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MODULE FOR TRAINING OF SPECIALIST IN
PEDIATRICS ON NEWBORN CARE
Module - A
(Management of Common Neonatal Problems)
Developed by:
Dr. M.L. Gupta Associate Professor Deptt. of Paediatric Medicine SMS Medical College & J.K. Lon Hospital, Jaipur
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INDEX
1. General objective of the training 1
2. Sessionwise plan 2
3. Resuscitation of Newborn 3-31
4. Management of Birth asphyxia 32-40
5. Management of Neonatal Convulsions 41-52
6. Management of Neonatal Jaundice 53-67
7. Management of Neonatal Sepsis 68-83
8. Management of Birth Injuries 84-91
9. Annexure : Questionnaire for Pre and Post test 92-94
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General objective of training
In modern times, improvement in knowledge and technology has
greatly influenced the health of children. However, past decade was marked
by limited progress in reducing infant mortality largely due to a failure in
reduction of neonatal mortality.
There is widely shared but mistaken idea that improvement in
newborn health requires advanced technologies and highly specialized staff.
The reality is that many conditions that result in perinatal death can be
prevented or treated without sophisticated and expensive technology. What
is required is essential care during child birth and immediate postpartum
period and a few critical interventions for the newborn during the first days of
life.
In this era of evidence based medicine the criteria of diagnosis and
management of illness changes frequently, hence, objective of this training
to specialists working at referral/ district level is to make them acquint about
the recent trends in the management of common newborn problems. The
module for training of pediatricians has been developed in three sections
"Module - A" contains care of newborn babies with common problems like
Birth asphyxia, Sepsis, Jaundice, Birth injuries and Convulsions, "Module -B"
contains Care of Low Birth Weight (LBW) babies and "Module - C" contains
Intensive Care of a Sick Newborn.
We hope that these modules will serve as a useful guide during
training and afterwards in practice for the specialist in Pediatrics working at
referral/district hospitals.
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TRAINING OF SENIOR/ JUNIOR SPECIALISTS IN PEDIATRICS
SESSION WISE PLAN
Day I II III IV
1 Resuscitation of Newborn
Management of Birth Asphyxia
Preparation and Initial steps of Resuscitation
Bag & Mask ventilation
Chest Compression,
Medication and Endotrached
Intubation
Practice of resuscitation on Baby Manikin
2. Management Convulsions
Management of Jaundice
Management of sepsis
Management of Birth injuries
3.
Management of LBW babies
Intensive Care of Newborn Including use of equipments in
NICU- e.g. Incubators phototherapy and warmer etc.
4. Visit to labour room and OT for demonstrate of
Neonatal Resuscitation
Setting up of nursery at district
level hospital (Group work)
5. Visit to nursery for intensive care of newborn and
demonstration of equipments used in NICU
Setting up of nursery at district
level hospital (Presentation)
6. Visit to Nursery for demonstration on care of LBW,
Asphyxia, convulsions, sepsis and Jaundice.
Post test Evaluation & Discussion
No. of participants in each batch 10
Duration of Training 6 days
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Day 1 : Session I –III (Resuscitation of Newborn)
Duration : 4½ Hours
Objectives : At the end of sessions the trainees should be able to :
• Understand the need and use of various equipments for neonatal
resuscitation.
• Set up a corner for neonatal resuscitation in labour room.
• Follow stepwise approach to neonatal resuscitation.
• Perform bag and mask ventilation and endotrached intubation in a
proper way.
• Administer drugs during resuscitation as required.
Methodology
• Lecture-Discussion
• Practical demonstration on baby manikin.
• Practice resuscitation on baby manikin in groups.
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RESUSCITATION OF NEWBORN
PREPARATION FOR RESUSCITATION
Anticipation and preparation are the key factors to effective
resuscitation, Anticipation of a likelihood of resuscitation is only possible if a
good antenatal history is available so that the high-risk neonate can be
identified. It is essential to go through the maternal documents before the
delivery and talk to the obstetrician concerned.
Personnel
Preparation for resuscitation requires having the right persons and
equipment available in the delivery area. At least 1 person skilled in initiating
neonatal resuscitation should be present at every delivery. An additional
skilled person capable of performing a complete resuscitation should be
available immediataly if required. Resuscitation of a severely depressed
newly born infant requires at least 2 persons, 1 to ventilate and intubate and
another to monitor heart rate and perform chest compressions. A team of 3
or more persons with designated roles is highly desirable especially during
medication administration. A separate team should be present for each
infant of a multiple gestation. Each team should have an identified leader,
and all team members should have specifically defined roles. It is preferable
that such teams have opportunities to practice together and have regular
"resuscitation drills" to keep their skills intact. New members should meet the
leader well in advance so that doubts can be clarified. Personnel should
wear gloves and other appropriate protective barriers when handling newly
born infants or contaminated equipment. Techniques involving mouth suction
by the healthcare provider should not be used.
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Equipment
Although the need for resuscitation at birth can often be predicted by
risk factors, in many cases it is not anticipated. A complete set of
resuscitation equipment and drugs should be maintained at hand and in fully
operational condition wherever deliveries occur. Equipment required for
resuscitation is life saving and procurement and maintenance of the same
should be given top priority. Essential resuscitation equipment is given in
Table 1. Two radiant warmers should be available in the labor room and the
obstetric OT at all times. It not available, a makeshift warmer (table and a
200 Watt bulb) may be used.
Environment
Prevention of heat loss is important for the newly born, Cold stress
can increase oxygen consumption and impede effective resuscitation;
however, hyperthermia should be avoided as it causes respiratory
depression. Whenever possible, the infant should be delivered in a warm,
draft-free area. Rapid drying of the skin, removing wet linen after delivery,
placing the infant under a radiant warmer, and wrapping the infant in
prewarmed blankets will reduce heat loss. Another strategy for reducing heat
loss is placing the newly born skin-to-skin on the mother's chest or abdomen
to use her body as a heat source.
Table 1: Neonatal Resuscitation Supplies and Equipment
Suction equipment
- Bulb syringe / Mucus extractor
- Mechanical slow suction (100 mm Hg) with tubing
- Suction catheters, 5F or 6F, 8F, and or 12F
Bag-and-mask equipment
- Neonatal resuscitation bag with a pressure-release valve and
/or pressure manometer and reservoir (the bag must be
capable of delivering 90% to 100% oxygen)
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- Face masks, newborn and premature sizes (masks with
cushioned rim preferred)
- Oxygen with flow meter (flow rate up to 10 L/min) and tubing
(including portable oxygen cylinders)
Intubation equipment
- Laryngoscope with straight blades, No. 0 (preterm) and No. 1
- Extra bulbs and batteries for laryngoscope
- Endotracheat tubes: 2.5, 3.0, 3.5, and 4.0, mm ID (No. 2 tube
not recommended)
- Sty let (optional)
- Scissors
- Tape for securing device for endotracheal tube
Umbilical vessel catheterization supplies
- Sterile gloves
- Scalpel or scissors
- Povidone-iodine solution
- Alcohol sponges
- Umbilical tape
- Three-way stopcock
- Flushing solution
Miscellaneous
- Gloves and appropriate personal protection
- Radiant warmer or other heat sources
- Firm, padded resuscitation surface
- Clock (timer optional)
- Warmed linens (at least two per delivery)
- Stethoscope
- Tape, 1/2 or 3/4 inch
- Oropharyngeal airways
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- Syringes, 1, 2, 5, 10, 20, and 50 ml
- Needles, 25, 21, and 18 gauge.
Medications
Administration of drugs is rarely indicated in resuscitation of the newly
born infant. However, in rare cases the following medications are used:
- Epinephrine 1:10 000 (0.1 mg/ml) Dilute 1 ml of 1:1000 solution
and keep ready
- Isotonic crystalloid (normal saline or Ringer's lactate) for
volume expansion 100 or 250 ml
- Sodium bicarbonate, dilute 7.5% solution 1:1 with DW to get
approximate concentration
- Naloxone hydrochloride 0.4 mg/ml 1-ml ampoules; 1.0 mg/ml
2-ml ampoules
Communication
Communication among caregivers of the mother and baby should
include details of maternal history and treatment that may affect the baby.
For example, maternal sedatives and analgesics, tocolytics, and
corticosteroids all can influence respiratory function at birth. Details of
antepartum and intrapartum monitoring and ultarasonography are important.
When time permits, the team responsible for care of the newly born should
introduce themselves to the mother and family before delivery. In case of
potentially lethal fetal malformations or extreme prematurity, the family
should be asked to express their desires regarding the extent of
resuscitation.
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INITIAL STEPS IN RESUSCITATION
Decide if a rewborn needs to be resuscitated
Within a few seconds you ask yourself the following questions:
• Is the amniotic fluid clear of
meconium?
• Is the baby breathing or crying?
• Is there good muscle tone?
• Is the color pink?
• Was the baby born at term
If the answer to all of these is 'Yes," the baby may receive routine
care to continue transition. If the answer to any one of these is "No," or the
baby was born pretern, the baby will require some form of resuscitation.
The initial steps in resuscitation includes the following:
1. Preventing heat loss and providing warmth
2. Opening and clearing the airway.
3. Drying, Stimulating and Repositioning
4. Evaluation and Oxygen administration if required.
Preventing heat loss is achieved by placing infant under radiant
warmer which has already been switched on manual mode before the baby
arrives. Infants who suffer heat loss have increased metabolic rate and
require more oxygen. All babies require this step in the resuscitation
protocol.
Opening the airway is achieved by
positioning and suctioning the infant's mouth
and then nose to clear the airway. The baby
should be placed on his back in a flat position
with the head slightly extended at the atlanto- Fig. 1
Fig. 1
Birth
• Clear of meconium? • Breathing or crying? • Good muscle tone? • Color pink? • Born at term
Routine care
• Provide warmth
• Dry
Yes
Needs resuscitation
No
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ocipital joint. There is no need to put the baby in a head-low position. Care
should be taken to prevent hyper or hypo extension since either may
decrease air entry (Fig 1).
We may place a rolled towel under the shoulders elevating them 1
inch off the mattress. This is specially useful in babies with large occiputs
resulting from moulding, caput or prematurity. If the baby is correctly
positioned, he maintains an open airway. If copious secretions are seen in
the mouth, one may turn the head to one side. This will allow secretions to
collect in the mouth, rather than in the posterior pharynx, where they can be
easily removed.
The mouth should be suctioned first in order to make sure that there
is nothing for the infant to aspirate if he should gasp when the nose is
suctioned. (Fig.2)
Also, touching the posterior pharynx can stimulate the hypopharynx
and cause bradycardia or apnoea. The act of suction provides a degree of
tactile stimulation. In some cases this is all the stimulation that is needed to
initiate respiration. If material in the mouth and nose is not removed before
the infant establishes respiration, it can be aspirated into the trachea and
lungs. One can use a bulb syringe, DeLee suction catheter or mechanical
suction (at 100mmHg pressure) to remove secretions.
Fig.2
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Drying is done with the help of prewarmed towels. Body and head should be
dried to prevent evaporative heat loss. Care should be taken to remove the
wet towel from contact with the infant, otherwise evaporative heat loss will
continue. Keep the neonate euthermic at all times. Remember that
hyperthermia can also be harmful!
Providing tactile stimulation is required if the newborn does not breathe
after suction and drying (Fig3a). Quickly and firmly rubbing the infant's back
is another safe method trying to initiate respirations. (Fig3b).
Harmful actions Potential consequences
1. Slapping the back Bruising
2. Squeezing the rib cage Fractures, pneumothorax
3. Forcing thighs onto abdomen Rupture of liver/ spleen
4. Using hot/ cold compresses Hypothermia / hyperthermia,
Burns
5. Blowing cold oxygen onto face Hypothermia
Fig. 3a
Fig. 3b
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Evaluating the infant
If the newborn does not start breathing after TWO attempts of tactile
stimulation, bag and mask ventilation is initiated immediately. Continued use
of tactile stimulation in a newborn who does not respond is not warranted
and may be harmful since time is being wasted.
Evaluation of the newborn is based on three vital signs:
1. Respiratory effort
2. Heart Rate
3. Color
Steps in evaluation
1. Observe and evaluate the baby's respiration; if normal, go on to the
next sign; if not (absent or ineffective) begin positive pressure
ventilation.
2. Check the baby's heart rate. If > 100/min go on to next sign; if not
irrespective of respirations, initiate positive pressure ventilation.
3. If the baby is breathing and the heart rate is > 100/min, evaluate the
color. If central cyanosis is present, administer oxygen.
Use of free flow Oxygen
At birth, most babies have some degree of cyanosis. By 60-90 secs.
Most babies begin to become pink although peripheral cyanosis may still be
present. However there are times when baby has regular respiration and a
heart rate of > 100/min but central cyanosis persists. In such cases the
respiration may be adequate to provide enough oxygen to keep the heart
rate > 100/min but not adequate to fully oxygenate the baby. In this situation,
positive pressure ventilation is not immediately indicated. Instead, free flow
oxygen should be given to improve the color. Hence we should know how to
manage free flow oxygen
1. Initially - High concentration of oxygen (at least 80%)
2. Once the baby becomes pink oxygen should be gradually withdrawn
until baby can remain pink while breathing room air.
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3. If cyanosis persists the baby should continue to receive just enough
oxygen to remain pink.
What is free flow Oxygen?
Free flow oxygen refers to blowing oxygen over the baby's nose so
that the baby breaths oxygen enriched air. This can be done by holding the
end of an oxygen tube close to the nose within a cupped hand or by holding
the oxygen mask over the mouth and nose. To get the specific concentration
of oxygen, one must set the correct combination of (a) liter flow and (b)
distance from the end of the tube to the baby's nose. Research has shown
that the concentration can be controlled with a flow of 5 lits/min (Fig 4).
A Self-inflating bag should not be used to deliver free flow oxygen.
Oxygen should be heated and humidified before delivery. However, during
emergency dry oxygen may be used briefly to stabilize the baby's condition.
If a baby continues to require oxygen for maintaining a pink color for a longer
time, move the baby into an area where oxygen concentration in the blood
can be monitored.
Tube Distance Oxygen %
1/2" 80%
1" 60%
2" 40%
Oxygen by Mask %
(a) Held Firmly 60-80
(b) Held Losoely 40
Fig. 4
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BAG AND MASK VENTILATION
Almost 85% of newborns who would require resuscitation beyond the
initial steps respond to bag and mask ventilation alone. Before learning the
procedure let us familiarize ourselves with the equipment.
Resuscitation Bags: Two basic kinds of bags are available (Fig5). The
anaesthesia bags and self-inflatable bags.
