Birth Asphyxia

Birth asphyxia (also called perinatal asphyxia) occurs when a baby doesn't receive enough oxygen before, during, or just after birth, leading to hypoxia and hypercapnia. It is a major cause of neonatal morbidity and mortality worldwide.

Overview

Birth asphyxia results in hypoxic-ischaemic injury to multiple organs, with the brain being particularly vulnerable. The severity depends on:

Duration and severity of hypoxia

Gestational age of the infant

Timing of the insult (antepartum, intrapartum, or postnatal)

Incidence:

Affects 1-6 per 1,000 live births in developed countries

Higher rates (5-26 per 1,000) in developing countries

Major contributor to neonatal mortality (23% of neonatal deaths globally)

Aetiology

Birth asphyxia can result from factors affecting oxygen delivery at any point from mother to fetus.

Antepartum causes:

Maternal hypoxemia (severe anaemia, respiratory disease, carbon monoxide poisoning)

Placental insufficiency (pre-eclampsia, placental abruption, chronic hypertension)

Maternal drug use (opioids, anaesthetics)

Intrauterine growth restriction (IUGR)

Post-term pregnancy

Multiple gestation

Intrapartum causes:

Prolapsed cord causing compression during birth

Nuchal cord (cord wrapped around neck)

Cord compression (short cord, true knot)

Placental abruption

Uterine rupture

Prolonged or obstructed labour

Shoulder dystocia

Maternal shock or intrapartum haemorrhage

Uterine hyperstimulation

Maternal hypotension (from epidural, haemorrhage)

Postnatal causes:

Severe respiratory distress

Congenital heart disease with inadequate pulmonary blood flow

Persistent pulmonary hypertension of the newborn (PPHN)

Severe anaemia or shock

Fetal factors:

Prematurity

Congenital anomalies

Infection (sepsis, pneumonia)

Hydrops fetalis

Pathophysiology

Acute phase (minutes to hours):

Initial hypoxia → Redistribution of blood flow to vital organs (brain, heart, adrenals)

Persistent hypoxia → Cellular energy failure (depletion of ATP)

Anaerobic metabolism → Lactic acidosis

Cellular dysfunction → Loss of membrane integrity, cytotoxic oedema

Multi-organ dysfunction

Reperfusion injury (hours to days):

Restoration of blood flow paradoxically worsens injury

Free radical formation

Inflammatory cascade activation

Excitotoxicity (excess glutamate)

Apoptosis and necrosis

Secondary energy failure peaks at 6-15 hours after insult

Chronic phase (days to months):

Ongoing cell death

Glial scarring

Permanent neurological damage

Clinical Features

Immediate signs (delivery room):

Failure to initiate or maintain regular breathing

Poor muscle tone (floppy, hypotonic)

Bradycardia (heart rate <100 bpm)

Absent or weak reflexes

Pallor or cyanosis

Poor Apgar scores:

0-3 at 1 minute
<7 at 5 minutes
Persistent low scores at 10, 15, 20 minutes

Need for active resuscitation (PPV, chest compressions, drugs)

Metabolic abnormalities:

Metabolic acidosis: pH <7.0, base deficit ≥12 mmol/L (in umbilical cord blood or early neonatal sample)

Hypoglycaemia or hyperglycaemia

Hypocalcaemia

Hyponatraemia (SIADH)

Multi-organ involvement:

Central nervous system (most important):

Altered consciousness (lethargy, coma)

Hypotonia or hypertonia

Seizures (often within first 24 hours)

Poor feeding, weak suck

Abnormal reflexes

→ Hypoxic-Ischaemic Encephalopathy (HIE) - see below

Cardiovascular:

Hypotension

Poor perfusion

Myocardial dysfunction

Tricuspid regurgitation

Arrhythmias

Respiratory:

Persistent pulmonary hypertension (PPHN)

Respiratory distress

Pulmonary haemorrhage

Renal:

Acute kidney injury

Oliguria or anuria

Haematuria

Gastrointestinal:

Feeding intolerance

Necrotising enterocolitis (NEC)

Hepatic dysfunction (elevated transaminases, coagulopathy)

Haematological:

Thrombocytopenia

Disseminated intravascular coagulation (DIC)

Hypoxic-Ischaemic Encephalopathy (HIE)

HIE is the clinical syndrome of abnormal neurological function in the first days of life in term or near-term infants, resulting from birth asphyxia.

