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Birth Asphyxia

A. Definition

There is no accepted definition. It is a result of a combination of hypoxia and
hypoperfusion and affects many organ systems of which the cerebral complication is the
most devastating.

B. Incidence of Birth Asphyxia

Depends on definition used and ranges from 3.7 to 9/1000 livebirths (average of
6/1000 LBs)
Depression of Apgar score of  5 in 5 min. is 4/1000 (Levene 1986)
Hypoxic ischaemic Encephalopathy (HIE) 5-6/1000 term infants and
1 per 1000 dies or survives with neurological damage.1

C. Diagnosis

1. Meconium staining of amniotic fluid may be an indicator of foetal distress or
intrapartum hypoxia.

2. Abnormal CTG tracing is sometimes present.

3. Acidosis. A low umbilical cord pH is a better indicator of perinatal asphyxia than the
Apgar score 2-4 A pH of <7.0 is present if cerebral palsy results from birth asphyxia

4. Apgar Score. Poorly predictive of adverse outcome and not a useful method of
defining significant asphyxia. 50% of children with CP. evident at 7 years of age had
an optimal A/S of 7-10 at 1 min.

Use of the Apgar Score
5 min : Measures effectiveness of resuscitation.
20 min : All babies with Apgar < 6 at 5 min. should have a 20 min. score.
Apgar < 5 at 20 min.: an important prognostic indicator of poor CNS outcome
(most will be quadriplegic).

5. Delay in Establishing Respiration. . If there is no spontaneous respiration by 20
minutes despite adequate resuscitation - the neurological outcome of such
survivors is invariably bad.

6. Severity of Neonatal Encephalopathy (NE) is the best clinical method currently
available to predict subsequent outcome following asphyxia.
Staging of Neonatal /Hypoxic Ischaemic Encephalopathy (HIE)
Only constant in term infants or > 35 weeks. Not consistent in Prems.

(Stage II) (Stage III)
 Lethargy with   Comatose with little
 subtle abnormality  spontaneous movement spontaneous movement
days  Moro’s and other  Seizures prolonged and
 Irritable with exaggerated primitive reflexes lost in frequent. In very severely
and frequent Moro’s. early stages, tendon jerks asphyxiated babies no
 Hyperalert (look of exaggerated. seizures clinically or EEG
hunger, wide eye gaze,  Differential tone with due to completely
failure to fixate. LL>UL and neck exhausted brain energy)
 Normal tone extensors>flexors  Severely hypotonic
 Weak suck ( NG)  Seizures ++ (lip initially with lost of
 Sympathetic dominance smacking, sucking, tonic reflexes
with tachycardia and or clonic seizures.)   Death
mydriasis.  Poor suck (NG required)  If recovers there is
 No seizure clinically  Parasympathetic excessive hypertonia.
dominance with  Persistent abnormal
bradycardia and neurological signs beyond
constricted pupils. 6 weeks means CP.

No Impairment 25% Impaired 92% Impaired .

Important to note:

i) Absence of encephalopathy does not mean infant has not suffered significant intrapartum
asphyxia (kidney and heart may be affected).
ii) Encephalopathy can be caused by hypoglycaemia or cerebral haemorrhage and therefore have
to be excluded before diagnosing HIE.

D. Complications of Birth Asphyxia
 Brain: Periventricular haemorrhage and periventricular leukomalacia. Intracranial
haemorrhage (subdural (5%), subarachnoid (some), choroid plexus, cerebellum
and thalamus). Cerebral oedema occurs after 24-28 hours.
 Kidney: Acute tubular necrosis; oliguria; usually recovers with supportive Rx. Rule
out acute urinary retention.
 Heart: Hypoxic ischaemic damage (cardiogenic shock, hypotension, heart failure
with atrioventricular valve regurgitation, arrhythmia).
 Lungs: Meconium aspiration common
 GIT:stress gastric ulcer, feed intolerance and NEC
 Metabolic: SIADH (secondary to head injury) , hypoglycaemia, hypocalcaemia,
 Haematological : DIVC
E. Management

I. Good intrapartum care

II. Adequate and effective resuscitation

III. ICU monitoring for complications. Regular BP, respiratory, urine output, acidosis etc.

IV. General measures:
a) Nurse in thermoneutral environment. Avoid high environmental temperature as
fever is associated with adverse outcome
b) Avoid hypo or hyperglycaemia
c) Adequate ventilation and avoid hypoxaemia and hypercarbia or hypocarbia
d) Review infection risk and Rx with antibiotics
e) Maintain adequate hydration but do not dehydrate or overhydrate
f) Treat jaundice as necessary

V. CVS  Rx hypotension with plasma expanders and inotrope support.
Renal  Careful assessment of fluid status; if output < 1ml/kg/hr start renal
failure regime; peritoneal dialysis if needed.
Lungs  IPPV
Metabolic  In SIADH, restrict fluids. Rx hypoglycaemia.
DIVC  No specific Rx. Replace with fresh frozen plasma., cryoprecipitate,
platelet or packed cell as indicated
Nutrition  Enteral feeding is preferable to parenteral but avoid rapid increase in
feeding to decrease risk of NEC

