1238

Management of
Emergency Pediatrics
Made Easy
Management of
Emergency Pediatrics
Made Easy
S Letha
Professor and Head, Department of Pediatrics Government

Medical College Kottayam, Kerala
India
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Management of Emergency Pediatrics Made Easy
2008,Jaypee Brothers Medical Publishers
All rights reserved. No part of this publication and CD ROM should be reproduced, stored in
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photocopying, recording, or otherwise, without the prior written permission of the author and
the publisher.
This book has been published in good faith that the material provided author is original.
Every effort is made to ensure accuracy of material, but the publisher
, printer and author
will not be held responsible for any inadvertent error(s). In case of any dispute, all legal
matters are to be settled under Delhi jurisdiction only .
First Edition:2008
ISBN 978-81-8448-282-9
Typeset at JPBMP typesetting unit
Printed at Rajkamal Electronic Press, B-35/9, G.T. Karnal Road, Delhi-33
To
My beloved husband
R Sadasivan
who was my encouragement and
inspiration throughout this endeavor
PREFACE
Prompt recognition and appropriate management of a
critically ill child improves the quality of life. It prevents
morbidity as well as mortality. To identify a critically ill child
is the most important aspect of critical care management.
After identifying the sick child, a protocol oriented
management done by a team of trained personals is the next
step in the management of such a child.This book is intended
to help the young doctors in managing the common pediatric
emergencies in a simple way . Lack of sophisticated
instruments, costly equipments and drugs are often
compensated to a great extent by the sincerity and dedication
of the health personals and constant and careful personal
monitoring.
I express my sincere gratitude to all my teachers and my
students, my tiny patients and their parents who all inspired
me for putting in such an effort.
My thanks are due to Mr KVVarkey, Royal DTPCentre,
Gandhinagar, Kottayam for all the help he has rendered tome.
Lastly but of most importance, I would like to thank Mis
Jaypee Brothers Medical Publishers (P) Ltd, New Delhi for
their help extended to me for publishing this book.
S Letha
CONTENTS
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
12.
13.
14.
15.
16.
17.
18.
19.
20.
How to Identify a Sick Child? .................................. 1

Pediatric Cardiopulmonary Resuscitation ................ 9
Vascular Access....................................................... 25
Oxygen Therapy ..................................................... 35
IV Fluid Therapy ..................................................... 51
ABG Analysis ......................................................... 69
Mechanical Ventilation ........................................... 81
Management of Shock in Children ......................... 95
Status Epilepticus .................................................. 101
Coma ..................................................................... 107
Acute Respiratory Failure ...................................... 111
Acute Severe Asthma ............................................. 115
Hepatic Failure ...................................................... 121
Acute Renal Failure .............................................. 129
Diabetic Ketoacidosis ........................................... 135
Cardiac Emergencies ............................................ 141
Hypertensive Emergencies ................................... 153
Blood and Blood Component Therapy ................. 157
Envenomation ....................................................... 163
Poisoning in Children ........................................... 171
Index ...................................................................... 183
CHAPTER 1
How to Identify
a Sick Child?
MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY
Identifying a sick child is the first step in the management

of a critically ill child. Often the young doctor finds it difficult to recognize a child who needs immediate, emergency
management. A sick child or critically ill child is one who
is in vital compromise, having serious respiratory, cardiovascular or neurological illness who may have to face
mortality if not treated promptly. Timely and appropriate
emergency care will help save the life. He has to be assessed
rapidly through a step- wise approach-golden hour concept.
The golden hour is aptly termed as golden because it is
this critical duration which is vital for saving the child.
Rapid cardiopulmonary assessment is indicated if the
child is having the following features.
a. Tachypnea RR >60/mt
b. Tachycardia >180 in under 5 years >160 over 5 years.
c. Bradycardia <80 in under 5 years <60 over 5 years
d. Increased work of breathing
e. Cyanosis
f. Diminished level of consciousness
g. Seizures
h. Fever
i. Petechiae
j. Trauma
k. Burns
Very simple assessment of overall illness is by using
the pediatric assessment triangle
Appearance
Circulation
Breathing
HOW TO IDENTIFY A SICK CHILD?
Appearance
This denotes the neurological status of the child which is
determined by the oxygen and blood supply to the brain
which in turn is dependent on the cardiopulmonary
function and structural integrity of the brain.
Alertness
See if baby is alert, active, or lethargic, confused or comatose.
The consciousness can be roughly assessed by the AVPU
scale.
AAwake
VVerbal-response to voice
PPain-response to pain
UUnresponsive
Modified Glasgow scale also can be used for the rapid
assesment of critical function.
Glasgow Coma Scale
Eye opening
Spontaneous
To voice
To pain
None
Total points 5
4
3
2
1
Verbal Response Total Points 5

Older children
Oriented
Confused
Inappropriate
Incomprehensible
None
4
3
2
1
Infants
Appropriate words,
smiles, fixes, follows
Consolable crying
Persistently irritable
Restless, agitated
None
5
4
3
2
1
Motor Response Total Points 6

Obeys
6
Localizes pain 5
Withdraws
4
Flexion
3
Extension
2
None
1
GCS of 8 or less carry bad prognosis and need
aggressive management.
Distractibility and Consolability
By the parent is a useful observation. The most sick child
does not regard even the mother.
Eye Contact
Absence of eye contact even to mother is a grave sign.
Speach/cry
Identify the reason for cry and observe whether it is normal
or not. The quality of the cry also is important. Weak, shrill
or whimpering cry shows that the child is very sick.
Motor Activity
Assess whether it is normal or not.
Pupil Size
May be abnormal depending on the cerebral perfusion and
pressures. Unequal pupils are seen in raised intracranial
pressure.
Breathing
Respiratory rate is very important in the assessment of a
critically ill child. Tachypnea is an early sign of respiratory
distress whereas bradypnea is an omnious sign.
Respiratory Rate
NB
40-60 mt.
1-5 yr
26-22
>5 yr
22-20
>18 yr
18
Upper limit of RR is:

Newborns 60/mt
Infants
50/mt
Children
40/mt
Effortless or quiet tachypnea is seen in shock, cardiac
disease, acidosis, etc. A slow or irregular respiration in an
acutely ill child is an omnious sign.
Work of Breathing
Increased work of breathing is evidenced by working of
the accessory muscles of respiration like intercostals, and
sternocleidomastoids. There may be intercostal, subcostal
and suprasternal retractions, nasal flaring, grunting and
head bobbing indicating respiratory distress and potential
respiratory failure.
Child with impending respiratory failure will be having
tachycardia, which when severe produces bradycardia.
Hypoxia leads to catecholamine release producing pallor
of skin progressing to central cyanosis as hypoxia worsens.
Hypoxia and hypercarbia alters the level of consciousness.
Oxygen saturation can be assessed by pulse oximetry
which is very useful for the early detection of hypoxia.
CIRCULATION
Pulse and Heart Rate
Tachycardia is a very sensitive indicator of inadequate
oxygen delivery and the first response to circulatory failure.
Bradycardia in an acutely ill child is an omnious sign.
Normal heart rates in children
Tachycardia
Bradycardia
Newborns
Infants
Children
>160/mt
>150/mt
>120/mt
<100/mt
<80/mt
<60/mt
120-160/mt
100-120/mt
80-120/mt
Pulse Volume
Pulse volume is low during the early phase of circulatory
failure because of the peripheral vascular constriction, as
a compensatory mechanism to the vital organs. When
circulatory failure is established the peripheral pulses will
not be palpable. In early septic shock there is low systemic
vascular resistance and so there can be bounding pulse
during the early phase of warm shock.
Pulse Pressure
As cardiac output decreases pulse volume reduces and the
pulse pressure narrows and pulse became thready. As
cardiac output increases in warm septic shock and
anaphylactic shock pulse pressure widens and pulses
become bounding.
Blood Pressure
In early compensated shock BP is normal. Hypotension
develops when the compensatory mechanisms fail. Low BP
is an indicator of late, decompensated shock.
BP in Children
Normal
Newborn
1 yr
2-10 yr
>10 yr
Minimum acceptable level of systolic BP.

60 mmHg
70 mmHg
70+(age+2) mmHg
90 mmHg
Skin Perfusion
Skin perfusion can be assessed by temperature, color and
capillary filling time.
Temperature
Hands and feet become cold as cardiac output falls.
Color
Skin appears pale, cyanozed or mottled due to the
decreased perfusion to skin.
Capillary Filling Time
The capillary blood flow is reduced in shock. The normal
capillary filling time is 2-3 seconds. Prolonged CFT is a
useful sign in shock. But capillary filling time can be
prolonged in rising fever and exposure to cold ambient
temperature also.
Organ Perfusion
Poor organ perfusion occurs when shock progresses.
Cerebral hypoperfusion results in altered sensorium. Renal
hypoperfusion results in decreased urine output. Ischemia
of gut can produce GI hemorrhage.
So, with the help of the pediatric assessment triangle the

status of the critically ill child can be characterized as:
1. Stable
2. Respiratory distressRespiratory failure
3. Cardiovascular failureCompensated or decompensated shock
4. Disturbed neurological status.
If the child is not stable the initial management should
be aimed at stabilizing the child in an agressive manner
by maintaining the Airway Breathing and Circulation.
Monitoring is very important in the management of a
critically ill child. Being aware about the age specific
emergencies and current epidemics will help in the
management of critically ill children. All children brought
to the hospital should be thouroughly assessed for their
critical nature, stabilized within no time to be followed by
definitive management for specific management of the
underlying condition. Periodic reassessment is also very
important to detect the progress or deterioration. Last but
not of least importance is the management of the worried
parents and relatives. They should be explained about the
condition of the child and the doctor should have the
empathetic attitude.
CHAPTER 2
Pediatric
Cardiopulmonary
Resuscitation
10
The relevance and community participation of pediatric

cardiopulmonary resuscitation is often a neglected part of
our training. Many children develop cardiopulmonary
arrest outside the hospital and BLS training is to be offered
to all expectant parents, parents of young babies and highrisk children and also to those who are entrusted with care
of children like nursery teachers, school teachers, day care
personnel, etc. The content of such BLS courses should
include the preventive strategies, training in BLS techniques, access to EMS system which are to be developed in
our country.
Cardiopulmonary arrest in children is different from
that of adults. Primary cardiac arrest in young children
is very rare. More commonly it results from low oxygen
level secondary to respiratory difficulty or arrest. The
outcome of respiratory arrest alone is best with a prompt
resuscitation followed by aggressive ALS.
Pediatric cardiopulmonary arrest can occur in newborn to adolescence and the causes differ in different age
groups.
CAUSES IN INFANCY BEYOND NEWBORNS
1.
2.
3.
4.
5.
6.
7.
8.
9.
Injuries
ALTE (Acute life-threatening events)
SIDS (Sudden infant death syndrome)
Respiratory diseases
Airway obstructionFB aspiration
Smoke inhalation
Submersion
Sepsis
Neurological diseases
PEDIATRIC CARDIOPULMONARY RESUSCITATION
11
Beyond Infancy
Accidents and injuries are the leading causes for cardiopulmonary arrest. Airway obstruction leading to asphyxia
is a major cause of death and disability in children. It can
be due to a foreign body or edema due to infection.
Poisoning through accidental ingestion is most common
in 1-4 years age group.
The basic steps of CPR are the same in an infant, child
or adult. It includes the sequential assessment and motor
skills designed to support or restore effective ventilation
and circulation to the person in respiratory or cardiorespiratory arrest.
The steps are:
1. Determine responsiveness
This helps in assessing the presence and extent of injury
and determine the consciousness. This is done by tapping
the child and speaking loudly to elicit a response. The
victim should not be shaken or moved unnecessarily if
spinal cord injury is suspected because such handling may
aggravate the injury.
If child is unresponsive but breathing or struggling to
breathe he should be transported to an advanced life
support facility.
Once unresponsiveness has been determined the lone
rescuer should shout for help and then provide BLS to the
child.
2. Position of the victim
In order to provide an effective CPR the victim must be
lying on his or her back on a firm flat surface. Sometimes,
it is mandatory to move the child from a dangerous
12
location (e.g. in a burning building). Great care must be

taken while moving the child particularly if there is
evidence of trauma. The cervical spine should be
immobilized and the head and the body must be held as
a unit and the head and neck firmly supported so that the
head does not roll, twist or tilt.
3. Open the airway
Relaxation of the muscles and passive posterior
displacement of the tongue may lead to airway obstruction
in the unconscious victim. Opening of the airway is
essential for effective ventilation.
Head TiltChin Lift
Place one hand on the childs forehead and tilt the head
gently back into a neutral position. The neck is slightly
extended. Place the fingers not the thumb, of the other
hand under the bony part of ther lower jaw at the chin,
and lift the mandible upward and outward.
Be careful not to close the mouth or push the soft
tissues under the chin which may obstruct the airway.
Jaw Thrust
Safest method when neck or cervical spine injury is
suspected because it can be done without extending the
neck.
Place two or three fingers under each side of the lower
jaw at its angle and lift the jaw upward and outward.
If jaw thrust alone does not open the airway, slight
head tilt may be added in patients with no evidence of
cervical spine injury. Whenever head or neck injury is
suspected the cervical spine must be completely stabilized
13
when airway is opened. This can be accomplished by a

combined jaw thrust and spinal immobilization maneuver
using only the amount of manual control necessary to
prevent cranial cervical motion by pressing over the
forehead by the thumbs of the rescuer.
If two rescuers are present, the first rescuer can open
the airway with jaw thrust maneuver and the second can
immobilize the neck in the neutral position.
Breathing
After airway is opened the rescuer should determine if
the baby is breathing or not. He can look for the movement
of chest, listen for the exhaled air, feel for the exhaled air
flow at the mouth.
If the victim is breathing effectively he can be placed
in the recovery position.
The victim should not be moved if there is suspicion
of trauma or if he needs rescue breaths and CPR.
Recovery Position
Victim is moved on to his side moving his head, shoulders
and torso simultaneously. The leg not in contact with the
ground may be bent and the knee moved forward to
stabilize the victim.
Rescue Breathing
Rescue breaths are the single most important manuever
in assisting a non-breathing child victim. If a mask with
a one-way valve or other infection control barrier is readily
available it can be used. However, ventilation should not
be delayed while such a device is located.
14
If the victim is an infant place the mouth of the rescuer

over the infants nose and mouth creating a seal. In a large
infant or older child, make a mouth-to-mouth seal and
pinch the victims nose tightly with the thumb and forefinger of the hand maintaining head tilt. First inhale
deeply and then seal the mouth and nose or mouth as
required depending on the age of the baby.
Give two slow breaths (1 to 1 seconds per breath) to
the victim pausing after the first breath to a take a deep
breath. The volume and pressure of the rescue breaths
should be sufficient to cause the chest to rise. The breaths
should be delivered slowly. Slow breaths will allow
delivery of an adequate volume of air and ensure effective
lung and chest expansion. Taking a pause in between the
breaths maximizes the oxygen content and minimizes
carbon dioxide content in the delivered breaths.
If air enters freely and chest rises the airway is clear.
If not, either the airway is obstructed or more breath
volume or pressure is necessary. So the rescuer should reattempt opening the airway and re-attempt ventilation.
If there is no suspicion of neck or spine injury, the rescuer
should move the victims head into several positions of
neck extension until a position of optimal airway patency
results in effective rescue breathing. If rescue breathing
fails to produce chest expansion after several attempts, a
foreign body airway obstruction is to be suspected and
the necessary maneuvers are to be done to remove the
foreign body.
Rescue breathing especially if done rapidly may cause
gastric distension. Excessive gastric distension can
interfere with ventilation and so if a second rescuer is
15
there, he can apply cricoid pressure to displace trachea

posteriorly compressing the esophagus against the
vertebral column to prevent gastric distension and reduce
the likelihood of regurgitation.
In a single rescuer, delivering the rescue breaths slowly
will prevent gastric distension.
Circulation
Once the airway is opened and two rescue breathes have
been provided, the rescuer should determine the need for
chest compression.
Pulse Check
If cardiac contractions are ineffective or absent, there will
not be a palpable pulse. In infants, since the carotid artery
is difficult to palpate due to the short and chubby neck
the brachial artery palpation is recommended with the
thumb on the outside of arm, the index and middle fingers
are gently pressed over the brachial artery to feel the pulse.
In children the carotid artery on the side of the neck
is the most acceptable central artery to palpate. To feel the
carotid artery, locate the victims thyroid cartilage with
two or three fingers of one hand while maintaining head
tilt with the other hand. Slide the fingers onto the groove
on the side of the neck closer to the rescuer, between the
trachea and sternocleidomastoid muscle.
If pulse is present but spontaneous breathing absent,
provide rescue breathing alone at a rate of 20 breaths per
minute (Once in every 3 seconds) till spontaneous
breathing resumes. If not able to resume spontaneous
breathing child needs emergency medical care services.
16
If pulse is not palpable or heart rate is less than 60 and

signs of poor systemic perfusion are present child needs
chest compressions.
Chest compressions are serial rhythmic compressions
of chest to facilitate oxygen containing blood to be
circulated to vital organs like heart, lungs and brain until
advanced life support can be provided. To achieve optimal
chest compressions, the child should be supine on a hard,
flat surface. For an infant the hard surface may be the
rescurers hand or palm itself.
Chest Compressions in the Infant
1. Use one hand to maintain the infants head position
(unless the hand is under the childs back).
2. Use the other hand to compress the chest. Place the
index finger of the hand on the sternum just below the
level of the infants nipples. Place the middle finger
on the sternum adjacent to the index finger. Sternal
compression is done approximately the width of one
finger below the level of nipples. Compression to the
xiphoid process is to be avoided since it may damage
the liver, stomach or spleen.
3. Using two or three fingers, compress the sternum approximately one-third to one-half the depth of the chest.
This will correspond to a depth of about to 1 inch.
The rate of compression should be at least 100
times/minute.
Compressions should be co-ordinated with ventilation in a 5:1 ratio with pauses for ventilation. The
number of compressions will actually be at least
80/minute.
17
4. At the end of the each compression, pressure should

be released without removing fingers from the chest.
A smooth compression relaxation rhythm without
jerky movements should be developed with equal time
for compression and relaxation.
When the victim resumes effective breathing he may
be placed in the recovery position.
Chest Compression in the Child
For the purposes of BLS, 1 to 8 years old are considered
as child. If the child is large or more than 8 years chest
compression should be provided as for adults.
1. Use one hand to maintain childs head position.
2. Using fingers of the other hand the lower margins of
the victims rib cage is traced on the side near to the
rescuer. Reach the notch where the sternum and ribs
meet.
3. Place the heel of the hand over the lower half of the
sternum between the nipple line and the notch,
avoiding the xiphoid process. The long axis of the heel
should be over the long axis of the sternum.
4. Compress the chest as already mentioned as in the
infant to 1/3 to 1/2 of the depth. If the victim resumes
effective breathing, place him in the recovery position.
If not, he needs emergency care services.
Foreign Body Airway Obstruction
Foreign body airway obstruction should be suspected in
infants and children with sudden onset of respiratory
distress associated with coughing, gagging, stridor or
wheezing. Attempts to clear the airway should be
18

Summary of BLS in Infant Child and Adult
0-1 yr
1-8 yr
>8 yr
Determine responsiveness shake and

shout tapping and
speaking loudly
Yes
Yes
Yes
Call for help
Yes
Yes
Yes
Position the victim
Yes
Yes
Yes
Look, listen and feel

for breath
Yes
Yes
Yes
Open the airway
Yes
Yes
Yes
Rescue breaths
Yes
Yes
Yes
Check pulse
Brachial
Carotid
Carotid
Activate EMS
Yes
Yes
Yes
Locate the position of

chest compression
Lower
sternum
Lower
sternum
Lower
sternum
Compression with
2 fingers
heel of
one hand
heel of
two hands
Compression depth
-1
1-1
1 to 2
(1/3 or 1/2
(1/3 to 1/2
(1/3 to 1/2
of total depth) of total depth) of total depth)
Compression/
minute
at least 100
100
80-100
Compression
ventilation ratio
5:1
5:1
5:1
considered when foreign body aspiration is witnessed or

strongly suspected or when airway remains obstructed
during attempts to provide rescue breathing. Relief of
airway obstruction should be attempted only if signs of
complete obstruction is observed.
19
In InfantsBack Blows and Chest Thrusts

(Figs 2.1 and 2.2)
1. Hold the infant face down resting of on the forearm
of the rescuer. Support the infants head by firmly
holding the jaw. Rest the forearm on the thigh to
support the infant. The infants head should be lower
than the trunk.
2. Deliver up to 5 back blows forcefully between the
infants shoulder blades using heel of the hands.
Fig. 2.1: Back blows
Fig. 2.2: Chest thrusts
20
3. After delivering the blows, place the free hand on the

infants back, holding the infants head. Thus one hand
supporting the back, other hand supporting the head,
neck and jaw the baby is turned to the supine position
draped on the thigh. The infants head should be lower
than the trunk.
4. Give up to five quick downward chest thrusts in the
same location as in the manner of chest compression.
If the infant is large or rescuers hands are small, the
infant may be placed on the lap with head lower than the
trunk. After the five back blows, infant is turned as a unit
to the supine position and five chest thrusts are given.
All these steps are repeated until the object is expelled
or the infant losses conciousness.
If the infant losses consciousness open the airway
using a tongue jaw lift and remove the foregin body if it
is seen and attempt rescue breathing and relief of airway
obstruction.
Tongue Jaw Lift
Grasp both the tongue and lower jaw between the thumb
and finger and lift. This action draws the tongue away
from the back of the throat and may itself partially relieve
the obstruction and if a foreign body is seen it can be
removed.
THE CHILDTHE HEIMLICH MANEUVER
Victim Conscious
1. Stand behind the victim with arms directly under the
victims axilla encircling the victims torso.
21
Fig. 2.3: Abdominal thrusts
2. Place the thumb side of one first against the victims

abdomen in the midline slightly above the navel and
below the xiphoid process.
3. Grasp the fist with the other hand and exert a series
of quick upward thrusts. Each thrust should be a
separate distinct movement intended to relieve the
obstruction. Continue the abdominal thrusts till the
foreign body is expelled or the patient losses conciousness (Fig. 2.3).
Unconscious Child
Place the child supine. If the loss of consciousness is witnessed and foreign body aspiration is suspected open the
airway with a tongue jaw tilt and remove the object if it
22
is seen. Attempt rescue breathing. If ventilation is unsuccessful try re-position of head and re-attempt ventilation. If
ventilation is unsuccessful go through the following steps.
Kneel beside the victim or straddle the victims hips.
Place the heel of one hand on the childs abdomen in the
midline, below the xiphoid process and above the navel
place the other hand on top of the first and press with both
hands in to the abdomen with a quick upward thrust.
Perform a series of five thrusts. Each thrust should be a
separate and distinct movement. Open the airway and
with tongue jaw tilt, if the foreign body is seen, remove
it. If not repeat the steps till foreign body is expelled and
ventilation is successful (Fig. 2.4).
Advanced Life Support
ALS is done as a continuation of BLS which is initiated
immediately and then the victim is to be transferred to
a facility that can care for them appropriately.
Fig. 2.4: Head tilt-chin-lift maneuver
23
Fig. 2.5: Recovery position
RespiratoryAirway and Ventilation

