Neonatal Ventilation Made Easy

Neonatal VentilationMade Easy

Neonatal VentilationMade Easy

Sujoy ChakravartyMBBS, MRCPCH (UK), DCH (Lon)

Visiting Paediatrician and NeonatologistJain Hospital, Howrah

Woodlands Medical Centre, Kolkata

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Neonatal Ventilation Made Easy

© 2007, Sujoy Chakravarty

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First Edition: 2007ISBN 81-8448-165-9Typeset at JPBMP typesetting unitPrinted at Gopsons Papers Ltd, Sector 60, Noida

dedicated toSoumil and

Swapnil

Foreword

It is a pride and pleasure for me to introduce Dr SujoyChakravarty, my ex-student for his outstanding andchallenging contribution in writing this book on neonatalventilation. This book is intended for postgraduate trainees,junior doctors and medical personnel involved in level I, II,and III care of children in neonatal resuscitation unit.

Respiratory distress and/or failure is the common causeof pulmonary arrest in neonates which may be due tohypoventilation, diffusion mismatch, intrapulmonaryshunting. All these disturbances may finally lead torespiratory arrest calling for ventilatory support. The twoforms of ventilation practiced in NICU are—pressurecontrolled and volume controlled types—both discussedin this book. The author has also discussed some commonpulmonary and extra pulmonary conditions frequentlyencountered in daily neonatal practice.

I again congratulate this young doctor for his soundknowledge and expertise with a bold attempt in discussingneonatal ventilation in a concise and yet such user friendlyform. I sincerely wish this book will be of true help to allconcerned and hope he will go a long way in PediatricAcademy.

Prof (Dr) Manas MukherjeeEx-President Indian Academy of Pediatrics

Ex-Head of the Department of Pediatrics,NRS Medical College, Kolkata

Preface

This book is an effort to share my minimal knowledgeand experience with all my colleagues involved inneonatal care and in particular with all the junior doctors.I had my share of running around from one ventilatedbaby to another, of running blood gases, and of head-scratching with the results. The dilemma to call or not tocall your senior! (Better ask for help in these cases!). Ababy collapses on a ventilator! Of course shout for helpbut as a junior doctor I felt it is extremely stressful, if youare not sure what exactly you are supposed to doparticularly when you are the first port of call. There is nosubstitute for hands on experience, but I hope this bookwill be your constant companion and aid particularly inhours when you need urgent help. The book will also behelpful for aspiring Neonatologists who will be workingin India and abroad. This is not a substitute for a propertextbook, which should be consulted at the earliestopportunity.

Sujoy Chakravarty

Acknowledgements

I would like to thank my parents, my family for theirconstant inspiration and support. Also I would like tothank all my teachers and colleagues in neonatal unitsfrom whom I have learnt the ABC of Neonatology. Myspecial thanks to Dr Rashmi Gandhi without whose helpthis book would not have seen the light of the day.

I would like to extend my sincere thanks to thepublishers, and in particular to Mr Sabyasachi Hazra andMr Sandip Gupta for their tireless work and tenacity ingetting this book published.

Contents

1. Newborn Life Support .............................................. 1

2. Formulas Commonly Used in NICU ..................... 5

3. Acid-Base Balance ...................................................... 7

4. Continuous Positive Airway Pressure (CPAP) .... 11

5. Positive Pressure Ventilation—Introduction and Terminologies ............................ 17

6. Different Modes of Positive PressureVentilation ................................................................. 23

7. Ventilatory Adjustments According toBlood Gas Changes .................................................. 27

8. Volume Controlled Ventilation .............................. 31

9. High Frequency Ventilation ................................... 35

10. Nitric Oxide ............................................................... 41

11. Extra Corporeal Membrane Oxygenation(ECMO) ....................................................................... 45

12. Respiratory Distress Syndrome ............................. 49

13. Chronic Lung Disease .............................................. 53

14. Meconium Aspiration Syndrome .......................... 55

15. Transient Tachypnoea of Newborn ...................... 57

16. Collapse of a Baby on Ventilator ........................... 59

17. Necrotising Enterocolitis ......................................... 63

xiv NEONATAL VENTILATION MADE EASY

18. Jaundice ...................................................................... 65

19. Neonatal Feeding—Difficulties ............................. 69

20. Neonatal Vomiting—Common Causes ................ 71

21. Anaemia in Neonates .............................................. 73

22. Hypoxic Ischaemic Encephalopathy (HIE) .......... 75

23. Intraventricular Haemorrhage and PeriventricularLeucomalacia ............................................................ 77

24. Persistent Pulmonary Hypertension of theNewborn (Persistent Foetal Circulation) .............. 79

25. Sepsis in Neonates ................................................... 81

26. Tit-Bits ........................................................................ 85

27. Neonatal Formulary (Commonly usedMedications) .............................................................. 89

Index ............................................................................ 91

Chapter 1

Newborn LifeSupport

2 NEONATAL VENTILATION MADE EASY

The care of the newborn in the first few minutes after birthis extremely crucial with regards to the subsequent flowof events. The foetus was in a nice and warm atmosphereinside the womb requiring no effort to breathe and nothaving to worry about its nutrition as well. As soon as thecord is severed the newborn baby has to find ways ofindependent existence.

RESUSCITATION AT BIRTH

Preparation

It is always useful to reach for the delivery with a few minutesto spare (absolute necessity for preterm labours). A briefmaternal history is to be taken and all equipments (theoverhead heater, the laryngoscope, the suction apparatus,appropriate masks, proper size ET tube) to be checked.

Few dry towels should always be available.

Collecting the Baby

After the baby is born and cord is clamped the baby shouldbe collected in a dry and clean towel. In case of extremeprematurity, babies are put in a plastic bag immediatelyafter birth to minimize further chances of heat loss.

In the Resuscitaire

1. Start the clock.2. Dry the baby and transfer to a fresh and warm towel.3. Keeping the baby covered feel or listen for the heart beat.

(Heart rate can be felt by palpating the umbilical cord)Also assess the respiratory effort, colour and tone of thebaby.

4. If the heart rate is > 100 and regular, all the baby mightneed is gentle stimulation and the doctor’s patience.

NEWBORN LIFE SUPPORT 3

5. If the heart rate is slow (< 80), the baby will needstimulation by inflation breaths with a mask. Before doingthat it is important to check for the patency of the airway.Blind suction is strongly discouraged. Sometimessimple airway opening manoeuvres, e.g. head tilt andchin lift or jaw thrust might do the trick and thecondition of the baby might improve.

6. If these doesn’t work and after airway is reassessed5 inflation breaths are given and each breath should ideallylast for about 2 seconds. These breaths are given withthe aim to displace as much lung fluids as possible.The inflation breaths should measure about 30 cm H2Opressure. The important point to note here is the chestmovement with the inflation breaths. If the chest is notmoving then airway needs to be reassessed again. If the chestrises with each breath, the baby is examined after the5 breaths. If by this time the heart rate has improvedand the baby is making spontaneous efforts to breathe,masterly inactivity is what might be needed at thisstage. If heart rate has improved but the breathing isstill not satisfactory, ventilation breaths might beneeded till the baby establishes regular andspontaneous breathing. The ventilation breaths are ofmuch shorter duration compared to the inflation breaths.

7. If above methods have failed and the baby is still bradycardiacwith a very poor tone, the baby needs intubation for a definiteand a secure airway. If intubation is difficult (not possiblewithin 30 seconds, i.e. one attempt) revert to bag and maskventilation and ask for help. (According to Scandinavianstudies 1 in 500 babies only need intubation). Oncethe ET tube is in place and secured continue ventilationand reassess the heart rate. If the heart rate is still lowstart cardiac compression ( 3:1 ) with one hand or two handtechnique. If there is no improvement in heart rate


recheck the position of the ET tube (see for chestmovement and listen for air entry).

8. If the tube is in place continue ventilation and cardiacmassage. Consider adrenaline (0.1 ml/kg 1: 10,000)at this stage.

IMPORTANT POINTS TO REMEMBER1. Always ensure that the baby is kept warm and dry.2. Follow ABC (airway, breathing, circulation) in order.