Anaesthesia bags inflate only when they are connected to oxygen or
any other compressed gas source. Self-inflatable bags, as the name
suggests, remain inflated unless compressed. They have the following parts:
1. Air inlet
2. Oxygen inlet
3. Valve assembly
4. Patient outlet
Resuscitation bags used for neonates should be no larger than 750
ml in capacity and preferably 250-500ml; larger bag volumes make it difficult
to judge delivery of the small tidal volumes (5 to 8 ml/kg) that are required.
Self-Inflating Bags:
These refill- independently of gas flow. Most bags of this type have an
intake valve at one end that pulls in room air, diluting the oxygen flowing into
the bag at a fixed rate. Delivery of high concentrations of oxygen (90% to
Fig. 5
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100%) requires an attached oxygen reservoir. To maintain inflation pressure
for at least 1 second, a minimum bag volume of 450 to 500 ml may be
necessary. If the device contains a pressure-release valve, it should release
at approximately 30 to 35 cm H20 pressure and should have an
override/closure feature to permit delivery of higher pressures if necessary.
Bags that do not have this feature should be equipped with an in-line
manometer. They cannot be used to deliver oxygen passively through the
mask because the flow of oxygen is unreliable unless the bag is being
squeezed.
Flow-Inflating Bags:
The flow-inflating (anesthesia) bag inflates only when compressed
gas in flowing into it and the patient outlet is at least partially occluded.
Proper used requires adjustment of the flow of gas into the gas inlet,
adjustment of the flow of gas out through the flow-control valve, and creation
of a tight seal between the mask and face. Because a flow inflating bag is
capable of delivering very high pressures, a manometer should be
connected to the bag to monitor peak and end-expiratory pressures. More
training is required for proper use of the flow-inflating bag than the self-
inflating bag but the flow-inflating bag can provide a greater range of peak
inspiratory pressures and more reliable control of oxygen concentration. It
can also be used to provide free-flow oxygen and provides a certain amount
of PEEP during this process which may be useful for preterm babies.
While some bags have pressure gauge attachment (Fig 6), in others
pressure gauge could be connected to the patient outlet directly with the
help of an adaptor which is interposed between the patient outlet and mask.
The pressure gauge helps in delivering the desired pressure.
Fig. 6
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An additional safety feature is the pressure release valve - this is set
to release or pop off at pressures exceeding 30 - 35 cms H2O (Fig 7).
Even though room air resuscitation may be adequate in some patients,
ventilation with 100% oxygen is ideal. Such high concentrations are achieved
by connecting oxygen supply to the oxygen inlet and oxygen reservoir at the air
inlet. Two commonly available reservoirs are shown in Fig 8
Oxygen concentrations delivered when the bag is connected to
oxygen at 05 litres per minute is 40% without and 90-100% with the oxygen
reservoir. In the absence of O2 resuscitation must be continued with room
air. Any bag with capacity between 240 to 750 ml is acceptable. However, a
bag with capacity of 450 ml is deal.
Fig. 7
Fig.8
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Face Masks
Two basic kinds are available - masks with cushioned rims and masks
with noncushioned rims. Masks with cushioned rims form a better seal and
prevent injury to the face and eyes. Amongst masks 0,1 and 2 sizes are
available and should be appropriately chosen. Size 00 is used for smaller
infants while size OI is used for larger infants. Two shapes available are
round and conical. Masks with conical shape (with conical end towards
bridge of nose) provide better seal and do not damage the eyes (Fig 9).
Oxygen
An oxygen sources should be available. A flow meter, air source and
blender are also preferred so that during free flow of oxygen the
concentration can be adjusted more accurately.
Checking the equipment
Checking the bag is essential to ensure that there are no tears or
leaks.
It is always recommended to check the bag by blocking the patient
outlet tightly and compressing the bag. It is also a good idea to practice
delivering the following pressures if a pressure gauge is available -
1. 15 - 20 cms H2O
2. 20 - 30 cms H2O
3. 30 - 40 cms H2O
Do not ever forget to connect the oxygen source and reservoir before
putting it to use. Pressure valve should be checked by keeping it open and
Fig. 9
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hearing the release of air if higher pressure is applied. In an anesthesia bag
the flow-control valve and flow meter should be adjusted to ensure adequate
filing.
Cleaning the equipment:
Most bags and masks are autoclavable. They can also be sterilized
by immersing in 2% glutaraldehyde for 20-40 min and washing with distilled
water. They should be dried before used. Gas sterilization, if available, is
also useful.
Indications of Bag and Mask Ventilation
1. Apnoea or gasping respiration
2. Heat rate less than 100 per minute despite respirations
In addition, any newborn who has spontaneous respiration, normal
heart rate (i.e. heart > 100/min) and persistent central cyanosis may be
given a trial of bag and mask ventilation if free flow oxygen fails to relieve the
cyanosis.
Procedure for Bag Mask Ventilation (BMV)
• Position the infant correctly on a firm surface in a supine position with
head in slightly extended position to open the airway by placing a
small roll of cloth under the shoulder blades.
• An appropriate sized mask (adequate to cover chin, mouth and nose
of the infant) should be selected and attached to the bag. Position the
mask correctly and apply a firm seal so that air does not escape
between face and the mask. The upper end of the mask is at the
bridge of the nose with the lower end being at tip of the chin. Cupping
the chin and the mask is helpful in maintaining this. Care should be
taken not to apply pressure on the trachea or eyes and to position
oneself so as not to obstruct the view of the chest. The bag should be
attached to the oxygen source.
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• Test the adequacy of seal by giving two to three breaths and seeing
for the chest rise. If the chest does not rise, take the following
corrective actions sequentially.
Action Condition Corrected
Reapply mask Inadequate seal
Reposition infant's head Blocked airway
Check for secretions and suction if present Blocked airway
Increase the pressure slightly Inadequate pressure
Ventilate with mouth slightly open Blocked airway
Squeeze the bag adequately enough to cause a slow and easy rise of
the chest. Although the pressure required for establishment of air breathing
is variable and unpredictable, higher inflation pressures (30 to 40 cm H2O or
higher) and longer inflation times may be required for the first several
breaths than for subsequent breaths. Visible chest expansion is a reliable
sign of appropriate inflation pressures. A manometer attached to the bag
and mask assembly is also useful to determine the amount of pressure
required. Saying "squeeze 2-3" while bagging is helpful in maintaining a
rhythm. If the chest does not rise try a new bag. When adequate chest rise is
seen begin ventilation.
Ventilate at 40 breaths per minutes. Rate of 30 to 60 breaths per
minute are acceptable. In case the neonate requires chest compression 30
breaths are given in a minute and one breath is delivered after every three-
chest compression. Pressures required to inflate lungs are as follows -
Normal lungs - 15-20 cms H2O
Diseased lungs - 20-40 cms H2O
Evaluate heart rate - After 30 seconds of bag and mask ventilation, count
the heart rate for 06 seconds and multiply by 10 to obtain the heart rate in
beats per minute. Take the following decisions as per the heart rate -
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1. The heart rate is above 100 and the infant has spontaneous
respirations Discontinue ventilation, provide tactile stimulation and
give free flow oxygen. However, if spontaneous respirations are
absent, ventilation must be continued.
2. Heart rate between 60 &100 - continue ventilation.
3. Heart rate < 60 beats per minute - ensure ventilation with 100%
oxygen and initiate chest compression.
An orogastric tube (8F) must
be passed if bag and mask
ventilation is continued for more
than 02 minutes. The stopcock is
left open. This is done to relieve
gastric distension, which invariably
result following prolonged bag and
mask ventilation (Fig 10).
Any infant requiring ventilation must have periodic monitoring of heart
rate and respiration till both parameters become normal. In case the
parameters fail to become normal the patient may require further
resuscitative measures such as chest compression, medications and
endotracheal intubation.
Contraindications to Bag and Mask Ventilation
• Diaphragmatic Hernia - Since bag and mask ventilation result in
gastrointestinal distension and since stomach and bowel are in
thoracic cavity, bag and mask ventilation leads to further aggravation
of cardio-respiratory compromise. In case these patients need
positive pressure ventilation as they normally do, they must be
intubate.
Fig. 10
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• In infants who have history of Meconium stained amniotic fluid and
have respiratory depression, intrapartum and intratracheal suctioning
precedes positive pressure ventilation.
CHEST COMPRESSIONS
In severe asphyxia both heart rate and myocardial contractility are
decreased resulting in bradycardia and less powerful contraction. This
results in decreased tissue perfusion and hence decreased oxygenation to
vital organs. Chest compressions provide an artificial heartbeat, thus
restoring circulation to life-sustaining level. Positive pressure ventilation with
100 % oxygen must accompany chest compression to oxygenate circulating
blood.
What Is chest Compression?
Rhythmic compressions of the sternum that
1. Compress the heart against the spine
2. Increase the intrathoracic pressure
3. Circulate blood to the vital organs of the body. When pressure on the
sternum is released, blood enters the heart form the veins.
Indications For Chest Compressions
If in spite being ventilated with 100% oxygen, a newborn fails to
achieve an adequate heart rate, chest compressions must be performed. In
most infants positive pressure ventilation (PPV) with 100% oxygen itself
raises heart rate to adequate levels. Therefore, the decision to perform chest
compression should be based on the heart rate obtained after 30 seconds of
PPV and not on the heart rate obtained at delivery. If the heart rate is less
than 60/min despite good assisted ventilation for at least 30 seconds,
chest compressions should be started. Once the heart rate reaches 60,
chest compression are withdrawn.
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Positioning For Chest Compression
By now, the baby is already positioned for PPV and is being ventilated
with 100% oxygen. A person performing chest compression must gain
access to the chest and two persons should position in such a way that each
one can do an effective job with the other.
Methods of chest compression:
Two methods are used:
1. Two thumb method (Fig 11): This is recommended.
2. Two finger method (Fig 12).
Fig. 11
Fig. 12
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Location of Compression:
Pressure is applied to the lower third of sternum strictly avoiding
applying pressure on the xiphoid. The lower third of sternum is just below the
line joining the two nipples. (Fig 13).
Depth of Compression:
Enough pressure
should be used to
compress the sternum to
approximately 1/3 of the
antero-posterior diameter
of the chest to generate
a palpable impulse (Fig
14). One compression consists of the downward stroke plus the release.
Shorter compression phase than the relaxation phase has been proved to be
more effective.
Rate of Compression:
Compression/release action should be repeated 90 times per minute
and ventilation 30 times per minute making the ratio as 3:1. This will be done
by counting 1-2-3 for three compression and 4 for the PPV (interposed
ventilation) which together should take 2 seconds. (1/2 seconds for each
event).
Fig. 13
Fig. 14
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Checking Effectiveness of Compression:
Heart rate should be checked every 30 seconds. It should be checked
for no longer than 6 seconds. (this causes minimal interruption in chest
compressions).
Ventilation should be discontinued while the heart rate is being
checked so that breath sounds do not obscure the heart sounds. It is
important to know whether the blood is being circulated effectively as a result
of chest compression. The pulse should be checked periodically if at all
possible. This cab be done at carotid, brachial and femoral.
Dangers of Chest Compression:
Broken ribs, lacerated liver, pneumothorx
Precautions :
1. Do not remove the finger or thumb in between compressions.
2. Feel the pulse for effectiveness of compression.
3. Do not squeeze the chest.
4. Continue positive pressure ventilation. It using bag and mask,
interpose a ventilation every third compression.
Evaluation and Follow up Action:
After 30 seconds of chest compression, check the heart rate with
cessation of procedure for six seconds
If HR < 60/ min (i) Continue compression
(ii) Continue ventilation
(iii) Initiate medication
If HR > 60/min (i) Discontinue compression
(ii) Continue ventilation till HR > 100/min
and good respiratory efforts
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DRUGS IN NEONATAL RESUSCITATION
Neonatal resuscitation, as any other resuscitation procedure, is a
team effort and before any medication is administered to a neonate, the
team leader has to ponder over the above 4 questions.
Why Should Drugs Be Given To A Neonate During Resuscitation?
• To provide substrate and stimulation to the heart so that it can supply
oxygen and nutrition to the body, primarily to the brain.
• Give support to the myocardium by administration of inotropic and
chronotropic drugs.
• Correct acidosis, if it's documented and resuscitation is prolonged.
• Ensure adequacy of blood volume.
• Combat depression due to narcotic administration in the mother.
When Should Medications Be Administered During Ressuscitation?
Medications should be administered during resuscitation when in spite
of adequate ventilation and cardiac massage, together for more than 30
seconds, the heart rate remains < 60/min and is not improving or if there is
initial asystole after 30 sec of BMV. Do not 'wait', to take 'weight', use
approximation - 1, 2 or 3 kg?
What Drugs May Be Required By the Neonate?
• Epinephrine
• Sodium bi-carbonate/THAM
• Naloxone
• Volume expanders
• For special situation - calcium
How (Or What) Should Be The Route Of Administration?
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Endotracheal: This route can be used to give epinephrine. Effect is rapid
and safer than intra-cardiac route. Can also be used to administer naloxone
when mother has been given narcotic analgesia.
Intravenous: Most rapid and convenient intravenous route is through
umbilical vein catheterization. Catheeter should be inserted about 2-3 cm
past the abdominal wall at the point of easy return of blood. In this position
catheter will be in or just below the ductus venosus. After any medication the
catheter should be flushed since there is no flow through the umbilical vein
after the separation of the cord.
Other routes: Intraosseous route may be tried.
Epinephrine
• 0.1-0.3 ml/kg IV 1:10,000 of epinephrine solution (prepared in normal
saline); may be repeated every 3-5 min if required.
• Endotracheal route is easier and effective. Dose remains the same.
Sodium bi-carbonate
Indication:
Documented acidosis (pH <7.14) and/or after prolonged resuscitation
acidosis is suspected. It should be given after effective ventilation has been
esalished; otherwise it will increase Pa CO2, leading to Respiratory acidosis
and compounding the clinical situation.
Dose:
• 2 meq/kg of 7.5% solution (1meq/ml) diluted in equal amount of
distilled water (not in dextrose or normal saline).
• 50% of the dose should be given stat at the rate of 1 meq/kg/min IV
and remaining as IV infusion over 3-4 hours with monitoring of ABG.
Sodium bi-carbonate should not be mixed with epinephrine, calcium
and phosphates.
28
Complications:
• Hypercarbia
• Hypernatremia
• Hyperosmolality
Naloxone
Indication:
If the mother has been given narcotic analgesia within 4 hours of
delivery, the neonate may manifest with respiratory depression. This
presents as apnoea, bradycardia and cyanosis that improves with bag and
mask ventilation but recurs on stopping respiratory support. Naloxone should
be administered and respiratory support maintained till spontaneous
respiration is established.
Dose:
0.1-0.2 mg/kg or 0.25-0.5 ml/kg (each ml contains 0.4 mg), IV or
through endotracheal route. It can be repeated 3 times if there is no
response. It should not be used if mother is a chronic user of narcotics.