Respiratory problems are common resulting in cardiopulmonary arrest and if respiratory failure is promptly treated
intact survival of the child is likely. If not it may progress
to cardiac arrest and the prognosis is poor.
Most important is to anticipate and recognize
respiratory problems and to support the child.
Alert children with respiratory distress should be
allowed to remain in a position of comfort to them,
preferably with their parents and airway equipment with
oxygen should be introduced in a non-threatening
manner. If the child is uncomfortable with one method
of oxygen support, alternative methods are to be tried. If
the child is somnolent or unconscious see that the airway
is not obstructed by neck flexion, relaxation of the jaw,
posterior displacement of the tongue and collapse of the
hypopharynx. If necessary, airway is to be cleared off
secretions, mucous or blood (Fig. 2.5).
CHAPTER 3
Vascular Access
26
Establishment of a vascular access is highly essential in

the emergency care setting. It helps in successful resuscitation because infusion of the fluids and drugs are
possible through it. Endotracheal tube may help in administering some drugs used in resuscitation but intravenous
or intraosseous access is preferred for administration of
fluids and drugs.
Venous Access
Peripheral venepuncture provides a satisfactory route if it
can be achieved within a few minutes. It can be performed
in veins of arm, hand, leg and foot. But cannulation of
small veins may be difficult when patient is in shock or
cardiopulmonary arrest. In such circumstances, large veins
are to be tried like femoral or jugular. Cannulation of scalp
veins are less desirable because the catheters in these veins
may infiltrate when fliuds and medications are infused
rapidly and forcefully and may interfere with control of
the airway and ventilation.
Intraosseous route is a reliable alternative to
venipuncture in infants and children who are in shock if
peripheral venous access is not achieved within a few
seconds. The proximal tibia is the preferred site of
intraosseous puncture. The main contraindication is the
presence of fracture in the bone chosen or proximal to it.
During CPR intraosseous route is to be tried if a venous
access is not achieved within 3 attempts or within 90
seconds whichever comes first. Since the tibial marrow is
more difficult to cannulate as age advances, in children
older than 6 years, percutaneous central venous access or
saphenous vein cut down should be established if reliable
venous access cannot be obtained within first 90 seconds
VASCULAR ACCESS
27
of resuscitation. The preferred site of venous access remains

the largest vein that can be rapidly accessed without
interfering with CPR.
Intraosseous Cannulation (Fig. 3.1)
Complications following intraosseous infusion are
reported in fewer than 1% of patients. But when they occur
they are often more serious and so intraosseous cannulation is done in the treatment of critically ill infants and
children only as a temporary measure until other venous
access sites become available.
Fig. 3.1: Intraosseous cannulation
Devices
Two types are available, specially designed intraosseous
infusion needles and Jamshidi type bone marrow
aspiration needles. In an emergency short wide gauge
spinal needles with internal stylets can be used if no
alternatives are available. All commonly used drugs during
resuscitation, crystalloids, colloids and blood can be given
through intraosseous route. The drugs administered should
be followed by a sterile saline flush of at least 5 ml to ensure
that the drug is delivered to the central circulation. The
complications reported include tibial fracture, compartment
syndrome, skin necrosis and osteomyelitis.
28
Site
The flat anterolateral surface of the tibia approximately
1-3 cm below the tibial tuberosity is the preferred site.
Insertion of the needle is successful if the following
conditions are present:
A sudden decrease in resistance occurs as the needle
passes through the cortex to the marrow cavity.
The needle remain up wright without support.
Marrow can be aspirated into a syringe but this is not
consistantly achieved.
Fluid flows freely through the needle without evidence
of subcutaneous infiltration.
If the cannulation is blocked it can be replaced with a
second needle provided no infiltration. If evidence of
infiltration occur a second attempt on the other tibia is to
be tried.
Central Venous Cannulation
This enables delivery of the infusate directly into the central
circulation and delivery of medications at or near their site
of action. It allows monitoring of central venous pressure
during post-resuscitation stabilization. In addition, there
is little risk of infiltration of drugs. Complications of the
procedure include local and systemic infections, venous
or arterial bleeding, arterial cannulation, thrombosis,
phlebitis, pulmonary thromboembolism, hydrothorax,
hemothorax, cardiac tamponade, arrhythmias, air
embolism and catheter fragment embolism. The incidence
of the complications depends on the site, experience of the
clinician and clinical condition of the patient. Since
complications are more in pediatric age group central
VASCULAR ACCESS
29
venous cannulations are done only if the benefits outweigh

the risks.
Devices and Techniques
Though the needle catheters can be used, great care must
always be exercised during placement of a through the
needle catheter because the catheter tip can be sheared off
by the sharp needle. If any resistance is encountered during
catheter advancement the catheter should not be withdrawn through the needle. Instead, the entire assembly
should be withdrawn as a unit to prevent catheter shearing
and potential fragment embolism.
Modified Seldingers Technique for Insertion of
Catheters and Introducing Sheaths
Pressure monitoring catheters are catheters of relatively
low compliance that allow measurement of central venous
or intracardiac pressure. A catheter introducing sheath
consists of a dilator within a large bore sheath. Once the
catheter-introducer is placed in to a central vein, the dilator
is removed and the sheath may be used for fluid infusin
or to guide the insertion of a central venous catheter.
The Seldingers (Guidewire) technique is especially
useful for establishing vascular access in children. This
technique allow the introduction of catheters into the
venous circulation after the initial venous entry using a
small gauge, thin walled needle or an over the needle
catheter. Once the free flow of blood is achieved through
the needle or catheter a guidewire is threaded through the
needle or catheter into the vessel and the small gauge
needle or catheter is withdrawn over the guidewire while
30
the guidewire is held in place. A large catheter or a catheter

introducing sheath is then passed over the guidewire into
the vessel and the guidewire is withdrawn. If the catheter
introducing sheath is used both the sheath and the dilator
are then removed simultaneously, leaving the sheath in the
large vein.
SitesFemoral Vein
Femoral vein is used most frequently during emergency
because it is relatively easy to access with lower rates of
complications. Leg is restrained with slight external rotation.
The femoral artery is identified by palpation of the femoral
artery. If pulses are absent, the mid point of anterior superior
iliac spine and the symphysis pubis is taken. After
scrubbing, cleansing and anesthetizing the skin flush the
needle, syringe system and catheter with sterile saline. The
thin walled needle or over the needle catheter is introduced
one fingers breadth below the inguinal ligament just medial
to the femoral artery. Gentle pressure is applied with an
attached 3 ml syringe and slowly the needle is advanced
with direction towards umbilicus at 45 angle. Once a free
flow of blood is achieved the syringe is disconnected and
a guidewire is advanced through the needle during a
positive pressure breath or spontaneous exhalation. Remove
the needle over the guidewire leaving the guidewire in
position. Then pass a catheter or catheter introducing
sheath over the wire. Advance the catheter in to the inferior
vena cava to the right atrium. The guidewire may then be
removed. Secure the catheter or introducer in place with
suture material or tape and attach the infusion set. A sterile
occlusive dressing is applied to the catheter insertion site.
VASCULAR ACCESS
31
A chest radiograph is taken to verify that the catheter tip

is correctly placed at the inferior vena cava right atrial
junction. After introducing the needle if no free flow of blood
through the needle occur, with gentle aspiration slowly
withdraw the needle and syringe so that it may unkink a
vessel which has become kinked during the entry.
External Jugular Vein
External jugular vein is actually a peripheral vein with an
excellent portal to the central venous circulation. It is tried
when other peripheral venous access is unsuccessful. Not
preferred much in CPR because it requires extension and
rotation of neck. Child is restrained in 30 head down
(Trendlenberg) position with the head turned away from
the side to be punctured, right side is preferred for better
access. After cleansing and anesthetising the skin, the
saline flushed needle is used to puncture the skin slightly
distal to or to one side of the visible external jugular vein
with a 16 or 18 gauge needle to facilitate entry of the
catheter through the skin. Do not enter the vein with the
needle. Temporarily occlude the vein just above the angle
of the mandible by applying gentle pressure with the tip
of the long finger of the non-dominant hand to mimic the
effect of a tourniquet. Stretch the skin over the vein just
below the angle of the mandible using thumb of the nondominant hand to immobilize the vein after allowing it to
distend fully. If peripheral cannulation desired, insert a
short length over the needle catheter. If central venous
cannulation is desired, insert a long length through the
needle catheter or catheter-over-guidewire and proceed as
for any central venous cannulation.
32
Arterial Access
Arterial catheters are extremely useful for patient
monitoring, for monitoring blood pressure and blood
sampling. But their use is associated with complications
including local and systemic infection, air or particulate
embolization, thrombosis of artery with associated ischemia
and growth failure in the affected limb.
Sites
Radial, brachial, axillary, femoral, dorsalis pedis and
posterior tibial arteries can be used but radial and femoral
arteries are the preferred sites of cannulation.
TechniqueRadial Artery
Collateral circulation to the hand may be evaluated before
radial artery cannulation is done with modified Allens test
or Doppler flow evaluation. Regardless of the method of
evaluation of collateral flow before cannulation, it is
imperative that hand circulation is closely monitored
following radial artery catheterization. If any evidence of
hand ischemia is observed, the catheter should be removed.
Cannulation of radial artery is done as follows. Hand
is dorsiflexed at wrist 45 to 60 and secure both the hand
and the lower forearm to a board. Dorsiflexion is
maintained by a roll of gauze placed behind the wrist.
Tape the hand down, leaving all fingers exposed so that
perfusion of the hand can be assessed. Thumb may be
taped aside to prevent movement during attempts at arterial
cannulation. Radial pulse is located. After sterile precautions, anesthetize the skin with 1% lidocaine. Puncture the
skin at the site of maximal pulsation with a 20 gauge
VASCULAR ACCESS
33
needle. Advance a 20-24 gauge heparin flushed catheter

at 30 angle and advance till the blood appears in the hub.
Two techniques are frequently used. Pass the catheter
and the needle through the artery to transfix it. Withdraw
the catheter very slowly until there is a free flow of blood.
Advance the catheter slowly through the lumen of the
artery.
Puncture only the anterior wall of the artery, advance
the catheter slowly until blood appears in the needle.
Lower the needle carefully to a 30 angle. Ascertain that
blood flow is continuing and advance the catheter slowly
over the needle into the lumen of the artery.
Remove the needle and attach the catheter to a T connector to permit continuous infusion of heparinized saline
1-5 units/ml. Apply sterile dressing and tape the puncture
site. Remove the gauze roll and secure the wrist in a neutral
position. Label the arterial line so as to prevent accidental
administration of drugs through it. Catheter should be
removed immediately if any evidence of ischemia is
developing and microvascular surgeon is to be consulted.
Modified Allens Test
Compress or clench the childs hand several times. Elevate
the hand above the heart and compress or clench the hand
tightly. Occlude both ulnar and radial artery and lower the
hand to the level of heart open the hand but do not hyperextend the fingers. Release pressure over the ulnar artery.
If color returns to hand within 6 seconds while radial artery
is occluded, the Allens test is negative and radial catheterization can be done because the flow through ulnar artery
and palmar arch is adequate when the radial artery is
occluded.
CHAPTER 4
Oxygen Therapy
36
Oxygen therapy is very important in the management of

critically ill children. Oxygen is a drug which is to be used
judiciously. Patients on oxygen needs close monitoring.
Reduced oxygen content of blood is hypoxemia and
impaired oxygen utilization is hypoxia. If spontaneous
ventilation is effective oxygen may be administered via a
number of delivery systems determined by the childs
clinical status and desired concentration of oxygen.
OXYGEN DELIVERY SYSTEMS
The oxygen delivery systems can be of two types.
Low Flow Systems
The low flow system provides an FiO2 that varies with the
patients inspiratory flow. Here the room air is entrained.
The low flow system is often insufficient to meet all
inspiratory flow requirements. They can provide an oxygen
concentration of 23 to 90% although not reliably.
High Flow Systems
The high flow system provides a specific FiO2 at flows that
meet or exceed patients inspiratory requirements.
Oxygen Mask
The simple oxygen mask is a low flow device that delivers
35-60% oxygen with a flow rate of 6-10 l/minute. The
inspired oxygen concentration can be increased only
modestly (up to 60%) because the inspiratory entrainment
of room air occurs through exhalation ports in the sides
of the mask and between mask and the face. Oxygen
concentration delivered to the patient will be reduced if the
OXYGEN THERAPY
37
patients spontaneous inspiratory flow requirement is high,

the mask is loose or the oxygen flow into the mask is low.
A minimum oxygen flow of 6 l/min must be used to
maintain an increased inspired oxygen concentration and
prevent rebreathing of exhaled carbon dioxide.
Partial Rebreathing Mask (Fig. 4.1)
Consists of a simple face mask with a reservoir bag. It
reliably provides an inspired oxygen concentration of 5060%. During exhalation the first third of the exhaled gases
flows into the reservoir bag and combines with fresh
oxygen. Since the initial portion of the exhaled gas remains
in the upper airway and is not involved in respiratory gas
exchange during prior breath it remains oxygen rich.
During inspiration the patient draws gas predominantly
from the fresh oxygen inflow and from the reservoir bag,
so entrainment of room air through the exhalation port is
minimized. Rebreathing of exhaled carbon dioxide from the
mask is prevented if the oxygen flow rate into the bag is
consistently maintained above the patients minute
ventilation. If the oxygen flow rate is sufficient and the
mask fit secure, the reservoir bag will not empty completely
Fig. 4.1: Partial rebreathing mask
38
during inspiration. An oxygen flow rate of 10-12 l/min

generally is required.
Non-rebreathing Mask
Consists of a face mask and reservoir bag with the
following additions.
1. A valve is incorporated into the exhalation port to
prevent entrainment of room air during inspiration.
2. A valve is placed between the reservior bag and the
mask to prevent flow of exhaled gas into the bag. On
inspiration the patient draws 100% oxygen flow.
Oxygen flow into the mask is adjusted to prevent
collapse of the bag. An inspired oxygen concentration
of 95% can be achieved with an oxygen flow of
10-12 l/min and the use of a well sealed mask.
Venturi Mask
This is designed to reliably and predicably provide
controlled low to moderate (25-60%) inspired oxygen
concentrations. Venturi valves deliver air oxygen mixture
at high flow rates the ratio of which will not varry at any
point of time and thus fixed FiO2 is delivered to the patient.
They are advantageous because humidification may not
be necessary as a much greater air flow than oxygen is there
resulting in the delivery of essentially room air humidity.
Moreover it is economical and cheap.
Face Tent (Fig. 4.2)
A face tent or face shield is a high flow soft plastic bucket
often better tolerated by children than a face mask. Even
with a high oxygen flow (10-15 l/min) stable inspired
OXYGEN THERAPY
39
Fig. 4.2: Face tent
oxygen concentration greater than 40% cannot be reliably

provided. An advantage of the face tent is that it permits
access to the face (e.g. suctioning) without interrupting the
oxygen flow.
Oxygen Hood (Fig. 4.3)
An oxygen hood is a clear plastic shell that encompasses
the patients head. It is well tolerated by infants, allows easy
access to the chest, trunk and extremities, permits control
Fig. 4.3: Oxygen hood
40
of inspired oxygen concentration, temperature and

humidity. A gas flow rate equal to or greater than
10-12 l/mt maintains an inspired oxygen concentration of
80-90%. The hood is usually not large enough to be used
for more than 1 year old.
Oxygen Tent
It is a clear plastic shell that encloses the childs upper
body. It can be used to deliver more than 50% oxygen with
high flows but cannot reliably provide a stable inspired
oxygen concentration. Room air is entered into the tent
whenever the tent is entered and the inspired oxygen
concentration falls. The tent limits access to the patient
when humidified oxygen is used the mist limits observation
of the patient. In practice it does not provide greater than
30% concentration of inspired oxygen.
Nasal Cannula
Simple low flow oxygen delivery device suitable for infants
and children who require only minimal amounts of
supplemental oxygen. The cannula contains two short
plastic prongs arising from a hollow face piece. The prongs
are inserted into the anterior nares and oxygen is delivered
into the nasopharynx. The inspired oxygen concentration
cannot be reliably be determined because it is influenced
by other factors including nasal resistance, oropharyngeal
resistance, inspiratory flow rate, and tidal volume. A high
oxygen flow rate (>4 l/min) irritates the nasopharynx and
may not appreciably improve humidified oxygen.
OXYGEN THERAPY
41
Nasal Catheter
It is a flexible, lubricated catheter with multiple holes in
the distal 2 cm. The catheter through one nostril is
advanced into the pharynx behind the uvula.
This method is discouraged because it has no advantage
over the nasal cannula and it may cause trauma to
adenoids, gastric distension if inadvertently placed in the
esophagus.
AIRWAYS
Oropharyngeal Airway
It consists of a flange, a short bite block segment and a
carved body made of plastic. The carved body is designed
to fit over the back of the tongue to hold it and the soft
hypopharyngeal structures away from the posterior
pharyngeal wall. This is indicated in an unconcious infant
or child if the procedures to open the airway fail to provide
and maintain a clear airway.
Airway sizes differ from 4-10 cm in length. (Guedels
sizes 0000-4). The proper size is estimated by placing the
oropharyngeal airway next to the face with the flange at
the corner of the mouth, the tip of the airway should reach
the angle of the jaw. It is not of correct size whether large
or small will result in airway obstruction.
Nasopharyngeal Airway
It is a soft rubber or plastic tube that provides a conduit
for airflow between the nares and posterior pharyngeal
wall. They are available in sizes 12F to 36F. 12F corresponds approximately to the size of 3 mm endotracheal
tube and will generally fit to a newborn baby. The outside
42
airway diameter should not be so large as to cause

sustained blanching of alae nasi. The proper length is
approximately equal to the distance from the tip of the nose
to the tragus of the ear.
Management of Respiratory Failure or Arrest
As soon as respiratory failure or inadequate ventilation is
identified clinically or by blood gas analysis, rapid
initiation of assisted ventilation is the only appropriate
therapy.
BAG- VALVE-MASK VENTILATION
Ventilation Face Mask
A ventilation mask consists of a rubber or plastic body, a
standardized 15-22 mm connecting port and a rim or face
seal. Ideally the face mask should be transparent, permitting
the rescuer to observe the color of the childs lips and
condensation on the mask (indicating exhalation) and to
detect regurgitation (Figs 4.4 and 4.5). They are available
in variable sizes. The proper mask size is selected to
provide an air-tight seal. The mask should extend from the
bridge of the nose to the cleft of the chin, enveloping the
nose and mouth but avoiding compression of the eyes. An
airtight seal is essential for an effective ventilation.
Two hands must be used to provide bag-valve-mask
ventilation. The mask is held on the face with one hand
as a head tilt chin lift maneuver is performed. The other
hand compresses the ventilation bag. In infants and
toddlers, the jaw is supported with the base of the middle
or ring finger. In older children the fingertips of the third,
fourth and fifth fingers are placed on the ramus of the
mandible to the hold the jaw forward and extend the head.
OXYGEN THERAPY
43
Fig. 4.4: Bag and mask ventilation
Fig. 4.5: Proper area of the face for mask application
This creates a one handed jaw thrust maneuver. When two

rescuers are available one uses both hands to open the
airway and make an airtight mask to face seal while the
second rescuer compresses the ventilation bag.
A neutral sniffing position without hyperextension of
the head is usually appropriate for infants and toddlers.
Children older than 2 years may require some anterior
44
displacement of the cervical spine to obtain optimal airway

patency. This may be achieved by placing a folded towel
under the neck and head.
If the child demonstrates spontaneous ventilatory effort
and partial airway obstruction application of 5-10 cm H2O
continuous positive pressure (CPAP) via a face mask may
maintain adequate airway patency and oxygenation
without the need for assisted ventilation. This requires a
tight mask fit and a breathing circuit capable of delivering
CPAP.
Gastric inflation in an unconcious child can be
minimized by applying cricoid pressure (Sellick
maneuver). This occludes the proximal esophagus by
displacing the cricoid cartilage posteriorly, the esophagus
is compressed between the cricoid ring and the cervical
spine. Cricoid pressure is applied by the second rescuer
using a finger tip in infants and the thumb and index
finger in children. Excessive pressure must be avoided
because it may produce tracheal compression and
obstruction in infants.
Self Inflating Bag-valve Ventilation Devices
Self inflating bag-valve device with a face mask provides
a rapid means of ventilating a patient in an emergency.
The bag recoil allows the self inflating bag to refill
independent of inflow from a gas source. During inflation
the gas intake valve opens, entraining room air or
supplemental oxygen if a fresh oxygen inflow reservoir is
provided. During bag compression the gas intake valve
closes and a second valve opens to permit gas flow to the
patient. During patient exhalation, the bag outlet valve
OXYGEN THERAPY
45
(non-breathing valve) closes and the patients exhaled

gases are vented to the atmosphere to prevent rebreathing
and retension of carbon dioxide.
A self inflating bag-valve device delivers room air (21%
oxygen) unless supplemental oxygen is provided. At an
oxygen inflow of 10 l/min, pediatric self inflating valves
without oxygen reservoirs deliver 30-80% oxygen to the
patients. Reservoir equipped bag-valve device can provide
oxygen concentration of 60-95%.
Before initiating ventilation the flow of oxygen to the
bag is to be confirmed by listening to the sound of oxygen
flow. Many self inflating bags are equipped with a pressure
limited pop off valve set at 35-45 cm H2O to prevent
barotrauma. Bags used for resuscitation should have no
pop off valve or one that is easily occluded since pressures
required for ventilation during CPR may exceed the pop
off limit, particularly during bag-valve-mask ventilation.
The bag-valve device must be appropriate to patient size
and condition. When assisted ventilation is provided the
administered tidal volume should be approximately 10-15
ml/kg. Neonatal size (250 ml) are usually inadequate to
support effective tidal volume and even in infants it should
have a minimum of 450 ml.
CPAP
It is a simple way of improving the oxygenation in patients
with normal ventilatory activity.
CPAP improves oxygenation by
1. Increasing the FRC and thus reducing the work of
breathing.
46
2. Increasing static compliance of lungs. Recruiting the

alveoli for gas exchange.
3. Improving ventilation perfusion relationship.
CPAP can be given
Without intubation
a. Nasal prongs
b. Nasopharyngeal catheters
c. Tightly fitting mask
With intubation
a. With ventilator
b. Without ventilator
CPAP partially obstruct the expiratory flow and thus
prevent the complete collapse of lung at the end of
expiration. Simple devices can be made from a bottle with
a glass tube immersed in it for the intended depth to deliver
the desired CPAP.
Patient is weaned from CPAP at a point when the
patient maintains adequate saturation on FiO2 of 30%.
Then the CPAP is reduced slowly.
Endotracheal Airway
Ventilation via an endotracheal tube is the most effective
and reliable method of assisted ventilation.
Endotracheal Tube
The basic design of the endotracheal tube is standardized.
The connector fits into the tube at the proximal end with
a standard 15 mm outside diameter permitting connection
to the mechanical ventilator circuit, bag-valve-mask device
or anesthesia devices. The tube body has a standard
OXYGEN THERAPY
47
curvature with markings that allows determination of the

depth of insertion. The distal tip has a bevelled edge and
in murphy type there is a hole just opposite the bevelled
edge- the murphys eye. This allows ventilation even when
the bevelled edge is blocked. A vocal cord marker may also
be present at the level of glottic opening to endure that the
tip of the tube is in the mid tracheal position. Cuffed
endotracheal tubes are used in children older than 8-10
years and adults. The normal anatomic narrowing at the
level of the cricoid cartilage provides a functional cuff in
children younger than 8 years.
Size of the Endotracheal Tube
3-3.5 mm internal diameter - newborns.
4 mm - 1year 5 mm - 2 years
Above 2 years
Age (yr)
Endotracheal tube =
+4
4
or the size of the 5th finger of the baby, roughly.
Depth of Insertion
(alveolar edge to mid trachea)
Older than 2 years of age.
Age (yr)
+ 12
2
Another calculation is by using the internal diameter
of the tube.
Depth of insertion is internal diameter 3 in cm.
Oral intubation is preferred in emergency as it is easier
to insert.
48
Preparation and Technique of Intubation

