exposure code of personnel 265 definition ............................... 92
feeding ................................. 261 feeding .................................. 97
follow-up . .. ..... 261 glucose rate calculation ........ 95
immunization ....................... 262 management ......................... 93
investigations to confirm ..... 262 maternal beta-blocker ............ 9
management in delivery room medications ........................... 95
........................................ 260 operational threshold ........... 92
perinatal TB ......................... 253 refractory hypoglycemia
perinatal transmission ... 10, 257 investigations ................... 99
post-exposure prophylaxis .. 262, risk factors ............................. 92
266 seizure ................................. 210
526

Hypokalemia ......................... 63 nitrogen dioxide .......... 151, 155


Hypospadias ........................ 338 stopping .............................. 153
Hypothermia weaning ............................... 154
definition ............................... 46 Inhibin A ............................... 12
management ......................... 52 I-No ............................... 25, 242
prevention ............................. 49 Insensible water loss
signs ...................................... 47 maintenance fluids ................ 54
Hypothyroidism, maternal ...... 9 radiant warmer ..................... 51
Hypoxic ischemic Intestinal obstruction ..... 329-33
encephalopathy (HIE) .. See also Intra-cranial hemorrhage 20 ]-{),
Asphyxia See also Intra-ventricular
brain lesions ........................ 103 hemorrhage
early course ......................... 191 neuro-imaging ..................... 202
hearing screen ..................... 363 types ................................... 201
management ...................... 106 Intra-uterine growth retardation
role of EEG ........................... 107 (IUGR)
role of neuroimaging ........... 107 maternal risk factor ................. 9
seizure ................................. 210 risk of polycythemia ............ 171
staging ................................. 103 Intra-uterine transfusion (JUT)
Immature to total ratio (!TR) cordocentesis ........................ 14
···································· 228, 229 Intravenous fluids
Immunization .................. 36, 39 indications ............................. 54
Inborn errors of metabolism Intravenous immunoglobulin
(!EM) ............................ 311-18 (!VIG)
approach to diagnosis ......... 313 for hyperbilirubinemia ........ 194
feeding contraindication ....... 69 for sepsis ............................. 236
inheritance .......................... 313 Intra-ventricular hemorrhage
investigations ....................... 315 (IVH)
management ...................... 317 bloody CSF ·························· 201
onset in neonatal period ..... 311 grading ................. .............. 203
presentation ........................ 312 hearing screen .................... 363
seizure ................. 211, 212, 215 management ....................... 203
when to suspect .................. 320 neuroimaging ...................... 107
Incubator ............................... 49 prevention .......................... 204
humidification ....................... 50 prophylactic indomethacin. 342
oxygen ................................. 123 risk with opioids .................. 204
Indirect inguinal hernia ....... 3 3 7 seizure ................................. 210
Inhaled nitric oxide (iNO). 149- withdrawal of care .............. 356
56 Investigation Folder .............. 26
circuit ................................... 150 Iron
dose and titration ................ 152 supplement for preterms ...... 72
echocardiography, prior to .. 149 supplementation with EPO .170
for CDH ................................ 328 supplementation with HMF .. 74
indications ........................... 149 Isolation, of infected baby ... 224
methemoglobinemia ........... 153
monitoring ........................... 153
527

Jaundice ....... 183-200, See also desired increase .................... 77


Double volume exchange Liley's chart .......................... 14
transfusion (DVET); and Livebirth register ................... 25
Phototherapy (PT} LSCS
age of onset ........................ .185 for maternal herpes ............ 249
approach in iso-immunized .196 for maternal HIV .................. 258
approach in non-isoimm unized Magnesium
........................................ 195 in TPN .......................... 305, 307
Bhutani's nomogram ............. 36 Magnesium sulphate, maternal 9
breast milk jaundice ............. 198 Malnutrition, maternal... ........ 10
clinical assessment .............. 183 Mal presentation ....................... 9
conjugated ........................... 199 Maternal risk factors ................ 9
definition of pathological ..... 183 Measles vaccine ................... .40
early discharge ....................... 37 Meconium
etiology ................................ 184 first passage .................. 32, 331
fluid supplementation ......... 193 Meconium aspiration syndrome
hearing screen ..................... 194 (MAS)
immunoglobulin ................... 194 use of CPAP ......................... 128
in congenital syphilis ............ 255 ventilator settings ............... 136
in neonates on TPN .............. 304 Medium chain triglycerides
in UTl. ................................... 232 (MCT) ..................... 75, 79, 159
investigations ....................... 186 Meningitis
MRI ...................................... 194 antibiotics ............ 232, 233, 234
near term infants ........... 36, 187 follow-up ............................. 234
pre-discharge bilirubin ... 22, 187 hearing screen ..................... 362
prolonged unconjugated ..... 198 prevalence in sepsis ............ 229
short-term follow-up ........... 366 repeat LP ............................. 230
transcutaneous bilirubinometry seizure ................................ 211
(TcB) ............................... 183 Metabolic acidosis
treatment ............................ 187 anion gap .......... . ........ 87
AAP guidelines ................ 188 correction in PPHN ....... ...... 145
preterm .......................... 188 etiology ................................. 87
Jitteriness ............................ 209 management ......................... 87
Kangaroo Mother Care ... 77, 78 Metabolic alkalosis
Karyotyping ........ 323, 418, 425 etiology ................................. 88
Labor room (LR) hypokalemia .......................... 63
monitoring neonates in .........42 management ........................ 88
Late onset sepsis (LOS)See also Metabolic profile
Sepsis before discharge .................. 24
antibiotic duration ............... 234 Microbiological investigations
approach to ......................... 228 ............................................. 410
presentation ........................ 226 Microbiology labs .............. .409
Left ventricular output (LVO) Micro-erythrocyte
............................................ 289 sedimentation rate (µESR)
Length cut-off values ..................... 229
528