Volume expanders:
Normal saline
Ringer's lactate
Plasma/plasma expanders
Whole blood
Indication:
• In Shock
• Acute bleeding
• Poor response to resusctitative efforts
Dose:
10 ml/kg IV over 5-10 min; slower in preterm neonates
29
Special situation
When mother has been given Magnesium sulphate for control of
eclampsia, baby will require calcium gluconate, 1-2 ml/kg slow IV with heart
monitoring.
ENDOTRACHEAL INTUBATION
Indications
These will vary depending on the presence or absence of meconium,
gestational age of the infant, degree of respiratory depression, response to
bag-valve-mask ventilation, and skill and experience of the resuscitator.
Endotracheal intubatin may be indicated at several points during neonatal
resuscitatio:
• When tracheal suctioning for Meconium is required
• If bag-mask ventilation is ineffective or prolonged
• When chest compressions are performed
• when tracheal administration of medications is desired
• Special resuscitation circumstances, such as congenital
diaphragmatic hernia or extremely low birth weight (for administrating
surfactant)
Equipment (Fig 15)
Tubes should be of uniform diameter, without a shoulder, with a
natural curve, radiopaque, and with a mark to indicate the appropriate depth
of insertion. If a sty let is used, it should not protrude beyond the tip of the
Fig. 15
30
tube. Appropriate size and depth of insertion depends on birth weight and
gestational age (Table 2). A laryngoscope with straight blade size 0 (7.5 cm)
for premature infants, size 1 (10 cm) for term infants is preferred.
Table 2: Chart to decide tube size required.
Tube size ID (mm) Weight (grams) Gstational age
2.5 <1000 <28 weeks
3 1000-2000 28-34 weeks
3.5 2001-3000 >34-38 weeks
4 >3000 >38 weeks
Technique of Endotracheal Intubation
Tracheal intubation by the oral route is recommended. The tip of the
laryngoscope should be inserted into the vallecula or on top of the epiglottis
and elevated gently to reveal the vocal cords (Fig 16).
Fig. 16
31
Cricoid pressure may be helpful. The tube should be inserted to an
appropriate depth through the vocal cords, as indicated by a black mark on
tip of the tube (Fig 17).
Another method of determining the depth of insertion is to calculate
the mark at the lip as "weight of the baby + 6 ". The tube should be tightly
secured with the appropriate centimeter marking located at the upper lip.
Tube fixation should be good as it is the most important determinant to
prevent displacement of the tube and its consequences.
Verification
After endotracheal intubation, confirm the position of the tube by the
following:
• Listening for equal breath sounds, especially in the axillae, and for
absence of breath sounds over the stomach
• Confirning absence of gastric inflation
• Watching for a fog of moisture in the tube during exhalation
• Noting improvement in heart rate, color, and activity of the infant on
ventilation
• An exhaled-C02 monitor may be used to verify tracheal tube
placement though it may not always be accurate.
Fig. 17
32
Bag to tube ventilation
The assisted ventilation rate should be 40 to 60 breaths per minute
(30 breaths per minute when chest compressions are also being delivered).
Signs of adequate ventilation include bilateral expansion of the lungs, as
assessed by chest wall movement and breath sounds, and improvement in
heart rate and color. After 30 seconds of adequate ventilation with 100%
oxygen, spontaneous breathing and heat rate should be checked as usual. If
spontaneious respirations are inadequate or if heart rate remains below 100
bpm, assisted ventilation must continue with bag to tube. If the heart rate is
<60 bpm, continue assisted ventilation & begin chest compression.
WHEN TO DENY OR STOP CPR AT BIRTH
Resuscitation at birth may be denied or abandoned when it is
considered futile in terms of survival or survival is likely to be associated with
gross neuromoter disability with extremely poor quality of life. It is justified
and ethical to deny resuscitation to infants with gross non-correctable lethal
congenital malformations and micropremies (<750 g in developing
countries). The resuscitation efforts may be abandoned in fresh still born
babies (zero apgar score at one minute) if there are no signs of life at 10
minutes or if spontaneous breathing is not established by 30 minutes.
REFERENCE
• NRP guidelines of American Academy of Paediatrics : 2000.
• Text book on Care of Newborn – Meharban Singh, VI Edition 2004.
• Manual of Neonatal care – John P. Cloherty V Edition 2004.
• Nelson Text Book of Pediatrics – 17th Edition 2004.
• Ghai Essential Paediatrics- VI Edition, 2004.
34
Day 1 : Session - IV (Management of Birth Asphyxia)
Objectives
At the end of the session the trainee should be able to understand :
1. The criteria of perinatal asphyxia.
2. Organ system involved in birth asphyxia.
3. Management of Birth asphyxia and
4. Prognostic factors for prediction of neurological outcome.
Methodology
- Lecture - Discussion
35
PERINATAL ASPHYXIA Perinatal asphyxia is one of the most important cause of neonatal mortality
and morbidity in developing countires of the world. There is wide variation in
the definition of asphyxia in medical literature. The American Academy of
Pediatrics Committee on foeus and newborn has therefore suggested the
following essential criteria for defining a case of perinatal asphyxia (Table 1
and 2)
Table 1: Essential criteria for perinatal asphyxia
• Prolonged metabolic or mixed academia (pH < 7.00) on an umbilical cord
arterial blood sample.
• Persistence of an Apgar score of 0-3 for > 5 minutes.
• Clinical neurological manifestations e.g. seizure, hypotonia, coma or
hypoxic-ischaemic encephalopathy in the immediate neonatal period.
• Evidence of multi-organ system dysfunction in the immediate neonatal
period.
Table 2: Multi-organ system dysfunction in perinatal asphyxia
C.N.S. Hypoxic ischaemic encephalopathy, cerebral oedema, neonatal seizure, long term neurologic sequelae.
Pulmonary Pulmonary hypertension, meconium aspiration, surfactant disruption.
Renal Oliguria, acute renal failure.
Metabolic Metabolic acidosis, hypoglycaemia, hypocalcaemia, hyponatraemia.
Gastrointestinal Necrotizing enterocolitis, hepatic dysfunction.
Haematologic Thrombocytopenia, disseminated intravascular coagulation.
Death
36
HYPOXIC – ISCHEMIC ENCEPHALOPATHY
Neonatal encephalopathy, following severe birth asphyxia or perinatal
hypoxia is refered to hypoxic ischemic encephalopathy (HIE). Cerebral
ischemia occurs as a consequence of cerebral edema (which compresses
cerebral vessels) and reduced cerebral perfusion due to myocardial
dysfunction as a result of hypoxic cardiomyopathy. Following severe birth
asphyxia, 25 percent infants are likely to develop the syndrome of HIE.
CLINICAL FEATURES
The clinical features of HIE are well described in term babies and can
be graded by Sarnat staging system (Table 3).
Table 3: Clinical Staging of hypoxic-ischemic encephalopathy (Sarnot
staging)
Features Stage I Stage II Stage III
Consciousness alert lethargic comatosed
Muscle tone normal hypotonic flaccid
Tendon reflexes brisk exaggerated absent
Myoclonus present present absent
Sucking active weak absent
Moro response exaggerated incomplete absent
Grasping normal exaggerated absent
Oculocephalic reflex (Doll's eyes)
normal over reactive reduced or absent
Pupils dilated and reactive
constricted dilated and fixed
Respiration regular periodic apneic attacks
Heart rate normal bradycardia bradycardia
Seizures absent common uncommon
EEG normal low voltage periodic/or paroxysmal
periodic, isoelectric
37
In preterm babies multiorgan dysfunction may dominate the clinical
picture leading to high risk of mortality. Seizures occur in approximately 50
percent of affected infants mostly within 6 to 12 hours after birth and
invariably by 36 hours of age. Term babies produce gross seizures while
preterm infants usually mainfest subtle seizures. Persistence of neurologic
abnormalities beyond 7 days is usuallly associated with poor neuromoter
outcome on follow up. Associated metabolic and electrolyte disturbances
may produce additional clinical features.
MANAGEMENT
Efforts should be made to prevent further hypoxic damage to the brain
and correct any associated acid base and metabolic abnormalities. If despite
active resucitation efforts, 5-minute Apgar score is less than 5, the infant
should be admitted in the neonatal intensive care unit for close monitoring
and management.
Clinical monitoring
� Vital signs should be monitord preferably with the help of a multi-
channel vital sign monitor.
� Color of the baby should be closely watched for cyanosis, greyness,
pallor (hypotension) and jaundice.
� Detailed record should be maintained to assess CNS integrity with the
help of Sarnat staging system. The clinical features of HIE are not
well described in preterm babies because Sarnat staging system
outlines early neurologic consequences of HIE in term babies.
� Tissue perfusion should be evaluated by capillary refilling time on
blanching which should be less than 2 seconds. When gradiant
between the core and peripheral body temperature is more than
2.5°C, it is also indicative of poor tissue perfusion.
� Development of respiratory distress following birth asphyxia may
occure due to meconium aspiration syndrome, hyaline membrane
disease, congenital malformations (diaphragmatic hernia, tracheo-
38
esophageal fistula) and pneumothorax following aggressive
ventilation at the time of resuscitation.
� Abdominal girth should be monitored to identify abdominal distension
and look for occult blood and reducing substance in the stools as
early markers of necrotising enterocolitis.
� Periventricualr-intraventricular hemorrhage is best diagnosed with the
help of ultrasound examination but can be clinically suspected by
features of sudden pallor/ jaundice, fall in hematocrit, subtle seizures,
bulging anterior fontanel and marked hypotonia.
� Renal perfusion shold be monitored by recording urine output which
must be kept above 2 ml/kg/ hr.
� Infants with severe birth asphyxia are predisposed to develop
septicemia which should be monitored by undertaking frequent
screening tests for sepsis.
Biochemical monitoring
� Acid base parameters and blood gases should be monitored as soon
as the infant is transferred to the NICU.
� Blood glucose should be frequently checked to indentify
hypoglycemia and hyperglycemia.
� Serum electrolytes should be monitored. Hyponatremia may occur as
a consequence of inappropriate secretion of antidiuretic hormone
while hypernatremia may occur due to frequent administration of
sodium bicarbonate for correction of acidosis. Hyperkalemia is
ominous and can occur due to acute renal shut down or tissue
catabolism.
� Tissue injury as a consequence of perinatal hypoxia leads to release
of phosphate in the blood stream and consequent hypocalcemia due
to inverse relationship between calcium and phosphate.
� Non-oliguric renal failure may occur in infants with profound birth
asphyxia and is diagnosed by elevation of BUN and creatinine.
39
Laboratory investigations
� Skiagram of chest should be taken in all cases to exculde
pneumothorax, diaphragmatic hernia and congenital pneoumonia.
� Sepsis screening and blood culture should be taken to make an early
diagnosis of bacterial infection.
� When facilities are available, EEG should preferably be taken during
first three days of life to identify any abonormalities like burst
supprssion, low voltage or isoelectric pattern.
Brain-oriented Resuscitaiton
Infants with absence of spontaneous breathing efforts by 10 minutes
or those with clinical evidences of hypoxic-ischemic encephalopathy demand
energetic measures to reduce cerebral edema, improve cerebral perfusion
and prevent ongoing neuronal damage due to hypoxia, ischemia and
metabolic disturbances. Brain-oriented resuscitaiton demands availability of
highly sophisticated supporative and nursing care and assisted ventilatory
facilities.
� The baby should be nursed in a thermoneutral environment with head
raised by 30° to prevent further elevation of intracranial pressure.
� The infant should be intubated and attached to a mechanical
ventilator and provided with hyperventilation to maintain paO2 above
80 mm of Hg and PaCO2 between 25-30 mn Hg. Hypocarbia should
be maintained to prevent vasodilatation and is extremely useful to
reduce intracranial pressure.
� During first 48 hours, infuse 10% dextrose solution (two-third of
maintenance requirements) without sodium and potassium.
� Acidosis, hypoglycemia, hyperkalemia and hypocalcemia (Qo Tc >
0.2 sec) should be identified and appropriately managed.
� Blood glucose should preferably be maintained between 60-100 mg/
dl.
� Calcium gluconate (150-200 mg/kg/day) should be administered
intravenouslly for initial 48 hours to counteract hypocalcemia due to
40
intracellular flux of calcium, elevated serum potassium and phosphate
levels. This may be given as a constant infusion or half-dilluted slow
boluses under cardic mointoring.
� Hypotension and poor tissue perfusion should be identified and
promptly managed by administration of normal saline or Ringer’s
lactate and by use of dopamine and dobutamine when myocardial
dysfunction is strongly suspected.
� Fluid restriction and use of osmotic diuretics like 20 percent mannitol
are useful to reduce cerebral edema. The use of mannitol is
controversial and must be avoided in preterm babies due to potential
risk of causing IVH.
� Furosemide in a dose of 1.0 mg/kg every 12 hours intravenously for 4
doses is recommended especially when there is oliguria to ensure
diuresis and reduce intracranial pressure.
� The use of cortocosteroids is not recommended for tratment of
cerebral edema. It has been shown that corticosteroids may reduce
vasogenic cerebral edema but they are useless for the treatment of
cytotoxic brain edema in infants with HIE.
� Neonates with moderate and severe HIE may manifest seizure
activity within 12 hours after birth. Prophylactic administration of
phenobarbitone is controversial and should be undertaken only in
centers which are equipped to provide assisted ventilation.
Therapeutic utility of phenobarbitone in infants who devleop seizures
following birth asphyxia is unquestionable and it is the anticonvulsnat
of choice for management of HIE-related seizures once metabolic
conditions are excluded or appropriately managed. When seizures
are unresponsive to a loading dose of phenobarbitone (20mg /kg IV
loading followed by 10 mg/kg, every 15 min. may be repeated to total
dose of 40 mg /kg), it is recommended to administer a loading dose of
phenytoin 20 mg/kg followed by maintenance dose of 5-7 mg/ kg/d
intravenously.
41
� In majority of neonates with HIE, seizure activity usually disappears
within 3 to 10 days. At the time of discharge, all anticonvulsants
except phenobarbitone should be stopped. The infant should be re-
evaluated at the age of 3 months, if there is no recurrence of seizures
and both CNS status and EEG examination are normal,
phenobarbitone should be stopped. When phenobarbitone is
continued beyond 3 months, the infant should be re-evaluated at the
age of six months to decide whether phenobarbitone therapy should
be continued as in a case of epilepsy or terminated at this stage.
PROGNOSIS
Birth asphyxia is an important cause of neonatal mortality accounting
for a case fatality rate of 15-50 percent depending upon the definition of birth
asphyxia and quality of newborn care facilities. Mortality among preterm
asphyxiated babies is much higher as compared to term babies.
Following severe birth asphyxia, 25 percent infants are likely develop
evidences of HIE. Infants with severe HIE have increased risk of long term
neurological sequelae and it is a better predictor of subsequent handicap
than poor Apgar scores or biochemical changes alone.