Before intubation, ventilation should be provided by bagvalve-mask device using 100% of oxygen. Monitoring of
heart rate and oxygen saturation by pulse oximetry should
be performed because ventilation may be interrupted
during intubation. Intubation attempts should be brief and
if longer than 30 seconds patient may be provided
ventilatory support with bag and mask.
Intubation should be done with direct laryngoscopic
examination. Heart rate is to be continuously monitored
during the procedure. In the incidence of reflux bradyarrhythmia atropine 0.02mg/kg may be given IV during
intubation in a spontaneously breathing child. However in
an emergency, intubation should be done without atropine
in order to avoid delay in intubation. Continuous evaluation
of oxygen saturation monitoring is important if the heart rate
response to hypoxemia has been blunted with atropine.
The laryngoscope handle is held in the left hand, and
the blade is inserted into the mouth in midline following
the natural contour of the pharynx to the base of the
tongue. Once the tip of the blade is at the base of the tongue
and the epiglottis is visualized, the proximal end of the
blade is moved to the right side of the mouth sweeping the
tongue toward the middle. Alternatively the blade may be
inserted in the right side of the mouth to the base of the
tongue. Once the epiglottis is visualized, the proximal end
of the blade and the handle are swept to the midline. This
movement toward the midline provides a channel in the
right third of the mouth through which the endotracheal
tube will be passed while direct visualization of the
laryngeal structures is maintained.
OXYGEN THERAPY
49
Either a curved or straight blade may be used for

intubation of children. The tip of the curved blade is
inserted into the vallecula to displace the tongue anteriorly.
With the straight blade, the tip of the blade is used to lift
the epiglottis and visualize the glottic opening. The tip
should rest beyond the vallecula. Then traction is exerted
upward in the direction of the long axis of the handle to
displace the base of the tongue and the epiglottis anteriorly
exposing the glottis. To avoid visual obstruction of the
glottic opening, by the endotracheal tube, the ETT is
inserted from the right corner of mouth not down the barrel
of the lanyngoscope blade. In this way the rescuer will
be able to see the ETT as it passes through the glottic
opening.
It will be helpful if an assistant can displace the corner
of the mouth to the right so as to enable the visualization
of the passage of ETT through the glottic opening.
Application of pressure at the cricoid also can facilitate
visualization of glottic opening. The black glottic marker
of the ETT is placed at the level of the vocal cord so that
the tip of ETT is in mid tracheal position. Immediately after
intubation, the position of the ETT is clinically assessed
by observation of chest movements and auscultation of the
chest. If not in the right position tube is to be removed,
patient is stabilized with bag and mask ventilation and
then intubation is re-attempted. After intubation, the ETT
should be secured to the patients face to prevent
unintentional extubation. Before ETT is taped, correct
position is confirmed once again. The distance marker at
the lips should be noted to allow detection of unintentional
extubation.
50
Complications Associated with Endotracheal

Intubation
During the intubation procedure
Vomiting with possible aspiration

Trauma - laryngeal, pharyngeal, tracheal and dental
Bradycardia caused by vagal stimulation
Hypoxemia caused by delay in procedure
Cardiac arrhythmias
Right mainstem intubation
Esophageal intubation
While the Tube is in Place
Tube malpositiontoo high, too low

Right mainstem intubation
Laryngeal or tracheal erosion, necrosis
Pharyngeal edema
Mouth lip or nares pressure sore development
Inadequate ventilation or oxygenation as a result of tube
obstruction or kinking
Loss of cuff integrity
Self extubation
Aspiration
Sinusitis/otitis media.
CHAPTER 5
IV Fluid Therapy
52
Proper maintenance of fluid and electrolytes is very

important in the supportive care of critically ill children.
Even when they dont have any changes in fluid and
electrolytes they may have to be supported with the
maintenance therapy for a few days in the intensive care
setting.
Maintenance of Water
The total body water content in an average adult or
adolescent is about 60% of body weight and in a newborn
it is as high as 80% of body weight. The total body water
is distributed in the body in two major compartments, the
extracellular fluid and the intracellular fluid.
Two-third is in the intracellular compartment and 1/
3 is in extracellular compartment. ICF is rich in potassium
and ECF is rich in sodium. The maintenance fluid therapy
has to take into consideration the insensible fluid loss
which is usually lost through skin, respiratory tract and
kidneys. The basic principles of parenteral fluid therapy
were laid by Holliday and Segar in 1957. It should contain
5% dextrose to minimize the endogenous breakdown of
proteins and fats thus preventing formation of ketones. It
should also contain sodium and potassium (3 mEq/kg/
day and 2 mEq/kg/day respectively).
Maintenance Fluid and Electrolytes
Body wt Water
Na
K
Glucose
0-10 kg 100 ml/kg/day 3 mEq/kg/day 2 mEq/100 ml 5 gm/100 ml
11-20 kg
1000 ml + 50 ml/kg
20 ml/kg for each kg above 20 kg
1500 + 20 ml/kg
IV FLUID THERAPY
53
Rate of Fluid Infusion

1000 ml in 24 hrs. Roughly 40 ml/hr or 4 ml/kg/hr. For
microdrop set 1ml = 60 micro drops and conventional IV
set. 1ml - 15 drops.
Maintenance fluid has to be modified in certain clinical
situations.
Increased Requirement
1.
2.
3.
4.
5.
Radiant warmer (20 ml/kg/day)

Phototherapy (20 ml/kg/day)
Fever 10-15% for each 1 C above normal
Tachypnea
Bypassing upper airways
Decreased Requirement
1. Increased ambient humidity
2. Humidification of inhaled gases.
Most of the commercially available maintenance fluids
are approximately 1/6th saline having 25 mEq/1000 ml.
There is an increasing concern over development of
hyponatremia especially in older age groups.
Administration of parenteral fluids has its own
deleterious effects on health and so as far as possible
enteral fluids are to be preferred and IV fluid therapy
should be as short period as possible and those on IV fluids
should be closely monitored. Younger babies need more
careful monitoring.
54
IV FLUIDS IN SPECIFIC SITUATIONS

Acute Diarrheal Disease
IV fluids are indicated only if the child is having:
1. Severe dehydration
2. Severe purging - purging more than 3 times/hour or
if fluid lost is >15ml/kg stools
3. Persistent vomiting - more than 3 times/hour
4. Abdominal distension
5. Associated illnesses
6. Severe dyselectrolytemia
Fluid preferred is Ringers lactate or 1/2 Darrow
solution. If both are not available N. saline may be used.
Amount of fluids for a chlid with severe dehydration:
30 ml/kg
70 ml/kg
<12 months
1 hour
5 hours
>12 months
1/2 hours
21/2 hours
DYSELECTROLYTEMIAS
Hyponatremia
Commonest electrolyte disturbance in critically ill children.
It is defined as S. sodium less than 135 mEq/L.
Causes
Can be due to loss of sodium (hypovolemia).
Renal Losses
Diuretics
Recovering ATN
Congenital adrenal hyperplasia
Adrenal insufficiency
IV FLUID THERAPY
55
Hypoaldosteronism
Bartters syndrome
Extrarenal
Gastrointestinal- ADD
Excessive sweating
Gain of Water (Hypervolemic hyponatremia)
Nephrotic syndrome
Cirrhosis liver
CCF
ARF, CRF
Gain of Water (Euvolemic hyponatremia)
Pain, stress, anxiety, drugs
Hypothyroidism, Cortisol deficiency , SIADH.
Pseudohyponatremia
Methodology dependent artifact when serum sodium is
estimated by flame emission spectrometry which measures
sodium in total serum. When the serum solids are increased
as in hyperlipidemia or hyperproteinemia the serum
sodium appear low. When serum sodium is measured by
ion specific electrode, measurements are made directly in
the fluid compartment of serum which gives the correct
measurement of sodium.
Factitious Hyponatremia
Presence of osmotically active particles (e.g. glucose) rises
the serum osmolality and so water is drawn from ICF to
ECF and thence the S. sodium becomes low.
56
In pseudohyponatremia the serum osmolality is

normal. In factitious hyponatremia the serum osmolality
is high. In other causes, hyponatremia is associated with
hypoosmolality.
Symptoms of hyponatremia are non-specific and may
simulate a primary neurologic disorder. A high index of
suspicion is necessary to detect hyponatremia in a critically
ill child.
Differential diagnosis of hyponatremia can be done by
estimating the urine sodium.
Hypovolemic
U Na <20 mEq
Extrarenal
U Na>20
Renal
CAH
Euvolemic
Hypervolemic
U Na >20
Drugs
Hypothyroidism
Glucocorticoiddeficiency
Pain
SIADH
U Na <20
N syndrome
Cirrhosis
CCF
U Na >20
ARF
CRF
Treatment
Whatever be the type or cause of hyponatremia serum
sodium above 130 mEq/L is usually asymptomatic and no
treatment is necessary. When serum sodium falls rapidly
to 125 mEq/L or less cerebral edema can occur and CNS
symptoms can occur. The child is to be treated with
hypertonic saline, 3% NaCl 10-12 ml/kg over a period of
2-4 hours (1 ml NaCl= 0.5 mEq Na). Once the acute
symptoms are controlled further correction is done
gradually over a period of 48 hours. The sodium required
is calculated as per the formula.
0.6 body weight (135 measured serum sodium)
135 is the expected serum Na
IV FLUID THERAPY
57
This should be given over 48 hours. Serum sodium is

to be increased at a rate 0.5 mEq/L per hour or not more
than 12 mEq/day
Hypovolemic Hyponatremia
Hypovolemia is corrected with the bolus of 20 ml normal
saline. After the serum sodium concentration has been
corrected to approximately to 125 mEq/L the rest of the
deficit should be corrected slowly in 18 to 36 hours. The
fluid to be given is determined on the basis of water deficit.
The water deficit is decided by the weight loss or by
assessing the level of dehydration by the clinical signs. 10%
dehydration in a 10 kg child would mean a water deficit
of 1000 ml.
Hypervolemic Hyponatremia
Occurs due to water gain and in fact total body sodium
is high despite the low serum sodium. Administration of
sodium may worsen edema and may result in fluid
overload. The treatment would consists of fluid restriction.
Fluids given should be less than the total amount of
insensible water loss and urine output. The fluid excess
can be calculated as follows.
TBW (1 measured sodium/expected sodium)
Fluid restriction will slowly correct the hyponatremia.
In addition, furosemide if given will correct the hyponatremia more rapidly.
Euvolemic Hyponatremia
Most common condition is SIADH. Restrict the fluids to
insensible water losses. Fluid replacement is done with
58
isotonic saline. Furosemide is administered to improve free

water clearance. If serum sodium is less than 120 mEq/
L and accompanied by CNS symptoms, administration of
3% NaCl is given.
In slowly developing hyponatremia CNS cells adapt to
the hypotonic milleu. The cells do so by extruding
osmotically active particles and lowering the intracellular
osmolarity. If the serum sodium level is corrected rapidly,
the ECF tonicity becomes normal but since Na cannot enter
the cells the ICF is unable to increase its tonicity rapidly.
This osmotically challenged cells undergo osmotic
demyelination and can result in psuedobulbar palsy,
quadriparesis and even death. The changes in autopsy or
MRI are seen as central pontine myelinolysis. Therefore
unless symptomatic, hyponatremia should be corrected
gradually, not more than 12 mEq/L day.
Hypernatremia
Serum sodium level above 150 mEq/L is hypernatremia.
It is rare compared to hyponatremia. It is often due to
increased free water loss or due to a true gain in sodium.
Often occurs in infants with ADD especially when they
are offered high solute containing fluids like inappropriately prepared ORS, salted kanji water or when large
amounts of fluids are given IV as Ringers lactate. Extremely
premature babies who have large insensible water losses
through immature skin can develop hypernatremia.
Exclusively breast fed infants when there is lactation failure
or in hot weather can develop hypernatremia. Central or
nephrogenic diabetes insipidus can result in excessive
water loss and result in hypernatremia.
IV FLUID THERAPY
59
Accidental or intentional salt poisoning, sea water

drowning, administration of hypertonic saline or sodium
bicarbonate are other causes.
Marked thirst and irritability inappropriate for other
signs of dehydration are the characteristic features in
infancy. Other CNS symptoms can follow.
The cause of hypernatremia can be made out by clinical
evaluation with specific attention to the volume status,
urine output, urine osmolality and specific gravity.
S. sodium >150 mEq/L with dehydration
Urine output >3 ml/kg/hour Urine output decreased
Sp gravity < 1005
Sp gravity >1020
Urine osmolality < 200
Diarrhea
Diabetes Insipidus
VLBW
Lactation failure
S. sodium >150 mEq/L with overhydration
Urine output normal or high
Urine Na high
Salt poisoning
Excess hypertonic saline or soda bicarb
Treatment
The more common problem is hypovolemic hypernatremia
or hypernatremic dehydration which is due to free water
deficit. Correction should be done by slow rehydration. The
fluid deficit should be corrected in 48 hours or longer. The
volume of fluid to be given is 2 maintenance fluid +
calculated deficit to be given equally spread over 48 hours.
No fluid bolus unless the child is in shock. The free water
deficit can be calculated as:
60
Free water deficit = 0.6 Wt (S. sodium expected

sodium) 1 l
This deficit is pure water. In diarrhea there will be
sodium losses also. So the total free water deficit can be
calculated and the rest of the fluid can be given as isotonic
saline. Since the total sodium lost is very little the total
calculated fluid can be given as 0.2 N saline also. The rate
of fall of sodium should not be not more than 0.5 mEq/
L/hr or not more than 12 mEq/L/day.
A sudden fall in S. sodium is to be avoided as this can
result in several complications. If the serum sodium is
lowered rapidly, the serum osmolality, and tonicity gets
lowered rapidly. To protect the cell from shrinkage cells
generate idiogenic osmoles to maintain osmotic
equilibrium. During correction of hypernatremia the cells
are unable to dissipate these idiogenic osmoles rapidly. As
the intracellular osmolality is high water moves to the cells
leading to cerebral edema, which can result in seizures,
respiratory and pupillary irregularities and even death.
This may even necessitate infusion of 3% NaCl to prevent
rapid fall in serum sodium. Rapid correction of hypernatremia again result in extrapontine myelinolysis as evidenced by MRI. Hyperglycemia is frequently encountered
in hypernatremic dehydration as the high serum sodium
has an inhibitory effect on insulin secretion. Insulin should
not be given as this will worsen cerebral edema. Glucose
in IV fluids can be reduced to 2.5% or patient is allowed
free water orally by nasogastric tube as hourly instalment
to prevent worsening of hyperglycemia.
In polyuric children with DI the concentration of fluid
administered should not exceed 0.2 DNS. The total fluid
for 24 hours should include.
IV FLUID THERAPY
61
Maintenance fluid + 1/2 deficit + hourly replacement

of urinary losses.
The deficit can be given as free water orally or by
nasogastric tube as infusion or hourly instalment. Central
D1 needs vasopressin as specific therapy. When the
response to vasopressin occurs (Urine output < 2ml/kg/
hour) the administration of hypotonic fluids should be
limited to prevent hyponatremia.
Hypokalemia
is defined as serum potassium of < 3.5 mEq/L.
Can occur in.
PEM
GI losses in diarrhea or vomiting
Ketonuria
RTA
Bartters syndrome
Steroid therapy
In these conditions, total body potassium also is low.
Hypokalemia without decrease in body potassium can
occur due to transcellular shift of potassium as in
Administration of glucose
Insulin
Catecholamines
Bicarbonate
Clinical history along with analysis of urine
potassium, acid base balance and urine chloride gives the
right diagnosis.
62
Urine K < 20 mEq/L

Low BicarbonateDiarrhea
High BicarbonateVomiting
Urine K > 20 mEq/L
Low BicarbonateRTA
Urine K > 20 mEq/L, Urine Cl < 10 mEq/L
Vomiting
Urine K > 20 mEq/L, Urine Cl > 10 mEq/L
Diuretics
Bartters syndrome
Mg depletion, Extreme K depletion
Treatment
Hypokalemia need to be corrected slowly, orally if feasible.
If given IV it should be diluted and given with fluids, upto
40 mEq/L. Up to 80 mEq/L can be given if required under
continuous ECG monitoring in ICU set up. One ml KCl
yields 2 mEq of potassium. Rapid correction may be
necessitated in severe hypokalemia resulting in cardiac
arrhythmias, bradycardia, slow respiration and severe
muscular weakness where 0.5 to 1 mEq/kg can be given
suitably diluted over 1 hour with continuous ECG
monitoring. Should never be given as a bolus.
Persistent hypokalemia should arouse suspicion of
hypomagnesemia. In co-existant hypocalcemia and
acidosis correction should be deferred since bicarbonate
can still lower serum potassium and administration of
calcium can precipitate cardiotoxicity.
IV FLUID THERAPY
63
Hyperkalemia
Defined as serum potassium more than 5 mEq/L.
Causes
Often renal as kidney is the main route of excretion of
potassium- Renal failure.
Drugs like ACE inhibitors
Aldosterone antagonists
Adrenal insufficiency
Transcellular shifts of potassium from ICF ECF
occurs in acidosis, blockers
Crush injuries, burns
Spurious hyperkalemia occur during excessive pressure
of tissues during the collection of blood.
Mild hyperkalemia
K level is < 6.5 mEq/L No ECG changes.
Moderate
K levels 6.5 mEq/L ECG changes -peaking of T waves.
Severe
K levels >8 mEq/L or regardless of plasma K levels ECG
shows. Widened QRS complexes, flattenig of p waves or
ventricular arrhythmias.
Treatment
Measures aims at:
Shift of potassium into cells
Antogonism of effects of potassium
Removal of potassium from body.
1. Sodium bicarbonate 2 mEq/kg IV diluted and as a rapid
push in 3 to 5 minutes
64
2. Calcium gluconate 10% 0.5 to 1 ml/kg IV as a rapid

push over 3 to 5 minutes
3. Glucose 0.5 to 1 gm/kg IV over 30 minutes
accompanied by regular insulin 0.1 to 0.2 u/kg
4. Na/K cation exchanger orally or as a retention enema
over 30 to 45 minues.
Finally, if these measures fail or because of accompanying renal failure, peritonial or hemodialysis must be
instituted.
Hypocalcemia
Defined as total serum calcium less than 8.5 mg/dl in
children, less than 8 mg/dl in term neonates and less than
7 mg/dl in pre term babies. Cause of hypocalcemia varry
with age. In children the causes are:
Vitamin D deficiency
Pancreatitis
Hypoalbuminemia
Hungry bone syndrome
Alkalosis
Hypophophatasia
Hypoparathyroidism
Renal failure
Malabsorption syndrome
Treatment
Asymptomatic hypocalcemia is treated with oral Ca. 100200 mg/kg/day of elemental Ca as calcium gluconate or
carbonate. Vitamin D supplements may be required in
patients with renal disease and vitamin D deficiency states.
In critically ill patients IV calcium is given as 10%
calcium gluconate in a dose of 1-2ml/kg IV over 3-5 minute
upto a total of 10 ml with cardiac monitoring. Calcium
gluconate contains 9.8 mg/ml or 0.45 mEq/ml of elemental
IV FLUID THERAPY
65
calcium. Calcium chloride 10% contains 27mg/ml and so

is more irritating to the veins. The bolus can be followed
by 100-200 mg/kg of IV calcium gluconate infusions over
24 hours in children. If magnesium is low, 50% magnesium
sulfate may be given as 0.1 - 0.2 ml/kg IM every 12-24
hours as needed.
Hypercalcemia
Defined as S. calcium levels >12mg/dl. It is rare as
compared to hypocalcemia.
Causes
Varry with age and in infants and children the causes are
Vitamin D excess.
Primary hyperparathyroidism
Idiopathic infantile hypercalcemia
Williams syndrome
Severe autosomal recessive hyperphosphatasia
Thiazide diuretics
Treatment
Primary line of treatment is to augment urinary losses of
calcium by saline diuresis coupled with IV furosemide.
1.5- 2 times the maintenance fluid requirement is given
with close monitoring of S. electrolytes and urine output.
If serum calcium is greater than 14 mg/dl calcitonin
2-4 units/kg every 6-12 hours may be used. Biphosphonates such as pamidronates at 0.5 to 1 mg/kg/dose
over 4-5 hours can be tried but rarely used in children. In
severe hypercalcemia dialysis is life-saving.
66
Hypomagnesemia
Defined as serum Mg < 1.8 mEq/L.
Causes
Diarrhea, nasogastric suction
IBD
Renal losses with drugs like
Thiazides
Loop diuretics
Aminoglycosides
Amphoterecin B
Poorly controlled diabetes, recovery of diabetic ketoacidosis.
Treatment
If mild and asymptomatic oral replacement with 10-20 mg/
kg/day of elemental magnesium in 3-4 divided doses is
enough. In symptomatic hypomagnesemia IV magnesium
can be given 1 mEq/kg over 2-6 hours on day 1 followed
by 0.5 mEq/kg over 2-4 hours for next 3 days. 50% Mg SO4
contains 4 mEq per ml (48 mg). The total replacement
recquired would be about 4 mEq/kg. Careful monitoring
of electrolytes and blood pressure is required during IV
magnesium infusion due to the chance of developing
hypotension, hypocalcemia and hypermagnesemia.
Hypermagnesemia
Is defined as serum magnesium levels above 2.5 mEq/L.
IV FLUID THERAPY
67
Causes
Patients in renal failure with excessive intake of Mg.
Trauma, shock, burns.
Initial dehyrated phase of DKA.
Treatment
IV calcium gluconate 1 ml/kg diluted is given slowly with
cardiac monitoring to antagonize the effects of Mg at the
cardiac membrane and neuromuscular level. When urine
output is good, saline diuresis can be given. Non Mg
containing enemas or cathartics may be given to enhance
GI clearance. In hypermagnesemia with S. Mg >8 mEq/L
dialysis is indicated and also in any patient with cardiovascular or neuromuscular effects of hypernagnesemia,
irrespective of the serum level.
CHAPTER 6
ABG Analysis
70
Knowledge of blood gas analysis is essential in critical care

management. Analysis is normally performed in the blood
obtained from the peripheral artery. Radial artery is the
commonly used one. After the Allens test, radial artery is
punctured and 2-3 ml of blood is taken in a 5 cc syringe
that is coated on the inside with 1:1000 solution of heparin.
0.05 ml of heparin is enough anticoagulant for 1 ml blood
and up to 0.1 ml for 1 ml of blood shall not interefere with
the blood gas values. It is to be immediately immersed in
ice to prevent the continued gas consumption of the blood
cells which can alter the values. The syringe to be used
should be made of glass since the air bubbles adhering to
the sides of the plastic syringe may increase the value of
oxygen. Heparin has high H+ ion concentration and so the
values can get altered if the amount of heparic used is
more.
Values Obtained
pHrepresents a measure of the overall acid-base balance.
PCO2represents arterial CO2 levels and thus gives a
measure of the ventilatory status.
PO2represents the oxygen tension in the arterial blood
and gives the oxygenation status.
HCO 3Base excess or deficit indicate the metabolic
component of acid-base status.
Normal Status
pH
PCO2
PO2
Saturation
Arterial
7.4
40 mmHg
97 mmHg
97%
Venous
7.37
45 mmHg
40 mmHg
75%
ABG ANALYSIS
71
>7.45 Alkalosis
<7.35 Acidosis
pH
PCO 2
PO2
Hypoxemia
Mild
Moderate
Severe
Normal
7.3-7.4
30-50 mmHg
>80 mmHg
range
7.35-7.45
35-45 mmHg
60-80 mmHg
40-60 mmHg
<40 mmHg
What are the steps in analyzing the values?