method ................................ 393 apnea .................................. 109


Microtech lab ...................... 396 definition ............................... 46
Middle cerebral artery (MCA) New Ballard Score ................ 25
doppler ............................ 13, 14 NJCU Data Manager (NDM)
Minimal enteral nutrition dextrose calculation .............. 97
(MEN) ........................... 71, 309 discharge summary ............... 21
MMR vaccine ....................... 40 TPN calculation ................... 306
Monitoring ...................... 42-45 NIPPY
MRI ELBW babies ........................ 339
for intra-cranial hemorrhage indications ........................... 131
....................................... 202 settings ................................ 132
for cerebral palsy ................. 372 weaning ............................... 132
for herpes encephalitis ........ 249 Non-nutritive sucking ............ 72
for HIE .................................. 107 Non-stress test (NST) ...... 11, 12
for hyperbilirubinemia ......... 194 Nutritional requirements ....... 68
for intra-cranial hemorrhage Occipito-frontal circumference
....................................... 204 (OFC)
for NTD ................................ 335 desired increase .................... 77
for PVL ......................... 207, 208 follow-up ............................. 367
Multiple pregnancy ................. 9 meningitis ........................... 234
Murmur, cardiac .................. 285 open NTD ............................ 335
Nappy rash ............................ 36 spastic children ................... 375
Near term babies ............. 36, 42 Oil massage ........................... 38
Necrotizing enterocolitis (NEC) Oligohydramnios ........... 10, 116
···································· 298-302 Omphalocele ....................... 333
approach to stage 111 ............ 302 O-No .............................. 25, 242
in AREDF ................................ 79 OPV ................................. 22, 39
in term neonates ................. 301 Ortolani, test for dislocation .. 31
management ....................... 300 Osteopenia of prematurity
perforation ..................... 300 (OOP) ............................ 350-52
platelet count ...................... 181 prevention .................... 73, 351
probiotics ............................. 298 risk factors ........................... 350
rapid feed advancement. ....... 70 screening ............................. 351
risk factors ........................... 298 treatment ............................ 351
staging ......................... 298, 299 Out-patient department (OPD)
Neonatal examination ........... 30 admissions from .................... 19
Neonatal follow-up clinic morning consultation .......... 366
(NFC) neonatal follow-up clinic ..... 365
appointment system ............ 365 postnatal clinic .................... 366
Friday clinic .......................... 367 Oxygen
home oxygen therapy .......... 161 appropriate concentration .... 122
responsibilities of residents.366 delivery systems .......... 122, 123
Neonatal proforma ................ 25 Oxygenation index (01)
Neural tube defect (NTD) ... 334 calculation & interpretation 121
alphafetoprotein ............. 12, 14 iNO indication ..................... 149
Neutral thermal zone (NTZ) sildenafil dose ..................... 146
529