The commonest neuromotor sequelae following birth asphyxia is CP
of varying grades and severity. Isolated mental retardation without CP is
usually not attributable to birth asphyxia. Birth asphyxia is an important
cause of CP accounting for about 10 percent of cases but it is not the
leading cause. A large number of clinical, biochemical and laboratory
parameters are reliable predictors of occurrence of cerebral palsy (Table 4)
Table 4 Clinical correlates of adverse neuromotor outcome following
birth asphyxia
1. Low birth weight and prematurity.
2. Apgar score of <4 at 10 minutes or later
42
3. Assisted ventilation for >24 hours.
4. Severe metabolic acidosis (cord umbilical aartery blood pH ≤ 7.0).
5. Hypoglycemia
6. Polycythemia
7. Intractable seizures or brain stem signs (poor sucking,pooling of oral
secretions, pupillary changes etc )
8. Severity of HIE (Sarnat stage two and above).
9. Abnormal neurological behaviour for more than 7 days.
10. Multiorgan failure especially development of acute renal failure.
During follow up detailed neurological and development examination
should be conducted to identify early clinical markers of CP (Table 5 )
Table 5 Early clinical markers of cerebral palsy
∗ Episodes of inconsolable crying, chewing movements, excessive
senstivity to light or sound etc
∗ persistent asymmetric neck tonic posture beyond 4 weeks.
∗ Clenched fists (Cortical thumb) beyond 8 weeks
∗ Lack of social smile by 12 weeks
∗ Abnormalities in tone (Hypertonia in lower limbs and hypotonia in
neck/ upper limbs)
∗ Paucity or absence of fidgety limb movements during 6-12 weeks.
∗ Persistence of automatic reflexs beyond 4-5 months
∗ Slow head growth.
REFERENCES
• Text book on Care of Newborn – Meharban Singh, VI Edition 2004.
• Manual of Neonatal care – John P. Cloherty V Edition 2004.
• Ghai Essential Paediatrics- VI Edition, 2004.
• Nelson Text Book of Pediatrics – 17th Edition 2004.
• Managing Newborn Problems. A guide for doctors, nurses, and
midwives: WHO Publication, 2003.
43
Day 2: Session I (Management of Convulsions)
Objectives :
At the end of the session the trainee should be able to understand :
• Common causes of convulsions in newborn.
• Drugs used to control seizures on short and long term basis.
• Prognostic factors for outcome.
Methodology
• Lecture- Discussion
44
NEONATAL CONVULSIONS
In the newborn infant, seizures may occur due to an underlying
cerebral or biochemical abnormality. Their incidence varies from 0.5 to 0.8
percent in term babies and 6-12 percent in babies weighing less than 1500
g> Newborn babies do not manifest febrile convulsions. Jitteriness which is
characterized by stimulus-sensitive rhythmic tremors peculiar to newborn
babies should not be confused with seizures.
JITTERINESS
Jitteriness is extremely common in newborn babies and generally
carries good prognosis. It is characterized by symmetrical tremors of
extremities which are provoked by stimulus and aborted by restraining the
limbs. The amplitude of tremulous movements is equal and its rate is around
5-6/sec. There are no associated eye movements, autonomic changes or
EEG abnormalities. The common correlates of jitteriness include hypoxic-
ischemic encephalopathy, hypoglycemia, hypocalcemia and narcotic
withdrawal syndrome.
TYPES OF SEIZURES
Generalized tonic and clonic convulsions, as in grandmal epilepsy,
are usually not seen in the neonates, due to incomplete development of
axons, dendritic processes, arborization and poor myelination. The
manifestations are more subtle and pleomorphic. The clinical type of the
seizures generally offers little clue to the etiology.
Subtle seizures They account for over 50 percent of all seizures and are
more common in preterm babies. They can be easily overlooked, Jerking of
eyes (with or without conjugate deviation), blinking or fluttering of eyelids,
staring look, sucking, chewing, or smacking oro-buccal movemets and
apneic attacks are included among subtle seizures. Oral, facial and lingual
phenomenon are common due to advanced maturation of the limbic System.
45
There is tachycardia at the onset followed by bradycardia after the apnea
and hypoxemia.
Multifocal clonic seizures Tonic convulsive movements migrate
haphazardly from one limb to another. The twitching may be pedominantly
limited to one side of the body. They may occur due to hypoxic-ischemic
encephalopathy and birth trauma.
Focal clonic seizures. They are well localized and often associated with
loss of consciousness. Even focal seizures in a newborn baby are a
manifestation of bilateral cerebral disturbance. They are common due to
metabolic disorder, birth trauma and cerebral infarction.
Tonic seizures. There is generalized stiffening, similar to decerebrate (tonic
extension of all limbs) or decorticate (flexion of upper limbs and extension of
lower limbs) posturing and may be associated with stertorous breathing and
eye signs or occasional clonic jerks. They may be associated with
intraventricular hemorrhage and kernicterus. In general, the prognosis of
tonic seizures is poor.
Myoclonic seizures. Sudden jerky movements produced by episodic
contractions of a group of muscles are rare in the newborn. These are more
common in babies with developmental defects including anencephaly.
Apnea as a manifestation of seizure
Apneic attacks with bradycardia are common in extremely pretern
babies as a manifestation of immaturity of respiratory center. Subtle seizures
in term babies may manifest with apneic attacks. During convulsive apnea
the heart rate either remains normal or there may be tachycardia. It is often
associated with subtle seizures like eye opening, staring gaze and conjugate
deviation of eyes. EEG may show abnormalities. The inadvertent use of
respiratory stimulants in these babies would worsen the seizures activity.
46
CAUSES
Common causes of convulsions in the newborn, in the decreasing
order of their frequency, are given below:
Perinatal complications. Birth asphyxia and intracranial injuries together
account for about half of the neonatal seizures. In babies with 5-minute
Apgar score of less than 3, the convulsions may occur on the first day of life
due to hypoxic ischemic encephalopathy. The convulsive manifestations of
intracranial bleed appear between 2 to 7 days of age.
Hypocalcemia Hypocalcemia (serum calcium <7mg/dl) is the commonset
biochemical abnormality causing neonatal seizures (10 percent).
Convulsions occur on the first day or at the end of the first week. In the
absence of perinatal complications, the prognosis in this group is excellent.
Hypoglycemia. The diagnosis is suspected if any of the situations known to
predispose to hypoglycemia such as severe IUGR, large-for-dates babies
and infants of diabetic mothers coexist.
Infections. Intrauterine infections or neonatal septicemia may be associated
with meningitis. About one-third of patients with neonatal menigitis, present
with convulsions. The clinical diagnosis of meningitis in the newborn is often
difficult. Therefore, lumbar puncture is mandatory in all babies with fits to
exclude this potentially treatable condition. Tetanus neonatorum is an
important cause of spasms which should not be confused with convulsions.
Inborn errors of metabolism. If convulsions are intractable to therapy and
when there is a history of similar disorder in the previous sibling, metabolic
causes should be excluded. Symptoms appear after introduction of milk
feeding. Apart from seizures, look for evidences of vomiting, severe
jaundice, hepato-splenomegaly, virilization and malodorous urine.
Developmental defects. Presence of facial or caput asymmetry should
arouse the suspicion of underlying developmental defects of brain such as
47
microcephaly, hydrocephalus, dysgenesis, microgyria, porencephaly,
hydranencephaly and agenesis of corpus callosum.
Acute systemic illness. The babies with severe respiratory distress and
septicemia may develop fits as a result of hemorrhagic infarction due to
disseminated intravascular coagulation and hypoxia.
Miscellaneous Conditions
Drug toxicity. The use of large doses of phenothiazines for the
management of eclampsia in mother may evidenced by excessive jiteriness,
rigidity and opisthotonus. Theophylline, doxapram, propylene glycol (diluent
in IV nutritional formulations) can cause seizures in newborn babies.
Local anesthetics. During paracervical block, inadvertent injection of local
anesthetic into the fetal scalp, may result in intractable convulsions.
Hypomagnesemia. The suspicion is aroused when in a baby with
hypocalcemia, biochemical or therapeutic improvement does not occur with
calcium therapy alone.
Pyridoxine dependency. Prolonged maternal administration of vitamin B
during pregnancy may predispose to this condition. Seizures may be focal
or generalized having onset during first 12 hours and are resistant to
conventional therapy. There may be a history of severe or fatal cryptogenic
convulsive disorder in a sibling. There may be consanguinity among the
parents. Seizures are controlled with intravenous administration of
pyridoxine and they reappear within 3 weeks of withdrawal of pyridoxine.
Dyselectrolytemia: Hypo and hypernatremic states may be associated with
convulsions.
Neonatal narcotic withdrawal or abstinence syndrome
48
BENIGN SEIZURES IN NEONATES
Benign neonatal sleep myoclonus has onset during first week of life
and occur as synchronous myoclonic jerks during REM sleep. There are no
seizures when baby is awake, EEG is normal and seizures spontaneously
disappear by 2 months of age .
Benign familial neonatal convulsions occur as self-limiting isolated
clonic seizures on second or third day of life. The condition is autosomal
dominant with spontaneous recovery within 1-6 months of age.
Benign idiopathic 'fifth day' seizures The multifocal clonic seizures
classicaly occur on day 5 and usually disapper on day 15. The cause is
unknown though low CSF zinc level has been reported in few cases.
DIAGNOSIS
The time of onset of seizures
First day
Hypoxic-ischemic encephalopathy, cerebral contusion, 'first day'
hypocalcemia, pyridoxine dependency, accidental injection of local
anaesthetic.
Between 1-3 days
Intracranial hemorrhage, hypoglycemia, narcotic withdrawal, inborn
error of metabolism.
4th to 7th day
Tetany, meningitis, TORCH infections, developmental malformations
and kernicterus. positive
Family history of convulsions in the previous sibling(s)
• Inborn errors of metabolism
Maple syrup urine disease, hyperglycinemias, organic acidemias,
proline aminoaciduria, galactosemia, glycogen storage disease and
fructose intolerance.
• Developmental defects of central nervous system.
49
• Narcotic abstinence (withdrawal) syndrome.
• Pyridoxine dependency.
• Kernicterus due to rhesus iso-immunization.
• Benign familial seizures.
Presence of associated conditions as mentioned above, may aid the
clinical diagnosis. The readily treatable conditions like metabolic disorders
(Hypocalcemia, hypoglycemia) and bacterial meningitis must be identified
promptly. The following investigations are often necessary for precise
etiological diagnosis and for assessment of prognosis.
First line investigations
� Check hematocrit, blood glucose, calcium, phosphorus, magnesium,
sodium, venous pH and base excess. Hypocalcemia can be rapidly
suspected by looking for prolonged QTc interval (> 0.2 sec) on EKG.
� CSF examination and blood culture should be taken in all cases to
exclude pyogenic meningitis.
� Cranial ultrasound and EEG should be done once metabolic
disorders are excluded.
Second line investigations
� When convulsions persist and first line investigations are unable to
identify the cause, MRI or CT scan is advised to exclude structural or
developmental defects like cerebral dysgenesis, lissencephaly and
neuronal migration disorders.
� Appropriate tests including serology for TORCH infections should be
undertaken to exclude intrauterine infections.
� Screening tests for exclusion of inborn error of metabolism include
ABG, blood ammonia, lactate/pyruvate level, plasma and urinary
amino acid profile etc.
� Therapeutic trial with pyridoxine is usually reserved as a last resort.
50
Electroencephalography
Polygraphic EEG recording and video monitoring have greatly
facilitated classification and management of neonatal seizures. Neonatal
seizures may be associated with EEG abnormalities and at times EEG
abnormalities are seen without any clinical seizures.
� The 5-7 Hz "comb-like" rhythm on EEG is suggestive of maple syrup
urine disease.
� Patients with pyridoxine-dependency may have generalized 1-4 Hz
sharp and slow wave activity.
� Herpes encephalitis is characterized by multifocal periodic pattern on
EEG.
� Unifocal diphasic spike or sharp wave pattern carries good prognosis.
� Multiple foci with periods of virtual electrical silence interrupted by
bursts of irregular polymorphic and asynchronous activity or flat EEG
ddenote poor outcome.
MANAGEMENT
� After taking relevant blood samples and collection of cerebrospinal
fluid, intravenous line should be established in a peripheral vein. This
facilitates injection of medicines and avoids risk of aspiration of feeds.
Infant should be nursed in a thermoneutral environment and special
attention should be paid to his perfusion and ventilation.
� Biochemical abnormalities should be looked for and treated
appropriately.
EKG shows QoTC >0.2 sec or serum calcium < 7 mg/dl
Calcium gluconate 200mg/kg of 10 percent solution (2ml/kg) diluted
with equal volume of water is injected slowly in 5-10 minutes under cardiac
monitor. For maintenance, repeat the same dose through constant infusion
every 6-8 hr. Give 0.2 ml/kg 50% solution of magnesium sulfate I.M. single
dose daily if there is no or poor response to calcium therapy.
51
Dextrostix shows hypoglycemia (< 40mg/dl)
Glucose 2 ml/kg of 10 percent solution as a bolus followed by 10
percent dextrose at a rate of 8 mg/kg/minute. The blood glucose should be
maintained between 70-120 mg/dl.
When seizures persist even after correction of hypocalcemia, and
hypoglycemia, anticonvulsants should be given.
Anticonvulsant Therapy
� In case there is no improvement and / or no biochemical abnormality
has been detected, parenteral loading dose of phenobarbitone 20
mg/kg is administered slowly intravenously over 20 minutes. If there is
no response in 15 minutes, additional doses of phenobarbitone 10
mg/kg every 15 minutes are administered intravenously till the
seizures are controlled or a total dose of 40 mg/kg has been given.
� If convulsions are still uncontrolled despite maximal dose of
phenobarbitone, phenytoin is administered intravenously in a loading
dose o 20 mg/kg. It is diluted in normal saline and administered slowly
at a rate of 1 mg/kg/min. If seizures persist an additional dose of
5mg/kg may be used.
� The maintenance therapy with phenobarbitone and phenytoin is
started after 12 hours of loading dose and given in a dose of 5
mg/kg/day in two divided doses.
� If convulsions are intractable and baby is in a status convulsicus, give
lorazepam 50ug/kg IV slowly over 2-5 min. Alternatively, clonzepam
100-200 ug/ kg can be given IV over 30 sec. Benzodiazepines can be
repeated as and when needed. Midazolam 0.05-0.15 mg/kg/dose is
effective when given through intramuscular route because it is highly
soluble in water. Diazepam should be avoided as it has a short
duration of action, carries the risk of inducing apneic attacks and may
predispose the baby to develop kernicterus by displacement of
bilirubin from the binding sites in the protein because it contains
sodium benzoate as a preservative.