1. What is the overall acid-base status given by pHacidosis or alkalosis?
2. What is the ventilatory status given by the PCO2 and
oxygenation status given by PO2?
3. What is the metabolic status given by HCO3?
4. What is the problem?.
Acute? Compensated? Uncompensated?
Partially Compensated?
Simple? Mixed?
Chronic?
The primary alteration can be four types:
1. Acidosis
2. Alkalosis
Respiratory Acidosis
Respiratory Alkalosis
Metabolic Acidosis
Metabolic Alkalosis
Mixed disorders are those where there are more than
one primary disorder. A normal expected compensation in
a primary disorder does not make it a mixed disorder.
What is physiological compensation
respiratory acidosis?
In ventilatory failure respiratory acidosis occurs and there
is an increase in PCO2 due to inadequate CO2 wash out.
72
This is buffered initially by non bicarbonate buffers like

proteins in ECF and phosphate, hemoglobin and lactate
in the cells. If hypercapnea is sustained the renal
compensatory mechanism comes in to play resulting in.
1. Excretion and secretion of H+ ions.
2. Formation and excretion of ammonium ions.
3. Retension of bicarbonate ions and excretion of chloride
ions. An increase in bicarbonate is approximately the
same as the decrease in serum chloride and so there
is no change in anion gap.
Additionally, respiratory acidosis causes a shift of
electrolytes leading to a rise of serum potassium
concentration. This hyperkalemia may increase to toxic
levels to produce cardiac toxicity.
Many patients with respiratory acidosis may over
compensate leading to metabolic alkalosis associated with
hypokalemia which a may warrant therapy with potassium chloride
Examples
pH
7.25
PCO2
58 mmHg
HCO3
25 mEq/L
There is obvious acidemia, PCO2 levels are , but
bicarbonate is still low.
Impression
Simple respiratory acidosis with inadequate time for compensation or have a renal pathology. The compensatory
mechanisms take time to be effective. Respiratory responses
occur rapidly, 50% in 6 hours and 100% in 16 hours. Renal
mechanisms are slower and renal acid excretion is still
ABG ANALYSIS
73
slower compared to base excretion. 50% of base excretion

occurs in 8 hours and 100% in 24 hours whereas in renal
acid excretion 50% occurs in 36 hours and 100% occur in
72 hours. Renal compensation for respiratory alkalosis
occurs faster than for respiratory acidosis.
In the presence of a single acid-base disorder even after
compensation has occured pH will still be in the direction
of the primary disorder. A physiological compensation
never over compensates. So in such a case either the data
is wrong or it is a second primary acid-base disorder.
Example
pH
PCO2
HCO3
7.23
58 mmHg
17 mEq/L
Here the pH is acidic. There is CO2 retention. But

instead of expected high HCO3 there is low HCO3.
Impression: Mixed respiratory and metabolic acidosis.
There are certain rules for compensation by which we can
predict certain values and interpret the results.
Rule No I
An acute change in PCO2 of 10 mmHg is associated with
an increase or decrease of pH by 0.08 units. This is by
considering the normal pH as 7.4 and normal PCO2 as
40 mmHg. If the predicted pH is equal to the measured pH
it is respiratory in origin. If the measured pH is greater than
the predicted pH there is associated metabolic alkalosis
also and if less than the predicted value there is associated
metabolic acidosis.
74
Example
pH
7.26
50 mmHg
PCO2
Predicted pH for PCO2 of 50 is 7.32 but the actual pH
is 7.26 (less than expected). There is a deficit of 0.06 units
which is indicative of metabolic acidosis combined with
respiratory acidosis.
Rule No II
Helps us to estimate the magnitude of the metabolic
component. It says that the pH change of 0.06 units is as
a result of a base change of 0.67 mEq/L. So the base deficit
can be calculated by multiplying the difference with 0.67.
So 0.06 0.67 is roughly 4 mEq/L.
Rule No III
Helps in calculating the total base deficit. It is based on
the fact that HCO 3 is located in the extracellular
compartment which consists of 30% of body weight. So the
total base deficit is calculated by.
Base deficit (mEq/L) wt 0.3 in kg.
10 kg Child4 10 0.3 = 12 mEq.
Only half the calculated dose is to be given in 2-3 hours
Due to the detrimental effects encountered with
bicarbonate therapy (tetany, cardiac arrhythmias, intraventricular hemorrhage in newborn) base deficit is not
corrected until the serum bicarbonate value is < 10 mEq /L
or the pH is <7.2 unless there is cardiopulmonary instability.
In chronic acid-base disturbances the appropriate
compensation occurs and in long standing metabolic
ABG ANALYSIS
75
acidosis the normal expected degree of respiratory

compensation can be recognized by inspection of the last
2 digits of pH and PCO2. If the two digits are close, the
respiratory response is adequate.
pH
expected PCO2
7.25 25
7.3
30
7.35 35
In case of metabolic acidosis next thing to be done is
to look for the anion gap.
Anion gap = [Na + K] [Cl + HCO3]
Normal is 8-16 mEq/L
This represents the unmeasured anions which, along
with bicarbonate and chloride counter balance the positive
charges of Na and K.
Increased Anion Gap Acidosis
Diabetic Ketoacidosis
Lactic acidosis
Inborn errors of metabolism
Renal failure
Poisoning-alcohol, ethylene glycol, paraldehyde,
salicylates.
Normal Anion Gap Acidosis
Renal tubular acidosis
Carbonic anhydrase inhibitor
Chronic diarrhea.
How to determine whether there is coexistence of other
metabolic disturbances with an anion gap acidosis?
To find out this one has to determine if there is an
increase in anion gap and whether there is additional
76
variation in HCO3 existing. If no other metabolic disturbance exists the following calculation should result in
24 mEq/L.
Corrected HCO3= Measured HCO3 + (Anion gap 12)
If corrected HCO3 varries above or below 24 there is a
mixed or complex metabolic disturbance. To be more
specific, if the corrected HCO3 is more than 24 a metabolic
alkalosis coexists and if the corrected HCO3 is less than
24 a non-anion gap acidosis coexists.
E.g.: Corrected HCO3 = 10 + (26 12)
10 + 14 = 24
There is only anion gap metabolic acidosis.
The Practical Approach to Rapid Analysis of ABG
1. Look at pH
< 7.35 Acidosis

> 7.45 Alkalosis
Normal pH does not rule out an ABG disorder
2. Look at bicarbonate. Is it normal?
If bicarbonate is responsible for the pH change, the pH
will change in the direction of the change in
bicarbonate.
3. Look at PCO2. Is it normal?
If CO2 is responsible for the change in pH then the pH
will change in the opposite direction of the change in
PCO2. Increase in PCO2 will decrease pH and vice versa.
4. Now look for the compensation
Metabolic acidosis PCO2=1.5 [HCO3] + 8 + 2
Metabolic alkalosis PCO2 increases by 7 mmHg
for each 10 mEq/L increase in
the serum HCO3
ABG ANALYSIS
77
Respiratory acidosis: HCO3 increase by 1 for each

acute
10 mmHg increase in PCO2
Chronic
HCO3 increases by 3.5 for each
10 mmHg increase in PCO2
Respiratory alkalosis: HCO3 falls by 2 for each
acute
10 mmHg decrease in PCO2
Chronic
HCO3 falls by 4 for each
10 mmHg decrease in PCO2
Another method for looking for compensation is
Metabolic acidosis
Expected PCO2 = last 2 digits of pH
(If pH is 7.22 expected PCO2 is 22)
Metabolic alkalosis
PCO2 = rise of 6 mm per 10 mEq rise in Bicarbonate.
Respiratory acidosis
Acute:
For every rise of PCO2 by 10 mmHg pH fall by 0.08
Chronic:
For every rise in PCO2 by 10 mmHg pH fall by 0.03.
Respiratory alkalosis
Acute:
For every fall in PCO2 by 10 mmHg pH rise by 0.08
Chronic:
For every fall in PCO2 by 10 mmHg pH rise by 0.03.
Look for mixed disturbance
pH is normal and
Bicarbonate is high (Metabolic alkalosis + Respiratory
acidosis)
78
Bicarbonate is low (Metabolic acidosis + Respiratory

alkalosis).
Bicarbonate is low and anion gap is high (Metabolic
acidosis + Metabolic alkalosis).
Bicarbonate is low and pH acidic (Chronic respiratory
acidosis + Respiratory alkalosis).
Bicarbonate is normal and pH in alkalemic range
(Metabolic alkalosis + Metabolic acidosis)
pH is acidic, PCO2 , Bicarbonate (Respiratory
acidosis + Metabolic acidosis)
pH is alkalemic PCO2 Bicarbonate (Respiratory
alkalosis + Metabolic alkalosis)
In presence of predominent involvement of two systems,
often coupled with therapeutic intervention the patient may
present with acid-base disturbances both respiratory and
metabolic (e.g. respiratory acidosis and metabolic acidosis).
Additive disturbances are proven to be more fatal
compared to counter balancing ones (e.g. respiratory
acidosis with metabolic alkalosis).
Treatment
Respiratory Acidosis
Maintenance of ventilation and hemodynamic status is the
mainstay of treatment. Correction of the specific underlying
disorder also is essential. Alkali therapy is not indicated
unless the patient has severe hyperkalemia and ventricular
fibrillation.
Chronic respiratory acidosis per se does not require
specific therapy but hypoxemia must always be treated. If
chronic respiratory acidosis is over compensated then
metabolic alkalosis may occur and in such situation
patient may be treated with potassium chloride.
ABG ANALYSIS
79
Respiratory Alkalosis
Most common cause is functional hyperventilation. Other
causes are Gram ve sepsis, salicylate intoxication,
asphyxiants and cerebral diseases with involvement of
respiratory centre producing hyperventilation.
Treatment is to correct the underlying disorder. In
hyperventilation rebreathing into a bag will usually
terminate the attack.
Metabolic Acidosis
Look for anion gap. Wide anion gap means addition of an
acid load. Bicarbonate therpy is given when pH is < 7.2
after ensuring good perfusion and ventilation.
Metabolic Alkalosis
Classified according to urinary chloride.
Low urinary chloride (<10 mEq/L) Chloride responsive
Hypovolemic
Diuretic therapy
Nasogastric suction
Vomiting
Secretory diarrhea
High urinary chloride (> 20 mEq/L) normo or hypervolemic
Bartters syndrome, Cushings syndrome
Hyperaldosteronism, Potassium depletion
Alkali administration
Treat the underlying cause first and correct by normal
saline if indicated.
80
Anion Gap and Acidosis

Increased anion gap acidosis
DKA
Lactic acidosis
In born error of metabolism
Renal Failure
Normal anion gap

RTA
CA inhibitor therapy
Chronic Diarrhea
Wide Anion Gap Mnemonic

(MUDPILES, KUSMAL, MULIPAK)
Methanol, uremia, DKA, paraldehyde, infections, lactic
acidosis (from different causes), ethylene glycol, salicylates.
Normal Anion Gap
HCO3 loss diarrhea, small bowel damage, ureteroenterostomies, proximal RTA
HCO3 regeneration- distal RTA, hyperkalemic RTA,
CRF, adrenal insufficiency
Commonly used mnemonic ACCURED
Acid infusion, compensated respiratory alkalosis, CA
inhibitor, RTA, Ureteral divertion, Extra-alimentation,
hyperalimentation and diarrhea.
CHAPTER 7
Mechanical
Ventilation
82
Normal ventilation occurs when chest expands to create

a negative intrathoracic pressure. Air is then drawn in to
the lungs. Expiration is passive due to elastic recoil of lung
which expells air out. Intermittent negative pressure
ventilation (INPV) is the method which mimics
physiological ventilation. But this cannot be used in clinical
situations due to the cumbersome equipment and difficulty
in nursing the patient.
The method which is used in clinical situations is
intermittent positive pressure ventilation (IPPV). In IPPV
inspiration is accomplished by applying a positive pressure
to the upper airway to drive in air into the lungs. Expiration
is passive. So the airway pressure (Paw) is positive and
the mean intrathoracic pressure during IPPV is greatly
increased leading to adverse side effects on the
cardiovascular system and barotrauma on the airways and
lungs. Though unphysiological IPPV has become popular
because of its ease of clinical application.
Artificial Airways
Artificial ventilation for any length of time mandates the
use of artificial airways. This is to make the ventilation
optimal and also to protect the lung from the danger of
aspiration. Two types of artificial airways are used.
Endotracheal Tubes
Endotracheal tubes are made of non irritant tissue
compatible materials like polyvinyl chloride (PVC), e.g.
portex tubes. They can be passed through oral or nasal
route. Nasotracheal is used for prolonged use. For children
upto 8 years uncuffed tubes are used. For children above
MECHANICAL VENTILATION
83
8 years cuffed tubes with low pressure baloon are used.

In younger children the narrowest portion of the airway
is below the vocal cords at the level of the nondistensible
cricoid cartilage and the larynx is funnel shaped and so
there is no necessity of a cuffed endotracheal tube. Though
there can be problems like dislodgement of the tube,
difficulty in removing the secretions, subglottic stenosis,
etc. with proper care they can be used for 7-10 days.
Tracheostomy
When the need for artificial airway exceeds for more than
7-10 days tracheostomy is resorted to. Tracheostomy is
done as an elective procedure. Removal of the secretions
is easy through the tracheostomy tube and dislodgement
can be managed easily.
MECHANICAL VENTILATOR
Basic System
The driving force in a ventilator is contributed by either
compressed air or oxygen or both. A compressor giving
50-75 pounds/sq inch is used (PSI). The concentration of
oxygen and air can be adjusted by the blender to the
required concentration (FiO2). A flow meter regulates the
flow between air and oxygen.
The use of artificial airways bypasses the natural
humidifier, the nose. Breathing dry air will lead to
decreased mucociliary activity, encrustation of secretions
and infection. So ventilators are equipped with efficient
humidifier to provide water vapour.
The inspiratory limb has a pop off valve set at 5070 cm of H2O pressure as a safety measure for the patient.
84
The humidifier present in the inspiratory limb humidifies

air to a temperature close to body temperature (37oC). The
inspiratory limb has a bacterial fitter to sterilize the
inspiratory air given to the patient. Pressure gauges are
there to measure the mean airway pressure (MAP) and
peak inspiratory pressure (PIP) and peak end expiratory
pressure (PEEP). Finally, an expiratory valve is added to
the system. When the valve is open a continuous flow will
occur through the system preventing CO2 accumulation in
the tubing. When this valve is closed the pressure will
increase in ventilator tubing and patients airway until
desired pressure level is attained. The ventilator is cycled
by the opening and closing of the expiratory valve.
Present ventilators are driven by electrical power. The
controls and alarms are electronically operated. A piston
and bellows is classically used to drive in air into the
lungs. Mechanical ventilators always use atmospheric air
to ventilate the lungs. Oxygen is used only if it is indicated
by patients condition and laboratory data. The aim of
ventilation is to achieve satisfactory PaO2 using minimum
oxygen.
PEDIATRIC VENTILATORS ARE MAINLY OF
TWO TYPES
Pressure Limited Ventilators
Pressure limited ventilators deliver gas at a predetermined
flow rate until a preset pressure is reached, regardless of
tidal volume delivered. This is generally simple and cheap
but less versatile.
Pressure limited ventilators are extensively used in
NICUs for the following reasons.
1. Simplicity of design, low cost and easy operation
85
2. Peak inspiratory pressure (PIP) the key parameter

related to barotrauma and bronchopulmonary
dysplasia can be controlled directly.
Disadvantage
The tidal volume depends on the compliance of the lungs.
Hence, there is likelihood of hypoventilation when lungs
are less compliant and hyperventilation when they are
more compliant.
Volume Limited Ventilators
The ventilator delivers a preset tidal volume over a given
inspiratory time regardless of the pressure generated.
Advantage
Because of the constant tidal volume there is no hypo- or
hyperventilation with change in compliance.
Disadvantages
1. Not ideal for newborns. Tidal volume in neonates
being small may be lost in the ventilator circuit. Since
uncuffed endotracheal tubes are being used an
unknown amount of preset volume may leak from the
airway.
2. As the tidal volume is constant the normally compliant
areas tend to get preferentially ventilated. The atelectatic
areas which require higher opening pressure continue
to remain unventilated.
3. The design is complicated, the cost is high and
operation is more difficult.
86
Other types are also there

Time limited- Inspiration ends with a preset time.
Flow limited - Inspiration ends when the flow has reached
a critical level.
Mixed cycling can occur when two or more independent
parameters are considered.
High frequency ventilatorsthe ventilators are capable of
cycling at a rate of >150 per minute.
TYPES OF VENTILATION
Controlled Mechanical Ventilation
When the ventilator completely take over the ventilatory
function of the patient it is termed Controlled Mechanical
Ventilation (CMV). This is easy in a completely apneic
patient but in others to facilitate controlled mechanical
ventilation, sedatives and neuromuscular blocking drugs
will have to be used. So in many instances CMV cannot
ensure a normal PaO2 and PaCO2 and cannot improve gas
exchange. And also to ease transition from mechanical to
spontaneous ventilation other types of ventilatory modes
are used.
Constant Distending Pressure (CDP)
It is often seen that mechanically ventilated patients show
a gradual decline in PaO2 in spite of increased FiO2. An
FiO2 of more than 0.5 (inspired oxygen concentration of
50%) is dangerous. This reduction in PaO2 is due to a
gradual closure of distal airways leading to decrease in
FRC. It has been shown that if a positive pressure is applied
to the airway during expiration or throughout the
respiratory cycle this pressure will be transmitted to the
87
distal airways to keep them open leading to an increase

in FRC which improve PaO2. Two types of CDP can be
used.
CPAP, continuous positive airway pressure is used in
spontaneously breathing patients who are usually not
intubated. This is generally given by various means namely
nasal prongs, naso pharyngeal prongs or endotracheal
tubes. It is supplied on to a spontaneously breathing
neonate to produce a functional residual capacity at the
end of each expiration. It is the fundamental management
to be instituted on atelectatic disease.
Indications for CPAP
1.
2.
3.
4.
5.
6.
7.
Respiratory distress syndrome with FiO2 < 0.4

Meconium Aspiration Syndrome
Apnea of prematurity
Weaning patients from mechanical assistance
As adjunct to intermittent positive pressure ventilation
Sleep apnea
Bronchomalacia.
CPAP is a simple device which contains 3 parts

a. A circuit for continuous flow of gases (oxygen and air)
b. Air oxygen blender to deliver appropriate oxygen
c. Patient device.
Positive end Expiratory Pressure (PEEP)
PEEP is used along with IPPV. PEEP can be gradually
increased till a satisfactory PaO2 is obtained.
PEEP 0-2 cm of H2O low
4-7 cm of H2Omediumstandard
> 8 cm of H2Ohigh unusual
88
Intermittent Mandatory Ventilation

In IMV the machine is presenting a certain frequency of
breaths per minute. Patient breathes spontaneously but the
ventilator provides mandatory breaths at rate set by the
operator. Sometimes the spontaneous breaths and
mechanical breaths may not coincide and this can lead to
inefficiency or fighting with the ventilator. Hence adequate
sedation is required to overcome this.
Synchronized Intermittent Mandatory Ventilation
(SIMV)
In this mode the mechanically delivered breaths are
synchronized to the onset of spontaneous breaths of the
patient. It allows the patient to breathe spontaneously
between mechanical breaths. SIMV may be either pressure
controlled or volume controlled. At set intervals the
ventilators timing circuit becomes activated and if the
patient initiates a breath in the expected time the ventilator
delivers a mandatory breath. If no spontaneous breath
occur in the expected time, the ventilator delivers a
mandatory breath at a fixed time. In pressure support
mode spontaneous breaths by the patient is allowed. The
ventilator assists a predetermined amount of airway
pressure above the set PEEP. Here fighting with the
ventilator is absent. This mode is useful in a spontaneously
breathing child.
Assist Control Mode of Ventilation
This modality involves the delivery of a synchronized
mechanical breath each time a spontaneous breath is taken
by the patient (assist) or the delivery of a mechanical breath
89
at a regular rate in the event that the patient fails to take

a spontaneous breath (control).
In assist control mode of ventilation and SIMV there is
synchrony between the patients and ventilated breath and
the need for sedation is minimal.
Pressure Support Ventilation
In many situations baby has poor muscle power to sustain
effective spontaneous ventilation. For these patients during
transition from CMV to complete spontaneous respiration
support can be provided by PSV. The patient is allowed
to breathe spontaneously and each inspiration is supported
by the ventilator. The support is gradually decreased
allowing the patients system to be on its own.
Mechanical ventilation is indicated in different clinical
set ups where there can be a normal lung or an abnormal
lung. The abnormal lung can either with a decreased lung
compliance or increased airway resistance or both.
Compliance means the unit change in volume for a given
change in pressure. Airway resistance is the resisting force
to expiration.
Diseases with Decreased Lung Compliance
Various diseases like AIDS, atelectasis, pneumonia,
pulmonary edema and pulmonary hemorrhage have
decreased lung compliance. In all these diseases FRC is
reduced as terminal air spaces are flooded or collapsed
owing to the presence of abnormal fluid in the alveoli or
atelectasis due to lack of sufactant. Intrapulmonary shunt
is increased as blood is flowing through poorly ventilated
lung tissues. So the aim of mechanical ventilation is to
90
decrease the intrapulmonary shunt by improving FRC by

increasing mean airway pressure in order to recruit more
atelectatic areas of lungs. This can be achieved by higher
PEEPs although higher PIPs also can increase mean
airway pressure. Decreased compliance requires a higher
pressure gradient or a higher rate of respiration. If neither
the pressure nor the rate is increased to compensate for the
decreased compliance, hypercarbia will result.
Diseases with Increased Resistance
Resistance is increased in diseases that decrease the caliber
of the airway lumen by edema, spasm or obstructing
material. Because the airways decrease in caliber during
exhalation increase in resistance affects expiratory flow
more than inspiratory flow. The diseases in which the
airway resistance is increased include asthma, bronchiolitis, bronchopulmonary dysplasia, smoke inhalation and
cystic fibrosis. These diseases with increased airway
resistance are often accompained by both increased intrapulmonary shunt and dead space ventilation. Shunt
occurs because of the impedance of gas flow to the lungs.
Dead space ventilation occurs if the increasing resistance
lead to gas trapping in areas of lung that contain
hyperinflated alveoli. These hyperinflated alveoli exert
pressure on the surrounding tissues and it results in
reduction in pulmonary capillary blood flow. The increases
in both shunt and dead space produce significant
hypoxemia and hypercarbia. Increased resistance requires
higher pressure for the gas to reach the terminal air sacs.
Therefore if volume controlled ventilation is used, an
increase in PIP is required to deliver a given VT. If pressure
91
controlled ventilation is used, tidal volume is lower than

in a normal lung at the same pressure. Increased resistance
may result in significant increase in time constant. A longer
time constant is necessary. If the ventilator frequency is too
high gas trapping can occur as the ventilator cycles back
into inspiration before the lung has had sufficient time to
empty. More and more gas is trapped leading to lung
hyperinflation a predisposition to pneumothorax and
chronic barotrauma and reduction in compliance.
Initial Setting of Ventilator
The initial settings are different for normal lung and
diseased lung.
Normal Lung
Volume controlled ventilation
Respiratory Rate
Ventilator frequency may be slightly lower than the normal
respiratory rate.
Tidal Volume
Set higher than a healthy patients VT 5-7 ml/kg.
Pressure controlled ventilation
An initial PIP of 20-25 cm of H2O is sufficient to move an
adequate VT but this must be immediately assessed by
observation of chest expansion and measurement of VT.
Lung with Decreased Compliance
Mean airway pressure need to be higher. A higher PEEP
is necessary. PEEP is titrated in an attempt to provide
92
adequate oxygenation at an FiO2 less than 0.6. If volume

