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Paediatrics: Cerebral haemorrhage and ischaemia

Periventricular haemorrhage (PVH) and intraventricular haemorrhage (IVH)

Cerebral haemorrhage and ischaemia


Periventricular haemorrhage (PVH) and intraventricular haemorrhage (IVH)


Rare >32wks gestation. Haemorrhage starts in the vascular germinal ma-trix (subependymal). Bleeding may then extend into, and may dilate, the lateral ventricles (IVH). Haemorrhagic periventricular infarction may then occur secondary to impairment of cerebral venous drainage by intraven-tricular haemorrhage.


Incidence: 710–15% of infants born <32wks. Risk ‘rise’with ‘rise’prematurity.


Causes: related to rapid alteration in cerebral blood flow, e.g. severe RDS, pneumothorax, hypotension, hypoxia, i/d PaCO2.


Presentation: most occur within 72hr of birth. Seldom occur before birth unless there is alloimmune thrombocytopenia. Up to 50% are asympto-matic. Larger bleeds may present as sudden catastrophic systemic col-lapse, bulging fontanelle, neurological dysfunction (e.g. seizures or paucity/ abnormal movements), anaemia, and jaundice. Diagnosis confirmed using cranial US.

   At risk groups or preterm infants <32wks should be screened by cranial US (at 1wk, and at 1mth, or after sudden deterioration). Several grading systems exist, but it is better to describe the location and extent of haemorrhage as one of:

   subependymal only; or

   IVH ± ventricular dilatation; or

   IVH ± parenchymal involvement.



Antenatal steroids reduce incidence. Prophylactic neonatal indometacin treatment reduces incidence, but does not improve long term neurodevelopmental outcome.



Supportive. Irrigation of lateral ventricles following surgical drain insertion is experimental.




   Post-haemorrhagic ventricular dilatation (PHVD): s to obstruction of CSF flow or absorption. Clinical features include: increasing OFC; wide cranial sutures; apnoea; seizures; feed intolerance; ‘sun setting’ eyes. Diagnosis confirmed and monitored by measuring ventricular index on cranial US. 50% resolve spontaneously. Progressive symptomatic PHVD requires CSF drainage either by serial LP or intracranial reservoir and then by insertion of ventriculo-peritoneal shunt.


   Haemorrhagic periventricular infarction: occurs in 15%. Blood in the lateral ventricles impairs adjacent venous drainage, which results in adjacent cerebral infarction. Cranial US: cystic parenchymal area(s) adjacent and communicating with lateral ventricle (porencephalic cyst).



Sub-ependymal or uncomplicated IVH does not affect neurode-velopment. Cerebral palsy is common if either PHVD present and treat-ment is required (50%), or there is parenchymal extension (80%).


Term intracranial haemorrhage


Subdural: increased risk with difficult extraction.


Subgaleal: potential massive blood loss with systemic collapse. Boggy swelling all over scalp, not limited by sutures.


Subarachnoid: asymptomatic, or may present with seizures/irritability.


Parenchymal or intraventricular: is usually haemorrhagic infarction— seizures possible.


Cephalohaematoma: subperiosteal bleed, limited by suture lines, may take weeks to resolve, and may partially calcify.


Periventricular leucomalacia (PVL)


Severe HIE can lead to cortical neuronal necrosis, basal ganglia injuries, focal cerebral infarctions or subcortical leukomalacia. PVL is characterized by periventricular white matter lesions: ‘rise’echogenicity; cysts.

Cause: poor cerebral perfusion or ischemia, inflammation.

Risk factors: extreme prematurity; hypotension; severe illness; hypocarbia.

May not be apparent for several weeks after birth.

Diagnosis: periventricular echodensities or cysts seen on cranial US.

Prognosis: higher risk of cerebral palsy (especially spastic diplegia), particularly if there is cyst formation.



Cerebral infarction (perinatal stroke)


Incidence: 1:1600 to 1:5000 births.


Neurological signs and symptoms caused by a vascular event around the time of delivery.


Presentation depends on timing and nature of event; focal seizures, encephalopathy, apnoea, poor feeding, asymmetrical reflexes/ movement/tone.


May be associated with maternal/neonatal coagulation disorders (e.g. Factor V Leiden, Protein C or S deficiency).


Management: supportive, cover infection, correct any metabolic (e.g. hypoglycaemia) or haematological (e.g. polycythemia) abnormalities. Start CFAM and treat any seizures.


Investigation: FBC/Coag/U&E(Ca2+, Mg2+)/LFTs/Glucose/CFAM/ MRI/ EEG.



Prognosis: depends on site and nature of lesion. 750% of affected children will carry some neurological impairment into childhood.


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