52
� Pyridoxine-dependent seizure : Give pyridoxine 100 mg IV under EEG
control and close clinical observation. Repeat 100 mg pyridoxine IV
every 10 min till seizures are controlled or a cumulative dose of 500
mg is given. Watch for prolonged depression of cerebral activity or
vital functions during next 12 hr. The maintenance dose of pyridoxine
is 5 mg / kg (or 50 mg/d) single oral dose daily. There is no need to
administer any other anticonvulsant agent. If pyridoxine is stopped,
seizures would reappear within 3 weeks.
Table : Acute Management of Neonatal Seizures
After each step below, evaluate the infant for ongoing seizures. If seizures
persist.
Step 1. Stabilize vital functions
Step 2 Correct transient metabolic disturbances
a. Hypoglycemia (target blood sugar 70-120 mg/dl)
10% dextrose water IV bolus dose 2 mL/kg
+/- continuous infusion @ 8 mg/kg per minute
b. Hypocalcemia 5% calcium gluconate IV @ 4 mL/kg (need cardiac
monitoring)
c. Hypomagnesemia 50% magnesium sulfate IM @ 0.2 mL/kg.
Step 3 Phenobarbital 20 mg/kg IV load
Cardiorespiratory monitoring
10mg/kg IV (may be repeated every 15 minutes, max. total dose of
40 mg/kg)
Consider continuous EEG monitoring
Consider intubation/ventilation
Step 4 Phenytoin 20 mg/kg slow IV load
5 mg/kg slow IV (may repeat to total dose of 30 mg/kg)
Step 5 Lorazepam 0.05 mg/kg IV (may repeat to total dose of 0.1 mg/kg)
Step 6 Pyridoxine 50-100 mg/kg IV (with EEG monitoring)
Step 7 Other agents.
53
� Paraldehyde can also be given in a dose of 200-400 mg/kg IV as 5%
solution in 5% dextrose or diluted with double volume of olive oil or
coconut oil and given per rectum. Lidocaine 2 mg/kg IV bolus followed
by 6 mg/kg/hr as a constant infusion has been used with success to
abort intractable seizures. However, it should never be co-
administered with phenytoin due to potential risk of myocardial
damage and arrhythmia. Sodium valproate 20 mg/kg oral as a loading
dose followed by 10 mg/ kg every 12 hr has been used in newborn
babies. It is associated with a serious risk of hepato-toxicity.
Vigabatrin in a dose of 50 mg/kg/day has been used in neonates with
refractory infantile spasms.
The duration of anticonvulsant therapy
It is guided by neurological status of the infant at discharge, cause of
the seizures and EEG findings. All anticonvulsants are stopped except
phenobarbitone when seizures are controlled. At discharge, if CNS
examination is normal, phenobarbitone may be stopped. Phenobarbitone is
continued if there are any CNS abnormality and infant is reassessed at one
month. If there is no recurrence of seizures, CNS examination, EEG and CT
scan or MRI are normal, phenobabitone is tapered over 4 weeks. When
phenobarbitone is continued, child is evaluated at the age of 6 months. The
infant is treated like a case of epilepsy, if seizures are recurrent or there are
any evidences of neuromotor disability and / or EEG abnormalities at 6
months. Additional and alternative anticonvulsants may have to be
administered when prolonged anticonvulsant therapy is required.
PROGNOSIS
� About one-fourth of neonates with convulsions die and amongst
survivors prognosis regarding recurrence of seizures and neuromotor
sequelae is determined by the underlying disease process and ECCG
findings.
54
� The onset of fits within 24 hours of age, presence of myoclonic or
stiffening attacks and their persistence for more than 48 hours
suggest poor outcome.
� Prematurity, perinatal hypoxia, birth injury leading to intraventricular or
subdural hemorrhage, developmental and metabolic abnormalities,
hypoglycemia and meningitis are associated with high rate of
sequelae.
� Uncomplicated hypocalcemia, narcotic withdrawal and subarachnoid
hemorrhage carry good prognosis.
� Flat or periodic and polyphasic EEG signifies poor prognosis. The
overall risk of epilepsy and brain damage among survivors of neonatal
seizures is 30 to 40 percent.
REFERENCES
• Text book on Care of Newborn – Meharban Singh, VI Edition 2004.
• Ghai Essential Paediatrics - VI Edition, 2004.
• Manual of Neonatal care – John P. Cloherty V Edition 2004.
• Nelson Text Book of Pediatrics – 17th Edition 2004.
• Managing Newborn Problems. A guide for doctors, nurses, and
midwives: WHO Publication, 2003.
55
Day : 2 Session II ( Management of Jaundice)
Objectives :
At the end of the sessions the trainee should be able to understand :
• Common causes of Jaundice depending on day of onset.
• Diagnostic work up and management.
• Criteria for starting phototherapy and exchange transfusion and their
complications.
Methodology
• Lecture - Discussion
56
NEONATAL JAUNDICE
CLINICAL ESTIMATION OF JAUNDICE
In newborns, jaundice is detected by blanching the skin with digital
pressure. This reveals the underlying skin and subcutaneous tissue. A
bilirubin level of more than 5 mg/dl
manifests as clinical jaundice or icterus
in neonates whereas in the adults the
skin would look icteric with as little as 2
mg/dL. This dermal icterus is first noted
in the face and as the bilirubin level
rises it proceeds caudal to the trunk and
then to the extremities. Infants whose
jaundice is restricted to the face and
part of the trunk above the umbilicus,
have a bilirubin <12 mg/dL. All those,
whose palms and sloes are yellow,
have serum bilirubin over 15 mg/dL.
Correlation of dermal zones and levels of jaundice
Derma zone Bilirubin (mg/dl)
1 5
2 10
3 12
4 15
5 > 15
NON - INVASIVE MEASUREMENT OF JAUNDICE
These methods are more accurate and less subjective in estimating
jaundice.
57
Ingram ictermoeter
This is piece of transparent plastic on which are painted five
transverse strips of graded yellow lines. The instrument is pressed against
the nose an the yellow color of the blanched skin is matched with the
appropriated yellow stripe and a bilirubin level is assigned.
Transcutaneus bilirubinometer
This is costly and sophisticated equipment. It is hand-held, portable
and a xenon tube generates a strobe light. This light passes through a
fiberoptic filament, penetrates the blanched skin and enters the
subcutaneous tissue. The reflected light returns through a second fiber-optic
bundle to the spectrophotometric module. The intensity of the yellow color in
this light, correcting for the hemoglobin, is measured and instantly displayed
in arbitrary units.
PHYSIOLOGICAL JAUNDICE
Most neonates develop visible jaundice due to elevation of
unconjugated bilirubin concentration during their first week. This common
condition is called "physiological jaundice". This pattern of hyperbilirubinemia
has been classified into two functionally distinct periods.
Phase one lasts for five days in term infants and about seven days in
preterm infants, when there is a rapid rise in serum bilirubin levels to 12 and
15 mg/dL, respectively.
After this, in phase two, there is a decline to about 2 mg/dL, which
lasts for two weeks, after which adult values attained. Phase two may last for
more than a month in preterm infants and those babies who receive
exclusive breastfeeding.
The factors responsible for physiological jaundice are shown in Table
below. Once confirmed, physiological jaundice does not require any
treatment.
58
Table : Possible Mechanisms in Physiological Jaundice.
1. Increase bilirubin load on liver cells
• erythrocyte volume
• early labeled bilirubin
• enterohepatic circulation of bilirubin
• erythrocyte survival
2. Defective hepatic unptake of bilirubin from plasma
• ligandin (y protein)
• binding of Y proteins by other nations
• hepatic uptake especially in Phase II
3. Defective bilirubin conjugation
• UDPG activity
4. Defective bilirubin excretion
Exaggerated physiological jaundice. Certain common occurrence in
newborns may increase the level of physiological jaundice, which may be
prolonged and even require treatment as shown in table below.
Table : Possible Factors Responsible for Exaggerating "Physiological
Jaundice"
Factor Clinical Correlates
Bilirubin load to liver Infants with polycythemia, infants of
diabetic mothers, delayed cord
clamping, collection of extravasated
blood like cephallhematoma,
intraventricular hemorrhage
Defective uptake from plasma Decreased Y protein due to caloric
deprivation
59
Factor Clinical Correlates
Defective bilirubin conjugation Due to decreased UDPG activity as
seen in hypothyroidism and due to
inhibitors in breast milk
Decreased hepatic excretion Congenital infections
Inadequate hepatic perfusion Hypoxia, congenital heart disease
Increased enteropatic circulation Unfed babies, delayed passage of
meconium
Breastfeeding Jaundice and Breastmilk Jaundice
There is a strong association between exclusive breastfeeding and
neonatal jaundice. Studies have found a higher peak bilirubin level in the first
few days of life in breast fed babies as compared to those who are formula
fed. This has been classified as breastfeeding jaundice. A few babies who
remain on exclusive breast feeds develop jaundice in the second week of life
and continue well into the third month. This is called breastmilk jaundice. A
bilirubin level of over 20 mg/dL may be attained. It is presumed t be due to
inhibitory substances in the breastmilk that interfere with bilirubin conjugation
e.g. pregananediol and free fatty acids. Temporary interruption of breastmilk
feeds will dramatically reduce the serum levels of bilirubin. There may be a
slight increase in bilirubin when breastfeeding is resumed, but it never
reaches the previous levels.
UNCONJUGATED HYPERBILIRUBINEMIA
Definition
Any of the following features characterizes pathological jaundice.
1. Clinical jaundice appearing in the first 24 hours.
2. Increase in level of total bilirubin by more than 0.5 mg/dL/hour or 5 mg
/dL/24 hours.
3. Total bilirubin >15 mg/dL (hyperbilirubinemia).
60
4. Direct bilirubin > 2.0 mg/dL.
5. Jaundice persisting beyond 14 days.
Causes
A variety of pathological conditions as shown in tables below, may
result in sever and / or prolonged jaundice where the predominant or
exclusive pigment that accumulates in the serum is indirect bilirubin.
Table 1 : Causes of Unconjugated Hyperbilirubinemia
Increased production
1. Fetomaternal blood group incompatibility : Rh, ABO.
2. Hereditary spherocytosis.
3. Non-spherocytic hemolytic anemia : G6PD deficiency, pyruvate
kinase deficiency, alpha thalassemia, vitamin K induced hemolysis.
4. Sepsis.
5. Increased enterohepatic circulation : pyloric stenosis or large bowel
obstruction.
Decreased clearance
1. Inborn errors of metabolism : Criggler-Najjar syndrome type I & II.
2. Drugs and hormones : Hypothyroidism, breastmilk jaundice.
61
Table 2: Causes of Jaundice on the basis of age of onset
Within 24 hours of birth
• Hemolytic disease of the newborn due to feto-maternal blood group incompatibility in the Rhesus, ABO and minor blood group systems.
• Intrauterine infection* such as toxoplasmosis, cytomegalic inclusion disease, syphilis, rubella, hepatitis - B, herpes simplex and bacterial infections.
• Deficiency of red cell enzymes such as glucose-6-phosphate dehydrogenase, pyruvate kinase, hexokinase, phosphoglucose isomerase and unstable hemoglobins.
• Administration of large amounts of certain drugs such as vitamin K, salicylates, sulfisoxazole etc. to the mother.
• Hereditary spherocytosis.
• Crigler-Najjar syndrome.
• Lucey-Driscoll syndrome
• Homozygous alpha-thalassemia
Between 24-72 hours of age
Physiological jaundice appears during this period but can be aggravated and prolonged by immaturity, birth asphyxia, acidosis, hypothermia, hypoglycemia, drugs, cephalhematoma or concealed hemorrhage and bruising, polycythemia, high altitude, cretinism, breast feeding, infections and mild hemolytic states due to fetomaternal blood group imcompatibility, spherocytosis and deficiency of red cell enzymes.
After 72 hours of age (and within first 2 weeks)
• Septicemia.
• Neonatal hepatitis including other causes of intrauterine infections.
• Extra-hepatic biliary atresia.
• Breast milk jaundice.
• Metabolic diseases such as galactosemia, tyrosinemia, hereditary fructosemia, organic acidemias, cystic fibrosis and alpha 1-antitrypsin deficiency.
• Hypertrophic pyloric stenosis and intestinal obstruction.
62
DIAGNOSTIC WORK OF NEONATAL JAUNDICE
SEQUELAE OF UNCONJUGATED HYPERBILIRUBINEMIA
The recognition that unconjugated bilirubin may penetrate brain cells
under certain circumstances and result in neurological dysfunction and death
is reason enough for carefully monitoring serum bilirubin in neonates.
63
Transient encephalopathy
Early bilirubin induced neurologic dysfunction is transient and
reversible. This is suspected by increasing lethargy with rising bilirubin levels
but recovery following or prompt exchange transfusion.
Kernicterus
This term has been traditionally used to describe the pathological
findings of bilirubin toxicity within in the basal ganglia, hippocampal cortex,
subthalamic nuclei and cerebellum followed by gliosis of these areas, should
the baby survive. The cerebral cortex is generally spared, but 50% of babies
have extraneuronal lesions with necrosis of renal tubular cells, intestinal
mucosa and pancreatic cells, hematuria. Clinically, kernicterus is described
in phases, which may progress over 24 hours to 7 days :
Phase I : poor suck, lethargy, hypotonia, depressed sensorium.
Phase II : fever, hypertonia progressing to opisthotonus.
Phase III : high pitched cry, convulsions, death.
Long term survivors demonstrate choreoathetoid cerebral plasy,
upward gaze palsy, sensorineural hearing loss and mental retardation.
TREATMENT
The following options are currently available
- Exchange transfusion. This removes bilirubin mechanically. But it is
an invasive procedure requiring vascular access.
- Phototherapy. This converts bilirubin into photoisomers that can
bypass the conjugating system of the liver and be excreted in the bile
or urine without further metabolism.
- Drugs. They act by interfering with heme degradation, accelerating
normal pathways of bilirubin clearance and by inhibiting enterohepatic
circulation. There is very little role for this modality practice.
64
Phototherapy
This has emerged as the most widely used form of treatment for
unconjugated hyperbilirubinemia and has reduced considerably the need for
exchange transfusions.
Mechanism of action
1. Geometric photoisomerization of unconjugated bilirubin resulting in a
more soluble form of bilirubin. This account for 80% of conversion.
2. Converting bilirubin to lumirubin through structural isomerization,
which can then be excreted into the bile without the need for further
hepatic conjugation.
3. Oxidation mechanism resulting in colorless by products and excreted
by liver and kidney without need for conjugation. This is the least
important mechanism.
Indications. Phototherapy should be used when the level of bilirubin may be
hazardous to the infant if it were to increase, even though it has not reached
exchange transfusion levels. Prophylactic phototherapy may be indicated in
very special circumstances such as extremely low birth weight or severely
bruised infants.