controlled ventilation is used the PIP may be much greater
than in normal lungs and clinicians should pay attention
to pressure alarms.
If pressure controlled ventilators are used the initial PIP
may exceed 30 cm of H2O. The VT has to be monitored
closely. Significant hypoxemia results from these diseases
and it is customory to start with FiO2 of 100% and then
reduce. The ventilator frequency may be set higher than
normal. A common inspiratory time is 0.8-1 second.
Diseases with Increased Resistance
Ventilator frequency may need to be set as low as 12-16
breaths per minute. PEEP is to be minimized to minimum
2-3 cm of H2O to reduce the risk of gas trapping.
Tachycardia is the earliest sign of too much PEEP. Fall
in blood pressure and metabolic acidosis are late signs of
excessive PEEP. Increasing CO2 is also a sign of excessive
PEEP.
Inspiratory Time
Inspiratory time is an important aspect in controlling MAP
and hence oxygenation. Inspiratory time is to be
individualized on the understanding of the time constant
of that lung. Time constant TC= C R (C, the lung
compliance and R the airway resistance). In conditions
where the lung compliance is reduced like HMD the TC
is extremely short and so the complete emptying of alveoli
can be effected by a longer inspiration time (IE ratio of 1:1).
In MAS where the airway resistance in high the TC is long
and the IE ratio would be in the region of 1:1.8 to 1:2.5
93
depending on the oxygenation. This well help in

producing sufficient expiration and hence less air trapping.
Control of CO2 Elimination
CO2 elimination is simple when compared to the complex
process of oxygenation. The CO2 elimination depends on
minute ventilation MV= TV RR(tidal volume and
respiratory rate). The tidal volume is related to PIP.
Monitoring
Close monitoring of the system as well as the patient is
very important.
Patient
Clinical
1.
2.
3.
4.
5.
6.
Colour-pink
Adequate chest expansion
Absence of chest retraction
Adequate air entry
Prompt capillary filling
Blood pressure
Pulse Oximetry
Oxygen saturation (SaO2) to be kept between 88-95%.
ABG
PaO2 50-80 mmHg
PaCO2 35-45 mmHg (chronic cases upto 60 mmHg)
pH 7.35-7.45
94
System
Needs monitoring for set parameters and alarms.
Weaning
Gradual reduction of ventilatory support after the recovery
stage has reached. In 70-80% cases no weaning may be
required, e.g. upper airway obstruction. In severe lung
disease and neuromuscular disease weaning is required.
It is not necessary that a complete resolution of the disease
process has occured when you start weaning. The pace is
more important than the method.
The modes used are.
Pressure support , volume support, proportional assist,
volume assured pressure support, mandatory minute
ventilation, CPAP or T piece trials, PSV and SIMV of which
SIMV may take a longer period of weaning time.
Extubation Exiteria
1. Primary cause should be resolving (not necessarily
resolved).
2. Reasonbly free of secretions.
3. Should be able to protect the airway.
4. Should have enough muscle strength to generate good
cough.
5. Should not be on high cardiovascular support.
CHAPTER 8
Management of
Shock in
Children
96
Shock is an acute state of circulatory dysfunction resulting

in failure to deliver sufficient amounts of oxygen and
nutrients to meet the tissue metabolic demands. If
prolonged it will result in multiorgan failure and death.
Pathophysiologically it can be divided into three
phases:
1. Compensated: Blood is maldistributed so that the vital
organ function is maintained.
2. Uncompensated: Microvascular perfusion is compromised resulting in reduction of circulating volume.
3. Irreversible: Inadequate perfusion of vital organs leading
to irrepairable damage.
Shock can be classified into four functional categories.
Hypovolemic Shock
Most common cause in children is hypovolemia due to loss
of fluid and electrolytes as in diarrhea, bleeding and acute
blood loss, relative loss as in anaphylaxis or sepsis.
Cardiogenic Shock
Occur in cardiac conditions like myocarditis, cardiomyopathy or dysrrhythmias.
Obstructive Shock
Occur in aotic or mitral stenosis, pulmonory embolism or
cardiac tamponade.
Distributive Shock
Occur in sepsis, neurogenic or anaphylaxis.
MANAGEMENT OF SHOCK IN CHILDREN
97
Dissociative Shock
Occur in heat stroke, carbon monoxide or cyanide
poisoning.
Symptoms: Early symptoms are sinus tachycardia,
giddiness, irritability, apprehension, delayed capillary
refill, decreased urine output.
Late Signs
Altered mental status like lethargy and coma, hypotension,
anuria, mottled skin, acidotic breathing, cold extremities,
hypotonia, DTR, chyne stokes breathing.
Management
Whatever be the cause the first thing is to assess
Airway, Breathing and Circulation (ABC)
Hypovolemic Shock
There is fluid or blood loss producing low preload leading
to decreased stroke volume and decreased cardiac output.
Compensation occurs with increase in heart rate and
systemic vascular resistance.
Mainstay of therapy is administration of fluid and
treatment of the specific cause for fluid or blood loss. If
blood loss is the cause replacement therapy is necessary
with measures to arrest bleeding.
Rapid fluid replacement to expand the intravascular
volume is the most important step in the management of
shock Which fluid? Colloids or crystalloids?
Many studies and many meta-analysis has shown that
both are equally good and in usual clinical set up normal
98
saline is the first choice. In dehydration and shock due to

acute diarrhea Ringers lactate is the fluid of choice. In
hypovolemic shock the initial resuscitation usually is
about 20-30 ml/kg as the first bolus and repeated if
necessary. It can be as much as 200 ml/kg during the first
4-6 hours. Patients who do not respond to initial fluid
boluses should be considered for invasive hemodynamic
monitoring. It usually does not occur in diarrhea or
external blood loss. Constant and continuous monitoring
is needed to reassess perfusion, urine output and vital
signs.
Septic Shock
Classically described as warm shock and cold shock but
such chronologic differentiation may not be possible in a
given patient. Often the children are commonly seen in cold
septic shock.
In warm shock there is bounding pulses, tachycardia,
tachypnea, wide pulse pressure, increased cardiac
output, mixed venous saturation, decreased systemic
vascular resistance, hypocarbia, elevated lactate and
hyperglycemia.
In late shock there is cyanosis, cold clammy skin, rapid
thready pulses, shallow respiration, decreased mixed
venous saturation, decreased cardiac output and CVP,
increased SVR, thrombocytopenia, oliguria, myocardial
dysfunction, capillary leak, metabolic acidosis, hypoxia,
coagulopathy and hypoglycemia.
Monitoring is very important in assessing the clinical
improvement.
MANAGEMENT OF SHOCK IN CHILDREN
99
Steps in Management of Shock

Assess ABC. Secure the airway. Start oxygen with mask
or cannula. Oxygen supply is optimized by maintaining
the oxygen saturation. If adequate ventilation and
oxygenation cannot be achieved endotracheal intubation
and mechanical ventilation should be initiated.
Mechanical ventilation minimize the work of breathing,
reduces the oxygen consumption and improves
oxygenation. Early respiratory support will help patients
with severe shock and also children with cardiogenic shock
complicated with pulmonary edema.
Secure IV line- peripheral, intraosseous or central
whichever is feasible.
Saline is infused 20-40 ml/kg in 20-40 minutes,
followed by 20 ml/kg in 20 minutes.
Hydrocortisone 1 mg/kg IV statum and 8 hourly.
In warm shock- (wide pulse pressure > 40 mmHg)
Nor adrenaline can be given 0.2 mcg/kg/minute
(maximum of 1 mcg/kg/minute).
In cold shock, continue IV fluids 20-40 ml kg and start
on dopamine 10 mcg /kg/minute.
Use fluids to keep the CVP 10-15 mmHg.
With the above measures if the child is not improving,
Diastolic BP <30 mm of Hg in <8 years and < 40 mmHg
in > 8 years if contractility is poor, calcium gluconate is
given (10% 0.4 ml/kg/hour). If contractility is still poor add
adrenaline 0.01mcg/kg/minute. If > 0.5 mcg/kg/minute
is needed child needs ECMO, respiratory support and
plasma filtration. If contractility is acceptable, injection
vasopressin is given in the dose of 0.001 mcg/kg/minute.
100
Ventilatory support may be needed with minimum FiO2

to maintain SaO2 to >90%, PEEP as needed. Ventilate to
keep pH >7.3 but minimum PCO2 (35 mmHg and peak
expiratory pressure 35 cm of H2O. If pH is 7.1 and base
deficit >10 mmol/L consider bicarbonate IV over 1 hour.
On ventilatory support, and is on ionotrope if lactate
is >4 mmol/ L plasma filtration may be tried.
CHAPTER 9
Status
Epilepticus
102
Status epilepticus is referred as seizures persisting for more

than 30 minutes or two or more seizures occuring
consecutively without an intervening period of full
recovery of conciousness. It is estimated that 20-30 minutes
is the duration necessary to cause injury to central nervous
system. Majority of seizures resolves spontaneously within
a few minutes time. A child is who is still having
convulsion on arrival in to the emergency department may
be considered to have status, since they usually continue
to have convulsions until he receives active treatment. And
if a child needs a second dose of anticonvulsant for the
control of seizure also deserves special care treatment in
the emergency department.
STEPS IN MANAGEMENT
The most important step is the provision of proper
oxygenation and ventilation. So the airway and breathing
is assessed and supported by:
a. Positioning of the head and mandible to keep the
airway patent.
b. Suction with a large bore suction catheter to remove oropharyngeal secretions.
c. 100% oxygen is provided with a non rebreathing mask.
d. If feasible, an oropharyrngeal airway is introduced. May
not be feasible if there is clenching of the jaws during
the convulsion.
e. The stomach is decompressed with a nasogastric tube
to prevent vomiting and aspiration.
f. If the patient is not breathing, bag and mask ventilation
is to be tried.
g. If the patient is not ventilating due to convulsion and
becoming cyanosed, the airway is secured using an
STATUS EPILEPTICUS
103
orotracheal intubation. A high dose of midozolam and

a short acting neuromuscular blocking drug may be
required.
h. Though mentioned last, the most important aspect of
management is the control of seizure. Airway compromise is not a contraindication for anticonvulsant
therapy but may be a necessity for assisted ventilation.
Seizure control is to be done as quickly as possible.
Circulation and vascular access is very important for
seizure control and also for other supportive measures.
Intravenous access is to be tried and if not possible in a
child with shock, it can be given through the intraosseous
route. If not in shock, but difficult to get an IV line, drugs
can be tried, rectally or intramuscularly (Midazolam). In
hypovolemia fluid correction is to be done with saline
bolus. If not in shock give only 2/3 of the maintenance
fluid.
Hypoglycemia can cause severe disruption of
autoregulation of cerebral blood flow. If hypoglycemia is
documented or if it is not possible to measure blood
glucose, a bolus of 2 ml/kg of 25% dextrose may be given
intravenously.
Anticonvulsants
During drug administration, attention should be paid to
the possibility of apnea or hypoventilation. This
complication may be due to the effect of anticonvulsant
drugs or due to seizure activity itself. So be prepared for
assisted ventilation.
Benzodiazepine is the drug of choice as the first line
drug. Apnea is not a contraindication provided the airway
104
and breathing are simultaneously looked after. Diazepam

is the most commonly used one and it controls the seizure
in 1 minute. Lorazepam controls the seizure in 3 minutes
and has a longer duration of action of about 12-24 hours
and has less respiratory depression than diazepam.
Inj diazepam 0.2 mg/kg/IV slowly upto a maximum
of 10 mg/dose.
OR
Inj Lorazepam 0.05 mg to 0.1mg/kg upto a maximum
of 4 mg/dose, slow IV infusion with a rate of 2 mg/minute.
If diazepam is given, the effect will be lasting only for
30 minutes and so even when the seizure is controlled there
is the chance of recurrence and so phenytoin may be given
to prevent recurrence. A second dose of benzodiazepine is
required after 5-10 minutes if the seizures are not controlled.
IV midazolam has no advantage over diazepam or
lorazepam. But if an IV access is not available, it can be
given intramuscularly and can control the seizure.
After the two doses of benzodiazepines if seizures are
not controlled IV phenytoin is the second line drug except
in newborns and febrile status.
Phenytoin is infused in normal saline in the dose of
15-20 mg/kg as a bolus dose at the rate of 1mg/kg/minute.
The action is expected within 10-30 minutes. Rapid
infusion can produce hypotension, bradycardia,
dysarrhythmia and asystole. If convulsions are not
controlled, 5mg/kg increments can be given up to a
maximum of 30mg/kg. If the patient is already on
phenytoin the loading dose of the drug is to be avoided.
Phenobarbital is highly effective and the drug of choice
as a second line drug in febrile and neonatal status
epilepticus. The drug is given in the dose of 20 mg/kg as
STATUS EPILEPTICUS
105
infusion at the rate of 1-2 mg/kg/minute. The effect occurs

within 10-20 minutes. Phenobarbital can be given as bolus
dose even when the child was already on maintenance
dose of the drug. The disadvantages are depression of
mental status, respiratory depression and hypotension
especially when administered after benzodiazepines.
Fosphenytoin is a drug which liberates phenytoin when
metabolized. It can be given IM or IV. It has a faster action
also. The dose is 15 mg phenytoin equivalent/kg at a rate
of 3 mg/kg/minute (1 mg phenytoin is equivalent to 1.5
mg of fosphenytoin).
Valproate IV infusion 25 mg/kg at rate of 3-6 mg/kg/
minute can also be given.
Rectal administration of anticonvulsants are not
preferred in status epilepticus because the blood levels can
be erratic.
Refractory Status Epilepticus
Seizures not controlled by the administration of the above
said drugs within a period of 60-90 minutes have been
defined as refractory status epilepticus.
General anesthesia and assisted ventilation is the ideal
management for refractory status epilepticus if feasible.
If not, midazolam can be given, as IV bolus 0.15mg/
kg followed by a continuous infusion of 1mg/kg/minute.
Increase in increments of 1 mg/kg/minute every 15
minutes until the seizures are controlled. Maximum rate
of infusion is 10mg/kg/minute.
OR
Propofol 3 mg/kg/minute bolus followed by 1-1.5 mg
/kg/hour infusion.
106
OR
Thiopental 30 mg/kg bolus followed by infusion at a
rate of 5 mg/kg/hour.
Lidocaine 3 mg/kg IV bolus not faster than 25 mg/
minute followed by infusion at a rate of 5-10 mg/kg/hour
may be useful when refractive to other drugs.
Early Status 0-30 minutes
Drug used is benzodiazipines
Stage of established status 30-60 minutes
Drugs added are phenobarbital, phenytoin/
fosphenytoin followed by valproate infusion
Stage of refractory status >30-60 minutes
Drugs used are
Midazolam, thiopental or propofol infusion
These drugs are given in sufficient doses to maintain
a burst suppression pattern of EEG.
Treatment of specific causes if present should be paid
attention to, like infections, trauma, cerebral edema,
dyselectrolytemia, hypertensive encephalopathy, drug
toxicity etc.
Investigations
Blood is to be collected for glucose, S. electrolytes- Na, K,
bicarb, Ca, Mg, RFT, LFT, ABG and hematogical
parameters.
Vitals are to be monitored every half hourly, especially
while on continuous infusion of drugs. The cardiac
monitoring is very important while on infusion therapy
with phenytoin or lidocaine. Respiratory depression is a
risk with benzodiazepines especially when combined with
other drugs.
CHAPTER 10
Coma
108
A child presenting with altered consciousness is one of the

most difficult problem in pediatric critical care management.
The causes of coma can differ and the specific management
also. But the primary management is the same.
The causes of coma in a child
1. Infection
Meningitis
Encephalitis
Cerebral malaria
2. Drugs and poisons
3. Trauma
4. Vascular-intracranial hemorrhage, thrombosis
embolism
5. Epilepsy
6. Hypertensive Encephalopathy
7. Tumors
8. Hypoxic ischemic encephalopathy
9. DKA
10. Malignant hypothermia
11. Hypoglycemia
MANAGEMENT
The prime consideration is to assess the airway, breathing
and circulation. This is to be followed by a quick history
and systemic examination both general and CNS examination.
Bleeding-bruising and hematomas
Purpura, petechiae, mucosal bleed
Fever, seizures, meningeal signs
Focal seizures and focal
neurological signs
Abnormal smell
Trauma
Bleeding diathesis, e.g. ITP
Meningitis
Focal intracerebral pathology.
Hepatic failure, Metabolic error
COMA
109
Temperature, pulse, blood pressure, respiration are to

be recorded correctly and sometimes the diagnotic clue is
evident from them.
Examination of the pupils, eyes, and motor system also
may give clue towards the aetiology of diagnosis.
LAB EVALUATION
Blood CBC, coagulation screen, blood smear, blood sugar,
RFT, LFT, S. electrolytes, Calcium, Magnesium, ABG,
urine for sugar, ketone bodies.
X-RAY, ECG, EEG, CT SCAN, CSF ANALYSIS
S. ammonia, Lactate, Pyruvate in suspected metabolic
diseases.
TREATMENT
Start IV fluids
Normal saline bolus if in shock
Two-third maintenance if suspecting raised ICP
Give a dose of 10% dextrose if hypoglycemia is suspected
Gastric lavage in suspicion of poisoning
Antipyretics/anticonvulsants
Anti edema measures.
Care of eyes, skin and bladder is very important in a
comatose child.
CHAPTER 11
Acute
Respiratory
Failure
112
Respiratory system fails to meet the oxygen demand of the

body and/or remove carbon dioxide from pulmonary
circulation. Failure of optimal gas exchange in lung results
in hypoxemia and hypercarbia. Respiratory failure
exists when the arterial CO2 tension (PaCO2) is greater than
50 mmHg and/or the arterial O2 tension (PaO2) is less than
50 mmHg. But the laboratory values alone cannot be
considered in clinical set up. Because there are exceptions like.
1. PaO2 may be normal if a patient with respiratory failure
is breathing increased concentration of oxygen (high
FiO2).
2. PaCO 2 is increased in patients with right to left
intracardiac shunt despite having normal respiratory
function.
3. PaCO2 may be increased in patients with chronic
metabolic alkalosis as a compensatory mechanism in
spite of child having no respiratory failure.
Failure of ventilation and failure of arterial oxygenation
can occur individually but often both coexist. Ventilation
is the exchange of respiratory gases between the
atmosphere and lungs and minute ventilation is the volume
of air exchanged in one minute.
VE is divided into two components- alveolar ventilation
(VA) which participates in gas exchange and dead space
ventilation (VD) which does not. Because the bodys CO2
production (VCO2) is eliminated by VA the partial pressure
of CO2 in the alveoli (PA CO2) is approximately equal to
VCO2 divided by VA.
PA CO2 = VCO2/VA
This is known as alveolar ventilation equation and it
states that the PaCO2 (Which is equal to PA CO2 because
ACUTE RESPIRATORY FAILURE
113
the CO2 in the alveoli and the pulmonary capillary blood

is in equillibrium across the alveolar capillary membrane)
is directly proportional to the bodys CO2 production (V
CO2) and inversely proportional to alveolar ventilation
(VA).
So hypercapnia occurs when
VCO2 increases when VA does not
VA decreases when VCO2 does not
VD increases without a concomitant rise in VA
Causes for hypercapnia
Decrease in VA - hypoventilation
Increased VCO2
Increased VD.
Hypoventilation can occur in
1. CNS Causes:
Brainstem disease
CNS depression due to narcotics, anesthetics or
intracranial hypertension resulting in irregular
breathing or shallow breathing.
2. Respiratory muscle weakness
Poliomyelitis
GBS
3. Severe metabolic derangement as in hypokalemia,
hypophosphatemia, poor nutrition, diminished vital
capacity and total lung capacity
4. Abnormal lung mechanics leading to the secondary
event of respiratory muscle fatigue as a result of airway
obstruction or restrictive lung disease.
114
Increased CO2 Production (VCO2)

Occur due to: (1) fever, (2) severe burns, (3) hyper alimentation with high concentration of dextrose. In patients with
respiratory disease and minimal respiratory reserve will
go in for hypercapnia and acidosis.
Increased VD occurs in
1. Air trapping and overdistension as in asthma.
2. Loss of pulmonary capillary area as in vasculitis or
pulmonary embolism.
3. Respiratory diseases in presence of a large number of
gas exchange units with high ventilation/perfusion
ratios.
Effects of High Arterial CO2 Tension
For each 1 mm of acute rise in PaCO2 the pH increase by
approximately 0.01. Plasma bicarbonate remain stable for
a few hours after a PaCO2 change. An acute rise of 10 mm
of PaCO2 change the pH to 7.4 to 7.3. This causes severe
depression of cardiac function and may trigger lethal
arrhythmias. The rising PaCO2 also dilates cerebral blood
vessels and increased cerebral flow causes restlessness,
confusion or lethargy. This necessitates immediate action,
intubation, mechanical ventilation and specific treatment
for the cause of increased CO2 production.
Failure of Arterial Oxygenation
1. Low oxygen in the inspired air, e.g. high altitude.
2. Hypoventilation, alveolar hypoventilation causes
hypoxemia because less oxygen is available for gas
exchange. Increase in PaCO2 will cause decrease in PA
O2 and it will produce decreased PaO2.
CHAPTER 12
Acute Severe
Asthma
116
Any child with wheezing the first line management offered

is agonists either by MDI or nebulization.
Salbutamol 0.15 mg/kg repeated at 20 minutes interval
for 3 doses and if child is not improving, fits in with the
diagnosis of acute severe asthma. If inhaled salbutamol is
not available, terbutaline 0.01 mg/kg s/c or adrenaline
0.01mg/kg of 1:1000 solution s/c is administered and
repeated every 20 minutes for 3 doses. Beta agonists are
contraindicated in congestive cardiac failure and
tachycardia (HR>180/mt in < 1year old and HR>160/mt
in >1year).
Dose of Salbutamol Respiratory Solution for
Nebulization
> 20 Kg 1 ml in 3 ml N saline
< 20 Kg 0.5 ml in 3 ml N saline
Oxygen Therapy
Child should be given oxygen with the help of oxygen
hood, mask or cannula whichever is comfortable for the
child at a flow rate of 2-3 l/minute so that the oxygen
saturation is maintained at 90-95%.
Ipratropium Bromide
Salbutamol nebulization is combined with ipratropium in
the dose of 0.5 ml in <1 year.
Steroids
Steroid is the life-saving drug in acute severe asthma.
It can be either methyl prednisolone intravenously, 2 mg/
kg statum followed by 1mg/kg every 6 hourly or
ACUTE SEVERE ASTHMA
117
hydrocortisone 10 mg/kg statum followed by 5 mg/kg

every 6 hourly or prednisolone 1-2 mg/kg orally in 2-3
divided doses.
IV Fluid
IV fluid therapy is important in acute severe asthma.
Ideally the fluid offered should be 1-1.5 of maintenance
fluid.
Child should be monitored frequently for assessment
of deteriorating respiratory functions, dyselectrolytemias
and air leak syndrome.
If the child is not improving with the above mentioned
initial treatment, diagnosis is to be reconfirmed. X-rays and
ABG to be done if at all it was done earlier. Oxygen flow
is to be checked.
Clinical monitoring can be done by the pulmonary
score index.
Score
Respiratory rate
< 6 yrs > 6 yrs
Wheezing
Sternomastoid
activity
0
1
< 30
31-45
< 20
21-35
46-60
36-50
> 60
> 50
None
Terminal expiration
with stethoscope
Entire expiration
with stethoscope
Inspiration and
expiration without
stethoscope
No apparent activity
Questionable
increase
Apparent
increase
Maximal
activity
0-3 mild.
4-6 moderate
> 6 severe
If no wheezing (silent chest) the score is 3

If the score is >6 ICU management is necessary.
118
Oxygenation can be assessed by pulse oximeter.