It is completely irrelevant to sort out circulationwithout establishing the airway.

3. Always reassess after a manoeuvre. Start from airway.4. If there is presence of meconium and the baby is

screaming, it indicates open airway. Floppy babywith meconium demands a look inside the oral cavity.Suctioning is mandatory if meconium is presentbelow the vocal cords and if thick particulate meco-nium is seen inside oral cavity before administeringany inflation breaths.

5. Oropharyngeal airway can be sometimes be usefulprior to proceeding to the stage of intubation, (providedyou find one in the resuscitation trolley).

6. The only drugs used in newborn resuscitation areadrenaline and 10% dextrose (2.5 ml/kg). If the motherhas received pethidine prior to delivery sometimes adose of naloxone (IM) is given to the baby, if neededthough it’s precise role in resuscitation is debatable.

7. A fluid bolus of normal saline (10 ml/kg) is only neededif there is definite evidence of maternal blood loss, e.g.antepartum haemorrhage.

8. Consider stopping resuscitation, if there is nofunctional circulation established by the end of15 minutes of resuscitation.

9. Don’t forget the parents.10. Swallow your pride and ask for help without delay.

Chapter 2

FormulasCommonly Used in NICU


1. Size of ET tube—Gestation/10 (a baby of 25 weeksgestation needs a 2.5 mm size tube).

2. Length of ET tube—6 + weight of baby.3. Umbilical artery catheter—Birth weight (in kg) × 3 +

9 cm.For term babies a length of 16-17 cm suffice. Forpreterms 10-12 cm should be sufficient.

4. Umbilical venous catheter—1.5 × Birth weight (in kg)+ 5.5 cm.For term babies a length of 10 cm suffice. For preterms5 cm should be sufficient.

5. Half correction of bicarbonate—0.3 × weight (in kg)× base deficit (over 2 hours).

6. Dilutional (Partial) exchange transfusion—(DesiredHB-Current HB) × Blood volume/CurrentHaematocrit.

7. Blood transfusion (Packed cells)—15 ml/kg or (DesiredHb-Current Hb) × weight × 4.

8. Sodium requirement for neonates—3 mmol/kg (Addin 500 ml of 10% Dextrose).

9. Potassium requirement—2 mmol/kg (Add in 500 mlof 10% Dextrose).

10. Calcium requirement—1 mmol/kg (Add in 500 mlof 10% Dextrose).

Accepted position of catheters:• UVC—T-9• UAC—T6-T10• Long line tip (upper arms)—T3• Long line tip (lower limbs) —T9-T10

Chapter 3

Acid-BaseBalance


The understanding of acid-base balance and interpretationof blood gases is of prime importance in managingventilated neonates. Minimal changes in the ventilationcan produce significant alteration in the acid-base statusin the neonates, which can either be detrimental orbeneficial.

NORMAL ARTERIAL BLOOD GAS VALUES

• pH : 7.35-7.45• pO2 : 10.6-14 kPa• pCO2 : 4.7-6 kPa• Bicarbonate : 23-33 mmol/L• Base excess : +/- 2-3 mmol/L (Metabolic acidosis

is associated with a base excess below–5 mmol/L and metabolic alkalosiswith a base excess above +5 mmol/L

• Lactic acid : < 1 mmol/L

Acid-base Primary Effect on Base Compensatory

abnormality disturbance p H excess response

Respiratory Increased Decreased Negative Increasedacidosis pCO2 HCO3

Metabolic Decreased Decreased Negative Decreasedacidosis HCO3 pCO2

Respiratory Decreased Raised Positive Decreasedalkalosis pCO2 HCO3

Metabolic Increased Increased Positive Increasedalkalosis HCO3 pCO2

In general metabolic disturbances are compensatedacutely by changes in ventilation and chronically by renalresponses.

ACID-BASE BALANCE 9

Respiratory disturbances are compensated by renaltubular secretion of hydrogen ion.

Steps in Interpreting Blood Gas

1. First look at the pH whether it is acidotic or alkalotic.2. Then check the pCO2 and the bicarbonate—whether

it is respiratory or metabolic.3. Check pO2.4. Next look at the base excess—for the degree of acidosis

or alkalosis.5. Finally check the lactic acid.

Blood Gas Analysis

1. Arterial blood gas measurement: This is the gold standard inmonitoring the baby on the ventilator. Generally,indwelling arterial catheters are used when multiplesampling is necessary over a longer duration of period.

2. Continuous blood gas analysis (Neotrend): This methodis useful for rapid and continuous evaluation ofchanges in the clinical status of the baby. It gives acontinuous monitoring of pO2, pCO2 and pH. It alsominimizes the volume of blood sampling in thenewborns.

3. Capillary blood gas analysis: It is relatively easy to obtainand with the free flow of blood it provides a good estimate

of pCO2, but it is traumatic to the heel and can giveinaccurate results if the extremities are not well perfused.

4. Venous blood gas analysis: This is the least preferred methodused for monitoring blood gases in ventilated babies.Venous pCO2 is usually 6-10 mm of Hg higher thanarterial or capillary values.


5. Transcutaneous monitoring of pCO2: In this methodelectrodes are placed on the baby’s skin and give acontinuous reading of pCO2, but there are chances ofskin burns and inaccurate measurements.

SCENARIOS

1. pH: 7.25, pO2: 9.0, pCO2: 7.1, HCO3: 25, BE: 2, Lactate:1.2.Interpretation: This is an example of respiratoryacidosis. The pH is acidic and pCO2 is increased.

2. pH: 7.28, pO2: 8, pCO2: 5.3, HCO3: 17, BE: -7, Lactate:2.2.Interpretation: Those is an example of metabolicacidosis. The pH is acidic with a low bicarbonate andelevated base excess and lactic acid.

3. pH: 7.47, pO2: 8, pCO2: 3.2, HCO3: 23, BE: +2, Lactate:1.0.Interpretation: This is an example of respiratoryalkalosis. The pH is alkaline and pCO2 is decreased.

4. pH: 7.48, pO2: 9, pCO2: 5.4, HCO3: 34, BE: +7, Lactate:1.0.Interpretation: This is an example of metabolic alkalosis.The pH is alkaline with raised bicarbonate.

5. pH: 7.36, pO2: 2.2, pCO2: 4.9, HCO3: 24, BE: +2, Lactate:2.5.Interpretation: This is an example of gas of a hypoxicneonate. This type of blood gas can be suggestive ofcongenital cyanotic heart disease.

6. pH: 7.36, pO2: 8.2, pCO2: 7.0, HCO3: 34, BE: -2, Lactate:1.2.Interpretation: This is an example of compensatedrespiratory acidosis. The pH is in the normal rangethough the pCO2 is increased. An increased bicarbonatelevel compensates the respiratory acidotic component.

Chapter 4

ContinuousPositive Airway Pressure

(CPAP)


DEFINITION

Continuous Positive Airway Pressure (CPAP) is a form ofnon-invasive ventilation in which positive pressure is appliedto the airways both during inspiration and expiration.

BACKGROUND

In early 1970’s the use of CPAP was described in prematurebabies with respiratory distress. Due to reported incidenceof increased air leaks, gastric distension and also becauseof the introduction of more advanced ventilation CPAP fellout of favour in the 1980’s and 1990’s. But, because of itsnon-invasive nature there has been renewal of interest inthis form of ventilation.

METHODS OF DELIVERING CPAP

1. Nasal prongs (most common)2. Nasal masks3. Nasal cannula4. Face mask.

DEVICES

1. Infant flow driver: It is a variable flow positive CPAPdevice.

2. Bubble CPAP: In bubble CPAP a source of blended gasis administered to the baby via a nasal prongs and thedistal end of the tube is immersed in fluid to a depthof the desired level of PEEP.