Packed cell volume (PCV) .. See Persistent hyperinsulinemic


also Anemia; and Hemoglobin, hypoglycemia of infancy
normal values (PHHI) ................................... 99
method ........................ 171, 394 Persistent pulmonary
monitoring after discharge .... 77 hypertension of newborn
post-transfusion ................... 167 (PPHN) .......................... 144-46
pre-discharge ......................... 24 clinical features ................... 144
weaning from ventilator ...... 138 differential cyanosis ....... 273
Pain ............................... 378-83 echocardiography ............... 145
measures to alleviate in CDH ................................. 327
non-pharmacological ...... 380 management ....................... 145
pharmacological ............. 380 inhaled nitric oxide ........ 149
N-PASS ................................. 378 sildenafil. ........................ 146
opioids for ventilated neonates use of HFOV ........................ 140
........................................ 381 Phosphorus
procedural ........................... 382 in TPN .............•............ 310, 351
Partial exchange transfusion osteopenia prevention ........ 351
(PET) .............. 173-74, See also osteopenia treatment ......... 351
Polycythemia pre-discharge metabolic screen
Patent ductus arteriosus (PDA) ........................................ 24
...................................... 293-97 Phototherapy (PT). 189-90, See
cardiac murmur ................... 269 also Jaundice
cause of shock in ELBW fluid allowance .............. 55, 193
silent dangerous ductus .342 frequency ofTSB ................. 186
clinical .................................. 293 hyperbillrubinemia treatment
congenital rubella ................ 251 ....................................... 187
echocardiography ................ 294 intensive .............................. 188
follow-up ............................. 296 irradiance ............................ 189
in term infant ....................... 244 monitoring .......................... 190
shock in ELBW ...... 289, 339, 340 pre-discharge bilirubin ........ 187
treatment ............................ 294 protection of TPN solution .. 305
surgery ............................ 296 Pneumothorax
use of CPAP .......................... 128 cause of shock ..................... 288
Peak systolic velocity (PSV) prevention of IVH ................ 205
umbilical artery doppler ........ 13 rescue HFOV ........................ 140
Periventricular leucornalacia Polycythemia ................. 171-75
(PVL) definition ............................. 171
association with hypocarbia 137 fluid supplementation ......... 172
classification ........................ 207 long term outcome ............. 174
grading ................................. 207 management ....................... 174
hearing screen ..................... 363 risk factors ........................... 171
prevention ........................... 208 symptoms ............................ 172
risk factors ..................... 10, 207 Polyhydramnios ....................... 9
Poor free files ........................ 20
Post-hemorrhagic
hydrocephalus (PHH)
530

definition ............................ 205 NIPPV .................................. 132


management ....................... 205 surfactant ............................ 125
Potassium Resuscitation
in TPN .......................... 305, 307 atbirth .................................. 17
maintenance requirement ..... 55 in neonatal period ............... 109
Precipitate labor ...................... 9 Retinopathy of prematurity
Pregnancy induced (ROP) ............................ 347-49
hypertension (PIH) aggressive posterior ............ 348
risk for newborn ...................... 9 classification ........................ 347
Pregnant mothers .................... 9 risk factors ........................... 347
Preterm formula risk with erythropoetin ....... 170
as substitute for HMF ............ 75 screening ....................... 23, 348
osteopenia of prematurity .. 351 treatment ............................ 348
Problem sheet.. ...................... 25 visual problems ................... 362
Prolonged hypoglycemia .... See Rh -ve ............ See also Jaundice
Hypoglycemia:refractory approach in isoimmunized .. 196
Public health nurse approach in non·isoimmunized
family support ...................... 21 ....................................... 194
lactation support ............. 37, 77 blood group for DVET .......... 191
Pulmonary hypoplasia ......... 115 blood group for transfusion 166
Pulsatility index (PI) ............. 13 previous sibs ....................... 190
Quad test ............................... 12 Rheumatic heart disease,
Radiant warmer. .................... 51 matemal ................................... 9
fluid allowance ...................... 55 Rubella
Radiation, maternal exposure 10 diagnosis ............................. 251
Radiological investigations. 419 treatment ............................ 251
Refractory errors ................. 362 SID ratio ................................ 13
Resistive index (RI) .............. 13 Seizures ......................... 209-16
Respiratory acidosis .............. 89 age of onset ........................ 210
etiology .................................. 89 apnea .................................. 112
treatment .............................. 89 classification ........................ 209
EEG ...................................... 212
Respiratory alkalosis ............. 90
etiology ............................... 210
etiology .................................. 90
treatment .............................. 90
in HIE ................................... 210
in hypernatremia .................. 62
Respiratory distress
in hyponatremia .................... 59
approach to diagnosis .117, 118
assessment .................. 117, 120
in IEM .......................... 312, 320
investigations ...................... 212
clinical clues ......................... 115
management ........ 106, 212, 213
definition ............................. 115
weaning anti·epileptic drugs
initial management ...... 117, 119
oxygen therapy .................... 122 ·································· 215
prognosis ............................. 215
surfactant ............................ 124
Respiratory distress syndrome Sepsis .... 226-38, See also Early
(RDS) onset sepsis (EOS); and Late
HFOV .................................... 139 onset sepsis (LOS)
antibiotic treatment ............ 232
531