Technique. Bilirubin absorbs light maximally in the blue range (420-500
nm). Daylight and cool white lamps have a spectral peak between 550-600
nm and are less effective than special blue lamps, which have a range of
420-480 nm. Blue lamps interfere with observation of skin color in the baby
and cause headache and nausea to care givers. Hence, a combination of
white and blue lamps is preferred. A unit with 4 special blue and 4 daylight
lights will give an effective irradiance of 11µW/cm2/nm which is far above the
required 4-6 µW/cm2 /nm. With prolonged use, the irradiance of fluorescent
lights tends to diminish, hence lights are preferably changed every 2000
hours. Distance of the baby from the light source affects the effectiveness.
Typically, a distance of 45 cm used to be followed, although lesser distances
are now being used. Babies are kept naked, more effective is the
65
phototherapy. Skin pigmentation does not alter effectiveness. Eyes must be
shielded with eye patches to prevent potential adverse effects on retina.
Complications
1. Increase in environment and body temperature. Phototherapy causes
increase in insensible water loss especially in premature infants. In
addition, stools tend to be more loose and frequent. This loss must be
compensated for by increasing the fluid intake by 25% over that
required before phototherapy. Babies under phototherapy should
have a regular measurement of temperature and get weighted twice
daily.
2. Retinal damage : Effect of high intensity light on the growing retina in
uncertain. But animal studies indicate that retinal degeneration may
occur after several days of continuous exposure. It is essential
therefore, that the eyes of all newborns exposed to phototherapy be
covered with sufficient layers of opaque material.
3. Bronze baby syndrome. In this condition the skin, urine and serum
become brownish black after several days of phototherapy. It is seen
more often in neonates with conjugated hyperbilirubinemia. Babies
recover fully after several days once the phototherapy is discontinued.
4. Other. Electric shock due to poor grounding and unproven potential
long term effects on endocrine and sexual maturation.
Pharmacologic Therapy
1. Phenobarbitone : Administration of this drug to pregnant women and
babies has been shown to reduce the serum bilirubin in babies by
more than 50% in physiological jaundice. But it on is effective only if
given to the mother before delivery. Since onset of labor cannot be
predicted this has not gained in popularity. It leads to excessive sleep
in the baby and can be potentially addicting. Combining
phenobarbitone with phototherapy is no more effective than
phototherapy alone and hence is not used in routine clinical practice.
66
2. Metalloporphyrins. Tin (Sn) and Zinc (Zn) prophyrins and
mesopophyrins and under investigation for clinical use. These
compounds inhibit the activity of heme oxygenase and thus decrease
the formation of bilirubin.
3. Miscellaneous approaches: Frequent milk feeding will prevent
reabsorption of unconjugated bilirubin from the gut reducing
enterohepatic circulation. Bilirubin blinding agents like charcoal and
agar in the gut may prevent reabsorption of unconjugated bilirubin.
Exchange Transfusion
This is the standard mode of therapy for immediate treatment of
severe hyperbilirubinemia to prevent kernicterus and to correct anemia in
erythroblastosis fetalis.
Therapeutic guidelines for exchange transfusion are given in tables
below
Table : Management of idiopathic hyperbilirubinemia in healthy term
babies
Total serum bilirubin (mg/dl)
Age (Hours) (a) Consider Phototherapy (b)
Phototherapy (C)
Exchange transfusion if intensive
phototherapy fails (d)
< 24 - - -
25-48 >12 >15 >20
49-72 >15 >18 >25
>72 >17 >20 >25
(a) Jaundice during 1st 24 hours is always pathological and should be
investigated to identify the cause
(b) Based on individual clinical judgement.
(c) Phototherapy may be discontinued when TSB level falls below 15
mg/dl.
(d) Failure of intensive phototherapy is defined as inability to observe a
decline in TSB @ 1-2 mg/dl per 4-6 hours and its inability to keep the
TSB levels below the exchange range.
Adapted AAP Practice Parameters, Pediatrics 1994, 94 (4): 558-567.
67
Table : Indications for exchange blood transfusion (and phototherapy)
in preterm babies
Birth weight (g) Total serum bilirubin (mg/dl)
Normal infants High-risk* infants
upto 1000 10-12 8-10
1000-1250 12-14 10-12
1251-1500 14-16 12-14
1501-2000 16-18 14-16
2001-2500 18-20 16-18
>2500 20-22 18-20
* High risk factors include hemolysis, sepsis and perinatal distress factors
like birth asphyxia, hypothermia, hypoglycemia, acidosis etc. Start
phototherapy at a serum bilirubin level which is lower by 5 mg/dl than EBT
level. Due to increased risk of biliribin brain damage in high risk infants, they
are managed more aggressively and given an additional allowance of serum
bilirubin of 2 mg/dl both for phototherapy and exchange blood transfusion
Exchange transfusion is also indicated in following situations :
1. When phototherapy fails to prevent a rise inbilirubin to toxic levels.
2. To correct anemia and improve congestive cardiac failure in hydropic
infants.
3. To stop hemolysis and production by removing antibodies and
sensitized RBC's.
Type of blood. Most blood banks use blood anticoagulation with citrate
phosphate dextrose (CDP). Blood withdrawn <72 hours before is preferred.
In an emergency, frozen RBC reconstituted in saline or plasma may be
used. ABO compatible, Rh -ve blood is used for erythroblastosis fetalis and
O group Rh compatible blood is used for ABO incompatibility.
Quantity. 160 mL/kg (double the normal volume of 80 mL/kg) blood is used
for one exchange transfusion.
68
This ensures that 87% of blood volume is removed and exchanged by
the donor blood.
Procedure
The most commonly used technique is the push pull method in the
umbilical vein. For this, a single syringe and a special 4-way stopcock (two
three way stopcocks can be connected to make one 4 way system) are
required. Use of peripheral veins, or peripheral artery and vein has also been
described. The size of the aliquots during each push or pull should be small
(5-10 mL). Larger aliquots done rapidly causes acute depletion of blood
volume. A double volume exchange transfusion should take 1.5 to 2 hours
and probably longer in sicker infants.
Complications
These occur frequently and include bacterial
sepsis,thrombocytopenia, especially after repeated exchanges, portal vein
thrombosis, umbilical or portal vein perforation, arrythmia, cardiac arrest,
hypocalcemia, hypoglycemia, hypomagnesemia, metabolic acidosis,
alkalosis, HIV, hepatitis B & C infection, and graft vs host disease.
CONJUGATED HYPERBILIRUBINEMIA
This is rare in newborns but its presence always signifies pathology.
Conjugated hyperbilirubinemia is defined as a direct reacting fraction of >
2mg/dLor > 15% of the total bilirubin. Although clinicians commonly
associate direct bilirubin with biliary atresia or neonatal hepatitis, it must be
remembered that a large number of heterogenous disorders as shown in
table-3, are associated with laboratory evidence of conjugated
hyperbilirubinemia. Once a diagnosis of conjugated hyperbilirubinemia is
made extensive investigations are required for diagnosis.
Table 3: Common causes of conjugated hyperbilirubinimia
Sepsis
Intrauterine infection
69
Toxoplasmosis
Cytomegalovirus
Rubella
Herpes
Syphilis
Severe hemolytic disease
Biliary atresia
Giant cell hepatitis
Choledochal cyst
Cystic fibrosis
Galactosemia
Alpha1-antitrypsin deficiency
Tyrosinemia
REFERENCES
• Text book on Care of Newborn – Meharban Singh, VI Edition 2004.
• Ghai Essential Paeditrics- VI Edition - 2004.
• Manual of Neonatal care – John P. Cloherty V Edition 2004.
• Nelson Text Book of Pediatrics – 17th Edition 2004.
• Managing Newborn Problems. A guide for doctors, nurses, and
midwives: WHO Publication, 2003.
70
Day - 2 Session III (Management of Sepsis)
Objectives :
At the end of the session the trainee should be able to understand :
• How to diagnose sepsis.
• Relevance of laboratory tests.
• Rational use of antibiotics.
• Supportive treatment of sepsis.
Methodology
Lecture - Discussion
71
NEONATAL SEPTICEMIA
Neonatal sepsis is the most important cause of morbidity and
mortality especially among LBW and preterm babies in developing countries.
According to pooled hospital data based an NNPD survey, the incidence of
neonatal sepsis is around 3.8 percent. Neonatal sepsis can be divided into
two main subtypes depending on whether the onset is during the first 72
hours of life or later. In our experience there is almost equal distribution of
early-onset and late-onset cases.
Early-onset septicemia is caused by organisms prevalent in the
genital tract or in the labor room and maternity operation theatre. In the West
early-onset infections are mostly caused by group B streptococci and E. coli
while in our nursery most cases are due to Gram-negative organisms
especially E.coli, Klebsiella, and Enterobacter sp. Majority of neonates with
early- onset sepsis manifest as respiratory distress due to intrauterine
pneumonia. The onus for prevention of early-onset septicemia rests with the
obstetricians.
Early-onset bacterial infections occur either due to ascending infection
following rupture of membranes or during the passage of baby through
infected birth canal or at the time of resuscitation in the labor room. When at
least three of the following high risk factors are present, the baby is
considered to be infected and should be treated with appropriate antibiotics:
1. Very low birth weight (<2000 g) or preterm baby. The incidence of
early-onset sepsis is nearly 10 times higher in infants with birth weight
<1000 g compared to infants with normal birth weight.
2. Febrile illness in the mother during or within two weeks of delivery.
3. Foul smelling and/ or meconium stained liquor amnii.
4. Prolonged rupture of membranes (>12 hr).
5. More than three vaginal examination during labor.
6. Prolonged and difficult delivery with instrumentation.
72
7. Birth asphyxia and difficult resuscitation.
8. Pathological evidences of funisitis or presence of polymorphs in the
gastric aspirate.
Late onset septicemia is acquired as nosocomial infection from the
nursery or lying in ward. The onset is delayed for 72 hours after birth. In
most cases symptoms appear by the end of first week or during second
week of life. About two-third cases of late-onset septicemia are caused by
Gram-negative bacilli viz Klebsiella pneumoniae, Enterobacteria, Escherichia
coli. Pseudomonas aeruginosa, Alkaligenese fecalis, Salmonella
typhimurium, Proteus sp., Citrobacter and serratia, while the rest are
contributed by Gram-positive orgnaisms including Staphylococcus auerus
and albus.
The spectrum of bacterial pathogens analyzed from hospital- based
data collected by National Neonatal-Perinatal Database Network from
different centers in the country is shown in Table 1
Table 1 Blood culture isolates in neonatal sepsis (n = 837)*
1. Kelbsiella pneumoniae 29.7%
2. S. aureus 14.7%
3. E.Coli 13.9%
4. P.aeruginosa 9.2%
5. Enterobacter Sp. 7.9%
6. S.albus 7.2%
7. Candida sp. 4.8%
8. Acinetobacter 2.4%
9. S. viridans 1.4%
10. others 8.7%
* Based on National Perinatal Network Database, 1995
It is important to remember that bacterial flora is dynamic, different
from one place as compared to the other and it changes in the same place
73
over a period of time. It is essential to closely monitor the baccterial flora of
the NICU and the antibiotic sensitivity pattern of pathogens to evolve rational
antibiotic policy which is most suitable for your nursery.
The usual sources of nosocomial infection include incubators
(especially humidity tank), resuscitators, ventilators, solutions for cold
sterilization, feeding bottles, catheters, face masks and infusion sets and
sites etc.
CLINICAL FEATURES
Early onset neonatal sepsis is characterized by perinatal
hypoxia,resuscitation difficulties and evidence of congenital pneumonia in
the form of repiratory distress. The clinical presentation of late- onset
neonatal sepsis may be silent in a very small baby who may suddenly die
without exhibiting any signs and symptoms. The response may be modified
by the birth weight and maturity of the infant.
� The alteration in the behaviour and established feeding pattern of the
child are characteristic early features. The baby who had been
sucking normally, gradually or suddenly becomes lethargic, inactive,
unresponsive and refuses to suck. The previously alert and well baby
appears pale, sickly with grayish-blue circumoral cyanosis and vacant
stare.
� The baby just ‘does not look well’ may sound vague but is a most
useful clue to an experienced physician and nurse. Therefore, a high
index of suspicion and frequent evaluation of laboratory markers of
neonatal infections is mandatory to make an early diagnosis of
neonatal septicemia.
� Hypothermia is a common manifestation of sepsis in preterm babies,
while large babies may manifest with fever, especially in association
with Gram-positive infections.
� Diarrhea, vomiting and abdominal distension may precede or follow.
74
Table : Symptomatology of Neonatal Sepsis
General Respiratory system
• Lethargy • Cyanosis
• Refusal to suck • Tachypnea
• Poor cry • Chest retractions
• Poor weight gain/excessive weight loss
• Apnea/gasping
CNS Hypotension
• Not arousable, comatosed • Poor perfusion
• Sezuires + • Shock
• High pitched cry + • GI
• Excessive crying/irritability+ • Distension abdomen
• Neck retraction + • Diarrhea
• Bulging fontanel + • Vomiting
• Poor neonatal reflexes
Temperature problems Others
• Hypothermia • Sclerema
• Fever + • Excessive jaundice
• Bleeding
• Renal failure
� Onset of jaundice after the age of 3 days and elevation of direct
reacting bilirubin to more than2 mg/dl is suggestive of associated
hepatitis. Hepatosplenomegaly may or may not be present.
� Episodes of apneic spells with cyanosis may be th sole manifestation
of sepsis in preterm babies.
� In some babies, failure to gain weight or unexplained loss of weight
may be the only maifestation.
� In addition to the above features of disseminated infection, localizing
features may appear depending upon the predominant involvement of
different systems of the baby e.g. Pneumonia, Meningitis, UTI ,
Osteomyelitis and Septic arthritic etc.
DIAGNOSIS
There is no rapid and reliable test for confirmation of etiologic
diagnosis. The treatment is generally started when clinical picture is
supported by indirect early markers of neonatal infection. The appropriate
75
culture specimens are obtained before initiating antibiotic therapy which is
modified subsequently on the basis of the laboratory reports and response of
the patients to the treatment.
Leukocytes. The total leukocyte count has a low predicitive value for the
diagnosis of sepsis because of the wide range of normal counts from 8000 to
20,000/ mm3.
� Leukopenia (<5000/mm3) or absolute neutropenia (<1000/mm3) is
usually associated with neonatal sepsis.
� A band neutrophil is an immature neutrophil, wherein the width of the
narrowest segment of its nucleus is more than one-third of the
broadest segment. The band cell count of more than 20 percent and
band count to total neutrophil ratio of equal to or more than 0.2 has a
reported sensitivity of 82 to 90 percent for the diagnosis of septicemia.