MECHANISM OF ACTION OF CPAP

The main way CPAP acts is by generating PEEP (positive endexpiratory pressure), which is the pressure, needed to keep thealveoli open at the end of expiration. Before the advent of

CONTINUOUS POSITIVE AIRWAY PRESSURE 13

CPAP, end expiratory pressures would drop to zero at theend of delivering PIP (positive inspiratory pressure), whichliterally means the collapse of alveoli. By holding the alveoliopen at the end of expiration CPAP ensures adequate gasexchange and also less pressure is needed to inflate thelungs in inspiration (it is easier to inflate a already partiallyinflated balloon rather than a balloon which is completelydeflated). In babies who are grunting (breathing against apartially closed glottis) they effectively try to generate CPAPthereby preventing the collapse of alveoli and thereby theirlungs.

There are mainly two schools of thought regarding theamount of PEEP needed in newborns—the low pressuregroup and the high pressure group. Generally, a PEEP of4-6 cm H2O pressure is adequate for premature newborns.But pressures as high as 9-10 cm has been used whichmight accentuate possibilities of air-leaks and abdominaldistension causing more respiratory distress and reducelung compliance.

When a baby is already on CPAP and needs to comeout of it, the weaning is done as a gradual process. If thepressures are set quite high, it needs to be decreasedgradually over hours or days depending on how well thebaby tolerates the weaning process. If the PEEP is alreadyat 4 cm H2O, the weaning mode is time cycled allowingthe baby to come off CPAP for brief periods and increasingthe duration off CPAP gradually as tolerated by the baby.

Indications for CPAP Use

1. Babies born with immature lungs2. As a weaning mode of ventilation3. Atelectasis4. Apnoea of prematurity5. Obstructive apnoea.


Recent trials have shown the beneficial use of CPAP inbabies with extreme prematurity but more studies areneeded to validate these findings.

Contraindications of CPAP Use

1. Persistent and profound apnoeas and bradycardias inspite of being on NCPAP.

2. Congenital malformations, e.g. congenital diaphrag-matic hernia, choanal atresia, etc.

3. Respiratory failure.

Hazards of CPAP Use

1. Air trapping.2. Air-leaks (Pneumothorax, pulmonary interstitial

emphysema).3. CO2 retention.4. Gastric distension (orogastric tube might help).5. Local trauma to the nostrils from nasal prongs.6. Noisy.

GENERAL GUIDELINES FOR CPAP

1. Respiratory distress in newborn baby (grunting, chestrecessions, etc.).

2. Increasing oxygen requirement (about 40%, if oxygenrequirement is more than 60% or there is increasinghypercapnia—consider ventilation).

3. Initial PEEP is usually set at 4-6 cm of water.

Threshold for Intubation

Preterm infants with respiratory distress should beconsidered for intubation and surfactant treatment if:1. Early chest X-ray is consistent with RDS.

CONTINUOUS POSITIVE AIRWAY PRESSURE 15

2. Despite adequate CPAP FiO2 requirement > than 60 percent.

3. A lower threshold may be used for intubation andsurfactant for infants < 30 weeks’ gestation at high-riskof RDS and increasing oxygen requirements, parti-cularly if the X-ray is consistent with RDS.

NASAL VENTILATION

This mode of ventilation has been tried but with variablesuccess. It has been used as a weaning mode of ventilation,and also in treating apnoea of prematurity. To date thereis no concrete medical evidence to suggest its definite rolein ventilation though it is still used in some UK centres.

Chapter 5

Positive PressureVentilation—Introduction

and Terminologies


INTRODUCTION

Positive pressure ventilation is mainly of two types:1. Volume controlled ventilators—delivers the same amount

of tidal volume irrespective of pressure.2. Pressure controlled ventilators—delivers variable amount

of tidal volume depending upon the preset pressure.

Advantages of Pressure Controlled Ventilators

1. Simple design and lower cost.2. Is simple to operate.3. As the same pressure is delivered with each breath,

even with changes in lung compliance over-distensionof the lung is less likely.

VENTILATOR CONTROLS

Peak Inspiratory Pressure (PIP)

It is the main factor used to deliver tidal volume. In mostmodern ventilators the physician can directly adjust PIP. It

can also be manipulated by changing the flow rate or the I/E

ratio. The initial levels of PIP are selected depending onthe infant’s weight, gestational age, lung compliance andairway resistance. As a basic principle the lowest level of

PIP that adequately ventilates a neonate should be used. In mostinstances PIP of 20-24 cm H2O is adequate to ventilate anewborn.

Use of high pressures may be associated with side effects

like bronchopulmonary dysplasia and pulmonary air leaks. Onthe other hand uses of low pressures run the risk of thebaby receiving insufficient ventilation (Table 5.1).

POSITIVE PRESSURE VENTILATION 19

Table 5.1: Advantages and disadvantages of low PIP

Low PIP (< 20 cm H2O)

Advantages Adverse effects

1. Fewer side effects—BPD, PAL 1. Insufficient ventilation2. Normal lung development 2. Generalised atelectasis may

proceed rapidly occur

Positive End-Expiratory Pressure (PEEP)

The use of PEEP has been documented since early 1970’s.PEEP is continuous distending pressure, which prevent alveolarcollapse at the end of expiration. In most modern ventilators,like PIP the physician can directly adjust the PEEP as well.PEEP can be altered by changing expiratory time or if theairway resistance changes. The initial levels of PEEPdepend on the weight of the baby, the pathophysiologyof the disease process, and also on the aim of the treatment.

The benefits of PEEP are:a. Stabilization and recruitment of lung volume.b. Improvement in lung compliance.c. Improvement in ventilation-perfusion matching in

the lungs.In most instances the level of PEEP used is 4-7 cm of

H2O. Levels above 8 cm of H2O are associated withincreased risk of pulmonary air leaks, abdominaldistension and reduction of cardiac output. Pressuresbelow 4 cm may be too low to maintain adequate lungvolume.

Rate

CO2 elimination depends mainly on the amount of gasthat passes in and out of the alveoli. The total amount ofgas that passes in and out of the lungs is called minute


ventilation. Respiratory rate is one of the primarydeterminants of minute ventilation (MV) in mechanicalventilation (MV = RR × tidal volume).• In most instances the rate used is between 40 to

60 breaths per minute, but the adjustment in ratemight depend on the weight of the baby, type of therespiratory disease and on the clinical response. Thisrate mimics the normal respiratory rate of the babyand will effectively treat most neonatal lung diseases.

• Rates < 40/minute might be associated with increasePIP and its adverse effects, and rates > 60/minute maycause hypocapnia and inadvertent PEEP.

Fraction of Inspired Oxygen

Oxygen is probably the most commonly used drug in theneonatal intensive care, but it can act as a double edgedsword, if not used with caution. Inadequate O2 administrationcan lead to hypoxemia and consequently to severe neurologicinjury. On the other hand high oxygen concentration has beenimplicated as one of the precipitating factors for retinopathy ofprematurity and bronchopulmonary dysplasia.

The oxygen that is delivered to the neonate duringventilation is in a humidified form. Humidification preventsbronchospasm and airway injury in newborns.

Inspiratory to Expiratory Ratio

I:E is an important variable in the ventilatory managementin babies. The normal I: E is 1:1- 1:3. In most instances theTi (inspiration time) is selected along with the rate andthe I: E is automatically set. In general a starting Ti of 0.3to 0.4 seconds is used. This ratio mimics the naturalbreathing pattern of the baby. Increasing Ti increases themean airway pressure without increasing the PIP.

POSITIVE PRESSURE VENTILATION 21

If I: E is inversed (> 1 : 1) it may result in air trapping,pulmonary interstitial emphysema and also impairedvenous return to the heart, but it may also be used torecruit more alveoli in presence of atelectasis therebyimproving the oxygenation.

A prolonged I: E (< 1 : 3) may be useful in conditionssuch as meconium aspiration syndrome, but a lowinspiratory time can also result in decrease in tidal volumeand increase risk of intraventricular haemorrhage.

Mean Airway Pressure (MAP)

MAP is the measure of the average pressure to which thelungs are exposed during the respiratory cycle.Oxygenation increases linearly with increase in MAP. Theventilator variables which increase MAP are:

a. PIPb. PEEPc. I : Ed. Flowe. RateMAP as low as 5 cm H2O may be sufficient in babies

with normal lungs whereas pressure as high as 20 cm H2Omay be necessary in newborns with RDS.