catheter associated ............. 229 pre-discharge metabolic screen


clinical signs ......................... 226 ········································· 24
definition ............................. 226 Spoon feeds ........................... 72
in birth asphyxia .................. 107 Surfactant ...................... 125-27
in hypothermia ...................... S2 in CDH ................................. 328
in NEC .................................. 300 INSURE ........................ 128, 339
intravenous immunoglobulin preparations available.126, 127
........................................ 236 prophylactic in ELBW .......... 339
pulmonary artery hypertension Syphilis
........................................ 144 diagnosis ............................. 2S5
supportive care .................... 23S follow-up ............................. 256
Sepsis screen treatment .. ......................... 255
components .........................228 TB, perinatal
in EOS ........................... 226, 227 diagnosis ............................. 2S3
role in LOS ............................228 treatment ............................ 254
Shake test ............................ 394 Temperature
Shock ............................ 287-92 in delivery room .................... 48
definition ............................. 287 measurement ...................... 47
etiology ................................288 Thrombocytopenia
in HIE .................................... 106 approach to ......................... 178
investigations ....................... 289 definition ............................ 176
septic....... ........................ 236 fungal sepsis ........................ 237
treatment ............................ 290 immune-mediated .............. 180
Short stature, maternal .......... I 0 inhaled nitric oxide .............. 155
SIADH .................................. 60 lipid emulsion ...................... 304
in HIE .................................... 106 maternal APLA ......................... 9
in meningitis ........................ 234 maternal SLE .......................... 9
SIDS ................................ 37, 80 platelet transfusion ............. 178
Silverman-Anderson score ... 44, Thrombocytopenia, maternal
117 ............................................. 176
SIMV .................................. 134 TORCH .......... 244-56, See also
sedation during .................... 381 individual infections; and HIV
Skin servo mode .................... 49 co-infection with HIV .......... 260
Skin-to-skin contact ..... See a/so TORCH, maternal ......... I 0, 244
Kangaroo mother care (KMC} Total parenteral nutrition (TPN)
after birth .............................. 32 ...................................... 303-10
counseling ............................3SS calculations ......................... 306
for mild hypothermia ............. S2 complications.... ....... 308
transport ............................... 48 components ........ ............... 303
Small for gestational age (SGA) for NEC ................................ 301
feeding policy ........................ 81 fungal sepsis ................. ...... 242
monitoring ............................. 42 hyperglycemia ..................... 100
Sodium hypoglycemia ........................ 97
in TPN .......................... 305, 306 indications ........... ............... 303
maintenance requirements ... SS monitoring .......................... 308
monitoring after discharge .... 77 osteopenia .......................... 351
532

vit K...................................... 176 clinical signs ........................ 232


Toxoplasma ......................... 245 investigations following ...... 235
diagnosis .............................. 245 jaundice ............................... 198
treatment ............................ 245 Urinary tract infection (UTI),
Transient tachypnea of newborn matemal ................................. 10
............................................ 121 Urine
Transport analysis ................................ 232
for surgery ........................... 327 first passage .......................... 32
from emergency .................... 20 Varicella
incubator ......................... 20, 49 diagnosis ............................. 247
of lab samples ...................... 392 maternal infection .............. 247
procedure .............................. 20 treatment ............................ 248
to home ................................. 21 Vascular catheter
Trans-pyloric feeding ............ 80 policy for asepsis ................. 220
Triple test.. ...................... 10, 12 Ventilation, invasive ............ 132
Ultrasonography (USG) adjustment of settings 136, 137
before discharge .................... 23 breath synchronization ....... 134
diagnosis of PVL ................... 208 flow rate with iNO ............... 152
double bubble antenatally ... 330 indications ........................... 132
for bladder aspiration .......... 232 initial settings ...................... 136
for intestinal obstruction ..... 332 initiation .............................. 132
for intra-cranial bleed .......... 202 modes ................................. 134
for NTD ................................ 335 weaning ............................... 137
for PVL ................................. 207 Visiting hours ...................... 223
for seizures .......................... 212 Vitamin A
for suspected I UI ................. 244 prevention of BPD ................. 80
for UTl .................................. 234 supplementation of preterms73
grading IVH .......................... 203 Vitamin K
in fungal sepsis ............ 237, 238 birth dose .............................. 21
in HIE ................................... 107 bleeding neonate ................ 178
in pregnancy .......................... 10 deficiency ............................ 180
meningitis follow·up ............ 234 indications ........................... 176
nephrocalcinosis .................. 159 PIVKA .................................. 177
schedule in preterm infants.204 Weight
tibial bone conduction ......... 351 desired increase .................... 77
Umbilical artery (UA) follow-up schedule .............. 366
catheter ............................... 222 gain before extubation ........ 158
doppler .................................. 13 gain before weaning ........... 138
single ................................... 116 monitoring in PDA ............... 294
Umbilicus monitoring TPN ................... 308
cord care ................................ 36 NFC file ................................ 366
granuloma ........................... 337 Withdrawal of intensive care
hernia .................................. 337 autopsy ............................... 360
Universal precautions .......... 224 death certificates ................ 359
Urinary tract infection (UT!) indications ........................... 356
antibiotics ............................ 234 procedure ........................... 357
533

TELEPHONE NUMBERS
Only those telephone numbers that a ·e important from the perspective of
the Newborn Unit of PGIMER are I !sted below. For numbers not listed
here, see PGJMER telephone directm y or call enquiry 6565.