Diagnostic criteria for HIE (all must be present):

Evidence of metabolic acidosis (pH <7.0, base deficit ≥12) in cord or early sample

Apgar score 0-3 for >5 minutes OR need for resuscitation at 10 minutes

Clinical evidence of encephalopathy (altered consciousness, abnormal tone, seizures)

Multi-organ dysfunction consistent with asphyxia

Sarnat Staging of HIE

Feature	Stage 1 (Mild)	Stage 2 (Moderate)	Stage 3 (Severe)
Level of consciousness	Hyperalert, irritable	Lethargic	Stuporous, coma
Muscle tone	Normal or increased	Mild hypotonia	Flaccid
Posture	Normal	Flexion	Decerebrate
Tendon reflexes	Hyperactive	Hyperactive	Decreased or absent
Moro reflex	Strong	Weak or incomplete	Absent
Pupils	Dilated, reactive	Constricted, reactive	Variable, poor light reflex
Seizures	Absent	Common (often focal)	Uncommon or decerebrate
EEG	Normal	Low voltage, periodic discharges	Burst suppression, isoelectric
Duration	<24 hours	2-14 days	Days to weeks
Outcome	100% normal	80% normal or mild disability 20% severe disability or death	50% die Survivors have severe disability

Investigations

Blood tests:

Cord blood gases (or arterial blood gas within 1 hour):

pH <7.0, base deficit ≥12 mmol/L supports diagnosis

Full blood count (thrombocytopenia, anaemia)

Renal function (elevated creatinine, urea)

Liver function tests (elevated ALT, AST)

Coagulation profile (DIC screen)

Blood glucose

Electrolytes (Na⁺, Ca²⁺, Mg²⁺)

Lactate

Blood culture (if sepsis suspected)

Neurological investigations:

EEG (Electroencephalography):

Continuous amplitude-integrated EEG (aEEG) for seizure detection
Background pattern correlates with severity and prognosis
Abnormal: low voltage, burst suppression, isoelectric

Cranial ultrasound:

Bedside screening
May show increased echogenicity, oedema, haemorrhage
Limited sensitivity for HIE

MRI brain (preferred neuroimaging):

Most sensitive for detecting hypoxic-ischaemic injury
Timing: Optimal at 2-8 days of age (after reperfusion injury develops)
Patterns:

Watershed injury (parasagittal cortex)
Basal ganglia and thalamus injury
Diffuse cortical injury

Diffusion-weighted imaging (DWI): Shows restricted diffusion in acute injury
Prognostic value: Helps predict long-term outcome

Other investigations:

Chest X-ray (if respiratory distress)

Echocardiography (if cardiac dysfunction or PPHN)

Urine output monitoring

Management

Immediate resuscitation (delivery room):

Follow neonatal resuscitation protocol

Ensure effective ventilation (most critical)

Chest compressions if HR <60 despite ventilation

Medications as needed (adrenaline, volume)

Umbilical cord blood gas sampling

Supportive care (NICU):

Respiratory:

Oxygen therapy targeting SpO₂ 90-95%

Avoid hyperoxia (may worsen injury) and hypoxia

Mechanical ventilation if needed (target normal PCO₂ 35-45 mmHg)

Avoid hypocapnia (causes vasoconstriction) and hypercapnia

Cardiovascular:

Maintain adequate blood pressure (MAP >35-40 mmHg in term)

Inotropic support if needed (dopamine, dobutamine)

Fluid management (restrict to 40-60 mL/kg/day initially to reduce cerebral oedema)

Metabolic:

Maintain normoglycaemia (2.6-6 mmol/L)

Correct electrolyte abnormalities

Treat metabolic acidosis (optimize ventilation and perfusion)

Neurological:

Seizure management:

Phenobarbital (first-line): Loading 20 mg/kg IV, may repeat 10 mg/kg doses
Phenytoin/fosphenytoin (second-line): 20 mg/kg IV
Midazolam, levetiracetam (third-line)
Continuous EEG monitoring recommended

Renal:

Monitor urine output, fluid balance

Adjust fluid and medication doses for renal impairment

Haematological:

Correct coagulopathy (vitamin K, FFP, platelets if needed)

Nutritional:

Enteral feeding cautious due to NEC risk

May need parenteral nutrition initially

Therapeutic Hypothermia (Neuroprotection)

The most important specific intervention for moderate-severe HIE.