LIMITATION OF MAP

1. Increases in PIP and PEEP are more effective inenhancing oxygenation as compared to increases inI : E.

2. Very high MAP may cause lung over distension, right toleft intrapulmonary shunting, or decreased cardiac output.

3. Long Ti increases risk of air leaks.


Wave Forms

The two commonly used waveforms in neonatal ventilationare sine and square.

The sine wave breathing resembles normal spon-taneous respiration of infants. There is gradual increasein inspiratory pressure, which may be helpful in manyneonatal lung diseases.

The square wave breathing improves oxygenationwhen used with low rates and longer Ti. It provides ahigher MAP compared to sine wave breathing for identicalPIP. If longer Ti is used it can impede venous return to theheart and cardiac output may decrease.

Flow Rate

Flow rate is an important determinant of the ability of theventilator to deliver expected levels of PIP to the baby.Minimum flow of at least twice the baby’s minuteventilation is usually required but in practise the operatingrange can be much higher. (Normal neonatal minuteventilation ranges from 0.2-1 L/minute).

Chapter 6

Different Modes ofPositive Pressure

Ventilation


There are various modes of positive pressure ventilationthat are in practice and though each mode has its ownmerits and demerits, at the end of the day it comes downto the clinician’s choice and experience. The types usedcan be broadly divided into two main categories—asynchronized and synchronized. Due to reasons describedlater asynchronized type of ventilation has fallen out offavour.

Intermittent Mandatory Ventilation (IMV)

This is asynchronized form of mechanical ventilation. Herethe ventilator delivers a minimum number breaths perminute with which the baby has to be ventilated. The babiescan still breathe independently between ventilatorsdelivered breaths, but there can be asynchrony betweenthe two. Asynchronized ventilation can result in variable tidalvolume, lung over distension, air leaks and intraventricularhaemorrhage. To minimize the asynchronized ventilationthe baby should be adequately sedated and paralysed.

Synchronized IntermittentMandatory Ventilation (SIMV)

It is improvement over IMV in achieving the synchronizedmode of ventilation. This form of ventilation deliversintermittent positive pressure breaths at a fixed rate insynchrony with the baby’s inspiratory effort. Here the clinicianpresets a ventilator backup rate (e.g. 30/minute). Thisimplies that the ventilator is going to deliver 30 mandatorybreaths to the baby per minute irrespective of the baby’sown respiratory effort. If the baby is breathing at a ratehigher than the preset rate (e.g. 40/minute) 30 of thesebreaths will be synchronized and supported by theventilator. The remaining 10 breaths are the baby’s owneffort only and may or may not be effective breaths.

DIFFERENT MODES OF PP VENTILATION 25

The advantage of this mode of ventilation is that thereis lesser need for sedation and paralysis and is often usedas a weaning mode.

Synchronized Intermittent Positive PressureVentilation (SIPPV)/Assist Control (A/C)

In this mode each spontaneous breath that exceed triggerthreshold will result in the delivery of a completelysupported mechanical breath. If the baby does not breatheor if the breath fails to exceed the trigger threshold amechanical breath will be provided by the ventilator at arate preset by the clinician. For example, if the cliniciansets the rate of 30/minute it will imply that the baby willbe receiving 30 guaranteed breaths from the ventilator. Ifthe baby is breathing at a rate higher than this for example,40/minute then this will imply that all the 40 breaths willbe supported by the ventilator and the will effectively bebreathing at a rate of 40/minute. Weaning in this form ofventilation is generally by reduction of PIP as compared toSIMV where rate is the weaning parameter.

The advantage of this mode of ventilation is that itrequires minimal amount of patient effort and also hasthe safety of a guaranteed backup rate (all breaths aresupported by the ventilator and hence effective).

Chapter 7

Ventilatory AdjustmentsAccording to

Blood Gas Changes


1. To increase pO2:a. Increase PIPb. Increase PEEPc. Increase I/E ratiod. Increase flow.

2. To decrease pCO2:a. Decrease PIPb. Decrease PEEPc. Increase rated. Decrease flow.

3. To increase pCO2:a. Increase PIPb. Decrease ratec. Increase PEEP.

SCENARIOS

Always remember DOPE before any intervention(Displaced tube, Obstructed tube, Pneumothorax,Equipment failure).1. Baby on ventilator with high pCO2, acceptable pO2

( FiO2—50%, RR—40/m, IT—0.35 sec, P—22/4). Initiallikely ventilator adjustment to be made — Increase rate.

2. Baby on ventilator with low pCO2, acceptable pCO2(FiO2 80%, RR—40/min, P—22/4, IT—0.35 sec). Initiallikely ventilator adjustment to be made — Decrease rate/Increase PIP.

3. Baby on ventilator with low pCO2, acceptable pO2(FiO2 50%, RR—40/m, P—26/4, IT—0.35 sec). Initiallikely ventilator adjustment to be made — Decrease rate.

4. Baby on ventilator with high pCO2, acceptable pO2(FiO2 50%, RR—60/m, P—26/4, IT—0.35 sec). Initiallikely ventilator adjustment — Decrease PIP.

VENTILATORY ADJUSTMENTS ACCORDING TO BGC 29

5. Baby on ventilator with low pCO2, acceptable pCO2(FiO2 60%, RR—40/m, P—26/4, IT—0.35 sec). Initiallikely ventilator adjustment—Increase FiO2.

Answers

1. Increase rate.2. Increase FiO2/Increase pressure (PIP)—think PPHN!3. Decrease rate.4. Decrease PIP.5. Increase FiO2.

WEANING OF VENTILATION

It should be tried when the concentration of inspiredoxygen is 40 percent or less. The PIP is gradually reducedalong with the ventilator rate to allow the baby to breatheon his/her own. When the rate is weaned to around 10/minute or less the baby is extubated to CPAP with a PEEPof 4-6 cm of H2O. The infant should not be stressed beforeweaning and usually is kept nil by mouth for 6-8 hours.A loading dose of caffeine citrate is also administered 12 to24 hours prior to extubation.

Chapter 8

Volume ControlledVentilation


INTRODUCTION

The age old concept of pressure related trauma(barotrauma) is gradually being replaced by the under-standing that it is the over distention and stretching of thelungs (volume-trauma), which is, more damaging to thealveoli. The repeated stretching of the lungs cause ashearing stress which might lead to air-leak syndromes.

Why is Tidal Volume Important?

The normal tidal volume in babies is—5-8 ml/kg. Volumesgreater than 8 ml/kg will cause over distension.• Tidal volume less than total dead space (inadequate)

will produce insufficient exchange of alveolar gases.• Large tidal volume may produce alveolar over distention

and shear stress damage.• Lung over stretching and over distention are significant

in causing lung injury.• Extreme over distention may lead to impaired venous return

and subsequent cardiac compromise.

Volume Controlled Ventilation

The characteristic feature of this mode of ventilation isthat the ventilator delivers a specific volume of gas to thebaby irrespective of changes in pressure. In this the cliniciansets the tidal volume, frequency (therefore the minute volume)and inspiratory and expiratory times are set by default. Themost significant advantage of this mode of ventilation isthat even in the face of rapidly changing lung compliancethe actual tidal volume delivered to the patient remains constant.This is in contrast to pressure-limited ventilators wherepressures are preset but there is no guaranteed tidalvolume delivered. On the other hand because of theendotracheal tube leaks and poor lung compliance measurement

VOLUME CONTROLLED VENTILATION 33

of delivered tidal volumes can be erroneous at times. The chancesof endotracheal tube leaks are high because uncuffed ETTare used in babies as a standard practise. Also the tidalvolume that is delivered is measured more near theventilator than the baby which again increases the risk oferroneous measurement of tidal volumes.

There are various types of volume-targeted ventilation.

Volume-Assured Pressure Support (VAPS)

This modality combines the advantages of pressure andvolume ventilation on a breath to breath basis and can beused with other pressure support ventilation or by itselfin babies with reliable respiratory drive. The clinicianpresets the volume to be delivered. As long as thedelivered volume exceeds the preset level the breathbehaves as a pressure support breath. If the preset volumeis not achieved during the course of breathing inspiratorytime will be prolonged till the desired volume is reached.

