DOI: 10.1097/CCM.0b013e3182451e07

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PMID: 22511164

Issn Print: 0090-3493

Publication Date: 2012/05/01


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Novel insights into the pathophysiology and treatment of intraventricular hemorrhage*

David B. Seder; Richard D. Murray

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In a remarkable and innovative series of investigations, the CLEAR investigators (1) have worked for a decade to crack the nut of intraventricular hemorrhage (IVH). Among patients with spontaneous intracerebral hemorrhage (ICH), IVH often causes obstructive hydrocephalus and prolonged coma, and it is independently associated with poor outcome (2, 3). External ventricular drainage in such patients allows for reduction and monitoring of intracranial pressure (ICP) and is considered a standard of care. Nonetheless, the specific role of ventricular drainage is unclear–does it merely provide a means of monitoring and controlling ICP, or might the removal of hemoglobin breakdown products be important in reducing inflammation, fever, and delirium, in shortening the duration of coma, or in decreasing secondary brain injury?
The hypothesis undergoing evaluation in the CLEAR IVH trials (4, 5), and now in CLEAR-III (6), is that by rapidly clearing hematoma from the ventricular spaces using external drainage and a series of isovolumic intraventricular injections of recombinant tissue plasminogen activator (rt-PA), normal flow and resorption of cerebrospinal fluid (CSF) can be reestablished and neurologic outcomes can be improved. The first two prospective trials in this series have been completed, and in this issue of Critical Care Medicine, the investigators present a retrospective analysis of those data, attempting to better-understand the role of intracranial pressure in the pathophysiology of the disease and seeking lessons that might be extrapolated to other forms of brain injury (7).
Data from 100 patients were pooled. Most were young (mean age, 55 years) and had experienced small, deep, hypertensive hemorrhages (median ICH volume, 6 mL) with a large intraventricular component (median IVH volume, 35 mL). Patients were excluded if the ICH component was .30 mL or if a vascular lesion had precipitated the hemorrhage. They underwent a wide range of intrathecal treatments: 22 received placebo; 26 received 3 mg rt-PA twice daily; 26 received 1 mg rt-PA twice daily; 18 received 1 mg rt-PA three times daily; and 8 received 0.3 mg rt-PA twice daily. Intracranial pressure was recorded at least every 4 hrs, and the ICP readings contrasted with dichotomized 30-day mortality and modified Rankin Scale scores in multivariate models that also included stability ICH and IVH volumes, presenting Glasgow Coma Scale, presenting pulse pressure, age, and treatment with rt-PA.
After a primary insult to brain tissue, elevated ICP is a mechanism by which the initial damage is aggravated by causing cerebral ischemia. In the traumatic brain injury literature, which has been extrapolated to ICH, a general consensus exists for treatment of ICP .20 mm Hg (8). Less well-understood is the threshold at which secondary brain injury actually occurs, and it has been postulated that tolerating persistently elevated ICP in the absence of low cerebral perfusion pressure (9) or preserved markers of cerebral perfusion may be a reasonable option. In this cohort, the percentage of intracranial pressure measurements .30 mm Hg but not between 20 and 30 mm Hg was associated with poor outcome, independent of age, hematoma size, presenting neurologic examination, and other factors; unfortunately, episodes of low cerebral perfusion pressure were not evaluated in the model. It remains unclear whether elevated ICP, low cerebral perfusion pressure, or another factor such as inadequate ventricular drainage as in the case of an “entrapped” ventricle may be responsible for this increased morbidity. Nonetheless, these data provide reassurance that current ICP management recommendations (8, 10) may have a physiologic basis.
The authors noted higher ICP when ventricular drainage was performed ipsilateral to the larger IVH ventricle.
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