Dyselectolytemia is to be checked. Most common problem
is hypokalemia. So IV fluids should contain potassium.
If the Child is Improving
Nebulized salbutamol can be continued hourly or 2 hourly
till the improvement is consistent and then the interval can
be increased every 4 hourly.
Ipratropium is continued every 4 hourly
SteroidsHydrocortisone or methyl prednisolone
continued 6 hourly.
Children usually improve in 24 hours. After 48 hours
the drug interval can be increased and changed to oral
medication as per the clinical judgement.
If Child is Not Improving by the Initial Treatment
Terbutaline IV infusion should be started 10 mcg/kg bolus
followed by continuous infusion at a rate of 0.4-0.6 mcg/
kg/minute under cardiac monitoring. The rate of infusion
can be increased by 0.2 mcg/kgminute every 15 minutes,
to a maximum of 3-6 mcg/kg/minute.
If the child is not improving with the maximum doses
of terbutaline, aminophylline infusion should be tried.
When aminophylline is started, the dose of IV terbutaline
can be reduced to 50%. The dose of aminophylline is is
5-10 mg/kg in N saline to be infused statum followed by
0.5-1 mg/kg/hour infusion. If the child is not improving
with aminophylline infusion also, magnesium sulphate
can be given 20-40 mg/kg (maximun 2 gm) in 30 ml
N Saline over 30 minutes. The drug can be repeated after
6 hours.
ACUTE SEVERE ASTHMA
119
Heliox the mixture of oxygen and helium if available

can be given to improve oxygenation.
If child is not responding, general anesthesia with
halothane and supported ventilation is the last resort.
Indications for Mechanical Ventilation
1. Failure of maximum pharmacologic therapy
2. Cyanosis and hypoxia not relieved by oxygen- PaO2
< 60%
3. PaCO2 >50 or rising by 5 mm Hg/hour.
4. Deteriorating mental state
5. Pneumothorax or pneumo mediastinum
Mechanical ventilation may be given with ketamine
and midazolam or fentanyl IV infusion. Paralysis with
vacuronium if required.
When the child is better and discharged from ICU, long
term management is to be decided. Persistent asthma
should be offered preventor therapy. In a child who was
on local steroids, rescue steroids are to be advised during
an episode of acute asthma. If a child with mild intermittent
asthma develops acute asthma, he should be given rescue
steroids for about 2-3 days. Oral prednisolone 2mg/kg in
2-3 divided doses to be started at the onset of an acute
episode.
When the child improves and able to do, PEFR should
be measured with the Wrights peak flow meter. This will
help in assessing the asthma severity and will help in
further management. But this is often possible only in an
older child 5-6 years and above.
When clinical improvement is sustained for 4-6 hours
drugs can be discontinued as last in -first out principle.
120
Omit MgSO4 if used. Then omit aminophylline infusion in

next 24 hours. Then omit terbutaline infusion. Then
ipratropium nebulization in next 24-48 hours. Reduce
agonist 2-4 hourly, 4-6 hourly and then orally thrice a
day. Replace any steroid with oral steriod twice or thrice
a day.
There are centers using MgSO4 as the drug which is
used next to beta agonist inhalation steroids and
ipratropium before terbutaline infusion and aminophylline
which is actually the new recommendation but the the
authors experience is with the other regimen.
Discharge Criteria
Pulmonory score < 3, slept well at night, comfortable,
feeding well and no need of nebulization agonist as sos
basis.
On discharge, beta agonist can be given 6-8 hourly for
3-7 days
Rescue steroids for 3-7 days
Review or initiate long term preventor strategy.
CHAPTER 13
Hepatic Failure
122
Acute hepatic failure is one of the most challenging

problems in pediatric critical care.
Fulminant hepatic failure is defined as a potentially
reversible condition, the consequence of severe liver injury
with an onset of encephalopathy within 8 weeks after the
appearance of the first symptom and in the absence of preexisting liver disease.
The main features of acute hepatic failure are:
1. Hepatic encephalopathy
2. Coagulopathy
3. Metabolic changes
4. Acid-base disturbances
5. Electrolyte disturbances
6. Infections
7. Haemodynamic changes
8. Renal failure
9. Respiratory problems
10. Ascites
Encephalopathy
The West Haven criteria for semiquantitative grading of
mental state is acceptable and is based on the level of
conciousness, intellectual function and behavior.
Grade 1
Trivial lack of awareness
Shortened attention span
Grade 2
Inappropriate behavior
Lethargy or apathy
Disorientation to time and space.
Grade 3
Somnolence to semistupor or confusion
Grade 4
Coma
HEPATIC FAILURE
123
Very often the first two stages are missed and child is
received in the ICU in grade 3 or 4 encephalopathy and
the routine monitoring of a coma child with Glasgow coma
scale is an additional useful clinical parameter.
The early clinical signs of cerebral edema are subtle and
include changes in pupillary response, bradycardia,
hypertension and hyperventilation. Changes in muscle
tone, myoclonus, seizures and decerebrate rigidity are
signs of irreversible brain damage leading on to respiratory
failure and death. Simple procedures like mouth care or
endotracheal suction may precipitate a surge in intracerebral pressure.
ICP monitoring is indicated in grades 3 and 4 of
encephalopathy but not feasible everywhere. Since CT or
MRI are not sensitive enough to pick up the changes even
in presence of a high ICP, invasive monitoring with
placement of sensors in intraventricular, subarachnoid or
epidural spaces needed but they are not easily available
in many centers in our country and hazardous also.
As in any other critical care situation maintenance of
ABC is the first and foremost step.
Placement of a central venous line, an arterial line, an
indwelling urinary catheter and a nasogastric tube should
be done. An orotracheal tube is to be placed if encephalopathy is grade 3 or 4.
Management of Cerebral Edema
1. Head of the patient may be elevated to 10-20 degrees.
2. Avoid factors which may increase ICP such as sensory
stimulae.
3. Hydration - give IV fluids 75% of the maintenance
124
4. Mannitol -20% in the dose of 0.5-1 gm/kg over 10-20

minutes. Can be repeated every 6 hours.
5. If mannitol is not useful or in the presence of poor renal
perfusion thiopentone can be used. It has antioxidant
anticonvulsant activities and will reduce the cerebral
metabolic rate. Severe hypotension is an occasional
complication which should be agressively managed.
Pentobarbital can also be used . 3-5 mg/kg over 15 minutes
followed by continuous IV infusion 0.5-2 mg/kg/hour.
6. N. acetyl cysteine may reduce cerebral edema by
increasing cerebral blood flow and enhancing tissue
oxygen consumption. 100-150 mg/kg/day till INR falls
below 2. It also acts as a free radical scavenger.
The goal of the therapy is to maintain the ICP to
< 20 mmHg (normal is 10 mmHg).
Methods to Reduce Serum Ammonia
In order to reduce enteric production of nitrogenous toxins
protein feeds are to be stopped. Lactulose is an ammonia
lowering agent by many different mechanisms. It is
administered in a dose of 2 ml/kg with a goal to result in
2-3 semiformed stools per day.
Infections
Sepsis is the cause of death in 25-50% of acute hepatic
failure. The common sites of infections are chest, urinary
tract, blood and IV cannula site. Fungal infections are
possible after one week of hospital stay. Since systemic
staphylococcal infections are common the antibiotics
preferred are ampicillin and cloxacillin, ceftriaxone,
amoxycillin, metronidazole and vancomycin.
HEPATIC FAILURE
125
Unabsorbable antibiotics to decontaminate the bowel

is not necessary if on prophylactic systemic antibiotics.
When cultures are positive antibiotics can be given
accordingly. If no response in 72 hours- amphotericin
1.5 mg/kg/day or fluconozole 3-6 mg/kg/day can be
given.
L Ornitine, L Aspartate
These ammonia lowering agents can be given either orally
or as IV infusion. They provide critical substrates for both
uregenesis and glutamine synthesis, the key pathways for
ammonia detoxification thus lower the serum ammonia
level.
Fluid and Electrolytes
Maintenance fluids with additional dextrose is to be given
upto 75% of total maintenance fluid. The urine output is
to be maintained at 1ml/kg/hour. If the urine output is
less fresh frozen plasma may be given. Dopamine drip
2-5 mcg/kg/minute also may be given.
Sodium intake is 0.5-1 mEq //kg/day
Potassium intake is 3-6 mEq /kg/day
Hyponatremia, hypocalcemia, hypomagnesemia and
hypokalemia when present, are to be corrected.
Metabolic Problems
Hypoglycemia is a common problem. Blood sugar is to be
monitored and should be maintained above 70 mg% with
10% dextrose. If hypoglycemia is present, it should be
corrected with 50% dextrose.
Metabolic acidosis can occur due to tissue hypoxia and
hypovolemia which should be corrected with oxygen
126
therapy and proper volume replacement. N acetyl cysteine

given as a infusion can help in correcting the metabolic
acidosis in the dose of 150 mg/kg/24 hours.
Coagulopathy
Vitamin K can improve the clotting abnormalities in the
initial stages but FFP is to be given if there is evidence of
bleeding or any invasive procedures are planned.15-20 ml/
kg can be given as an infusion every 6 hourly. Platelet
transfusion is given to keep the platelet counts above 50000
. PRC are transfused if Hb is less than 8 gm% which will
help in improving tissue oxygenation.
Prevention of GI Hemorrhage
IV Ranitidine 3 mg/kg/dose 8 hourly.
Sucralfate 250-500 mg 4-6 hourly.
Proton pump inhibitors also can be used. Vitamin K is
to be given IV, 2.5 mg in < 6 months, 5 mg in 6 months
-2 yrs, 10 mg in > 2 yrs.
Renal Dysfunction
Circulating blood volume is to be maintained to prevent
pre -renal hypovolemia. If there is hypovolemia as evidenced
by low CVP a fluid challenge is given with normal saline
10 ml/kg. If CVP is > 8-10 ml of water, frusemide 1-2
mg/kg is given IV or 0.25mg/kg/hour by infusion.
In established renal failure hemodialysis may be required.
Ascites
Requires only correction of oncotic pressure by 50%
albumin.
HEPATIC FAILURE
127
Respiratory Problems
Elective mechanical ventilation guided by ABG should be
initiated in respiratory failure.
Nutrition
Protein intake to be limited to 1-2 gm/kg per day. Calories
should be adequate to maintain the blood glucose at
75 mg%.
Management of Seizures
Choice of anticonvulsants is very crucial. Phenytoin and
gabapentin are relatively safe in hepatic failure.
Agitation and Restlessness
It is often a problem in a child with hepatic failure.
Benzodiazepines are usually avoided because of the
respiratory embarassment and deepening of coma. If to be
used lorazepam is the better tolerated one. Haloperidol also
can be used which is relatively safe.
Liver Support Systems
The curative treatment may be liver transplant. Other
support systems are hemodialysis, hemofiltration, plasma
exchange and hemoperfusion. Molecular absorbant
recirculating system (MARS) enables albumin bound
toxins to be removed by dialysis along with other
dialyzable toxins. It comprises a double sided albumin
impregnated polysulphone or hollow fiber dialysis
membrane in a closed loop dialysis unit.
128
Bioartificial Liver Systems

They combine biological tissue with non-biological
materials. One such system contains human or pig
hepatocytes implanted to hollow fiber ultrafiltration
catridges. The patients blood or plasma circulates through
these bioreactors and after clearance of toxic compounds
and addition of synthesized products is returned to
patients. The two main types are (1) extra corporeal liver
assist device (ELAD) and bioartificial liver (BAL).
Liver Transplantation
Acute hepatic failure is responsible for 11% of pediatric
liver transplantation. Orthotopic liver transplant is the
treatment of choice whenever there is no potential for
recovery. Auxillary liver transplant is desirable for those
who have a chance of spontaneous recovery. The survival
rate is 70-80% in well recognized centers.
CHAPTER 14
Acute Renal
Failure
130
Acute renal failure is characterized by inability of the

kidneys to maintain body homeostasis and is manifested
as reduced urine output with increasing blood urea and
serum creatinine level. But 10% renal failures can have
good urine output- non oliguric or polyuric ARF. It occurs
secondary to sepsis, aminoglycoside toxicity and burns
and is a feature of multiorgan dysfunction in PICU setting.
The problems usually faced are- hypervolemia,
hyponatremia, hyperkalemia and metabolic acidosis.
Fluid Management
Majority of acute renal failure patients presents with
hypervolemia. The preferred route of fluid administration
is oral or through nasogastric tube. The parenteral fluid
is preferred only if there are gasterointestinal problems.
Fluid intake is restricted to insensible water loss on day
one and there after insensible fluid loss plus the previous
days urine output.
Insensible fluid loss comes to
30 ml/kg body weight for infants.
20 ml/kg body weight for older children
10 ml/kg weight for adolescents and adults.
OR
400ml/m2 BSA per day
If any other abnormal fluid loss is there, e.g. vomiting
or loose stools that also is to be replaced.
If fluid therpy offered is ideal the body weight is either
steady or child losses around 0.5% of previous days
weight.
If there is hypovolemia, in addition to the above said
fluids extra fluids to correct dehydration is to given.
ACUTE RENAL FAILURE
131
If child is hypervolemic and edematous, fluids are to

be restricted and if hypervolemia persists furosemide 2-4
mg/kg IV can be given.
Since they need first class protein the preferred oral
fluids is usally milk or curd. If IV fluids are planned the
maintenance fluid to be given is 5% dextrose. If child is
grossly acidotic. 5 mEq of soda bicarbonate per 100 ml of
fluid may be added and if the child is non acidotic 3 mEq/
100 ml may be given. If child is having hypokalemia 4 mEq
of potassium per 100 ml of fluid is added to the
maintenance fluid. In normokalemia or hyperkalemia no
potassium is to be added.
Daily estimation of serum electrolytes will decide about
the addition or substraction of electrolytes. Fluid loss and
hypovolemia is to be corrected with normal saline or
Ringers lactate as in any other child. In addition to the
signs and symptoms of hypovolemia elevation in blood
urea disproportionate to serum creatinine also shows
hypovolemia and dehydration.
In acute renal failure with edema say in AGN with
failure often there is dilutional hyponatremia which does
not necessitate sodium correction. But children with
tubulointerstitial disorders, post obstructive release
diuresis, recovering ATN and chronic renal failure normal
sodium requirement is to be given on a daily basis. If on
IV fluids 0.45% saline can be given.
Hyperkalemia is often a problem in ARF. It should be
anticipated and tried to delay it by avoiding potassium in
diet, discontinuation of ACE inhibitors and potassium
sparing diuretics, avoiding antibiotics containing high
potassium salt, rapid control of infection, debridement of
necrotic tissues and control of hemolysis.
132
Potassium is to be given only in the presence of

hypokalemia or in a child who is losing potassium. Tender
coconut water, orange and other fruits are to be given
initially. Later it can be given as potassium salts orally or
rarely as IV potassium only if there is severe hypokalemia.
Hypovolemia
Can occur in renal disease due to indiscriminatory use of
diuretics and restriction of salts and fluids. Child with
oliguric renal failure can present with hypervolemia and
non oliguric renal failure can present with euvolemia.
Children with hypovolemia should get 20 ml/kg of normal
saline over 1 hour and if no improvement, another 3 more
similar doses can be given if CVP monitoring is available
and two more doses if no CVP monitoring is available. If
CVP monitoring is not available the patient should be
carefully monitored for assessment of pulse volume, pulse
rate, liver size, onset of hypertension and basal
crepitations. If euvolemia is attained and urine output is
inadequate, diuretic therapy can be given with 2 mg/kg
body weight of furosemide intravenously. If no diuresis
occur even after IV furosemide with an elevated CVP or
clinical evidence of hypervolemia child is to be restricted
of fluids and dialysis or continuous renal replacement
therapy is indicated.
Problems of vascular leak is a common problem in PICU
where a child presents with volume overload but with
decreased effective circulating blood volume. This is
because of the vascular leakage, fluid shift from the
intravascular compartment to the extravascular
compartment. More fluids are needed to maintain the
ACUTE RENAL FAILURE
133
intravascular volume for renal and tissue perfusion but will

aggravate the clinical features of fluid overload. This can
occur in sepsis, dengue shock syndrome, leptospirosis,
burns, snake envenomation and hypoalbuminemic
conditions. If renal functions are adequate, diuretics can
be given as continuous infusion 0.0 4mg/kg per hour. If
renal function is inadequate, where in diuresis is not
possible, peritoneal or hemodialysis is needed to maintain
the fluid balance.
CHAPTER 15
Diabetic
Ketoacidosis
136
It is a usual medical emergency in a child who is known

to have Diabetes Mellitus. It may be the first presentation
of Diabetes Mellitus in a child.
The clinical presentation is characterized by
dehydration and acidosis.
Detailed history may sometimes yield the presence of
polydypsia and polyuria.
Dehydration and hyperglycemia should be treated with
caution as rapid treatment may result in cerebral edema.
As in any sick child stabilization of the child, ABC is the
first and the most important step.
DKA
Blood glucose > 300 mg/dl
Acidosis pH arterial < 7.3, serum bicarbonate < 15 mEq/L
Glucosuria (+++ to ++++)
Ketonuria (+++ to ++++)
Severe DKA
Moderate DKA
Mild DKA
Blood pH <7.1
pH 7.1 - 7.2
pH >7.2
S. bicarbonate <5 mEq/L

S. bicarbionate 5-10 mEq/L
S. bicarbonate 10-15 mEq/L
Hydration
Assess the level of dehydration. Usually it is around 10%.
IV fluids first started is either normal saline or Ringers
lactate. 15-20 ml/kg is given in the first hour to expand
the intravascular volume. If peripheral circulation is not
improving (CRT>3 seconds) a second bolus can be given.
If the child is still in shock colloids (e.g. Albumin) can be
given.
The rest of the deficit fluid and the calculated maintenance fluid for the next 24 hours should be given during
next 23 hour.
DIABETIC KETOACIDOSIS
137
IV fluids for a 30 kg child with 10% dehydration is as

follows.
Ist hour 15 ml/kg (450 ml) of 0.9% saline or Ringers
lactate as IV bolus.
2nd hour and subsequently
85 ml 30 + 1750 450 = 167 ml
23 hr
hr
as 0.45% saline with 10 mEq/L potassium phosphate
and 20 mEq/L potassium acetate.
Instead of potassium phosphate and potassium acetate,
potassium chloride can be used 20 mEq/L
Ongoing losses are to be corrected.
Dehydration should be assessed clinically and fluids
to be calculated accordingly. Potassium phosphate is
advised to replace phosphate. Though phosphate
depletion shifts the oxygen dissociation curve to left this
defect is neutralized in untreated DKA by acidosis. Thus
phosphate depletion does not appear to be mandatory. If
it is given, serum calcium is to be monitored. In severe
dehydration often there is associated hypokalemia. It is not
wise to wait for the serum potassium report. ECG can help.
In lead 2 if there is a flat T wave it is the evidence for
hypokalemia and potassium can be given even if the child
has not passed urine.
Five percent dextrose is added to the fluids when the
blood glucose approaches 250 mg/dl. It can be 5% dextrose
saline so that the insulin infusion can be continued
without risk of hypoglycemia till the acidosis is corrected.
Bicarbonate is not to be given because it may over correct
acidosis and produce true alkalosis, hypernatremia and
severe hypokalemia. Should be used only in emergency
138
situations with (a) severe hypokalemia (b) cardiovascular

instability with pH < 7.2, shock or renal failure (e) blood
pH is less than 7.
Though serum bicarbonate is low, true deficit is not
present because ketoacids and lactate are metabolized to
bicarbonate during therapy.
Insulin Therapy
Continuous low dose insulin is the method of choice.
A loading dose of 0.1 unit per kg body weight is given
as and when IV fluids are started. This is followed by an
infusion of 0.1 units/kg/hour (50 units of regular insulin
is added to 500 ml of normal saline and 50-60 ml is run
off to fill up the tubings). The infusion is then started with
the infusion pump.
If blood glucose does not fall by 50-100 mg/dl per hour
in 2-3 hours the insulin dose is doubled. When blood
glucose reaches 250 mg/dl 5% glucose is added to the
fluid. IV fluid should not be discontinued till acidosis is
corrected. (PH > 7.3, S bicarbonate>18 mEq/L). The insulin
dose can be reduced to 0.05 unit/kg/hour or 0.025 unit/
kg/hour depending on the blood glucose level till acidosis
is corrected, child is alert and oral feeds are tolerated. The
subcutaneous insulin can be started. The dose is 1 unit/
kg/day divided 6 hourly. Half an hour before the insulin
infusion has to be stopped, a subcutaneous dose of regular
insulin 0.25 units/kg is to be given.
Following this, a regimen of regular and intermediate
acting insulin in two or more daily doses can be started.
Oral feeds can be started as soon as the patient is
conscious, has no vomiting or abdominal distension, has
DIABETIC KETOACIDOSIS
139
normal bowel sounds and willing to eat. This usually takes

about 4-12 hours after initiation of therapy. Initially clear
fluids are offered, then soft solids and finally full diet. Oral
potassium may have to be continued for a few days if the
serum potassium is low.
Investigations
Blood - CBC, Glucose, S electrolytes, ABG, S phosphates,
Creatinine and Osmolatily.
Serum osmolality can be calculated by the following
equation.
Serum Na + K 2 + glucose + BUN
Urine - Glucose, acetone, culture and sensitivity
ECG for changes due to hypokalemia -flattening of T
waves (> 2 div), appearance of U waves and QRS
widening.
Screening for sepsis-blood culture, urine culture
Follow-up
Blood glucose hourly to 2 hourly bedside till child is stable
and free of acidosis. Serum potassium hourly till stabilized.
S sodium, pH, Bicarbonate, Osmolality 2, 6, 10, 24 hours.
Fallacies in Biochemical Tests in DKA
Hemoglobim and BUN may be elevated due to
dehydration
Leucocytosis may be due to ketosis
Creatinine is elevated since the assay also measures
aceto acetate
Pseudohyponatremia is common for every 100 mg% rise
of glucose so add 1.2 mEq/L to the actual sodium level.
140
Apparent increase in ketone bodies in starting treatment

as betahydroxybutyrate which is not detected by the
nitroprusside reaction will be converted to acetoacetate
and detected in urine.
Complications
A close monitoring is very essential which includes mental
status, vital signs, insulin dose, fluid and electrolytes given,
urine output and laboratory parameters like blood glucose,
urine ketones, (early transient rise is a good sign)
electrolytes and anion gap (narrows with treatment).
Hypoglycemia should be corrected with appropriate
measures but insulin should not be discontinued suddenly.
Most serious complication a child with DKA is cerebral
edema. Treatment is difficult and so should be avoided as
best as possible. It usually develops in 4-16 hours after
starting treatment and must be suspected if sudden
neurological deterioration occur after the initial response.
The signs include decreasing sensorium, headache,
vomiting, disorientation, agitation, deterioration of vital
signs, incontinence, pupillary changes, papilledema and
seizures. A decreasing heart rate or occasionally
tachypnea may be the earliest sign of impending cerebral
edema. At the earliest sign, supportive treatment is to be
started - IV mannitol and hyperventilation. Symptomatic
cerebral edema carries a high level of mortality.
Cerebral edema can be avoided by slow rehydration 3648 hours, after the initial circulatory stabilization,
avoidance of hypotonic fliuds, avoidence of hypertonic
fluids. (infusion of bicarbonate) and avoidance of rapid
correction of hyperglycemia.
CHAPTER 16
Cardiac
Emergencies
142
CONGESTIVE CARDIAC FAILURE