Pressure-Regulated Volume-Controlled (PRVC)

This form of ventilation has the features of volume andpressure control. The clinician sets a target tidal volumeand the maximum pressure level. The first deliveredbreath is at 5 cm water pressure, which is also used tocalculate the lung compliance. The next three breaths aredelivered at three quarters of the calculated pressureneeded to deliver the targeted tidal volume. After thispressure is increased by 3 cm of water each breath untiltarget volume is delivered.

Volume-Guaranteed Pressure-Limited

In this mode of ventilation the clinician presets the tidalvolume and the maximum pressure. The pressure set is


usually 15-20 per cent above the peak pressure needed toconstantly deliver the target tidal volume. The volumeguarantee is based on the expired tidal volume of thepreceding eight breaths. The volume guarantee can onlybe used in association with SIMV and Assist Control.

WEANING OF VENTILATION

Most babies can be extubated when they are able tomaintain the target tidal volume with delivered PIP ofless than 10-12 cm of H2O and FiO2 less than 35 per centand show a good sustained respiratory effort.

Chapter 9

High FrequencyVentilation


INTRODUCTION

This is a form of ventilation that uses small tidal volumeswith very rapid ventilator rates. Lunkenheimer first reportedthis method of ventilating babies in the early 1970’s. Sincethen there has been lot of advancement in this regard andcurrently is used extensively worldwide for ventilatingnewborns.

The exact mechanism by which HFV works is still notvery clear, but facilitated diffusion is thought to be one of themajor mechanisms for gas exchange. Generally, if the tidalvolume is extremely low, particularly, if lower than theanatomical dead space, chances of effective alveolarventilation is minimal. But, even with such low volumethere is still effective gas exchange in HFV mode ofventilation.

TERMINOLOGIES USED

1. Mean Airway Pressure (MAP): This is the point aboutwhich oscillation occurs and directly affects oxygenationas with all other forms of ventilation. It opens up theatelectatic areas of the lung and thereby minimizesventilation-perfusion mismatch and intrapulmonaryright-to-left shunting.

2. Amplitude: Also referred to as delta p. This influencesthe CO2 elimination and indicates the size of the swings(chest bounce) about the MAP. This is also one of thedeterminants of the oscillatory volume.

3. Frequency: This is measured in Hertz (1 hertz = 60breaths/minute) and influences both the oscillatoryvolume and the amplitude. Generally frequencies ofaround 10 Hz are used in newborns. As the frequencydecreases the volume and amplitude increase resultingin a drop in pCO2.

HIGH FREQUENCY VENTILATION 37

4. Oscillatory volume: This results from pressure swingsand essentially determines the effectiveness of CO2 removal.The target oscillatory volume is usually around2-2.5 ml/kg. The volume is directly proportional to theamplitude and related inversely to the frequency.

5. Gas transport coefficient (DCO2): CO2 elimination inHFV correlates well with (Oscillatory volume) 2 ×frequency. This is called the gas transport coefficientand measures the effectiveness of CO2 removal. Anincrease in DCO2 will result in decrease in pCO2.

Types of High Frequency Ventilators

High Frequency Positive Pressure Ventilators (HFPPV)

This refers to mechanical ventilators operating at ratesbetween 60-150 breaths/minute. This has been used inclinical trails to treat severe air leaks and lung diseasesunresponsive to conventional ventilation. In most casesHFPPV requires no special equipment, all that is needed is toturn the rate up in a conventional mechanical ventilator. But,because standard ventilators are not generally designed withsuch high frequencies in mind, minute ventilation decreasessignificantly at higher rates. Inadequate gas delivery duringinspiration and air trapping during expiration are also themajor factors limiting the use of HFPPV.

High Frequency Jet Ventilators (HFJV)

This mode of ventilation involves delivering ofpressurized gas in small aliquots into the upper airwaythrough a jet injector. It is used in tandem with theconventional ventilator that provides PEEP andbackground conventional breaths (Sigh breaths), whichhelps to prevent atelectasis. HFJV uses passive exhalationrelying on the elastic recoil of the lung to help drive the


exhaled gases. The frequency used in this mode varies from150-600 breaths per minute. Studies have demonstratedthe superiority of HFJV to conventional ventilation inresolving pulmonary interstitial emphysema. Also there isno evidence to suggest a link between the use of HFJV andchronic lung disease in infants.

High Frequency Oscillatory Ventilation (HFOV)

In this mode of ventilation piston pumps are used thatoperate at rates ranging from 400-2400 breaths/minute.During HFOV inspiration and expiration are both active.It applies continuous distending pressure to maintain anelevated lung volume and small tidal volumes aresuperimposed at a rapid rate. Pressure oscillationsproduce tiny tidal volumes, which are again determinedby the amplitude of the airway pressure oscillation. Sighbreaths are not used with HFOV.

INDICATION OF HIGH FREQUENCY VENTILATION

1. It can be used as a primary mode of ventilation inextreme prematurity.

2. As a rescue therapy for infants failing conventionalventilation.a. Reduced complianceb. RDSc. Air leaksd. Hypoplastic lungse. Meconium aspirationf. Atelectasis.

3. Primary pulmonary hypertension of newborn.4. Babies with established PIE.5. Diaphragmatic hernia.

HIGH FREQUENCY VENTILATION 39

The only relative contraindication for the use of HFV ispulmonary obstruction.

ADVANTAGES OF HFV

1. Achieves adequate ventilation while avoiding largeswings in lung volume.

2. There is more alveolar recruitment and improvementin ventilation perfusion matching because of the highMAP used.

Complications

1. Irritation: Babies require more sedation to avoidirritation by HFV.

2. Hemodynamics: High MAP can jeopardies venousreturn and cardiac output and also increase pulmonaryvascular resistance.

3. Intracranial haemorrhage (debatable).4. Over inflation: With higher frequencies there is a

possibility of lung over inflation specially withobstructive airway disease (e.g. meconium aspiration).

Management Strategies of Babies on HFV

Problems Suggested management

High pO2 Decrease FiO2Decrease MAP gradually

Low pO2 Increase MAPIncrease FiO2?Apply sigh manoeuvre

High pCO2 Decrease frequencyIncrease amplitudeIncrease MAP


Low pCO2 Increase frequencyDecrease amplitudeDecrease MAP

Over inflation Decrease MAPDecrease frequency?Discontinue HFV

Hypotension Give colloidGive dopamine/dobutamineReduce MAP

Chapter 10

Nitric Oxide


INTRODUCTION

In 1992, Science magazine named Nitric oxide as the“molecule of the year” for its potential as a revolutionarymedical gas therapy. Nitric oxide is a highly diffusible,colourless gas with a sharp and sweet odour. The NOmolecule is a free radical making it able to react with othermolecules.

Mechanism of Action of NO

NO is produced endogenously as the direct result of theenzyme nitric oxide synthase which oxidises the nitrogenatoms of L-arginine.

NO diffuses into the pulmonary vascular smoothmuscles and it activates the soluble form of guanylatecyclase and thereby increasing the “second messenger”cyclic guanosine monophosphate which results inpulmonary vasodilation. NO is a very potent short actingvasodilator with a half-life of 3-5 seconds. Once, it combineswith haemoglobin it is quickly inactivated. This results inthe formation of methaemoglobin, inorganic nitrate andnitrite, which are then renally excreted.

Functions of NO

1. Pulmonary vasodilatation.2. Kills bacteria and tumour cells in white cells.3. Acts as a synaptic transmitter in the brain and the spinal

cord.4. Releases adrenaline from the adrenal medulla.5. Stimulates gut peristalsis.6. Inhibits clotting.

Why NO?

NO has the unique ability to achieve potent and sustainedpulmonary vasodilation without decreasing the systemic vascular

NITRIC OXIDE 43

resistance. This ability of NO to selectively lower pulmonaryvascular resistance and decrease the extra-pulmonaryarteriovenous admixture justifies its use for the immediateimprovement and oxygenation in babies with persistentpulmonary hypertension. It also improves oxygenation byredirecting blood from poorly aerated lung regions to better-aerated air spaces.

