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. 2010 Mar;10(2):73-82.
doi: 10.1007/s11910-010-0086-6.

Management of intraventricular hemorrhage

Holly E Hinson  1 , Daniel F Hanley, Wendy C Ziai
Affiliations

Management of intraventricular hemorrhage

Holly E Hinson et al. Curr Neurol Neurosci Rep. 2010 Mar.

Abstract

Brain hemorrhage is the most fatal form of stroke and has the highest morbidity of any stroke subtype. Intraventricular extension of hemorrhage (IVH) is a particularly poor prognostic sign, with expected mortality between 50% and 80%. IVH is a significant and independent contributor to morbidity and mortality, yet therapy directed at ameliorating intraventricular clot has been limited. Conventional therapy centers on managing hypertension and intracranial pressure while correcting coagulopathy and avoiding complications such as rebleeding and hydrocephalus. Surgical therapy alone has not changed the natural history of the disease significantly. However, fibrinolysis in combination with extraventricular drainage shows promise as a technique to reduce intraventricular clot volume and to manage the concomitant complications of IVH.

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Conflict of interest statement

Disclosure No other potential conflicts of interest relevant to this article were reported.

Figures

Fig. 1
Fig. 1
Severe intraventricular extension in patients with subarachnoid or intracerebral hemorrhage treated with conservative therapy, external ventricular drainage (EVD), and EVD with fibrinolysis, based on a systematic review of the literature. a Mortality. b Percentage of patients experiencing a poor outcome. (Adapted from Nieuwkamp et al. [46])
Fig. 2
Fig. 2
Biochemical reactions within the cerebral ventricle after administration of intraventricular tissue plasminogen activator (t-PA, alteplase) in patients with intraventricular hemorrhage (IVH). Fibrin in the blood clot provides binding sites for alteplase and plasminogen. On the fibrin surface, alteplase and intrinsic t-PA have a high affinity for plasminogen, which is converted to plasmin. Plasmin breaks down the blood clot with release of fibrin degradation products. Urokinase does not have specific affinity for fibrin and activates both freely circulating and fibrin-bound plasminogen. Fibrinolysis is terminated by circulating inhibitors of plasminogen, plasminogen activator inhibitor (PAI) 1 and 2; by inactivation of plasmin by α2-antiplasmin; and by clearance of fibrinolytic factors through the liver. Normally, cerebrospinal fluid concentrations of plasminogen and t-PA are minute because of their high molecular weight. Plasminogen and t-PA incorporated within the clot itself likely are most responsible for clot resolution in IVH. IVC—intraventricular catheter
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