VI. Brain Orientated Management.

a) Cerebral perfusion: Maintain BP (Mean Arterial Pressure > 40 mmHg)
b) Seizure (Also see chapter on Neonatal Seizures)
o frequent convulsion ( over 3 per hour) or prolonged convulsion ( lasting 3
or more minutes) should be treated 4,5
o Phenobarbitone (loading dose 20 mg/kg with another 20mg/kg for
persistent seizures , and 5 mg/kg OD maintenance dose)
o Clonazepam, lignocaine or phenytoin for persistent seizure. Phenytoin best
avoided for maintenance.
o Prophylactic barbiturate therapy did not show any benefit
c) Intracranial Hypertension
o Fluid restriction and give enough fluid to keep infant on dry side of normal.
(usually less 20 % of daily fluid requirement).
o If full fontanel and seizures give 20% mannitol at 1 g/kg over 20 min.
Mannitol contraindicated in oliguria. Can repeat 6 hourly for maximum
2 - 3 doses.
o Ventilate and keep PaCO2 at 35-45 mmHg. Keeping the PaCO2 less
than this as it can cause cerebral ischaemia. Maintain for 24 - 48 hours
o Steroids are of no use.
F. Prognosis
a) Apgar score and mortality.
 Mortality in the first year of life for premature babies.
Babies < 2500g : mortality > 80% if Apgar is 0 - 3 at 15 min.
mortality > 95% if Apgar is 0 - 3 at 20 min.
Babies > 2500 g: mortality is 50% if Apgar is 0 - 3 at 15 min.
mortality is 60% if Apgar 0 - 3 at 20 min.
 Mortality very high in infants who do not breathe spontaneously at 30 min.
 Risk of CP. is 60% for BW > 2500 g if Apgar is 0 - 3 at 20 min.
 93% of babies with Apgar 0 at 1 min. and 0-3 at 5 min. were entirely normal
on follow-up. Therefore 15 min and 20 min score is important.

b) Severity of HIE and outcome (most accurate predictor)
 No infant with mild HIE alone developed impairment. Mild encephalopathy
carries an excellent prognosis irrespective of Apgar score and parents
should be strongly reassured of excellent outcome.
 The median risk for impairment is 25% in moderate NE and 92% in severe

c) CT scans done after 1st week of life.
 Extensive areas of low attenuation with apparent brightness of basal ganglia
are associated with very poor prognosis.

d) Doppler U/S appears to be an accurate predictor for full term babies done after 24
hours of life.
 Decrease Pourcelot’s resistivity index (PRI <0.55) i.e. relative increase in the
end diastolic blood flow velocity compared to peak systolic blood flow
velocity or high mean flow velocity (or anterior cerebral artery) > 3 SD of the
normal mean has a +ve predictive value for adverse outcome of 94%.

e) U/S of head can be done at discharge and at 2 - 3 weeks of life to look for
periventricular haemorrhage or periventricular leukomalacia.

f) EEG:
 severe abnormalities include burst suppression, low voltage or isoelectric EEG.
 moderate abnormalities include slow activity

 The overall risks for death or disability were 95% for severely abnormal EEG,
64% for moderately abnormal EEG and 3 % for normal or mildly abnormal EEG 7,8

 Continuous EEG monitoring in the first 6-12 hours after birth has been shown to
identify infants at risk of subsequent brain damage 9

Long term :

a. Phenobarbitone will be taken off on discharge if the child is neurologically normal
and feeds normally (by day 7-10).

b. If CNS is abnormal - the duration of phenobarbitone use is controversial.
Probably 3-6 mths. (Longer if EEG abnormal)
c. All doctors managing such infants should never reassure the parents the child is
"Normal" unless on prolonged follow up (at least up to 2yrs) - the milestones are
within normal limits (including normal speech - suspect deafness/mental
retardation if speech delayed).

1.Levene ML, Sands C, Grindulis H, Moore JR. Comparison of 2 methods of predicting outcome in perinatal
asphyxia. Lancet 1986;1:67-71
2. Silverman F, Suidan J, Wasserman J, Antoine C, Young BK. The Apgar score: Is it enough? Obstet Gynae
3. Low JA, Panagiotopoulos C, Derick EJ. Newborn complications afterintrapartumasphyxia with metabolic
acidosis in term fetus. Am J Obstet Gynecol 1994;170:1081-7
4.LeveneML. Management of asphyxiated full term infant. Arch Dis Child 1993;68:612-6
5. Evan D, Levene M. Neonatal seizures. Arch Dis Child 1998;78:F70-5
6. Levene MI, Evan DH Medical management of raised intracranial pressure after severe asphyxia. Arch Dis
Child 1985; 60:12-6
7Holme G ,Rowe J, Hafford J, Schmidt R. Prognostic value of EEG in neonatal asphyxia. Electroenceph Clin
Neurophysiol 1982;53: 60-72
8. Thornberg E. Ekstrom-Jodal B. Cerebral function monitoring: a method of predicting outcome in term
neonates after severe perinatal asphyxia .Acta paediatr 1994;83:596-601
9.Helllstorm-Westas L, Rosen I, Svenningsen NW. Predictive value of early continuous amplitude integrated
EEG recording on outcome after severe birth asphyxia in full term infants. Arch Dis Child 1995; 72: F34-8