Posthemorrhagic Hydrocephalus
Posthemorrhagic hydrocephalus is the most common type of hydrocephalus in the neonatal period. Posthemorrhagic hydrocephalus may be communicating or noncommunicating. It is usually the consequence of intraventricular hemorrhage. Intraventricular hemorrhage usually occurs as a consequence of germinal matrix hemorrhage. Germinal matrix hemorrhages are unusual after 34 weeks gestational age. Germinal matrix hemorrhages are classified based on brain ultrasound in four grades. Grade I intraventricular hemorrhage refers to the presence of subependymal bleed; Grade II intraventricular hemorrhage refers to extension of the subependymal bleed into the ventricles but without ventricular dilatation; Grade III intraventricular hemorrhage refers to subependymal bleed with extension of the bleed into the ventricles and hydrocephalus; and Grade IV intraventricular hemorrhage refers to subependymal bleed with extension of the bleed into the parenchyma as a result of venous infarcts.
Hydrocephalus following intraventricular hemorrhage can occur within days of a bleed (acute), more than a week later (subacute), or as late as 3 months after the bleeding (chronic).
Acute hydrocephalus may be communicating or noncommunicating. Acute communicating hydrocephalus occurs with large intraventricular hemorrhages due to obstruction of the arachnoid villi by blood clots. Acute noncommunicating hydrocephalus is due to obstruction by blood clots of the ventricular system at any of its narrow passages.
Subacute hydrocephalus (the term posthemorrhagic hydrocephalus is often reserved for this type of hydrocephalus) is usually communicating. It occurs with small and large hemorrhages. It is due to obstruction of the subarachnoid space. The obstruction occurs at the tentorial notch. The arachnoid adhesions block the normal flow of cerebrospinal fluid to the convexity of the brain.
Chronic hydrocephalus may be communicating or noncommunicating. It occurs with small and large hemorrhages. Communicating hydrocephalus results from permanent scarring of the corpuscle of Pachioni. Noncommunicating hydrocephalus results from disrupted ependyma or reactive gliosis. The blood clot or reactive gliosis obstructs the ventricular system at any of its narrow passages.
The diagnosis of hydrocephalus in the premature newborn is made by ultrasound. Computed tomography and MRI of the brain offer additional information that may help to define the site of obstruction. There is no general consensus regarding the best way to manage these patients. Serial lumbar punctures do not prevent hydrocephalus. They are used because they delay the need for ventricular drainage, thus allowing time for spontaneous resolution of the blockage. Fibrinolytic therapy is promising but its use is not recommended. Neonates with posthemorrhagic hydrocephalus may present with: (1) excessive increase in head circumference (>1 cm/week); (2) excessive increase in head circumference associated with a tense fontanelle; (3) ultrasonographic evidence of increased ventricular size without any other signs; (4) neurological signs of increased intracranial pressure such as encephalopathy or increased musculoskeletal reflexes; or (5) cardiovascular signs of increased intracranial pressure such as tachycardia and hypotension. The latter two presentations are infrequent.