INDICATIONS

1. Persistent pulmonary hypertension of the neonate(PPHN) (extrapulmonary right to left shunt).

2. Atelectasis, alveolar filling with meconium or blood(intrapulmonary right to left shunt).

3. Meconium aspiration (V•

/Q•

mismatch).4. Pulmonary interstitial emphysema (V

•

/Q•

mismatch).

TREATMENT STRATEGIES

Infants who have hypoxemic respiratory failure with evidence ofPPHN and requiring mechanical ventilation with high FiO2 aresuitable candidates for inhaled NO therapy. The most commoncriterion, which is generally used for starting NO, is theoxygenation index (OI). OI is calculated as:

MAP (cm H2O) × FiO2 × 100OI =

Postductal paO2 mmHg (kPa × 7.5)

NO is usually started at OI values of > 25.

Dose

The starting dose for NO varies among different units,but usually a maximum concentration of 40 ppm (partsper million) is used. In most instances a dose of 20 ppm willsuffice.


Duration of Treatment

In NOVO trial recommends that an increase of 3 kPa inpaO2 above baseline should be considered as an evidenceof a clinical response. If no response is seen within 15-30minutes of using the highest dose then cessation of therapyshould be considered. In most studies the typical durationof NO treatment has been less than 5 days. If required longerthan 5 days then investigations into other causes of pulmonaryhypertension should be considered.

WEANING

Continued weaning for inhaled NO should be tried dailyin infants in whom a clinical response is seen. When verylow levels of NO are reached (5 ppm) further reductionin dose should be very gradual and may take several days.

PATIENT MONITORING

1. Methaemoglobin: It should be measured 8-12 hourly.Levels above 4-5 per cent may be considered anindication to reduce NO concentrations and levelsabove 7-8 per cent may be an indication to stop NOtherapy. Methaemoglobinaemia is uncommon if lowerdoses of NO are used (< 20 ppm).

2. Clotting profile (because of the effect of NO on plateletfunction)

3. Environmental levels of NO and NO2 should bemonitored in the relevant clinical areas.

Side-effects of NO

1. Bleeding problems including intracranial haemorrhage.2. Methaemoglobinaemia.

Chapter 11

Extra CorporealMembrane Oxygenation

(ECMO)


This is a device of placing babies on heart-lung bypass. Itis used to support infants with severe respiratory and/orcardiac failure not responding to conventional ventilatorysupport. It is being used more frequently now withincreasing rate of success.

PROCEDURE

A venoarterial or a venovenous bypass is set up througha semipermeable silicone membrane that providesoxygenation and removal of carbon dioxide. In thevenoarterial bypass two large bore perfusion cannulas areused—one is placed in the right atrium via the rightinternal jugular vein and the other into the commoncarotid artery so that the tip is at the origin of theinnominate artery from the aortic arch. In the veno-venous type a double lumen cannula is placed in the rightheart.

SELECTION CRITERIA

There are various criteria used to select a baby for ECMOtherapy. The commonly used ones are:1. Oxygenation index > 402. Unresponsive to conventional treatment—increasing

oxygen requirement, persistent metabolic acidosis orvery high PIP (> 38 cm) requirement.

Indications

1. Severe case of meconium aspiration syndrome.2. Congenital diaphragmatic hernia—before and after

repair.3. Severe neonatal pneumonia.

EXTRA CORPOREAL MEMBRANE OXYGENATION 47

Contraindications

1. Weight < 2000 gm.2. Gestational age < 35 weeks.3. Severe pulmonary haemorrhage, gastrointestinal

haemorrhage or intraventricular haemorrhage (Gr IIand greater).

4. Lethal genetic condition.5. Nontreatable congenital cardiac malformation or

disease.

ADVANTAGE OF ECMO

It helps to avoid the barotrauma of high inspired oxygenconcentration associated with ventilation and gives thelungs the required time to heal by rendering them almostnon-functioning. All newborn babies receiving ECMO dohave a endotracheal tube in place with minimal mecha-nical ventilation.

The ECMO is generally successful in treating thepulmonary hypertension along with the right to leftshunting in the above mentioned group of babies.

Monitoring a Baby on ECMOThe following parameters need vigilant monitoring:1. FBC2. Urea and electrolytes3. Clotting4. Liver function test5. Blood culture6. Endotracheal tube culture7. Cranial ultrasound.

Side-effects1. Increased chances if intracranial haemorrhage.2. Auditory abnormalities

Chapter 12

Respiratory DistressSyndrome


Respiratory Distress Syndrome (RDS) equates to lungdisease in newborn due to surfactant deficiency but someNeonatologists prefer the terms ‘surfactant deficiency lungdisease’ or ‘hyaline membrane lung disease’.

AETIOLOGY

Deficiency of surfactant in the lungs.

Predisposing Factors

1. Prematurity2. Males3. Race-Black babies tend to suffer less from RDS4. Maternal diabetes.

Clinical Features

1. Chest recessions2. Tachypnoea3. Expiratory grunting4. Bradycardia (severe RDS)5. Hypotension.

Prevention of RDS

1. Prevention of prematurity (Neonatologists might bemade redundant though!).

2. Antenatal steroids—even a single dose of steroid 12hours before delivery makes the prognosis better. Twodoses of antenatal steroids are usually given, butmultiple doses have been used though benefit of thatis not very clear.

3. Prophylactic surfactant—The use of surfactant withinthe first few minutes of birth has been shown toimprove the oxygenation and also reduces morbidity.

RESPIRATORY DISTRESS SYNDROME 51

INVESTIGATION

Chest radiography Fine diffuse granular shadowing of bothlung fields with air bronchogram (the classical finding).

Treatment

1. Ventilation—if necessary2. Fluid balance3. Nutrition4. Antibiotics (as it is hard to differentiate RDS from early

onset sepsis)5. Surfactant therapy.

Complications

1. Air leaks2. Intraventricular haemorrhage3. Chronic lung disease4. PDA ( the incidence of symptomatic PDA increases, if

there is fluid retention).

Chapter 13

Chronic LungDisease


DEFINITION

Oxygen dependency after 28 days of age with charac-teristic chest X-ray changes.

AETIOLOGY1. Volutrauma.2. Prematurity/surfactant deficiency.3. Airleaks.4. PDA.5. O2 toxicity.6. Chorioamnionitis.

MANAGEMENT1. Ventilatory—Maintaining steady tidal volume and

ventilating at lower pressure helps.2. Oxygen therapy.3. Prompt treatment of chest infections.4. Blood transfusion.5. Nutrition.6. Drugs—Diuretics, bronchodilators, corticosteroids.7. Specialist team for home O2 therapy.

PROPHYLAXIS

1. Antenatal steroids.2. Avoidance of aggressive respiratory support in initial

stages.3. Vitamin E.4. Strict fluid management.

Complications1. Aspiration pneumonia.2. Gastro-oesophageal reflux.3. Right heart failure.4. Cor pulmonale.

Chapter 14

Meconium AspirationSyndrome


Meconium Aspiration Syndrome (MAS) occurs as a resultof inhalation of meconium antepartum, intrapartum orimmediate postpartum.

PROPHYLAXIS

Airway suctioning in time (before delivering the inflationbreaths in presence of thick meconium) can effectivelyreduce the incidence of MAS. There is no need to suctionairway if the baby cries spontaneously after birth even inpresence of meconium staining unless meconium is visiblebelow the cords or it is particulate type.

Effect on the Baby

1. Hypoxia2. Acidosis3. Raised pulmonary artery pressure4. PPHN.

Treatment

1. Oxygen2. Ventilation—IPPV, ECMO3. Pulmonary vasodilators—Nitrous oxide, Tolazoline4. Antibiotics5. Fluid balance and acid-base homeostasis.