Newborn Unit
Name/ Area Landline Mobile
NICU 6236, 6237
NNN 6244 '

Newborn unit office 5318 '

Dr Praveen Kumar 5308, 5318 8308


Dr Sourabh Dutta 5313 8313
Dr Kanva Mukhopadhvav 5316 8317
Dr S Venkataseshan 5340 8487
Store-keeper's office/
Computer room
5341 '

Neonatology SR's and 8355,


Senior Research ' 8359 to 8362,
Associates 8373 to 8377

Other Newborn Care Areas


Area Landline
Maternity ward 6228
Gvneco!ol!V ward 6224
Private ward 3A 6238
Private ward 4A 6239
Private ward 5A 6241
Private ward 40 6240
Private ward 50 6262
CLR 6215
SLR 6234
CLR-OT 6360
Emergency OT 6359
Pediatric Emergencv 5307,5327
APCOPD 5645,5651

Pediatric faculn excludin! Neonatolo gy)


Name Landline Mobile
Dr Sunit Singhi 5301 8301
Dr RK Marwaha 5303 8303
Dr Pratibha SinP"hi 5304 8304
Dr Suri it Sinl':u 5305 8305
Dr Meenu Sin!di 5306 8306
Dr A.K. Bhalla 5685 8307
Dr Prabhiot Malhi 5310 8310
Dr Jayashree M 5311 8311
Dr Arnita Trehan 5312 8312
DrMunni Ray 5320 9220
Dr DePnak Bansal 5317 8300
Dr Joseoh Mathew 5657 8357
Dr Devi Dayal 5657 8657
534

Name Landline Mobile


Dr Bhavneet Bharti 5327 8327
Dr Aniu Gunta 5315 8315
Dr Inusha Panii:i:rahi 5319 8319
Dr Arun Bansal 5328 8328
Dr Savita Verma 6080 9080
Dr Alka Khadwal 5322 8314
Dr Arun Baranwal 5309 8309
Dr Shectal Sharda 5334 8481
Dr Deeoti Suri 5316 8316
Dr Rakesh 5338 8380
Dr Amit Rawat 5682 8486
Dr Saniay Venna 5337 8482
Dr Shano Naseem 5329 8329

Facultv in allied departments


il\ame Landline Mobile
Obstetrics facultv
Dr Lakhbir Dhaliwal Unit I 6345 9345
Dr Jaswinder Kaur Unit II 6350 9350
Dr Vanita Suri Unit III 6346 9346
Dr Vanita Jain Unit II 6352 9352
Dr GRV Prasad Unit II 6348 9348
Dr Rashmi BaQ2a Unit I 6349 9349
Dr SC Saha Unit I 6353 9353
Dr "'.'Jcelam AuParwal Unit Ill 6344 9344
Dr Seema Chopra Unit Ill 6351 9351
Dr Mcenakshi Rohilla Unit II 6354 9354
Dr Shalini Gainder Unit I 5345 8345
Dr Pooia Unit Ill 9228

Pediatric Sure:eni faculty


Dr KLN Rao 5320 8320
Dr KL Narasimhan 5321 8321
Dr Ram Samuih 5688 8688
Dr JK Mahaian 5325 8325
Dr Prema Menon 5330 8330
Dr Ravi Kanoiia 8331

Other facultv
Dr. Akshav Saxena, Radiolorr" 6383 9383
Dr. K Sodhi, Radiolo11v 5634 8634
Dr. Malkiat Singh, Infection control 5153 8169
Dr. Manisha, Infection control 5151 8164
Dr. Pallab Ray, Microbio]ol!v 5157 8157
Dr. A Chakrabarti, Microbi0Jocn 1 5156 8156
Dr Vikas Gautam, Microbioloo-v 5152 8152
Dr. Ncelam Verma, HematoloP-v 5125 8125
Dr. Reena Dass, Hematology 5128,5566 8128
Dr Jasmina Ahluwalia, Hcmatolo "' 5129 8129
Dr. Prabhakar, Neuro\oav 6691 9691
Dr. P. Sudesh, Orthooedics - 9749
535
Name Landline Mobile
Dr Neelam Marwaha, Transfusion Medicine 6481 9481
Dr Suchet Sachdeva, Transfuion Medicine 6487 9487
Dr. B.R.Thana, Pediatric Gastrocnterolol!v 6607 9607
Dr. Manoi Rohit, Pediatric Cardiolol!V 6517 9517
Dr. Anish BhattachHrva, Nuclear Medicine 6726 9726
Dr. Raiendra Prasad, BiochemisTT\J 5178 8178
Dr MR Dogra, Qphthalmolocrv 6115 9115
Dr Rama Walia, EndocrinoloPv 6581 9872
Dr Ashim Das, HistonathoJogv 5139 8139
Dr Nandita Kakkar, Histonathology 5141 8141
Dr Kirti Guota, Histooathology 5135 8135
Dr Ashima Goval, Pediatric Dentistn. 1
6832 9836
Dr Raiendra Prasad. Biochemistrv 5178 8178