Heart failure characterizes the clinical syndrome resulting
from the inability of heart to pump blood and oxygen at
a rate commensurate with bodys metabolic demands.
80% of CHF occurs in infancy and is a common cardiac
emergency in infancy and neonate.
The causes of congestive cardiac failure differs in
different age groups and in infancy the structural defects
of the heart or great vessels is the commonest cause of heart
failure.
Diagnosis of cardiac failure in neonatal period is quite
difficult as a number of non cardiac conditions such as
infections, metabolic disturbances, and respiratory
problems can have a similar presentation with tachypnea
and tachycardia.
The clinical manifestations differ based on the age,
aetiology of heart disease, specific chambers involved and
rate and extent of impairment of cardiac performance
Cardiac failure can be insidiously merge into chronic
congestic cardiac failure.
Neonates and infants with cardiac failure grow slowly
because of increased caloric requirement and decreased
caloric intake. They feed poorly and feeding time is
prolonged. In severe cases babies are unable to suck because
of rapid breathing.
The respiratory effort is more and breathing is rapid
even in resting stage. Since babies cannot suck
continuously they cry frequently and excessively and the
sleep also is disturbed. They sweat profusely even in cool
environment and the head sweating during feeding is very
charecteristic. Due to orthopnoea, babies are distressed on
CARDIAC EMERGENCIES
143
supine position and comfortable when put on shoulders

of the caretakers. Increased pulsations of the precordium
may be noticed by some mothers. Edema is not a common
complaint in a small baby.
Physical Examination
The major manifestations in CHF in babies are tachypnea,
tachycardia, tender hepatomegaly and cardiac enlargement.
Tachycardia may be a cause or effect. A heart rate of
180/minute or more is seen in CHF. But of the heart rate
is sustained and more than 220/minute should raise the
possibility of SVT.
Bounding pulses seen in CHF should lead to the consideration of PDA, AV malformation, Truncus arterosus with
truncal value regurgitation and other run off lesions.
Ausculation may show systolic murmurs in many of
the conditions. Diastolic rumble is common in shunt
lesions with pulmonary over circulation. Gallop rhythm
is a very suggestive finding in CHF. Auscultation of
cranium (Vein of Galen malformation) and abdomen
(hepatic AVM) is very important in a newborn or young
infant presenting with CHF.
Respiratory rate of 60-80/minute is common in CHF.
Bilateral rales or ronchi may be heard. Raised jugular
venous pulsations is a reliable sign in a child but not in
an infant. Cool extremities, decreased peripheral pulses,
lowered blood pressure and mottled extremities are signs
of impaired peripheral perfusion and cardiogenic shock.
Central cyanosis can occur due to impaired gas exchange.
In general, intense cyanosis do not occur due to CHF.
144
Measurement of BP in all the four limbs is important

to rule out aortic obstructive lesion.
Investigations
Since cardiomegaly is an important sign of CHF, X-ray
chest is an essential investigation. Cardiothoracic ratio
more than 55% is considered cardiomegaly in infants and
neonates. Pulmonary vascular markings are increased in
pulmonary overcirculation. ECG is helpful in delineating
ventricular hypertrophy, atrial enlargement and rhythm
disturbances. A 14 lead ECG with rhythm strip is to be
taken.
Other laboratory investigations often indicated are
blood glucose and serum electrolytes. Septic work up, ABG
and metabolic work are sometimes needed.
Echocardiography is always needed to assess the
structural changes but to be done after stabilizing the child.
Causes of CHF in First 2 Hours of Life
1.
2.
3.
4.
5.
6.
7.
8.
Tricuspid regurgitation
Pulmonary regurgitation
AV fistula
Hypoplasia of left heart
Endocardial fibroelastosis
Birth asphyxia
Twin to twin transfusion
Paroxysmal tachycardia.
Causes of CHF in Day 1

1. Perinatal asphyxia
2. Severe anemia-Rh incompatibility, severe hemorrhage
CARDIAC EMERGENCIES
3.
4.
5.
6.
7.
145
Ebsteins anomaly
Absent pulmonary valve
Systemic AV Fistula
SVT
Neonatal myocarditis
CHF in First Week

1.
2.
3.
4.
5.
Aortic stenosis
Hypoplastic left heart syndrome
Co-arctation of aorta
Interrupted aortic arch
Critical pulmonary stenosis.
All these presents when the ductus arteriosus closes.
7. TAPVC,
8. Preterms with PDA.
Noncardiac
1. Acute renal failure
2. Neonatal hyperthyroidism
3. Adrenal insufficiency
CHFAround 1 Month of Age
1.
2.
3.
4.
5.
6.
7.
8.
Shunt lesions - VSD

TGV with VSD
Complete AV canal defect
PDA
AP window
Truncus arteriosus
Single ventricle
ALCAPA
146
Treatment
Immediate aim of treatment is to improve the contractile
performance of myocardium and to remove the excess salt
and water.
Establishing the IV line is crucial. Oxygen by mask is
started immediately. Baby is to be kept warm.
Mainstay of drug therapy is ionotropes, diuretics and
vasodilators.
Ionotropes
Digoxin is the preferred ionotrope over the years. Though
the role is controversial it remains the mainstay of
management in the medical management of CHF. This
cardiac glycoside blocks the myocardial cellular sodium
- potassium pump. Thus intracellular sodium concentration increases, stimulating the uptake of calcium exchange
mechanism. The intracellular calcium concentration allows
for more actin and myosin cross bridges to form during
activation of the cardiac muscle increasing efficiency of
contraction. Digoxin also causes sympathetic withdrawal
and relieves tachycardia, diaphoresis and other systemic
signs and symptoms of CHF. In addition, digoxin is a good
drug for the initial treatment of certain arrhythmias.
The dosage schedule is as follows:
Patient
total digitizing dose maintenance dose frequency
Newborn
Infant
Child
30 mcgm/kg
40-50 mcgm/kg
40 mcgm/kg
7.5 mcgm/kg/day
10 mcgm/kg/day
10 mcgm/kg/day
BD
BD
OD
CARDIAC EMERGENCIES
147
Dobutamine and Dopamine

These ionotropes are used when baby is not responding
to the initial treatment. Dobutamine is the preferred drug
due to its predominant beta 1 action and less conspicuous
alpha activity. Dose is 5 mcgm per kg per minute and upto
10-15 mcgm/kg/minute. It is the ideal drug when there is
cardiac dysfunction with maintained blood pressure.
Dobutamine is dissolved in 5% or 10% dextrose started
at 5 mcgm/kg/mt infusion tritrated to 10 mcg/kg/mt upto
a maximum of 20 mcgm/kg/mt.
1 ampoule 250 mg.
Formula for Drug InfusionRule of six
1. 6 wt in mgms of drug to be diluted in 100 ml.
2. 10ml/hour gives 10 mcgm/kg/mt.
e.g. 14 kg child needs dobutamine 10 mcgm/kg/hour.
6 14 = 84 mgms 84 mgm in 100 ml fluid
10ml/hour = 10mcgm/kg/mt.
Dopamine is another ionotrope which has beta 1 and
beta 2 activity and also act on dopaminergic receptors in
renal vasculature. It increases arterial vascular resistance
and could be useful in acute CHF with hypotension. The
dose is 5 mcgm/kg/mt titrated upto 15 mcgm/kg/mt. It
may increase the pulmonary capillary wedge pressure and
can worsen pulmonary congestion and so once BP is stable
it may be switched over to dobutamine for continued
ionotropic effect. Both can be used together with the
advantage of less doses of individual drugs with maximal
therapeutic effect. The dose is 5 mcgm/kg/mt. Each
catecholamine should be continued for at least 48 hours
and then tapered off.
148
OTHER PARENTERAL IONOTROPES

Amrinone and Milrinone
The dose of amrinone is 0.75 mcgm per kg as a bolus dose
over 2-3 minutes followed by an IV infusion of 5-10 mcgm/
kg/mt. Repeat bolus doses may be given if clinical response
is not adequate, 2-3 doses given 15 minutes apart. It is a
proarrhythmic. It can also cause severe diuresis,
hypotension and thrombocytopenia.
Milrinone is given as a loading dose of 50 mcgm/kg,
IV and a maintenance dose of 0.35 - 0.75 mcgm/kg.
Diuretics
The commonly used diuretic drugs are the loop diuretics
- furosemide, thiazides and aldosterone antagonists spiranolactone. Furosemide is the commonly used one and
the drug of choice. The dose is 1-3 mg/kg/dose IM, IV or
oral, repeated every 8-12 hourly. It is better to start as
parenteral doses initially. 0.1mg/kg/hour as infusion also
can be given.
Aldosterone antagonist, spironolactone is a weak
diuretic and is rarely used as an additional diuretic.
Vasodilators
ACE inhibitors are used in CHF. They augment cardiac
pump function by altering the resistance of the peripheral
vascular bed. Captopril is the drug of choice. The dose is
0.5 - 3 mgm/kg/day in two to three divided doses.
Maximum dose is 4 mg/kg/day. Contraindicated in renal
failure. Enalapril and prazocin is not well studied in
children.
CARDIAC EMERGENCIES
149
Isoprenaline may be used in CHF with very high pulmonary vascular resistance (PPHN) or with low heart rate.
Other Supportive Measures
IV fluids are necessary since child cannot take enough
orally. The fluid recommended is 2/3 of total maintenance
fluid. Potassium supplementation is necessary in children
on furosemide. Not necessary if the child is on ACE
inhibitors.
Oxygen therapy is needed till cardiac failure is
controlled.
Nutrition - Babies with chronic CHF the growth is
always affected and they need 150-170 kcal/kg/day to
achieve adequate growth. Nasogastric feeding may be
required. Supplementation of iron is necessary to avoid
anemia.
CYANOTIC SPELL
Cyanotic spell is one of the common cardiac emergency in
an infant. It is due to an increase in impedance of
pulmonary blood flow and reduction in systemic vascular
resistance. It is classically found in TOF. Can occur in VSD
with. pulmonary atresia, tricuspid atresia, and
occasionally in TGA.
The steps in management are Oxygen with mask to combat hypoxemia.
Knee chest position to elevate systemic vascular
resistance and to reduce right to left shunting and
improve pulmonary circulation.
Injection morphine 0.1mg/kg, half the dose IM/SC
immediately and rest of the dose once the IV line is
150
established. Morphine relaxes the infundibulum and

quieten the baby and reduces hyperpnea.
Once IV line is established normal saline is infused to
expand the intravascular compartment.
Sodium bicarbonate 2ml/kg is given as a bolus diluted
in equal amount of distilled water, to correct acidosis.
Beta blockers, propranalol in a dose of 0.1mg/kg is given.
Half the dose is diluted and given immediately and the
rest 10 minutes later. 0.5mg/kg may be given 4-6 hourly
orally. Esmolol can be given initially as a bolus, 500
mcg/kg IV followed by IV infusion at a rate of 50-200
mcgm /kg/mt. They reduce infundibular spasm, reduce
heart rate and increase systemic vascular resistance.
Vasopressors like phenylephrine or methoxamine can
be used to increase systemic vascular resistance.
Other modalities tried are abdominal compression,
packed RBCS transfusion (5ml/kg) and ketamine instead
of morphine (0.25 - 1mg/kg IV).
Refractory spell may need general anesthesia and
mechanical ventilation.
Arrhythmias
Common arrhythmias in children include SVT (supraventricular tachycardia) VT (Ventricular tachycardia) and
bradycardia due to complete heart block.
SVT
SVT is the most common arrhythmia in children. Majority
of them are paroxysmal. It is a narrow QRS tachycardia
with a cardiac rate of more than 200/minute with an
absent or buried P wave.
CARDIAC EMERGENCIES
151
Once diagnosed, hemodynamic compromise is looked

for - CCF or hypotension. An ECG of 14 leads with a long
lead II should be taken.
The drug of choice is adenosine, given as IV boluses
at frequent intervals. Each dose is given as a rapid push
through a large vein flushed immediately with saline at
an interval of 3-4 minutes.
The recommended schedule is an follows Dose 1 50 mcgm/kg push
2 100 mcgm/kg push
3 150 mcgm/kg push
4 200 mcgm/kg push
5 250 mcgm/kg push
6 300 mcgm/kg push
Usually, SVT breaks at a median dose of 200 mcgm/
kg.
The other drugs available are:
Amiadarone
3-5 mgm/kg/dose IV bolus administration for 10-20
minutes, followed by 10 mgm/kg/24 hours for 2 days.
Diltiazem
0.2 mg/kg IV bolus for 2 minutes
0.3 mg/kg can be repeated after 5-10 minutes.
Esmolol
500 mcgm/kg/mt bolus for 4 minutes followed by. 50-200
mcgm/kg/mt infusion.
152
Verapamil
Can be given in an older child.
0.2 mg/kg IV bolus slowly.
In less urgent cases digoxin, oral verapamil and
propranalol can be given. In refractory cases DC version
may be needed.
In a child with no hemodynamic compromise with SVT,
vagal maneuvers such as iceberg application to face and
carotid massage may be tried but with limited success.
CHAPTER 17
Hypertensive
Emergencies
154
Hypertensive emergencies exist when blood pressure is

markedly elevated for age and signs and symptoms directly
attributable to uncontrolled hypertension develops. In these
clinical situations the blood pressure elevation is associated with vital organ dysfunction and the bood pressure
has to be lowered in minutes to hours using parenteral
drugs so as to save the vital organs. Hypertensive
emergencies occur with rapid rise in blood pressure
because chronic elevations in blood pressure is usually
well tolerated as in chronic renal disease and end stage
renal failure. Rapid elevation in BP can occur due to
stoppage of antihypertensive therapy, inadequate fluid
restriction or stopping the dialysis.
Hypertensive urgencies are associated with severe
hypertension but with no vital organ dysfunction and the
reduction need be achieved over hours to days using even
oral drugs.
The causes for hypertensive emergencies can be renal
or nonrenal origin.
Renal
Acute glomerulonephritis.
Hemolytic uremic syndrome.
Reflux uropathy.
Chronic renal failure/end stage renal failure.
Renal artery stenosis.
Systemic lupus erythematous.
Transplant rejection.
Nonrenal
Pheochromocytoma.
HYPERTENSIVE EMERGENCIES
155
Volume overload.
Drugscyclosporine, erythropoietin, steroids
Signs and Symptoms
They may present with headache, blurring of vision,
scotoma or blindness, lethargy, coma, seizures and
abdominal pain. They can present with cardiovascular
accidents, congestive cardiac failure or retinopathy.
Treatment
The goal of treatment is to reduce the BP but without a
precipitous fall. The blood pressure is to be lowered by 25%
within 6 hours and remainder of BP reduction to normal
is to be by 24-36 hours. Too aggressive reduction is not
advisable as it may be counterproductive and a precipitous
fall may worsen organ damage.
Though the parenteral drugs like nitroprusside, labetalol and enalaprilat are effective and are recommended
drugs the use of these drugs are limited in our set up
because of their toxicity and the lack of careful monitoring
they demand.
Very good results are obtainable from nifidipine 0.250.5mg/kg/dose oral or sublingual. The onset of action is
within minutes and lasts for about 30-60 minutes. Can be
repeated once or twice if required. Captopril sublingual in
the dose of 0.5mg/kg can be used if there is no renal
impairment.
In very efficient ICU set up the recommended drugs and
dosages are as follows.
156
Sodium Nitroprusside is the Drug of Choice

It is an extremely potent vasodilator which reduces
systemic arterial and venous pressure. Its action begins
within seconds after infusion is started and disappears
rapidly when it is discontinued. Because of its potent
effect, nitroprusside should be administered in an ICU with
blood pressure recording every 5-10 minutes. The drug is
to be shielded from light to prevent degradation. The
metabolic product of sodium nitroprusside is cyanide
which is converted to thiocyanate in the liver and almost
exclusively removed by the kidneys. And so cyanide
poisoning is extremely rare. Nitroglycerin has a similar
mechanism of onset and duration of action as
nitroprusside. It is preferred to the latter in patients with
renal impairment.
The dose is 0.5 - 1mcg/kg IV initially titrated to 5-8
mcgm/kg/mt. The effect occurs within seconds. The side
effects are sweating, muscle twitching and thiocyanate
toxicity.
Esmolol
500 mcgm/kg IV in 2-4 minutes followed by an infusion
of 100-200 mcgm/kg every 10-20 minutes.
Phentolamine
0.1 - 0.2 mg/kg/IV can reduce the BP in a few minutes.
The drug can cause tachycardia, headache and flushing.
CHAPTER 18
Blood and Blood

Component
Therapy
158
Transfusion of blood and blood components are indicated

in restoring and maintaining the oxygen carrying capacity
of blood, circulating blood volume, hemostasis, leukocyte
and platelet function.
Whole blood transfusion is indicated only for
replacement of blood loss after trauma or surgery. In other
situations the components needed for the patient only is
transfused.
Red Cell Concentrate
Red cell concentrate is used for symptomatic anemia after
an acute blood loss or in chronic anemia secondary to bone
marrow suppression.
One unit of red cell concentrate is expected to increase
the hemoglobin level by 1gm/dl (Hct by 3%) in an average
sized adult. The dose recommended for pediatric
population is 10-15 ml/kg.
Platelet Transfusion
Transfusion of platelets is indicated in severe thrombocytopenia (Platelet count less than 10,000/ml). Platelet
transfusion may be required prior to an invasive procedure
in patients with thrombocytopenia with the count less than
50, 000/ml. The dosage is l unit/10 kg body weight. A
baby of 10 kg needs 1 unit and child of 20 kg needs 2 units.
The platelet increment after each unit transfused is
5000 to 10, 000 (single or pooled donor). If a single donor
unit apherised is used, it contains an equivalent of 6 units,
adequate for an average sized adult.
BLOOD AND BLOOD COMPONENT THERAPY
159
PLATELET TRANSFUSIONINDICATIONS
Non-immune thrombocytopenia
1. Platelet count <20, 000/ml
2. Platelet count <50, 000/ml with bleeding or prior to an
invasive procedure or minor surgery
3. Platelet count <100, 000/ml prior to major surgery
4. Platelet count <100, 000/ml with recent intracranial
hemorrhage
5. Qualitative platelet defect with bleeding or prior to any
invasive procedure or surgery.
Immune thrombocytopenic purpur
Platelet transfusions are given to tide over the crisis when
platelet count is below 20, 000/ml.
Neonatal alloimmune thrombocytopenia
Either matched antigen negative platelets or irradiated
maternal platelets are to be given. If both are not available,
routine platelet transfusion can be given in life-threatening
bleeds.
Thrombocytopenia due to maternal antibodies
Platelet transfusions are given only in life-threatening
bleeds.
Plasma Transfusion
Plasma obtained from one unit of whole blood (450 ml) has
a volume of 200-220 ml. Plasma is frozen at 80 C and
stored at 30 C within 6 hours of collection of blood (FFP).
FFP has a shelf-life of one year and has all the labile and
stable coagulation factors. Outdated plasma is designated
as single donor plasma and it contains only the stable
160
coagulation factors. This has a shelf-life of 4 years at

30C.
Plasma transfusion is indicated in
Coagulation factor deficiency - both congenital and
acquired
Replacement therapy in congenital antithrombin III
deficiency, protein C deficiency and protein S deficiency
Clinical evidence of coagulopathy pending laboratory
results
Vitamin K deficiency with coagulopathy
Cheap substitute for albumin infusion, in increasing
the serum albumin value in Nephrotic syndrome. The
dose of plasma is 10-15 ml/kg.
Cryoprecipitate
Cryoprecipitate is prepared from one unit of FFP. FFP
frozen at 80 C thawed at 4 C triggers the precipitation
of certain protein present in plasma.
Each unit of cryoprecipitate contains 80-120 units of
factor VIII activity and 150 mg of fibrinogen. It is stored
at 30 C and is thawed for transfusion. Once thawed, it
should be used within 6 hours.
Granulocyte Transfusion
May be used as an adjunctive therapy in severe bacterial
sepsis.
Warning - All components for transfusion should be
as close to the room temperature as possible. This is done
by placing the components at room temperature for about
30 minutes.
BLOOD AND BLOOD COMPONENT THERAPY
161
Flow rates
RBC 3-5 ml/kg/hour
FFP within 30 minutes if volume
dose not exceed 10-15 ml/kg.
Platelets within 2 hours
Vascular access: Blood transfusion sets should have filters.
The standard IV cannulas or scalp vein sets with size
ranging from 21-27 gauges can be used.
CHAPTER 19
Envenomation
164
Snake Bite
Snake bite and envenomation is one of the commonest
causes for ICU admissions.
Often the snakes are brought to the casualty and will
be of help if the snake can be identified to be poisonous
or not.
The three common poisonous snakes in Kerala are
viper, cobra and krait.
How to identify them?
Vipers
Broad belly plates, triangular head, scales with or without
pit on the head.
Cobras
Head is covered with shields. There is a hood and the
spectacle mark on the hood. Third shield on the upper jaw
extends from the eyes to the nostrils and the fourth one is
small and triangular.
Krait
Central prominent row of shields with bands on the body.
When you are in doubt your forensic colleague can help
you.
The patient care is based on the identification of the
signs and symptoms of envenomation. All alleged cases
of envenomation are to be admitted and kept in close
observation for a minimum of 24 hours.
Snake venom is a mixture of about twenty or more
components and 90% are proteins. It contains, neurotoxins,
myotoxins, cardiotoxins, hemolysins, autacoids, enzymes
ENVENOMATION
165
like hyaluronidase and so on. The neurotoxins can cause

pre- and post-synaptic block in the myoneural junction to
produce flacid paralysis. The endogenous autacoids
released by the venom increase the vascular permeability
producing fluid loss from intravascular to extravascular
compartment.
Hypovolemia, hyperalbuminemia, hemo-concentration,
serous effusions, facial edema and ARDS result from
capillary leak. Tissue necrosis is caused by myotoxin,
vascular thrombosis and compartmental syndrome.
Bleeding can occur due to DIC, endothelial damage,
defibrination and thrombocytopenia. Hypotension is due
to vasodilation, myocardial dysfunction and hypovolemia.
Hypovolemia is due to vomiting, reduced fluid intake,
capillary leak syndrome, bleeding and myocardial
dysfunction. Persistent hypotension, hypersensitivity
reaction to venom, acute tubular necrosis and direct
nephrotoxicity result in acute renal failure.
Clinical Features
Early symptoms are vomiting, abdominal pain, and
regional lymphadenopathy. Pain and sewelling at local site
may or may not be evident depending on the type of venom.
Severe envenomation is characterized by progressive
deterioration of sensorium, myasthenic paralysis,
respiratory, circulatory, renal and coagulation failures and
ARDS. Viper envenomation is characterized by severe local
changes, even leading to gangrene of the limb and
hemorrhagic manifestations. Krait envenomation is mainly
neuroparalytic and cobra can have neuroparalytic and
myocardial toxicity. Pain without bleeding and other local
166
changes occur in cobra and krait envenomation, there is

too minimal local reaction. Severity of envenomation is
influenced by many factors.
The severity can be graded as follows:
No envenomation
Grade 0
Grade I
Local swelling, and pain without
(mild)
progression
Grade II
Swelling and pain progressive with mild
(moderate) systemic and laboratory manifestations
Grade III
Marked local response, severe systemic
(severe)
manifestations, significant alteration in
laboratory findings
The interval between bite, envenomation signs and
death are as follows
Viper
Local changes within 15 mts
Lymphadenopathy within 30 mts
Serious manifestations and death within
2 hours to 9 days (mean 48 hrs)
Cobra Local pain within 5 mts
Systemic manifestations and death
may occur within 30 mts to
60 hours (Mean 8 hours)
Krait
Local pain is not usual.
Systemic manifestations and death
may occur within 3 hrs to 63 hrs
(Mean 18 hours)
Investigations
Step I
- Hemogram, clotting time, clot retraction,

grouping and cross matching
ENVENOMATION
167
Step II
- Bleeding time, clotting time, APTT.