Mechanism:

Reduces cerebral metabolic rate

Decreases secondary energy failure

Reduces inflammation, apoptosis, and excitotoxicity

Reduces risk of death or major disability by 25%

Inclusion criteria:

Gestational age ≥36 weeks

Evidence of perinatal hypoxia-ischaemia:

pH ≤7.0 or base deficit ≥16 in cord or first hour blood gas, OR

pH 7.01-7.15 or base deficit 10-15.9 AND prolonged resuscitation or sentinel event

Moderate to severe encephalopathy (Sarnat 2 or 3) OR abnormal aEEG

Age <6 hours at initiation

Exclusion criteria:

Major congenital anomalies

Severe chromosomal abnormalities incompatible with life

Moribund infant (imminent death expected)

Severe coagulopathy with active bleeding

Birth weight <1800 g

Method:

Whole body cooling (most common) or selective head cooling

Target temperature: 33-34°C (rectal or oesophageal)

Duration: 72 hours

Rewarming: Slow (0.5°C per hour) to 36.5°C

Monitoring: Continuous temperature, vital signs, aEEG/EEG

Complications of cooling:

Bradycardia, arrhythmias

Hypotension

Coagulopathy

Thrombocytopenia

Increased risk of sepsis

Subcutaneous fat necrosis

Metabolic acidosis

Post-cooling care:

Continue supportive care

MRI at 2-8 days

Long-term neurodevelopmental follow-up

Prognosis

Predictive factors (poor prognosis):

Severe metabolic acidosis (pH <7.0, base deficit >16)

Persistently low Apgar scores (0-3 at 10, 15, 20 minutes)

Sarnat stage 3 HIE

Early onset refractory seizures

Severe abnormality on aEEG (burst suppression, isoelectric)

Severe abnormality on MRI (extensive watershed injury, basal ganglia/thalamus injury)

Need for prolonged resuscitation (>10 minutes)

Long-term outcomes:

Stage 1 HIE (Mild):

100% survival

Normal neurodevelopmental outcome

Stage 2 HIE (Moderate) with therapeutic hypothermia:

~5-10% mortality

70-80% normal or mild disability

20-30% moderate-severe disability

Stage 3 HIE (Severe) with therapeutic hypothermia:

40-50% mortality in first year

Survivors: High risk of severe neurodevelopmental impairment

Neurodevelopmental sequelae:

Cerebral palsy (most common, especially spastic quadriplegia)

Developmental delay

Intellectual disability

Epilepsy

Visual impairment (cortical visual impairment)

Hearing loss

Learning difficulties

Behavioural problems

Follow-up:

Regular neurodevelopmental assessment at 3, 6, 12, 18, 24 months

Audiology and ophthalmology screening

Physical, occupational, and speech therapy as needed

Educational support

Prevention

Antenatal:

Good antenatal care and risk assessment

Management of maternal medical conditions

Fetal monitoring in high-risk pregnancies

Planned delivery for at-risk pregnancies

Intrapartum:

Electronic fetal monitoring (CTG) during labour

Fetal scalp blood sampling if CTG abnormalities

Prompt response to fetal distress

Appropriate use of assisted delivery or caesarean section

Avoid prolonged second stage of labour

Active management of shoulder dystocia, cord prolapse

Delivery room:

Skilled birth attendant at every delivery

Neonatal resuscitation team available for high-risk deliveries

Equipment prepared and functional

Immediate and effective resuscitation when needed

Delayed cord clamping (30-60 seconds) if baby stable

Postnatal:

Early identification of at-risk infants

Prompt initiation of therapeutic hypothermia

Multidisciplinary NICU care

Key Points: Birth asphyxia is a major cause of neonatal morbidity and mortality. HIE is graded using Sarnat staging. Therapeutic hypothermia within 6 hours is the cornerstone of treatment for moderate-severe HIE and significantly improves outcomes. Long-term neurodevelopmental follow-up is essential.