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 and1 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 Score5 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.

MILD (Stage I)

subtle abnormality days

Irritable with exaggerated and frequent Moro’s.

Hyperalert (look of hunger, wide eye gaze, failure to fixate.

Normal tone Weak suck ( NG) Sympathetic dominance

with tachycardia and mydriasis.

No seizure clinically

No Impairment

MODERATE ENCEPHALOPATHY(Stage II) Lethargy with

spontaneous movement Moro’s and other

primitive reflexes lost in early stages, tendon jerks exaggerated.

Differential tone with LL>UL and neck extensors>flexors

Seizures ++ (lip smacking, sucking, tonic or clonic seizures.)

Poor suck (NG required) Parasympathetic

dominance with bradycardia and constricted pupils.

25% Impaired

SEVERE ENCEPHALOPATHY(Stage III) Comatose with little

spontaneous movement Seizures prolonged and

frequent. In very severely asphyxiated babies no seizures clinically or EEG due to completely exhausted brain energy)

Severely hypotonic initially with lost of reflexes

Death If recovers there is

excessive hypertonia. Persistent abnormal

neurological signs beyond 6 weeks means CP.

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,

hypomagnesaemia 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 outcomeb) Avoid hypo or hyperglycaemia c) Adequate ventilation and avoid hypoxaemia and hypercarbia or hypocarbiad) Review infection risk and Rx with antibioticse) Maintain adequate hydration but do not dehydrate or overhydratef) 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 IPPVMetabolic In SIADH, restrict fluids. Rx hypoglycaemia.DIVC No specific Rx. Replace with fresh frozen plasma., cryoprecipitate,

platelet or packed cell as indicatedNutrition 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 benefitc) 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 only.

o Steroids are of no use.6

F. Prognosisa) 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 NE.

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).

References1.Levene ML, Sands C, Grindulis H, Moore JR. Comparison of 2 methods of predicting outcome in perinatal asphyxia. Lancet 1986;1:67-712. Silverman F, Suidan J, Wasserman J, Antoine C, Young BK. The Apgar score: Is it enough? Obstet Gynae 1985;66:331-63. Low JA, Panagiotopoulos C, Derick EJ. Newborn complications afterintrapartumasphyxia with metabolic acidosis in term fetus. Am J Obstet Gynecol 1994;170:1081-74.LeveneML. Management of asphyxiated full term infant. Arch Dis Child 1993;68:612-65. Evan D, Levene M. Neonatal seizures. Arch Dis Child 1998;78:F70-56. Levene MI, Evan DH Medical management of raised intracranial pressure after severe asphyxia. Arch Dis Child 1985; 60:12-67Holme G ,Rowe J, Hafford J, Schmidt R. Prognostic value of EEG in neonatal asphyxia. Electroenceph Clin Neurophysiol 1982;53: 60-728. Thornberg E. Ekstrom-Jodal B. Cerebral function monitoring: a method of predicting outcome in term neonates after severe perinatal asphyxia .Acta paediatr 1994;83:596-6019.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