Intraventricular Haemorrhage of Prematurity

Intraventricular haemorrhage of prematurity is bleeding from the germinal matrix of the preterm brain that extends into the lateral ventricles. It is graded by cranial ultrasound from grade I (germinal matrix only) to grade IV (haemorrhagic parenchymal infarction).

It affects about 20% of infants under 1500 g and up to 40% of those under 28 weeks in some units. About half occur in the first 24 hours of life and about 90% by 72 hours. Rates have fallen with antenatal corticosteroids and better early care.

Risk factors are prematurity, lack of antenatal corticosteroids, chorioamnionitis, vaginal delivery in very preterm infants, respiratory distress syndrome, pneumothorax, hypotension or hypertension, fluctuating cerebral blood flow, hypercapnia, rapid volume expansion, sodium bicarbonate boluses, coagulopathy and thrombocytopenia.

Pathophysiology.

The germinal matrix has a rich, fragile capillary bed with little support tissue and poor autoregulation, and it involutes by 34 to 36 weeks. Fluctuating or raised venous and arterial pressure ruptures these vessels.

Blood extends into the ventricles and can obstruct CSF flow, causing posthaemorrhagic dilatation. In grade IV disease, venous infarction of periventricular white matter follows obstruction of medullary veins.

• Over half of infants are asymptomatic, and the lesion is found on screening ultrasound.
• Catastrophic deterioration: sudden hypotension, bradycardia, apnoea, seizures, bulging fontanelle, fall in haematocrit, metabolic acidosis and loss of tone.
• Saltatory deterioration over hours to days with altered tone and activity.

Red flags.

• Falling haemoglobin or haematocrit with a bulging fontanelle.
• Rapid head growth (over 2 cm each week), sutural splitting or sunsetting eyes, indicating posthaemorrhagic hydrocephalus.
• Seizures or coma.

• Cranial ultrasound in all infants under 32 weeks at days 1 to 3, around day 7, at 2 to 4 weeks and at term equivalent age, with extra scans when unwell or if ventricles enlarge.
• Grade I: germinal matrix haemorrhage only. Grade II: blood in the ventricles with no dilatation. Grade III: blood with ventricular dilatation. Grade IV: parenchymal haemorrhagic infarction.
• Ventricular size measured by ventricular index on a centile chart, and head circumference measured daily.
• Full blood count, coagulation and blood gas in deteriorating infants. MRI at term for white matter injury.

Differential diagnosis. Periventricular leucomalacia, haemorrhage in a cerebellar or choroid plexus site, neonatal stroke, subdural haemorrhage and ventriculomegaly from other causes.

Prevention.

• Antenatal corticosteroids (betamethasone 12 mg IM, 2 doses 24 hours apart), delivery in a tertiary centre, delayed cord clamping for 30 to 60 seconds and avoiding hypothermia.
• After birth, midline head position, minimal handling, avoidance of rapid fluid boluses and sodium bicarbonate boluses, treatment of coagulopathy and tight control of PaCO2 (45 to 55 mmHg).
• Routine prophylactic indometacin is not advised because it lowers severe haemorrhage but does not improve neurodevelopmental outcome.

Established haemorrhage.

• Supportive care: maintain blood pressure with fluids and inotropes only when needed, normal acid base balance and glucose, and treat anaemia or coagulopathy (fresh frozen plasma 10 to 15 mL/kg, platelets when under 50 x 10^9/L).
• Treat seizures with phenobarbital 20 mg/kg IV over 20 minutes.
• Serial ultrasound twice weekly for 2 weeks if ventricles are enlarging, with head circumference each day. Refer to neurosurgery when ventricular dilatation progresses.

Monitoring. Serial ultrasound, head circumference, blood pressure, haemoglobin and neurodevelopment to at least 2 years of corrected age.

Referral and escalation. Refer to paediatric neurosurgery for progressive dilatation, and to neurodevelopmental follow up for grade III or IV disease.

Special groups. Infants under 28 weeks are at highest risk and need the strictest early care and the most frequent imaging.