The most common causes of perinatal asphyxia are complications during delivery. These are clinically recognized as asphyxial birth events (sentinel events) and include uterine rupture, placental abruptio, prolonged labour, obstructed labour, shoulder dystocia and cord prolapse. Both ante and intrapartum risk factors have been associated with perinatal asphyxia and HIE. They include;(4,5)

1. Inadequate access to skilled birth attendants
2. Lack of antenatal care
3. Inadequate maternal prenatal care
4. Home deliveries
5. Hypertensive disorder in pregnancy
6. Premature rupture of membrane
7. Chorioamnionitis i.e., intrauterine infection
8. Meconium-stained amniotic fluid
9. Maternal anemia
10. Preterm births

Depending on whether the baby receives prompt resuscitation at birth and the severity of asphyxia, neonates with perinatal asphyxia can manifest soon after birth with a weak or absent cry, decreased or lack of response to stimulation, poor or absent suck, cyanosis (bluish skin colour), weak breathing efforts or difficulty with breathing and low heart rate. Other features which may manifest later include feeding difficulties, abnormal neurological signs, and seizures.(6)

Clinical assessment includes evaluating the baby’s overall condition, respiratory effort, and heart rate. The diagnosis of perinatal asphyxia is based on pH ≤7.0 or Base Excess (BE) ≤ − 12 mMol/L in Umbical Artery or within 1 hour, 5th minutes Apgar <7, or need for resuscitation > 10 min. However, due to limited accessibility to blood gas analysis in most resource settings, Apgar scores remained the most used tool to assess newborns’ well-being immediately after. In terms of severity, perinatal asphyxia is said to be mild, if the fifth minutes Apgar score is 6, moderate, if the Apgar score is 4 – 5, and severe if the score is 0 – 3.

Consistent Apgar scores in conjunction with asphyxia sentinel events thus form the basis for the diagnosis of perinatal asphyxia in resource-poor settings. Clinically, newborns with perinatal asphyxia could have signs of poor oxygenation, such as cyanosis, and hypoxemia. The presence of multi-organ dysfunction may also be indicative of severe asphyxia. The Sarnat staging is mostly used to classify asphyxial-related encephalopathy into three (see below).

Differential diagnoses for perinatal asphyxia include;

• Neonatal sepsis
• Congenital heart defects
• Metabolic disorders

Blood gas analysis to detect acidosis

Oxygen saturation for detection of hypoxemia

Random blood glucose (asphyxiated babies are at risk of hypo or hyperglycemia)

Packed cell volume and complete blood count

Electrolyte profile

Chest X-Ray

Imaging studies like ultrasound and MRI

Electroencephalography to assess brain function.

Immediate resuscitation of a newborn with an Apgar score of less than 7 or babies who fail to initiate breathing spontaneously at birth is important. Most babies would require minimal intervention such as drying, gentle airway clearance, tactile stimulation and warmth. If response remains poor, a bag and mask ventilation with or without chest compressions will be required.

Subsequent treatments for hospitalised asphyxiated neonates would include;

1. Supplemental oxygen therapy in case of hypoxemia (<92%), starting from as low as 0.5L/minute. Flow rates could be titrated up to 6L/minute and 10L/minute with nasal cannular and simple face mask respectively
2. Respiratory support

– Continuous positive airway pressure (CPAP): if there is increased work of breathing and persistent hypoxemia despite oxygen therapy

– Mechanical ventilation: May be indicated in those with severe perinatal asphyxia with persistently poor respiratory efforts, apnea and hypoxemia unresolved with CPAP

1. Management of seizures – 10 – 20 mg/kg loading dose of phenobarbitone is effective. Additional doses of 10 mg/kg may be administered every 30 minutes (up to 40 mg/kg) if the seizure is not controlled. This initial dose is followed by a maintenance of 5mg/kg/day in two divided doses.

Alternatively, phenytoin at the same loading and maintenance doses would be preferred if a neonate has respiratory depression, hypotension or bradycardia either de novo or following the use of phenobarbitone. Also, phenytoin may be needed for seizures refractory to phenobarbitone. Intramuscular paraldehyde (0.1ml/kg up to 5 mls) is administered to abort seizures.(6–8)

1. Correction of hypoglycemia (glucose <50mg/dl), if present with 200mg/kg of dextrose solution (i.e., 2mls/kg of 10% dextrose or 0.5mls/kg of 50% dextrose). 50% dextrose should be double diluted before administration
2. Prevention of hypoglycemia

– Intravenous with glucose infusion rates (GIR) of 6 – 8 mg/kg/minutes but could be higher depending on blood glucose levels. A 10% to 12.5% plain dextrose solution in the first 48 hours with a switch to solute-containing dextrose solution after 48 hours

–  The GIR could be increased by using a higher glucose concentration or increasing the volume of IV fluids. However, severely asphyxiated term neonates are commenced on lo

w initial volume of 50 – 60ml/kg/day with a gradual increment of 10 to 15ml/kg daily up to 180ml/kg/day.(7)

– Feeding could be commenced for babies with mild-moderate asphyxia soon after the initial resuscitation. However, for severely asphyxiated neonates, especially those with encephalopathy, evidence of good perfusion (prompt capillary refill, pink colour) and the presence of bowel sound are a reasonable clue to commence enteral feeding.

1. Hypocalcemia – neonates with severe perinatal asphyxia are at risk of hypocalcemia, and if present a bolus of 40mg/kg 10% calcium gluconate (double-diluted) is administered slowly over 10 minutes while a dose of 200mg/kg/day is added to daily IV fluid to prevent hypocalcemia.(7)
2. Monitoring

– Temperature, heart rate, capillary refill time (CRT), colour, oxygen saturation (SpO2), respiratory rate – with chart

– Seizure – with chart

– Blood glucose – every 30 minutes if hypoglycemic and at least 6 hourly if blood glucose is normal

– Urinary output especially for neonates with severe asphyxia with multi-organ dysfunction

Follow-up care for infants who have suffered from birth asphyxia is essential to monitor development and detect any long-term complications e.g., seizure disorder, or cerebral palsies.

Preventive measures include improving maternal health, ensuring skilled attendance at birth, enhancing access to emergency obstetric care and strengthening healthcare systems to manage complications promptly. Education and training for healthcare providers are also crucial.

Birth asphyxia and hypoxic-ischemic encephalopathy are significant contributors to neonatal morbidity and mortality in sub-Saharan Africa. Limited access to skilled birth attendants, inadequate healthcare infrastructure, and delays in timely interventions worsen outcomes. Strengthening prenatal care, improving delivery practices, and enhancing neonatal resuscitation efforts are critical to reducing the incidence and long-term complications of these conditions in the region.