Non-Neonatolo!!v residents
Name/ Area Landline Mobile
Autopsy Resident Incharge
JR day 8614, JR
Night 8615, SR 8611
Blood Bank JR 6480 9480
Blood Bank SR 6486 9486
CTVSSR 5061, 5039 9549
Endocrinoloov SR 9584,9590
Hematolovv Lab SR - 8369
Hosnital Administration SR on call 6669 8687
Onhthalmoloo-y (Eve Bank) 6368 8711
<mbthahnoloo-v JR on call - 8710
Oohthalmolocrv ROP clinic 6111 -
Pediatric Cardiology SR - 8378
Pediatric Emereencv SR 5307,5327 8367, 8368
Pediatric GastroenteroloP'v SR 6211 9210
Pediatric Surl!erv SR - 8379
Virolo'"' SR - 8170
X-rav (Emere:encv) JR 6060 9060

Investigation facilities in PGIMER* (alphabetically arranged)


*facilities in labs outside PGJMER are listed in sections 34 10 1-10 1 and I-11
Name/ Area Landline Location
Room 21, Level II, A Block, Nehru
ABGRoom 6051
Boso ital
BERA, EEG, YEP lab
(APC) 5658 Room No. 5108, APC 5A
Room No. 441, ENT OPD, Level 4A,
BERA, ENT OPD 6983
New OPD Block
Room No. 3050, Level-III, Nehru
Biochemistry Lab (Adult) 6049,6052 Hospital
Biochemistry Lab Room No.23, Emergency Block Level II,
6058
(Emeru:encv) Nehru Host ital
Biochemistry Lab
(Pediatric) I Microtech 6073, 6074 3-C, APC
Lab,APC
Blood Bank 1n-roupin12 & 6480 Room No. 3053, level III, Nehru
536

Name/ Area Landllne Location


OCT) Hosoital
Room No H-12, Level V, Research
Bone Marrow Lab 6054
Block-A
Room No. H-7, Level V, Research Block
Coagulation Lab 6093
A,
Room No. 18-19, Ground fl,
6082
Radiodiagnosis Dept., Nehru Hospital.
(Brain),
CT Scan Fees & appointment; Radiology
6081 Reception (Counter No. I), Ground Floor,
(Body)
Nehru Hospital.
CT Scan (APC) 5631 2-C, APC
Room No. H-9, Level V, Research
Cytogenetics Lab (Adult) 5123 Block-A
Cytogenetlcs Lab
5671 Room No. 4108, Level 4-A, APC
(Pediatrics)
Room No. 339, Level Ill, Biochemistry
Dr Rajendra Prasad's Lab 5178 Lab, Research block- A
Level-II, Emergency Block, Nehru
ECG 6061
Hosoital
Room No.3027, Level III, Research
Endocrinology Lab 6065 Block-B
Hematology Emergency Room No. 24, Level II, Emergency
6057
Lab block, Nehru Hospital
Hematology Lab Room No. H-11, Level-V, Research
(Central)
5133,5132
Block-A
Room No. H- l l, Level V, Research
Hematology Main Lab 6054
block-A
Room No. H-16, Level V, Research
Hemolytic Work-up Lab 5132 Block-A
H.-natolom Lab
1 6334 A Block, Level I, Nehru Hosnital
Histovatholocrv Lab 5126 Level IV, Research block-A
Room No. 1002, Block-A, Nehru
Holter ECG 6063
Hospital
Room No.24, Level IV, Research Block-
lmmunopathology Lab 6088
A
Microbiology (Clinical
5164
Room No.208, Level II, Research Block-
(Blood),
Bacteriology) Lab A
6078 (Pus)
Microbiology Room 25, Level II, Emergency Block,
(Emergency) Lab
6059
Nehru Hosvital
Room No. H-4, Level V, Research
Molecular studies Lab 5130
Block-A
Ground floor, Cobalt block, Nehru
Hospital. Fees & appointment:
MRI scan 6083
Radiology Reception (Counter No. I),
Ground Floor, Nehru Hospital.
Room No. 221, Level-II, Research
Mycobacteriology Lab 5159
Block-A
Room No. 212, Level-II, Research
Mycology Lab 5172
Block-A
Nuclear Medicine Dept of Nuclear Medicine, Level I, A-
(Radionuclide studies)
6721
Block, Nehru Hosoital
Nuclear Medicine Lab 6724 Room No.20, Level-II, Nehru Hosoital
537