Complications

1. Airleaks2. PPHN3. HIE4. Renal failure.

Chapter 15

Transient Tachypnoeaof Newborn


This is probably the most common cause of respiratorydistress in neonates born by caesarean section. The reasonfor this condition is likely to be the delayed absorption oflung fluid, which can often be visualised in the X-ray.Treatment is supportive. The close differential for thiscondition in term babies is sepsis while in premature onessurfactant deficiency should be thought of as well.

Chapter 16

Collapse of a Babyon Ventilator


This is a common scenario one encounters while workingin intensive care unit. Along with ABC of resuscitation,the mnemonic to remember here is:

D—displaced tubeO—Obstructed tubeP—PneumothoraxE—Equipment failureThe primary approach to a baby who has collapsed on

ventilator remains the same as in resuscitation—ABC. Quiteoften, if the baby is not adequately paralysed and/or theET tube is not properly secured there is always thepossibility of the tube getting dislodged. In this situationthe tube needs to be changed.

In certain instances, if the endotracheal tube has beenin place for long there is always an increased chance ofthe tube getting blocked by secretions and therebyobstructing the airway. Similar problems might occur, ifa narrow diameter ET tube is used. In these circumstances,tracheal toileting may suffice or else might need a tubechange.

Pneumothoraces can be spontaneous, but more oftenit is iatrogenic caused by inadvertent high pressuresduring ventilation. After checking the position and thepatency of the tube, a cold light examination of the chestis to be done to rule out any airleak. A chest X-ray shouldbe arranged though in case of a tension pneumothoraxintervention is urgent without waiting for a X-ray. Atension pneumothorax needs urgent intercostal drainagewith a needle. Later as in case of a simple pneumothoraxa proper chest drain can be inserted.

Equipment failures are a common cause of collapse ofa ventilated baby. The ventilatory circuit must bethoroughly checked before making exotic diagnoses forthe collapse!

COLLAPSE OF A BABY ON VENTILATOR 61

In premature babies it is also very useful to do a cranialultrasound as intracerebral bleed can lead to a similarscenario. Also remember sepsis as a cause for collapseand it is worth checking the blood sugar as well.

Chapter 17

NecrotisingEnterocolitis


This condition commonly encountered in prematureneonates increases mortality and morbidity rates in NICU’sconsiderably.

Predisposing Factors1. Prematurity.2. Absent or reversed end-diastolic flow.3. Early introduction of feeds in high-risk cases.

Clinical Findings1. Blood stained stool.2. Abdominal distension.3. Vomiting/large NG aspirates.4. Apnoea.5. Feed intolerance.

Pathogenesis

Ischaemic necrosis and inflammation of the gut. Whetherthis condition is a direct result of a bacterial infection is amatter of controversy.

Diagnosis

1. Raised inflammatory markers in blood.2. Abdominal X-ray:

a. Pneumatosis intestinalisb. Portal vein gasc. Pneumoperitoneum.

Treatment

1. Nil by mouth.2. Antibiotics (Benzylpenicillin, Gentamicin, Metronida-

zole or Cefotaxime and Metronidazole.3. Surgery (Resection of the necrotic bowel) in cases of

bowel perforation.

Chapter 18

Jaundice


Mild unconjugated hyperbilirubinaemia is common innewborns, but conjugated hyperbilirubinaemia impliesserious underlying pathology (always check color of stoolsin jaundice-white in conjugated type).

PHYSIOLOGIC JAUNDICE

Usually starts by 2nd to 4th day of life and resolves by aweek. It happens probably due to increased breakdown offoetal red blood cells and thereby raised bilirubinproduction.

BREAST MILK JAUNDICE

This happens usually by 5th to 7th day and can persist aslong as 2-3 weeks. The cause for this condition is unclearbut glucuronidase might have a role to play. If breast-feedingis continued in the face of jaundice, the bilirubin decreasesgradually. Cessation of breast-feeding reduces hyper-bilirubinaemia drastically.

First Day Jaundice

This is always pathological. Common causes are:1. Sepsis.2. Blood Group incompatibility.3. Haematological disorders, e.g. G6PD deficiency,

Hereditary spherocytosis, etc.4. Hypothyroidism (a cause for prolonged jaundice).

Treatment

Phototherapy and Exchange Transfusion

Phototherapy usually acts by converting the bilirubin tolumirubin, which is excreted by the kidneys. There is no

JAUNDICE 67

agreed level at which phototherapy should be started. Butgenerally accepted figures are:

24-48 hrs – 15 mg/dl48-72 hrs – 20 mg/dl> 72 hrs – 20-25 mg/dl

These figures are applicable for term babies. Forpremature babies phototherapy is initiated at much lowerlevels.

Chapter 19

Neonatal Feeding—Difficulties


Feeding a newborn baby is an art, which has to be acquiredwith patience. Poor suck is a worrying sign and can bethe first indication of an unwell baby.

Common problem checklist of a breast-feeding baby:1. Positioning of the baby.2. Are the size of nipples to large or too small for the

baby.3. Any cracked nipples.4. Evidence of mastitis.

Checklist for bottle-fed babies:1. Positioning of the bottle.2. Size of the nipple.3. Size of the teat.4. Milk to water ratio.

Chapter 20

Neonatal Vomiting—Common Causes


NEONATAL VOMITING—COMMON CAUSES

1. Sepsis (UTI)2. Gastro-oesophageal reflux3. Over feeding4. Lack of burping after feeds.

Chapter 21

Anaemia inNeonates


COMMON CAUSES

1. Transplacental haemorrhage.2. Haemolytic disease of newborn.3. Maternal APH prior to delivery.4. Anaemia of prematurity.5. Repeated phlebotomy in neonatal units.

POLYCYTHAEMIA IN NEONATES

Common Causes

1. Twin to twin transfusion.2. Infant of diabetic mother.3. Trisomy-21.4. Hypothyroidism.5. Delayed clamping of cord.

Treatment

Treatment for symptomatic polycythaemia is dilutionalpartial exchange transfusion with normal saline. Theformula used is:

Volume of exchange =

Blood volume × (Observed – Desired Haematocrit)

Observed Haematocrit

Chapter 22

Hypoxic IschaemicEncephalopathy (HIE)


This is an important cause of neonatal mortality and ofcerebral palsy or learning difficulty in later life. HIE causespermanent damage to CNS cells.

The three stages of HIE are:1. Stage 1 – Hyper alert baby with normal tone and

posture.2. Stage 2 – baby with hypotonia.3. Stage 3 – Stuporous and flaccid baby with dece-

rebrate posture.

Treatment

Therapy is supportive. Procedures like total bodyhypothermia (TBHT) or local cranial cooling are undertrial.

Chapter 23

IntraventricularHaemorrhage and

PeriventricularLeucomalacia


Intraventricular haemorrhage (IVH) may result fromtrauma, asphyxia, etc. IVH occurs in the subependymalgerminal matrix, which is the site of embryonic neuronsand immature blood vessels.

Common predisposing conditions for IVH:1. Prematurity2. Pneumothorax3. HIE4. Increased or decreased cerebral blood flow due to any

reason.The pathogenesis of periventricular leucomalacia (PVL)

is still evolving, but it is thought to be as a result of distur-bance in regulation of cerebral blood flow compoundedwith maternal or foetal infection. The chances of PVL arehigh in infants with IVH. PVL is responsible for adverseneurodevelopmental outcome in infants.

Diagnosis

Serial cranial ultrasound is the mainstay of diagnosingIVH and PVL. But more advanced imaging techniqueslike MRI or CT may be required particularly fordiagnosing PVL which is characterized by focal necroticlesions in periventricular white matter or more extensivewhite matter damage.

Treatment

Treatment is supportive. Antenatal administrations ofcorticosteroids reduce both IVH and PVL. Indomethacinhas been used prophylactically to reduce the incidence ofsevere IVH but is not universally practised. A DRIFT studyis being practised in UK (Bristol) which aims at removingpooled blood in brain in IVH and thereby reducing needsof a V-P shunt in later stages.

Chapter 24

Persistent PulmonaryHypertension of the

Newborn (PersistentFoetal Circulation)


This condition happens when there is persistence of foetalcirculatory pattern of right to left shunting throughForamen ovale and PDA. This is due to high pulmonaryvascular resistance.