� In addition the neutrophilis may show abnormal morphology with the
appreance of Dohle bodies (aggregates of rough endoplasmic
reticulum which stain light blue with Giemsa stain), toxic granulations
(eosinophilic granules in the cytoplasm of neutrophils) and
vacuolization.
Micro-erythrocyte sedimentation rate
Micro-ESR is a simple inexpensive though not very reliable marker of
neonatal infections. Normal value is upto 6 mm in the first hour during the
first 3 days of life. By the end of first month, maximum fall may be upto 11
mm. During the neonatal period a value of more than 15 mm is considered
as suggestive of infection.
Acute phase proteins
A number of acute phase proteins serve as useful indicators of
infection in the neonates (Table 2). The best studies among them is the C-
reactive protein (CRP). Two proteins, Namely prealbumin and transferrin are
negative reactants because their levels fall with inflammation and increase
with recovery.
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Table 2 Acute phase protein
Those increasing with inflammation
• C-reactive protein
• Procalcitonin
• Cytokines (IL-6 and IL –1ra)
• Alpha 1 acid glycoprotein (orosomucoid)
• Haptoglobin (alpha-2 glycoprotein)
• Alpha 1- antitrypsin
• Elastase alpha-1 proteinase inhibitor
• Fibrinogen
Those decreasing with inflammation
• Prealbumin
• Transferrin
CRP has been found useful in differentiating pneumonia from other
causes of neonatal respiratory distress syndrome. Serial decline in CRP
levels with therapy is suggestive of adequate response to antibiotics and
recovery. Elevation of CRP level may precede relapse of infection.
C-reactive protein is synthesized in the liver. Levels rise following any
inflammation and it is the most reliable indicator of neonatal infection. A level
of more than 8mcg/ml is considered as abnormal in the neonate.When CRP
is negative at the onset of disease, it must be repeated after 12 hours.
Accurate measurement of CRP can be made by laser nephelometry or
single radio-immunodiffusion assay. A semi-quantitative bedside latex
agglutination technique gives results within 15 minutes by using capillary
blood sample. CRP levels have a sensitivity and specificity of 87 percent and
83 percent respectively.
The ‘sepsis screen’
A battery of above indirect markers of infection when collectively
studied provide an extremely reliable index of early neonatal sepsis and
serve as a useful guide for initiating antibiotic therapy. When at least two of
77
the indirect markers of infection are positive, it gives the sensitivity and
specificity of 93 percent and 88 percent respectively. The septic screen is
indicated at birth if an infant is born following prolonged rupture of
membranes, foul smelling liquor, peripartal maternal fever and severe birth
asphyxia with active resuscitation. After birth if baby develops RDS or non
specific features of neonatal sepsis. Septic screen is indicated to support or
refute the clinical suspicion so that unnecessary antibiotic usage is curtailed
during neonatal period.
Gram’s stain and culture studies
� Culture of blood should be taken before starting antimicrobial therapy.
Using spirit followed by povidone-iodine (for 20 seconds or more), the
venipuncture site overlying a peripheral vein should be thoroughly
sterilized before obtaining specimen of blood for culture.
� It is recommended to take once ml of blood in a 10-20 ml broth blood
culture, so that the inoculated blood sample constitutes 5-10 percent
of the amount of liquid broth medium.
� Bactec method of blood culture is superior because of faster result
and greater yield. Blood culture is, considered as the gold standard
for the diagnosis of sepsis but is positive in only 60% of cases.
� Lumbar puncture should always be done in a suspected case of
neonatal sepsis except when the infant is too sick to undergo the
procedure. Cerebrospinal fluid should be promptly inoculated for
culture and its smear subjected to thorough search for organisms
after Gram staining. The interpretation of CSF cytology and
biochemistry is often difficult.
� Suprapubic specimen of urine is ideal for cytology and culture studies.
� In the presence of evidence of superficial infection (abscess, pustule,
vesicle), pus smear should be stained and swab cultured to identify
pathogens. Diarrheal stools should also be cultured.
78
� Examination of a stained smear (methylene blue) of gastric aspirate
also help in the diagnosis of early-onset sepsis if more than 5
neutrophils per high power field are documented.
� The culture studies are time consuming, but the bacterial antigens
(even if the organisms are killed) can be identified by a simple and
quick bed side procedure by using counter immuno-electrophoresis
(CIE).
� Buffy coat smear examination involves Gram staining of buffy layer of
the blood obtained after centrifugation and separation of plasma. If
carefully done, bacterial pathogens can be identified in 57 to 70
percent cases of neonatal sepsis.
Evaluation of extent of the disease
The infection may localize in any system of the body. Lumbar
puncture should be done in all cases and most septic neonates withstand
the procedure well.
� Suprapubic puncture should be done to obtain a clean specimen of
urine for microscopic examination and culture.
� Skiagram of chest should be taken in all cases to document
pneumonia while abdominal film will show presence of ileus and
changes of necrotising enterocolitis (NEC).
� Stools should be examined for occult blood and reducing substance
to exclude impending NEC.
� Radionuclide bone and liver scan may be done if there is suspicion of
osteomyelitis and pyemic liver abscess.
Biochemical abnormalities
� Blood should be examined for glucose (to detect hypo and
hyperglycemia), bilirubin, urea and creatinine (to detect renal failure
due to disease or aminoglycosides) and electrolytes.
� Acid base parameters and arterial blood gases should be monitored
in infants with pneumonia.
79
MANAGEMENT
Early recognition, prompt administration of effective and appropriate
antibiotic therapy with optimal supportive management are mandatory to
improve their intact survival. In view of very high morbidity and mortality due
to neonatal sepsis, prevention must be accorded highest priority.
Specific antimicrobial therapy
Antibacterial agents are greatly over prescribed in the neonatal period
because of non specific clinical features of sepsis and delay in laboratory
confirmation of diagnosis. Nevertheless, early therapy based on high index
of suspicion and supported by ‘sepsis screen’ is mandatory for improved
salvage.
� The rational use of antimicrobial agents in neonatal sepsis is
governed by the knowledge of the prevalent bacterial flora of a
particular newborn nursery and their sensitivity pattern against
available antibiotics.
� The initial regimen must cover the most common pathogens. It should
be borne in mind that there can be no single universal
recommendation for the antimicrobial regimen. Each treating unit
should adopt a suitable protocol on the basis of considerations
highlighted above.
� Based on changes in the spectrum of etiologic agents and the
antibiotic senstivity pattern, the choice of antibiotic must be constantly
reviewed and modified.
� Periodic changes in antibiotic schedule is associated with delayed
emergence of antibiotic resistant bacteria.
� In a rural setting where antimicrobial resistance is less likely to be a
problem, rational choice of antibiotics would include a combination of
gentamicin (an aminoglycoside) with benzyle penicillin or ampicillin.
Gentamicin 4 mg/kg single dose per day IM is found to be effective for
ambulatory management of neonatal sepsis in the community.
80
� Since common organisms causing neonatal sepsis in most neonatal
units in our country are klebsiella, E. coli, enterobacter and
Staphyloccus aureus, the initial antibiotic regimen must cover these
pathogens.
� The logical initial choice would be a combination of an aminoglycoside
(gentamicin or amikacin) and amoxycillin-clavulanate or ceftizoxime
and cloxacillin.
� The newer antibiotic preparations like tobramycin, netilmicin,
vancomycin, cefotaxime, ceftriaxone, ceftazidime, cefoperazone,
cefepime and imipenem should be kept in reserve for treatment of
meningitis and life threatening infections.
� Ciprofloxacin should be used as a last resort in critically sick neonates
when bacterial isolates are resistant to all other antibiotics.
� Indiscriminate use of ‘shot gun’ antibiotic therapy is not only
unscientific but it is also unethical and fraught with risks of emergence
of resistant strains of bacteria.
� When etiological agent is identified or suspected on the basis of
characteristic clinical picture, antimicrobial therapy can be made
highly specific. Benzyle penicillin is most suitable for the treatment of
infections due to Group B streptococci. Septicemia due to
Pseudomonas aeruginosa carries a poor prognosis and is best
managed by ceftazidime or cefepime. Beta-lactamase resistant
penicillin and vancomycin are indicated for the treatment of infections
caused by Staphyslococcus aureus. Ampicillin is the drug of choice
for treatment of an occasional case of listeriosis.
� The presence of bacterial meningitis in association with septicemia
modifies the choice, duration and mode of administration of
antibiotics.
� Aminoglycosides, polymyxin and first generation cephalosporins do
not effectively cross the blood brain barrier.
� Cefotaxime and moxalactam, the third-generation cephalosporins, are
not only highly active against Gram negative enteric organisms but
81
also attain excellent CSF levels. A combination of amikacin and
cefotaxime or ceftazidime is ideal for treatment of neonatal meningitis,
Cefuroxine the only second-generation cephaloxporin with good CSF
penertrability, may also be used, though enough data regarding its
use among neonates is not available as yet.
� Chloramphenicol has superb penetration across all body cavities
including blood-brain barrier. For susceptible organisms or when
organisms are unknown, its use should be considered. When
administered in recommended doses there is no risk of gray-baby
syndrome.
� Co-trimoxazole, an antimicrobial drug combination with excellent
diffusibility into the CSF, has not been studied well in neonates
because of the possible ill-effects of sulphamethoxazole on bilirubin-
albumin binding. It should theoretically have a useful place in the
management of neonatal meningitis after first week of life.
� Intraventricular administration of antibiotics for treatment of
ventriculitis is controversial and not recommended due to risk of
development of porencephalic cysts with repeated needle punctures.
Serial ultrasound examination should be conducted to exclude
development of septae and loculations.
� Bilateral intraventricular shunts with fenestration of septae is indicated
for management of ventriculitis complicated by loculations and
hydroccphalus.
Mode of administration and duration of therapy
Antibiotics should be administered intravenously at least in the initial
phases of management and as long as intravenous fluids are being
administered. Subsequently, except for the more fulminant infections (e.g.
meningitis), it is perhaps practical to give antibiotics intramuscularly.
Maintaining intravenous lines for the full duration of therapy is difficult and
fraught with the risks of extravasations, swelling and infection in most
neonatal set-ups in our country. Duration of antimicrobial therapy should be
82
individualized. In general, antibiotics should be given for a period of 10 to 14
days in septicemia and pneumonia, 14 days for urinary tract infection and 21
days for meningitis.
Supportive care and treatment of complications
� Neonate must be nursed in the thermo neutral zone of ambient
temperature. If possible, servo-controlled incubator or open care
system should be used. Intravenous fluids are started and enteral
feeding is stopped in a sick child for a couple of days.
� In case of documented hypoglycemia and when facilities to check
blood sugar are not readily available, it is prudent to give a mini-bolus
of 10 percent glucose (200 mg/kg).
� Injection vitamin K 0.5 mg is given intravenously at admission and
twice a week till enteral feeds are re-established.
� Metabolic acidosis is corrected by using appropriately dilute sodium
bicarbonate.
� Peripheral perfusion is supported with transfusion (s) of fresh blood or
fresh frozen plasma.
� Anemia is corrected with aliquots of packed cells. Fresh blood or FFP
is useful to improve defense mechanisms by providing opsonins and
polymorphonuclear leukocytes.
� Shock is managed by careful volume expansion (preferably with
central venous pressure monitoring), dopamine and high doses of
dexamethasone. Corticosteroids are indicated in gravely sick
neonates with endotoxic shock, sclerema and adrenal insufficiency.
� A number of therapeutic products like monoclonal antibiotics, tumor
necrosis factor (TNF) and interleukin -1 (IL-1) have been tried with
success for treatment of shock in experimental models. In addition,
pentoxifylline, a phosphodiesterase inhibitor, has been tried to
decrease the production of TNF. The role of prostaglandins,
ibuprofen, ketoconazole and inhibitors of nitric oxide synthase is
under evaluation and holds promise.
83
� Hyperbilirubinemia should be managed more aggressively with
phototherapy and exchange blood transfusion. Bilirubin
encephalophathy is likely to occur at a lower serum bilirubin level in
the setting of septicemia.
� Oxygen and ventilatory therapy should be instituted in the event of
respiratory failure as per the standard indications.
� Bleeding tendency is managed by judicious administration of fresh
blood, fresh plasma, platelet concentrates and vitamin K.
� Efforts should be made to identify collection of pus (over the joint,
bone, parotid, liver etc. ) which must be drained.
� In meningitis, fluids are restricted because of risk of syndrome of
inappropriate antidiuretic hormone secretion.
� Seizures are treated with diazepam and phenobarbitone. In the
presence of manifestations of raised intracranial pressure, mannitol
can be used.
Immunotherapy
Exchange blood transfusion in infected neonates can theoretically
help achieve improved peripheral and pulmonary perfusion, correction of
coagulation abnormalities and removal of toxins; and provide specific
antibodies, complement and phagocytic cells. The procedure is
recommended in critically sick neonates with sclerema, DIC and
hyperbilirubinemia. Controlled studies are, however needed to further
evaluate the therapeutic utility of exchange blood transfusion.
Granulocyte transfusion (1 X 109 granulocytes/kg) is suggested as
an adjunct to immunologic therapy for septic newborn infants with
neutropenia and has been used successfully in a limited number of infected
babies to decrease mortality. Granulocyte transfusion may be associated
with serious graft versus-host disease. It is not established whether it is
desirable to irradiate white cells before transfusion. Precise indications to
institute this therapy are not elucidated as yet.
84
Immunoglobulin preparations containing type- specific antibodies to
Group B Streptococci have been shown to be beneficial. Data regarding
Gram-negative organisms is not available. There is evidence to suggest that
administration of single dose of IVIG 750 mg/ kg in critically sick preterm
infants (1g/kg for term infants) with sepsis is associated with improved
survival. In future, specific immune globulins harnessed in donors or
produced by monoclonal antibody technique are likely to be used.
Fibronectin therapy in a septicemic neonate is experimental at
present. No randomized controlled trial is available and the present evidence
is anecdotal . Fibronectin, a large molecular weight glycoprotein influences
neutrophil and macrohage response to infection.
Colony stimulating factors (rh G-CSF and rh GM-CSF) are
endogenous proteins which can enhance the production and functional
capabilities of granulocytes. They have been shown to increase the bone
marrow granulocyte pool by proliferation of progenitor cells and improve
neutrophil functions, macrophage chemotaxis, phagocytosis and neutrophil
oxidative metabolism. Recombinant technology has now made available the
human G-CSF and GM-CSF for commercial use Experimental animal
studies and limited controlled trials in human neonates have failed to
demonstrate the efficacy of G-CSF for improving neutrophil count and
survival. There is a need to conduct multi-centric trails to assess the utility of
colony stimulating factors in the management of neonatal sepsis.
PROGNOSIS
The outcome depends upon the weight and maturity of the infant, type
of etiologic agent and its antibiotic sensitivity pattern; and adequacy of
specific and supportive therapy. Associated congenital malformations like
meningomyelocele, tracheoesophageal fistula and surgical procedure
adversely effect the prognosis.
