Intraventricular haemorrhage and posthaemorrhagic ventricular dilatation remain an important challenge in the management of prematurity and are associated with significant permanent morbidity. Progressive ventricular dilatation causes white matter injury by pressure, distortion, free radical injury and inflammation. Therapeutic interventions include serial lumbar punctures, only useful when the ventricles remain in communication with the lumbar subarachnoid space, and repeated aspiration through a ventricular access device. Reduction of cerebrospinal fluid production by acetazolamide and frusemide in a large multicentre randomised trial showed a worse outcome in the treated arm. A trial of drainage, irrigation and fibrinolytic therapy did not demonstrate a reduced need for permanent cerebrospinal fluid diversion, but did show a significant reduction in severe cognitive disability at two years. Ventriculoperitoneal shunting is indicated when the ventricles continue to enlarge at a body weight of around 2.5 kg and cerebrospinal fluid protein levels are below 1.5 g /L.
This review summarises current concepts on the pathophysiology and management of posthaemorrhagic ventricular dilatation, underlining clinical challenges and ongoing research.
Although the percentage of small preterm infants developing intraventricular haemorrhage (IVH) has been greatly reduced in the last three decades, increased survival of very immature infants has meant that large IVH with subsequent posthaemorrhagic ventricular dilatation is still a serious unsolved problem.
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Competing interests None.
Ethics approval This study was conducted with the approval of the Southmead Hospital LREC.
Provenance and peer review Commissioned; externally peer reviewed.