Predisposing Factors

1. Perinatal asphyxia.2. Neonatal sepsis.3. Meconium aspiration syndrome.4. Polycythaemia.

Diagnosis

There is universal hypoxia with no or minimal responseto 100 percent O2. Echocardiogram with Doppler studiesis usually diagnostic.

Differential Diagnosis

Congenital cyanotic heart disease.

Treatment

1. Ventilation—HFV2. Tolazoline3. Nitric oxide4. ECMO.

Chapter 25

Sepsis in Neonates


MOST COMMON ORGANISMS

1. Streptococcus (Group B)2. E. coli3. Listeria Monocytogenes4. Staphylococcal epidermidis (in babies with central lines

in situ).

Manifestations

1. Apnoea2. Feed intolerance3. Desaturating episodes4. Not well5. Worried nurse.

Investigations

1. Blood for FBC, culture, CRP2. Chest X-ray3. Urine for M/C/S4. Lumbar puncture.

Predisposing Factors for Sepsis

1. Prolonged rupture of membranes (dribbling for > 18hours though most units will consider > 24 hours tobe significant).

2. Maternal pyrexia in labour (temperature > 38°C).3. Previous baby had proven sepsis after birth.

Treatment

Different units have their own guidelines regarding whenand how to treat. Gestational age of the baby should alsobe taken into consideration. Benzylpenicillin/Gentamicinor Ampicillin/Gentamicin is a reasonable choice to start

SEPSIS IN NEONATES 83

with. Gentamicin can be substituted by Cefotaxime.Supportive care is essential.

POINTS TO REMEMBER

1. Sepsis can cause either hypo- or hyperglycaemia.2. Sepsis can cause either thrombocytopenia or thrombo-

cytosis.3. Restrict fluid to two-third maintenance in case of

SIADH.

Differential Diagnosis

1. Surfactant deficiency respiratory distress.2. Transient tachypnoea of newborn.3. Total anomalous pulmonary venous drainage.

Chapter 26

Tit-Bits


TIT-BITS

1. Three common differentials for an unwell neonate:a. Sepsisb. Cardiacc. Metabolic.

2. Fluid therapy in neonates:a. D-1—60 ml/kg/db. D-2—90 ml/kg/dc. D-3—120 ml/kg/dd. D-4—150 ml/kg/de. D-5—180 ml/kg/d

Fluid therapy started a day ahead in IUGR babies.3. The mechanism of Rh incompatibility and alloimmune

thrombocytopenia are identical (for details refer toRoberton’s Textbook of Neonatology).

4. Baby collapses on D-3 or D-4—Think duct dependentheart problems.

5. Most common cause of organic heart murmur inneonates:a PDAb. Pulmonary stenosisc. VSD

6. Routine investigations for heart murmur:a. Chest X-rayb. ECGc. Echocardiogram (gives the definitive answer

provided the expertise is present).7. Weight along with length, OFC and mid-arm circum-

ference is a better indicator of the child’s nutritionalstatus than just weight alone.

8. Baby born to a mother with diabetes—remember tostart feeds early to prevent hypoglycaemia. Alsoremember hypocalcaemia and cardiomyopathy.

TIT-BITS 87

9. Neonate vomiting and crying after feeds—think aboutgastroesophageal reflux. Treatment—postural,Gaviscon, Ranitidine, Omeprazole, Nissen’s fundo-plication (a graded approach).

10. Remember UTI in neonates. Antenatal renal pelvicdilation of > 10 mm demands Trimethoprimprophylaxis after birth followed by postnatal renalultrasound scans the timings of which is againdictated by the degree of dilatation. Usually scansbefore D-3 may be less informative.

Chapter 27

Neonatal Formulary(Commonly Used

Medications)


• Adrenaline (IV)—10 μg/kg (0.1 ml/kg of 1 in 10,000).• Adrenaline (ET)—100 μg/kg (0.1 ml/kg of 1 in 1000).• Atropine sulphate (IV)—15 μg/kg slowly.• Benzylpenicillin (IV)—25 mg/kg twice daily.• Caffeine citrate (IV/PO)—20 mg/kg loading dose

followed by 5 mg/kg maintenance.• Calcium gluconate (Infusion)—0.5 mmol/kg over

24 hours for maintenance therapy.• Cefotaxime (IV)—50 mg/kg twice to thrice a day.• Chloral hydrate (PO/PR)—25 mg/kg.• Dobutamine (IV infusion—continuous)—5-15 μg/kg/

min (to be diluted in 5% Dextrose or 0.9% NaCl).• Dopamine (IV continuous infusion)—5-20 mcg/kg/

min (to be diluted in 5% Dextrose or 0.9% NaCl).• Frusemide (IV/PO)—1 mg/kg.• Gentamicin (IV)—4-5 mg/kg every 24 to 36 hourly

depending on the gestational age.• Indomethacin—200 μg/kg for 3 days (for PDA closure).• Midazolam (IV)—100 μg/kg single dose.• Morphine sulphate (IV infusion)—5-20 μg/kg/hour (to

be diluted in 5% Dextrose or 0.9% NaCl).• Nystatin (PO)—1 ml 4 times a day.• Pancuronium (IV bolus)—100 μg/kg.• Paracetamol (PO)—10-15 mg/kg (can be repeated

4-6 times).• Surfactant (natural)—100-200 mg/kg depending on

source.• Teicoplanin (IV)—16 mg/kg loading dose followed by

8 mg/kg maintenance.• Trimethoprim (PO)—2 mg/kg for UTI prophylaxis.

AAcid-base balance 7Anaemia in neonates 73

BBlood gas analysis 9

arterial blood gasmeasurement 9

capillary blood gas analysis 9continuous blood gas

analysis 9transcutaneous

monitoring of pCO2 10venous blood gas analysis 9

CChronic lung disease 53

aetiology 54complications 54management 54prophylaxis 54

Collapse of a baby on ventilator 59Continuous positive airway

pressure (CPAP) 11contraindication 14indications 13mechanism of action 12methods of delivering 12

EExtracorporeal membrane

oxygenation (ECMO) 45advantage 47contraindications 47indications 46procedure 46side effects 47

Index

FFormulas commonly used in

NICU 5

GGeneral guidelines for CPAP 14

increasing oxygenrequirement 14

initial PEEP 14respiratory distress in

newborn baby 14

HHigh frequency ventilators 37

advantages 39complications 39indication 38types 37

Hypoxic ischaemicencephalopathy (HIE) 75

treatment 76

IIntraventricular

haemorrhage andperiventricular

leucomalacia 77diagnosis 78treatment 78

JJaundice 65

breast milk jaundice 66physiologic jaundice 66treatment 66

LLimitation of MAP 21

flow rate 22waveforms 22


MManagement strategies of

babies on HFV 39Meconium aspiration

syndrome 55complications 56effect on the baby 56prophylaxis 56treatment 56

NNasal ventilation 15Necrotising enterocolitis 63

clinical findings 64diagnosis 64pathogenesis 64predisposing factors 64treatment 64

Neonatal feeding 69Neonatal vomiting 72Nitric oxide 41

functions 42indications 43mechanism 42patient monitoring 44side effects 44treatment strategies 43

Normal arterial blood gasvalues 8

PPersistent pulmonary

hypertention of thenewborn 79

diagnosis 80differential diagnosis 80treatment 80

Polycythaemia in neonates 74common causes 74treatment 74

Positive pressure ventilation 18advantages 18types 18

Positive pressure ventilation 24

RRespiratory distress

syndrome 49aetiology 50

clinical features 50predisposing factors 50prevention 50

investigation 51complications 51treatment 51

Resuscitation at birth 2

SSepsis in neonates 81

investigations 82manifestations 82most common organisms 82predisposing factors 82treatment 82

TTerminologies used in HFV 36Threshold for intubation 14Tit-bits 86Transient tachypnoea of

newborn 57

VVentilator controls 18Ventilatory adjustments 27Volume controlled ventilation 31Volume-targeted ventilation 33

types 33

WWeaning of ventilation 29, 34

Documents

Neonatal Ventilation Made Easy