85
� The early-onset septicemia due to Group B streptococci and
nosocomial infections due to klebsiella and Pseudomonas aeruginosa
are associated with adverse outcome.
� Early and aggressive therapy is mandatory for improved salvage
because extension of infection into various body organs and
development of complications such as endotoxic shock, sclerema,
NEC, DIC etc. is associated with extremely high mortality.
� The reported mortality rates in neonatal sepsis in various studies from
India range between 15 to 50 percent.
� Early institution of specific antimicrobial therapy with the aid of ‘sepsis
screen’, excellent supportive care, close monitoring of vital signs, and
judicious use of fresh blood, FFP and immunotherapy is likely to
improve the outcome of neonates with septicemia.
REFERENCES
• Text book on Care of Newborn – Meharban Singh, VI Edition 2004.
• Ghai Essential Paediatrics- VI Edition, 2004.
• Manual of Neonatal care – John P. Cloherty V Edition 2004.
• Nelson Text Book of Pediatrics – 17th Edition 2004.
• Managing Newborn Problems. A guide for doctors, nurses, and
midwives: WHO Publication, 2003.
86
Day 2 : Session IV (Management of Birth Injuries)
Objectives :
At the end of the session the trainee should be able to understand :
• Common birth injuries occuring in new born
• Management of birth injuries and needs for referral to other specialty.
Methodology
• Lecture -Discussion
87
BIRTH INJURIES
Birth injuries include avoidable and unavoidable trauma sustained by
the infant during the process of birth. The incidence of birth injuries in a
particular country or a center reflects the standard of obstetrical services in
that place. The common risk factors for birth injuries include primiparity,
osteomalacia or short statue of mother, prolonged or precipitate labor,
malpresentation, instrumental delivery, versions and vacuum extraction. Low
birth weight or preterm babies and large-for-dates or overgrown babies and
infants with congenital anomalies are at increased risk to develop birth
injuries.
Superficial Abrasions
These occur over the sites of forceps or vacuum application.
Accidental incision of the baby may occur during cesarean section. The
gaping incised wound may require stitching and should be protected from
infection by local application of 1.0 percent aqueous solution of
mercurochrome.
Petechiae and Bruising
Following prolonged delivery, the presenting part of the baby may
show cyanotic bluish tinge, petechiae and bruises (traumatic cyanosis).
Spontaneous recovery occurs within 2 to 3 days. Subconjunctival
hemorrhages are commonly seen in healthy babies and they disappear
spontaneously.
Cephalhematoma
Subperiosteal collection of blood may occur following normal or
complicated delivery due to rupture of superficial veins between the skull and
periosteum. Predisposing factors for this are uncertain. A cystic or fluctuant
swelling limited by suture lines appears a few hours after birth and at times
of the second day. The edges of the swelling may give a false impression of
88
depressed skull fracture due to organized rim of cephalhematoma. The
overlying scalp may show discoloration.
The swelling may appear at any site but unilateral parietal
cephalhematomas are most common as shown in figure. The condition
should be differentiated from Caput
succedaneum which is characterized by
diffuse edematous non-fluctuant swelling of
soft tissues on the presenting part of the scalp.
It is present at birth and often disappears
within 24 hours and is not limited by suture
lines. Cranial meningocele or encephalocele
is located in midline over the ocipital region
and can be differentiated from
cephalhematoma by positive crying impulse
and associated bone defect. At times massive subaponeurotic collection of
blood under the scalp may be seen in babies born by vaccum extraction
(Subgaleal hematoma). In view of its location over the surface of
periosteum, it is not limited by suture lines. The blood collection may be
massive causing hypovolemia or shock.
Most cephalhematomas disappear spontaneously after a variable
period of few days or weeks depending upon their size. Vitamin K1 1-2 mg
intramuscularly should be given to correct any co-existent coagulation
defect, especially in cases of subaponeurotic collection of blood. The incision
and drainage is indicated only when cephalhematoma gets infected or if it is
contributing to critical hyperbilirubinemia. Phototherapy may be required for
treatment of hyperbilirubinemia.
FRACTURES
Skull
Ability of the skull to mould during birth process protects it from injury
during normal uncomplicated labor. Linear skull fractures may be associated
in one-forth of infants with cephalhematoma and are of no therapeutic
89
significance. The depressed fractures may occur due to compression as a
result of forceps or against the maternal symphysis pubis and sacral
promotory. These also disappear spontaneously though surgical elevation
may be required in there are associated neurological manifestations.
Clavicle
Fracture of calvicle is the most common and often follows breech
extraction or shoulder impaction. The fracture of clavicle may occur following
uncomplicated vaginal delivery. The reported incidence of fractured calvicle
varies between 0.2 to 3.5 percent. The baby cries due to pain when handled.
Most newborn infants with fracture of clavicle have no or minimal physical
findings. A greenstick fracture may be asymptomatic at birth and picked up
by callus formation at 7 to 10 days of age. The movements of affected limb
may be limited and Moro reflex may be asymmetric. The crepitus may be
elicited at the site of fracture and supra calvicular depression on the affected
side is often obliterated. The associated fracture of the humerus and Erb's
palsy should be looked for and excluded. The prognosis is excellent and
callus may form within one week. Immobilization of the arm on the affected
side can be achieved by pinning the infant's sleeve to the shirt or by
wrapping the limb. Paracetamol (15 mg/kg/dose) is a safe analgesic for use
in newborn babies.
Humerus
The forcible manipulations and pulling at baby's arm during delivery
may result in fracture of the humerus
which is commonest at the junction
between upper one-third and he lower
two-third of humerus. The diagnosis is
suspected by pain and limitation of
movements of the affected limb,
asymmetric Moro response and crepitus at the site of fracture. The strapping
of the arm by the side of chest for two weeks is recommended for
90
immobilization. The prognosis is excellent unless the epiphysis is damaged,
in which case the limb may be permanently shortened.
Femur
Fracture of femur is rare and caused by forcible manipulation of legs
during breech extractin. Spontaneous healing with excess callus formation
occurs without any splintage.
BIRTH TRAUMA TO NERVOUS SYSTEM
Intracranial injury
The improved obstetrical management and early resort to cesarean
section has reduced the incidence of birth trauma. Precipitate delivery or
difficult forceps and vacuum extraction in a large baby, extraction of breech
and other abnormal presentations may be associated with intracranial
hemorrhage. The baby is generally asphyxiated at birth and spontaneous
respirations may not be established even after resuscitation. The abnormal
neurological behaviour (cerebral depression or irritability) often manifests
within the first 48 hours of life. The differentiation between the isolated
perinatal hypoxia and intracranial birth injury is difficult and is guided by the
nature of events during delivery rather than by any specific syndrome of
neurological manifestations.
Spinal cord transaction
This relatively rare form of birth injury follows difficult breech
extraction when fracture of cervical spine or avulsion of cervical cord may
occur. Sometimes, a click or crack may be heard during delivery. It is
characterized by flaccid paraplegia, with retention of urine and overflow
incontinence. Respiratory failure due to diaphragmatic paralysis may
dominate the clinical picture. Sensations may be dulled or absent below the
site of lesion. Prognosis is grave.
91
Peripheral Nerve Palsies
Facial palsy
It may occur with or without forceps application. Facial asymmetry,
inability to close the eye and absent rooting reflex on the affected side
suggest the diagnosis as shown in figure. The recovery is excellent and
complete. By and large, most peripheral nerve
injuries in the newborn carry a good prognosis
because of greater regenerative power and short
length of nerves. Bilateral facial palsy or its
association with 6th nerve paralysis suggests a
central lesion such as agenesis of seventh nerve
nucleus (Moebius syndrome).
Partial facial palsy or cogenital absence of
depressor anguli oris muscle is a relatively
frequent condition. Facial asymmetry on crying is
limited to the corner of the mouth and mandible which gets pulled
downwards on the normal side. Eye closure is unaffected but depth of
nasolabial fold is flattened on the normal side. There is high incidence of
cardiovascular, genitourinary and skeletal anomalies associated with
congenital absence or hypoplasia of depressor anguli oris muscle.
Brachial Plexus Palsy
Avulsion of brachial nerve roots may occur during difficult breech
extraction or shoulder impaction.
Erb's palsy. When upper cervical roots (C5, C6) are affected, the arm
hangs limply, adducted and internally rotated with elbow extended. Arm
recoil is lost. Respiratory distress may occur if diaphragmatic paralysis is
associated. The lack of spontaneous movements and asymmetric
Mororesponse would favour the diagnosis of Erb's palsy. It may be
associated with fracture of clavicle or involvement of lower cervical roots.
92
Klumpke's palsy. The involvement of lower cervical nerve roots (C7, C8,
T1) manifests as wrist drop and flaccid paralysis of hand with absent grasp
response. The presence of miosis, ptosis and anhidrosis (Horner's
syndrome) though uncommon would suggest associated damage to the
cervical sympathetic chain of the first thoracic root.
The arm should be kept in the position of abduction and external
rotation at the shoulder and flexion of elbow in infants with Erb's palsy. In
Klumpke's palsy, cotton ball should be placed in the baby's hand to avoid
contractures. Massage and passive movements of muscles would aid
recovery, which is generally complete but may take few weeks or months. In
severe cases especially when associated with laceration of nerves, the
affected limb may remain permanently short and stunted. The lesions of the
upper brachial plexus have a better prognosis than those of lower or total
plexus. If paralysis persists for more than 3 months, neuroplasty is indicated.
Phrenic nerve palsy
Phrenic nerve injury, though rare, is often associated with upper
brachial palsy. Diaphragmatic paralysis results in irregular labored thoracic
breathing without any visible abdominal movements. The diaphragm is
elevated on the affected side and breath sound is diminished. The
characteristic see-saw movements of two sides of diaphgram during
respiration is obvious on fluoroscopic examination. There is no specific
therapy but bay should be placed on the affected side. Administration of
oxygen and gavage feeding, depending upon the severity of respiratory
difficulty, are often indicated. The recovery is often complete but the course
may be complicated by respiratory infections. At times when recovery is
incomplete, the weak, flabby and elevated leaf of diaphragam may manifest
as eventration during infancy.
Visceral Trauma
Capsular laceration of liver and spleen and adrenal hemorrhage may
follow difficult breech extraction. The damage may also occur due to over
93
zealous attempts at external cardiac massage. The hemorrhage may remain
concealed as subcapsular hematoma or capsule may rupture with blood
flowing into the peritoneal cavity. The baby may manifest severe pallor,
tachycardia and evidences of shock. The presence of shifting dullness may
suggest the existence of blood in the peritoneal cavity, which can be
aspirated for diagnostic purposes. Enlargement of liver in association with
clinical evidence of blood loss should alert the physician to the possibility of
sucapsular hematoma. Hyperbilirubinemia may occur as in other cases of
hemorrhage in the tissues and body organs. Early recognition and
administration of vitamin K and blood transfusion with monitoring of central
venous or arterial pressure may salvage some of these babies. Adrenal
hemorrhage is rarely diagnosed in life but when detected at autopsy it is
impossible to say whether it was the result of direct trauma, anoxia or
endotoxin shock.
Sternomastoid 'Tumor'
During the second week of life, a firm mass 1-2cm in diameter may be
noted in the midportion of the steromastoid muscle. It is believed to be either
a small hematoma from injury to the muscle at birth or due to fibromatous
malformation of the muscle. The attention to the condition is often directed
by the presence of torticollis on the affected side. The mother should be
advised to overextend the affected muscle by turning the infant's head in the
opposite direction and flexing the neck towards unaffected side. The majority
of these tumors resolve spontaneously by six months to one year of age. If
torticolis persists beyond one year, surgical correction may be undertaken.
REFERENCE
• Text book on Care of Newborn – Meharban Singh, VI Edition 2004.
• Manual of Neonatal care – John P. Cloherty V Edition 2004.
• Nelson Text Book of Pediatrics – 17th Edition 2004.
• Managing Newborn Problems. A guide for doctors, nurses, and
midwives: WHO Publication, 2003.
• Ghai Essential Paediatrics- VI Edition, 2004.
94
QUESTIONNAIRE ON NEWBORN CARE FOR SPECIALIST IN PEDIATRICS
Pre/Post Test Duration: 15 Min.
1. Correct ratio of chest compression and artificial respiration during
resuscitation of Newborn is
a. 1:1 b. 2:1
c. 3:1 d. 4:1
2. What should be the desired pressure in the suction machine for
clearning the air ways during resuscitation:
a. < 50 mm of Hg b. 50-100 mm of Hg
c. 100-150 mm of Hg d. 150-200 mm of Hg
3. How long can expressed breast milk be stored at room temperature
before feeding a newborn
a. Upto 4 hours b. upto 8 hours
c. Upto 12 hours d. Upto 24 hours.
4. Which is the most common fracture occurring as a result of birth injury
a. Femur b. Humerous
d. Clavicle d. Skull
5. At what level of blood glucose the diagnosis of Hypoglycemia is
entertained in the neonatal period.
a. < 20 mg/dl b. < 30 mg/dl
c. < 40mg/dl d. < 50 mg/dl
6. In suctioning during resuscitation the rule is to first suction XXXX.
and then the XXXXXXXXXXXXXXXX........X
7. A newborn is still not breathing after tactile stimulation what should be
the next action?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
95
8. What attachment is required to deliver 100% oxygen by self inflating
ambubag during resuscitation ?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
9. In a newborn baby after 30 seconds of ambubaging and chest
compression the heart rate is 80/mt. what should be the next step ?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
10. What is the recommended dose of epinephrine for resuscitation of
newborn ?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
11. What is the first line of anticonvulsant for neonatal seizures ?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
12. At what level of bilirubin the exchange transfusion should be done in
term baby having jaundices within 24 hours ?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
13. At what apgar score at 5 minutes the birth asphyxia should be
considered as severe ?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
14. At what axillary temperature the hypothermia in newborn is
considered to be sereve ?
XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX
15. In a breast fed 3 days term newborn with jaundice at what level of
bilirubin phototherapy should be started ?
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16. List two conditions when the endotracheal intubation is required at the
beginning of resuscitation ?
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17. Name 2 drugs which can be given by endotracheal tube in newborn
during resuscitation ?
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18. If breath sounds are unequal on auscultation of chest while
resuscitating a newborn with bag and mask, what conditions should
be suspected ?
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19. List criteria of diagnosing pathological jaundice in newborn ?
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2. XXXXXXXXXXXXXX
3. XXXXXXXXXXXXXX
4. XXXXXXXXXXXXXX
20. List perinatal risk factors of developing early neonatal septicemia ?
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2. XXXXXXXXXXXXXX
3. XXXXXXXXXXXXXX
4. XXXXXXXXXXXXXX