Platelet count,
Peripheral smear, PCV, CXR,
Step III
- RFT, S electrolytes, ABG, SGOT,
CPK, S cholesterol, Fibrinogen,
FDP, ECG
Clotting time is to be done every 6 hourly. RFT and
Electrolytes, other tests for coagulation, clot retraction and
FDP are done 12-24 hourly when clinically indicated.
Urine is to be measured and urine routine examination
is done for albuminuria and microscopic hematuria.
Treatment
ASV is the specific treatment. Monovalent antivenom is not
available in India.
1 ml of ASV available in India is able to neutralize 0.45
mg of krait, 0.6 mg of cobra and 0.6 mg of viper venom.
ASV should be administered as early as possible but
should be given at any time if signs of envenomation are
present. The dose is judged by the degree of envenomation.
Since the ASV is horse derived, allergy or anaphylaxis
can occur. So all measures to counteract anaphylaxis are
to be taken. Parents are to be informed about the risks and
benefits and an informed consent is obtained.
The lyophilized ASV powder is diluted 5-10 times with
normal saline and given as IV infusion. Before starting the
infusion an intradermal test is given. In evidence of allergy
or if there is history of allergy previously and also in severe
envenomation where ASV is a must, each dose of ASV is
started under cover of adrenaline (0.01ml/kg 1:1000 soln
S/C, Injection chlorphenaramine maleate 0.03 mg/kg IV
168
or diphenhydramine/mg/kg IV to reduce the risk of

anaphylaxis. If some untoward effects develop the ASV
infusion may be stopped and adrenaline and steroids are
given. ASV is restarted at a lower rate after adrenaline 2030 mts prior to infusion.
The dose of ASV is repeated if signs of envenomation
persists, every 6 hourly, often 5-6 vials, till all signs and
symptoms disappear. At the end of 6 hours, if CT is normal
but the clot retraction is abnormal ASV is to be continued.
Dosage Schedule
Mild
Local edema
Upto of limb
Moderate > of limb
Systemic signs +
CT prolonged
Early paralysis
Extensive edema
Necrosis/blebs
Systemic signs ++, + + +
Bleeding, hypotension
CT prolonged
ARF
Tests for allergy.
3-5 vials
5-15 vials
followed by 5
vials 6 hrly
Severe -
20 Vials
followed by
5 vials
6 hrly
Skin Test
ASV 0.01ml of 1:1000 solution in normal saline is injected
subcutaneously. Positivity is the appearance of a wheal in
20-30 minutes with or without systemic signs. The test can
be false positive in 50% and false negative in 20% of cases.
ENVENOMATION
169
Conjunctival Test
One drop of 1:100 solution of ASV in normal saline is put
into the lower conjunctival sac. If sensitive, conjunctivitis
and tears will appear in 10-30 mts.
Supportive Therapy
In early phase 1-1.5 times maintenance fluid is to be given.
Fluid losses are to be replaced accurately. Fluids should
be modified based on clinical situations like renal failure,
hypotension, administration of blood and blood
component therapy. In early phase, proper fluid therapy
prevents renal failure.
Broad spectrum antibiotics are to be given to prevent
infection. The oral cavity of snake can contain G +ve, G
ve and anerobic organisms.
Chloromycetin 100 mg/kg/day in 4 divided loses
or
Ampicillin 200 mg/kg/day in 3 divided doses.
is an acceptable first line therapy. Aminoglycosides can
be given if indicated with special care being taken with
respect to renal status.
Tetanus prophylaxis is to be taken when necessary.
IV methyl prednisolone 30 mg/kg/day for 3 days may
be given in patients with increased capillary permeability.
In hypotension
CVP is decreased and PCV < 40%Blood transfusion is
indicated.
CVP is decreased and PCV normalN saline is to be
infused.
CVP is decreased and PCV increased - Albumin or
hemocele is the choice.
170
CVP is normal and BP decreased - Steroids, IV methyl

prednisolone 2 mg/kg/every 6 hours is given.
In DIC - if FDP are increased, above 80 mcgm/ml,
heparin may be given.
In cobra or krait envenomation with neurological
involvement IV neostigmine sulphate 0.04 mg/kg/dose is given.
every 4 hourly or more frequently if clinical situation
warrants, till recovery. IV atropine sulphate 0.01mg/kg/
dose 4 hourly is to be given to counteract the untoward
effects. The dose is titrated to get the clinical effects and
the interval of administration is increased as the clinical
state improves.
Most important aspect of treatment is the early and
optimum administration of ASV and proper fluid therapy
in the early phase. Prognosis is good if ASV is administered
within 3 hours after the bite. Better be late than never. ASV
is effective upto 21 days after the snakebite.
Surgical help may be necessary in for development of
compartmental syndrome, amputation of the limb, skin
grafting, etc.
In myocardial or circulatory failure - dopamine,
dobutamine and steroids may be necessary.
ARDS - needs mechanical ventilation.
CHAPTER 20
Poisoning in
Children
172
Poison is defined as a substance which introduced into

the body or absorbed by a living organism causes injury
or death. Poisoning in young children can often be
accidental but in older children and adolescents it can be
suicidal also. Small children are more prone because of
their ignorance regarding poisonous nature of the object
Outcome depends on the time lapsed after the injestion,
the dose, the treatment received and how the person reacts
to the poison.
Any child admitted with unexplained coma, convulsions and altered sensorium, the possibility of poisoning
is to be considered and the history and circumstances are
to be revaluated.
TYPES OF POISONS
Household Poisons
Drugs and Pharmaceuticals
Plant poisons
Depending of the action the poisons can be
Stimulant poisons
Sympathomimetics
They produce restlessness, sweating, tachycardia,
dilated pupils and flushing.
For example, amphetamines, caffeine, cocaine,
decongestants, theophyllines.
Anticholinergetics
They produce warm dry flushed skin, tachycardia, dilated
pupils, hyperthermia.
For example, datura, belladona alkaloids, mushrooms.
POISONING IN CHILDREN
173
Hallucinogens
LSD and its analogues, Marijuana.
Withdrawal Syndrome
Alcohol, antidepressants, beta blockers, narcotics,
sedatives, hypnotics.
Depressant Poisons
Sympatholytic agents
They produce bradycardia, hypotension, bronchoconsriction, sedation and depression
For example, adnergic blockers, anti arrhythmics,
antihypertensives, Ca channel blockers, digoxin.
Cholinergic Agents
They produce nausea vomiting, abdominal cramps,
diarrhea, involuntary defecation and micturition,
sweating, salivation, lacrimation, bronchorrhea, blurred
vision and weakness.
For example, organophosphorus, organocarbomate,
pyridostigmine, etc.
Narcotics, sedatives and hypnotic agents
Analgesics, antispasmodics, alcohol, babiturates,
benzodiazepines
GENERAL SIGNS AND SYMPTOMS OF POISONING
Skin
Pallor, insulin, sympathomimetics, aniline deivatives
Cyanosismorphines, sulpha, CO, drug causing
methemoglobinemia, e.g. dapsone.
174
Sweatingcholinesterases inhibitors, nicotine, pilocarpine

Dry hot skindatura, belladona alkaloids.
Eyes
Miosis
Cholinesterase inhibitors, barbiturates, nicotine, opium,
morphine, para sympathomimetics
Mydriosis
Cocaine, datura, thallium, cyanosis, sympathomimetics.
Blindness
Methyl alcohol
Blurring of vision
Choline esterases, datura, alcohol, ergot.
GIT
Corrosives, phenol, cresol, mushrooms, digitalis, morphine,
choline esterase inhibitors
Cocaine, salicylates.
CNS
Headache
Atropine, CO, phenol, benzene, strychnine, cadmium.
Convulsion
Mushroom, cyanides, salicylates, datura, cocaine,
strychnine, cholinesterase inhibitors.
Delirium
Datura, cocaine, lead, arsenic, gold, ergot, barbiturates.
175
Coma
Salicylates, mushrooms, cholinesterase inhibitors phenol,
CO, cyanates, lead, barbiturates, morphine and nicotines
Respiratory
Pulmonary edema
CO, cyanide, narcotics, salicylates
Tachypnea cough and wheezing nicotine.
CVS
Bradycardia
Beta blockers, antiarrythmics, Ca channel blockers, organic
phosphates and carbomates, digoxin, odollum.
Tachyarrythmia Ventricular
Antipsychotics, tricyclic antidepressants heavy metals,
lithium, Mg.
MANAGEMENT
ABC
Removal of the Poison
Gastric lavage and emesis help in removing the poison
from gut. Emesis is not advised in children for fear of
aspiration. Gastric lavage can be done in hospitals except
when there is a suspicion of corrosives.
Inhibiting the absorption of poison
Activated charcoal 1gm/kg statum folowed by 0.2 gm/kg/
hour.
176
Cathartics not advised in children for fear of dehydration and dyselecrolytemias.

Whole body irrigation helps in eliminating the poison not
adsorbed by activated charcoal. Polyethylene glycol
electrolyte solution orally via nasogastric tube20-40 ml/
hour until clean effluent occurs.
Forced diuresis ionizable drugs can be excreted either in
acid or alkaline media, e.g. phenobarbitone, salicylates.
Hemodialysis
Useful in poisoning with salicylates, methanol, ethylene
glycol, theophylline, barbiturates, methotrexate, procainamide, digitalis, chloral hydrate
Hemoperfusion
Hemoperfusion over activated charcoal resin is done in
theophylline, salicylate, paraquat poisoning.
ANTIDOTES
PHYSICAL ANTIDOTES
They impair the absorption of poison
For example, demulcents-fats, egg albumin, activated
charcoa.
CHEMICAL ANTIDOTES
They neutralize the effect by forming compounds which
are innocuous
For example, potassium permanganate barbiturates
Tincture of iodine heavy metals
177
PHYSIOLOGICAL OR PHARMACOLOGICAL ANTIDOTES

They act at tissue level counteracting the poison by
blockade of receptor stimulation, enzymatic inhibition or
reactivation, displacement of poison from tissue binding
sites.
For example, Naloxone for opiates, atropine for cholinergic agents
Pyridoxine for INH
Chelating agents for heavy metals
Universal antidote
Can be used when poison is not known or more than one
poison is suspected
Powdered charcoal adsorb alkaloid
Milk of magnesianeutralisation of acids
Tannic acidPrecipitation of alkaloids, glucosides,
and heavy metals
INDIVIDUAL POISONS
Kerosine
Accidental ingestion of kerosine is very common in
children. Often the child aspirate it while drinking, or
during the process of vomiting which may be spontaneous
or induced by the care taker. Fatal dose is 30 ml.
But often the amount taken is very small and the child
comes with respiratory symptoms.
Treatment is Supportive
Gastric lavage is not advised. Oxygen therapy is advocated
if necessary.
Antibiotics if infection is suspected. Observe for 24
hours since the fatal period is 24 hours.
178
Acids
Mineral acids are corrosives. They extract water from the
tissues and coagulate cellular proteins and form acid
albuminates. Hemoglobin is converted to hematin. Local
irritation, bleeding and sloughing of mucosa and skin
occurs. They damage esophagus and stomach resulting in
necrosis and perforation.
Management
They can be diluted with milk or milk of magnesia. Gastric
lavage is contraindicated.
Because the child will be unable to swallow IV fluids
are to be given. Corticosteroids for 2 weeks are given to
decrease the incidence of stricture formation. Prophylactic
antibiotics can be given. Supportive therapy for respiratiry
distress is to be given.
Caustic Potash or Soda
They act as corrosives when concentrate and simple
irritants when dilute.
They are rapidly absorbed from mucous membranes
and combine with fat and protein, forming soaps and
proteinates. They produce soft deeply penetrating necrotic
areas.
Emetics and lavage are contraindicated. Weak acids
such as lemon or orange juice can be given as diluents for
neutralizing the alkali. Dilution with water should not be
done.
179
Iron
Has got 5 stages
30 mts 2 hours characterized by GIT
Stage 1
symptoms
Stage 2
Apparent recovery 2-6 hours
Stage 3
Circulatory failure 12 hours
Stage 4
Hepatic necrosis 2-4 days
Stage 5
Gasrtic scarring 2-4 weeks
When serum iron is >50 mg/dl toxicity manifests.
TREATMENT
Gastric lavage should be done. X-RAY will confirm the
success of the procedure because the iron in GIT can be
demonstrated in X-RAY.
Chelating Therapy
Desferroximine 10-15 mg/kg IV followed by 50 mg/kg
every 4 hourly as IM. Maximum dose to be given is 6 gm.
When iron is being excreted the urine will be coloured
red. The drug is to be continued till the blood level is
< 30 mg/dl.
ORGANIC CHEMICAL COMPOUNDS
Organophosphorus
The presently available pesticides come in the group of
organocarbamates Baygon, furadan, malathion.
The poison can get absorbed through all the routes.
They inhibit the enzyme acetyl choline esterase.
180
TREATMENT
The first step is to remove poison from body. Cleaning the
skin will reduce the absorption of poison through the skin.
This should be followed by gastric lavage. The treatment
of carbamate poisoning is same except that pralidoxim the
cholin esterase activator is contraindicated in carbamate
poisoning.
The drug is atropine which can be given as frequent
doses intravenously.as per the clinical judgement.
Clinically, the pupil size can decide the dose of atropine.
When the pupils are fully dialated then the dose can be
reduced. The child with organocarbamate poisoning
should not die due to atropine poisoning.
PARACETAMOL POISONING
The poisoning can be of 4 stages
Stage 1 First 24 hours
Stage 2 Next 24 hours
Stage 3 48-96 hours
Stage 4 stage of resolution 4 days -2 weeks
Fatal dose is 20-25 gms
The drug used in paracetamol poisoning is N-acetyl
cysteine orally or through NG tube 140 mg/kg followed
by 70 mg/kg 4 hourly for for 17 doses.
PLANT POISONS
DATURA (ummam in Malayalam)
It contains hyocine and hyocyanin
They first stimulate the higher centers and then depress
Fatal dose is 0.6-1gm (50-75 seeds)
181
TREATMENT
Stomach wash is to be given
The drug to be given is physostigmine.
ODOLLUM (OTHALAM in malayalam)
It contains many alkaloids producing vomiting diarrhea
followed by bradycardia, irregular respiration, collapse
and death.
TREATMENT
Stomach wash
Atropine
Correction of hyperkalemia
JETROPHA CUREAS (Purging nut-Kadalavanakku)
Poisonous parts are seeds and juice. The juice can cause
burns, blindness, gastritis, diarrhea and vomiting.
TREATMENT
Stomach wash
The rest is symptomatic
ARBUS PRECATORIUS (Kunnikkuru)
Similar to Viperine snake venom
Fatal dose 90-120 mg
TREATMENT
Symptomatic
Anti abrin if available
INDEX
A
ABG analysis 69
Acute renal failure 129
fluid management 130
hypovolemia 132
Acute respiratory failure 111
Acute severe asthma 115
Airways 41
management of respiratory
failure or arrest 42
nasopharyngeal airway 41
oropharyngeal airway 41
Antidotes 176
chemical antidotes 176
physical antidotes 176
Arterial access 32
modified Allens test 33
sites 32
technique-radial artery 32
Artificial airways 82
Chest compression in the child 17

Chest compressions in the
infant 16
Child-the Heimlich maneuver
20
advanced life support 22
respiratory-airway and
ventilation 23
unconscious child 21
victim conscious 20
Circulation 6
blood pressure 6
BP in children 7
capillary filling time 7
organ perfusion 7
pulse and heart rate 6
pulse pressure 6
pulse volume 6
skin perfusion 7
temperature 7
Coma 107
lab evaluation 109
management 108
treatment 109
Congestive cardiac failure 142
investigations 144
physical examination 143
treatment 146
CPAP 45
complications associated
with endotracheal
intubation 50
during the intubation
procedure 50
B
Bag-valve-mask ventilation 42
Self-inflating bag-valve
ventilation devices 44
ventilation face mask 42
Blood and blood component
therapy 157
cryoprecipitate 160
granulocyte transfusion
160
plasma transfusion 159
platelet transfusion 158
red cell concentrate 158
184
depth of insertion 47 en
endotracheal airway 46
endotracheal tube 46
preparation and technique
of intubation 48
size of the cndotrecheal
tube 47
Cyanotic spell 149
arrhythmias 150
SVT 150
D
Diabetic ketoacidosis 135
hydration 136
insulin therapy 138
complications 140
follow-up 139
investigations 139
Dobutamine and dopamine
147
Dysclectrolytemias 54
causes 54
extrarenal 55
factitious hyponatremia
55
hyponatremia 54
pscudohyponatremia 55
renal losses 54
treatment 56
E
Endotracheal tubes 82
Envenomation 163
clinical features 165
investigations 166
treatment 167
Euvolemic hyponatremia 57
External jugular vein 31
F
Foreign body airway
obstruction 17
H
Hepatic failure 121
agitation and restlessness 127
ascites 126
bloartificlal liver systems 128
coagutopathy 126
encephalopathy 122
fluid and electrolytes 125
liver support systems 127
liver trnnsplnntation 128
management of cerebral
edema 123
management of seizures 127
metabolic problems 125
methods to reduce serum
ammonia 124
nutrition 127
renal dysfunction 126
respiratory problems 127
Hypercalcemia 65
causes 65
treatment 65
Hyperkalemia 63
causes 63
treatment 63
Hypermagnesernia 67
causes 67
treatment 67
Hypematremla 58
Hypertensive emergencies 153
causes 154
nonrenal 154
renal 154
signs and symptoms 155
treatment 155
INDEX
Hypervolemic hyponatremia 57
Hypocalcemia 64
treatment 64
Hypokalemia 61
Hypomagnesemia 66
causes 66
treatment 66
Hypovolemic hyponatremia 57
I
Identifying a sick child 2
alertness 3
appearance 3
breathing 5
distractibility and
consolability 4
eye contact 4
glasgow coma scale 3
motor activity 4
pupil size 4
respiratory rate 5
speech/cry 4
work of breathing 5
Increased anion gap acidosis 75
Ionotropes 146
IV fluid therapy 51
decreased requirement 53
increased requirement 53
maintenance fluid and
electrolytes 52
maintenance of water 52
rate of fluid infusion 53
IV fluids in specific situations 54
acute diarrheal disease 54
M
Mechanical ventilator 83
basic system 83
Metabolic acidosis 79
Metabolic alkalosis 79
185
N
Normal anion gap acidosis 75
O
Other parenteral ionotropes 148
amrinone and milrinone 148
diuretics 148
vasodilators 148
Oxygen delivery systems 36
face tent 38
high flow systems 36
low flow systems 36
nasal cannula 40
nasal catheter 41
non-rebreathiug mask 38
oxygen hood 39
oxygen mask 36
oxygen tent 40
partial rebreathing mask 37
venturi mask 38
Oxygen therapy 35
P
Pediatric cardiopulmonary
resuscitation 9
causes in infancy beyond
newborns 10
beyond infancy 11 brea thing
13 circulation 15
head tilt-chin lift 12 jaw
thrust 12
pulse check 15 recovery
position 13 rescue breathing
13
Pediatric ventilators 84
pressure limited ventilators
186
84
disadvantage 85
volume limited ventilators 85
advantages 85 disadvantages
85 Physiological or
pharmacological antidotes
177
Plant poisons 180
arbus precatorius 181
treatment 181 datura 180
treatment 180 jetropha
cureas 181 treatment 181
odollum 181 treatment 181
Poisoning in children 171
general signs 173
management 175 symptoms
173
types 172
depressant poisons 173
household poisons 172
Practical approach to rapid
analysis of ABG 76
R
Respiratory acidosis
Respiratory alkalosis 79
78
shock 99
Status epilepticus 101
steps in management 102
anticonvulsants 103
investigations 106 refractory
status epilepticus 105
T
Tracheostomy 83
Types of ventilation 86
assist control mode of
ventilation 8
constant distending pressure
(COP) 86 controlled
mechanical ventilation 86
diseases with decreased lung
compliance 89 diseases with
increased resistance 90
intermittent mandatory
ventilation 88
positive end expiratory
pressure (PEEP) 87 pressure
support ventilation 89
synchronized intermittent
mandatory ventilation (SIMV)
88
V
S
Shock 96
cardiogenic shock 96
dissociative shock 97
management 97 symptoms
97 distributive shock 96
hypovolemic shock 96,97
obstructive shock 96 septic
shock 98
steps in management of
Vascular access 25
central venous cannulation
28 devices 27
devices and techniques 29
intraosseous cannulation 27
modified Seldingers
technique for insertion of
catheters and introducing
sheaths 29 venous access 26

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Management of

Professor and Head, Department of Pediatrics Government

JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD

How to Identify a Sick Child? .................................. 1

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

Identifying a sick child is the first step in the management

HOW TO IDENTIFY A SICK CHILD?

Verbal Response Total Points 5

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

Motor Response Total Points 6

HOW TO IDENTIFY A SICK CHILD?

Upper limit of RR is:

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

HOW TO IDENTIFY A SICK CHILD?

Minimum acceptable level of systolic BP.

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

So, with the help of the pediatric assessment triangle the

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

The relevance and community participation of pediatric

PEDIATRIC CARDIOPULMONARY RESUSCITATION

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

location (e.g. in a burning building). Great care must be

PEDIATRIC CARDIOPULMONARY RESUSCITATION

when airway is opened. This can be accomplished by a

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

If the victim is an infant place the mouth of the rescuer

PEDIATRIC CARDIOPULMONARY RESUSCITATION

there, he can apply cricoid pressure to displace trachea

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

If pulse is not palpable or heart rate is less than 60 and

PEDIATRIC CARDIOPULMONARY RESUSCITATION

4. At the end of the each compression, pressure should

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

Determine responsiveness shake and

Call for help

Position the victim

Look, listen and feel

Open the airway

Locate the position of

considered when foreign body aspiration is witnessed or

PEDIATRIC CARDIOPULMONARY RESUSCITATION

In InfantsBack Blows and Chest Thrusts

Fig. 2.1: Back blows

Fig. 2.2: Chest thrusts

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

3. After delivering the blows, place the free hand on the

PEDIATRIC CARDIOPULMONARY RESUSCITATION

Fig. 2.3: Abdominal thrusts

2. Place the thumb side of one first against the victims

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

Fig. 2.4: Head tilt-chin-lift maneuver

PEDIATRIC CARDIOPULMONARY RESUSCITATION

Fig. 2.5: Recovery position

RespiratoryAirway and Ventilation

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

Establishment of a vascular access is highly essential in

of resuscitation. The preferred site of venous access remains

Fig. 3.1: Intraosseous cannulation

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

venous cannulations are done only if the benefits outweigh

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY

the guidewire is held in place. A large catheter or a catheter

A chest radiograph is taken to verify that the catheter tip

MANAGEMENT OF EMERGENCY PEDIATRICS MADE EASY