1

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

2

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

3

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.

4

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

5

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.

6

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.

7

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)

8

- 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

9

- 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.

10

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

11

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

12

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

13

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.

14

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

15

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

16

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

17

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

18

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

19

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.

20

• 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 -

21

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

22

• 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.

23

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

24

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

25

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

26

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?

27

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.

33

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.

76

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 ?

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

16. List two conditions when the endotracheal intubation is required at the

beginning of resuscitation ?

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

17. Name 2 drugs which can be given by endotracheal tube in newborn

during resuscitation ?

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

96

18. If breath sounds are unequal on auscultation of chest while

resuscitating a newborn with bag and mask, what conditions should

be suspected ?

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

XXXXXXXXXXXXXXXXXXXXXXXXXXXXXXX

19. List criteria of diagnosing pathological jaundice in newborn ?

1. XXXXXXXXXXXXXX

2. XXXXXXXXXXXXXX

3. XXXXXXXXXXXXXX

4. XXXXXXXXXXXXXX

20. List perinatal risk factors of developing early neonatal septicemia ?

1. XXXXXXXXXXXXXX

2. XXXXXXXXXXXXXX

3. XXXXXXXXXXXXXX

4. XXXXXXXXXXXXXX