Name/ Area LandJine 1,ocation


(TFI)
~ .oom No. 4075, ENT OPD, Level-4A,
OAE, ENTOPD 6955
New OPD Block
Parasitology Lab Jc.oom No.126, Level-I, Research Block-
(Toxoplasma) 5124, 5169
A
Nuclear Medicine Department, Level-I,
Radionuclear studies 6721
A Block, Nehru Hosoital
Room No. 224, Level-II, Research
STD Lab 5163
Block-A
Ultrasound CAPCl 5634 Room No. 2315, APC-2C
t-.iain USG Room, Level I, Cobalt Block,
Ultrasound (Doppler) 6084
X-ray Dept, Nehru Hospital
6095, 85- Emergency Ultrasound Room, Level-II,
Ultrasound (Emergency)
9095 Emer1tencv Block, Nehru Hospital
Room No. 30, Level I, Cobalt Block, X-
Ultrasound Room (Main) 6084
rav Deoartment, Nehru Hosoital
Room No.33, Level-JV, Research Block-
VCTC (HIV) 5)98
A
Room No. 109, Level I, Research Block-
Viral Hepatitis Lab 5184
A
Room No. 107, Level-I, Research Block-
Virology Lab (serology) 5183, 5184
A
X-ray (Portable) 5384, 85-
-
Technician 8384
6060, 85- Emergency X-ray Room, Level-II,
X-ray Emergency (JR)
9060 Emer~ency Block, Nehru Hospital

Emer!!encv & sunnort services


Name/ Area Landline Mobile
AC Plant 5867
Biomedical 5874 7403
Chief Fire Officer,
0172-2703236
Chandi1Zarh
Child Line 6170 1098 (Toll Free)
Electricity Department 6343 9343, 7421, 8875
Night Sunerintendent 93)5
Fire brigade, sector 11 2747820
Fire Control Room 6101, 6110 9101, 8905
Chief Securitv Officer 6000
Gevser & Fan Section JE 9343
Main Fire Station I 01, 0172-2702333
Manifold Room 5889 8887
Oxvg-en Plant 5889
Refril!eration 5870
Securitv Control Room 6100,6109
5100, 2744262,
Police post, PGI
2741 JOO-x-343
Blood banks in PGIMER & Tricitv area
Blood Bank Land.line Mobile Location
PGIMER Blood
6480 Room No. 3053, Level
--Bank
--- --------------- - --- - ---- - ---- - ---- Ill, Nehru Hospital
Consultant on call 6482 9482
---- --- --- - --- ------ - --- -- - - ---- ------- ----
538

Blood Bank Laodline Mobile Location


JR on call 6480 9480
---- ------------- -----------
-s-R ~~ ~~f1- ---- 6486 9486
---------- ----
- - ---- - -------- -- - - ------ --------- - --- --- --- --- --
~ ~l~-~~~~ _s~~!~t)'__ 6484
------ - - -----I- - - - - - ---- - --- --- --- - -- ----- ------
Blood bank donation 6485
2665253-x- Level-I, D block, GMCH,
GMCH-32 Sector 32, ChandiQarh
1166, 1155
2768244, Room No. 164, GMSH,
GMSH-16 2768248. Madhya Marg, Sector 16,
toll free I 02 Chandi!!arh
Rotary blood bank
Rotary 2696057 society, Sec 37-C,
Chandi!!arh
5096720,
Fortis 4692222-x- Phase 8, Mohali
6192
2225264,
Mohali civil hospital
2273782
Panchkula civil 2580058, - -
hospital 2583858

Chemists in and around PGIMER


Chemist Landline Mobile Location
Shop No. 1, under
Super chemists 2740220 9872005024 ramp-8, gd. Floor,
Nehru Hospital
Shop No. 2, under
Consumer Medical Hall 2740220 9914748295 ramp-B, gd. Floor,
Nehru Hosnital
Shop No. 9, Old
6183, 6184.
Sai Medicos 2749592 Super Market,
9814137518
Nehru Hosnital
Child Care Chemists 2748494,6576504 9212165637 Basement, APC
Shop No. 2, New
Shopping Complex,
Well Being Chemists 5051785 9855137518
Near SBI, PG!
camnus

Other areas and miscellaneous


Name/ area Landline Mobile Location
Within PGIMER
Advanced Cardiac
Centre
5004 - PG! campus

Advanced Eye Centre 5701 - PG! campus


APC Reception 5858 - Level II, APC
Assistant PRO 6004 9004, 9023 Emen:rencv Recention
Autopsy Room 5144 - -
Brij Lal
9981, Rom No. 20, A block, Ground
Clinical Photography 6177
Ku Ideep floor, Nehru Hospital
9177
9015, 9016, Room No. 698, Cobalt block,
CRD 6015
9017 I" floor, Nehru Hosoital
539
Name/ area Landline Mobile Location
CTVS ICU 5052 4w floor, Advanced Cardiac
Centre
5052, 41h floor, Advanced
CTVSOT 5054,5055
Cardiac Centre
6767 (adm.
Main Emergency, Nehru
Emergency Reception card), 6566,
Hospital.
6565
Fee Section, Window No Main Reception, Ground
16 5665
Floor, Nehru Hospital.
Hans Rai Dharamshala 6197 Behind SBI, PGI campus
Immunization room 5693 Room No. 2422, APC 2-D
4w floor, C block, Nehru
Kitchen 6044,6045 hospital
Lifeline 9217916440
Main Reception 6566 Entrance, Nehru hosoital
Medical Social Worker
MS office, ground floor,
with MS poor fund, Mrs. 6006 8009
Nehru hospital
Surinder Kaur
Ground floor, F block, Nehru
MS Office 6666 9666
hosoital
Nehru hospital Old Sarai
6171 - -
New OPD Receotion 6868,6969 - Level II, New OPD block
NSICU (Ped. Sureerv 1 5632 8323 Level V~ B block, APC
Onhthalmoloirv office 5742 Advanced eve centre, Gd floor
Optium Exceed
9915342773,
glucometer
representative
9356407742
Pediatric Level II, F block, Nehru
Gastroenterolouv Ward
6211 -
hosoital
Pediatric Suruf>T'\/ Office 5320 - Level III, A block, APC
Pediatric Surgery OT 5660,5661 - Level VI, A block, APC
Pediatric Surj!;ery Ward 5642 - Level VI, C block, APC
Pediatrics office 5301, 5626 - Level III & II, A block, APC
Room No.202, l"' Floor, Oral
Pedodontics OPD 6838 -
Health Sciences Building
Pharmacy 6012 9012 Ground floor, Nehru hosnital
Physiotherapy (Mr. Room No. 2409, Level II, D
5690 9782
Pradeeo Sarkar) block, APC
Public Relation Officer 6003 znaFloor, A Block, New OPD
Rotary Sarai, Hari Sarai
6168 -
and Janta Sarai
APC:
Level II, D block, APC;
2743508 Room No. 19, Nehru Sarai,
Sewa Bharti
PG!:
Nehru hospital, PG!
2745560
Yaccinator for inborn
9815310131
IOPVl
9592315814
(Mon, Wed,
Vaccinators for inborn
Fr)
(BCG)
9646307950
(Tue, Thu,
540

Name/ area Landline Mobile Location


Sat)

Outside PGIMER
Chaitanya Hospital 2604613-x- Side 1 & 2, Sector 44-C;
NICU 311 - Chandigarh
Command hospital 2867658,
NICU 2867519 - Chandimandir
4692222-x-
Fortis Hospital NICU Phase 8, Mohali
6192
Dr Deepak
2665253-x- 3'd Floor, Block A, GMCH,
GMCHNICU Chawla
1108, 1300 Sector 32
9646121559
2768278, GMSH, Sector 16, Madhya
GMSH Nursery
2768277 - Marg, Chandil!arh
2543889,
Red Cross Bhawan, Madhya
Haryana Red Cross 2546330,
Marg, Sector 16, Chandigarh
2546328
Opposite Bal Bhawan, Sector
Missionaries of Charity 2705156 - 23-A,Chandil!arh
Sector-388, Dakshin Marg,
Prayas 2690872
n...-. Dainik Bhaskar
9779950037
2780827, Punjab Red Cross, Madhya
Punjab Red Cross (Mrs.
2548192 Marg, Sector-16, Chandigarh
K.aooor)
2na floor, Karuna Sadan
2744188,
UT Red Cross
2742000 - building, Sector 11-B,
Chandigarh
541
NOTES
542

NOTES

f"ellho!oJJ ovi Co!/} ~f_


g:shr
__;;-------
543

NOTES
544

NOTES
545

NOTES
546 r--1,· t_
J

-r-rl?e-Jr..,~,,~ ~­
NOTES

< 1~l.L-:J
-rr:: ,_~,,gt:.

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