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      Clinical review: Critical care management of spontaneous intracerebral hemorrhage

      review-article
      1 , 2 ,
      Critical Care
      BioMed Central

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          Abstract

          Intracerebral hemorrhage is by far the most destructive form of stroke. The clinical presentation is characterized by a rapidly deteriorating neurological exam coupled with signs and symptoms of elevated intracranial pressure. The diagnosis is easily established by the use of computed tomography or magnetic resonance imaging. Ventilatory support, blood pressure control, reversal of any preexisting coagulopathy, intracranial pressure monitoring, osmotherapy, fever control, seizure prophylaxis, treatment of hyerglycemia, and nutritional supplementation are the cornerstones of supportive care in the intensive care unit. Dexamethasone and other glucocorticoids should be avoided. Ventricular drainage should be performed urgently in all stuporous or comatose patients with intraventricular blood and acute hydrocephalus. Emergent surgical evacuation or hemicraniectomy should be considered for patients with large (>3 cm) cerebellar hemorrhages, and in those with large lobar hemorrhages, significant mass effect, and a deteriorating neurological exam. Apart from management in a specialized stroke or neurological intensive care unit, no specific medical therapies have been shown to consistently improve outcome after intracerebral hemorrhage.

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          Most cited references138

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          Spontaneous intracerebral hemorrhage.

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            The ICH score: a simple, reliable grading scale for intracerebral hemorrhage.

            Intracerebral hemorrhage (ICH) constitutes 10% to 15% of all strokes and remains without a treatment of proven benefit. Despite several existing outcome prediction models for ICH, there is no standard clinical grading scale for ICH analogous to those for traumatic brain injury, subarachnoid hemorrhage, or ischemic stroke. Records of all patients with acute ICH presenting to the University of California, San Francisco during 1997-1998 were reviewed. Independent predictors of 30-day mortality were identified by logistic regression. A risk stratification scale (the ICH Score) was developed with weighting of independent predictors based on strength of association. Factors independently associated with 30-day mortality were Glasgow Coma Scale score (P /=80 years (P=0.001), infratentorial origin of ICH (P=0.03), ICH volume (P=0.047), and presence of intraventricular hemorrhage (P=0.052). The ICH Score was the sum of individual points assigned as follows: GCS score 3 to 4 (=2 points), 5 to 12 (=1), 13 to 15 (=0); age >/=80 years yes (=1), no (=0); infratentorial origin yes (=1), no (=0); ICH volume >/=30 cm(3) (=1), <30 cm(3) (=0); and intraventricular hemorrhage yes (=1), no (=0). All 26 patients with an ICH Score of 0 survived, and all 6 patients with an ICH Score of 5 died. Thirty-day mortality increased steadily with ICH Score (P<0.005). The ICH Score is a simple clinical grading scale that allows risk stratification on presentation with ICH. The use of a scale such as the ICH Score could improve standardization of clinical treatment protocols and clinical research studies in ICH.
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              Efficacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage.

              Intracerebral hemorrhage is the least treatable form of stroke. We performed this phase 3 trial to confirm a previous study in which recombinant activated factor VII (rFVIIa) reduced growth of the hematoma and improved survival and functional outcomes. We randomly assigned 841 patients with intracerebral hemorrhage to receive placebo (268 patients), 20 microg of rFVIIa per kilogram of body weight (276 patients), or 80 microg of rFVIIa per kilogram (297 patients) within 4 hours after the onset of stroke. The primary end point was poor outcome, defined as severe disability or death according to the modified Rankin scale 90 days after the stroke. Treatment with 80 microg of rFVIIa per kilogram resulted in a significant reduction in growth in volume of the hemorrhage. The mean estimated increase in volume of the intracerebral hemorrhage at 24 hours was 26% in the placebo group, as compared with 18% in the group receiving 20 microg of rFVIIa per kilogram (P=0.09) and 11% in the group receiving 80 microg (P<0.001). The growth in volume of intracerebral hemorrhage was reduced by 2.6 ml (95% confidence interval [CI], -0.3 to 5.5; P=0.08) in the group receiving 20 microg of rFVIIa per kilogram and by 3.8 ml (95% CI, 0.9 to 6.7; P=0.009) in the group receiving 80 microg, as compared with the placebo group. Despite this reduction in bleeding, there was no significant difference among the three groups in the proportion of patients with poor clinical outcome (24% in the placebo group, 26% in the group receiving 20 microg of rFVIIa per kilogram, and 29% in the group receiving 80 microg). The overall frequency of thromboembolic serious adverse events was similar in the three groups; however, arterial events were more frequent in the group receiving 80 microg of rFVIIa than in the placebo group (9% vs. 4%, P=0.04). Hemostatic therapy with rFVIIa reduced growth of the hematoma but did not improve survival or functional outcome after intracerebral hemorrhage. (ClinicalTrials.gov number, NCT00127283 [ClinicalTrials.gov].). Copyright 2008 Massachusetts Medical Society.
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                Author and article information

                Journal
                Crit Care
                Critical Care
                BioMed Central
                1364-8535
                1466-609X
                2008
                10 December 2008
                : 12
                : 6
                : 237
                Affiliations
                [1 ]Department of Medicine, Cooper University Hospital, The Robert Wood Johnson Medical School University of Medicine and Dentistry of New Jersey, Camden, NJ 08501, USA
                [2 ]Neurological Intensive Care Unit, Division of Stroke and Critical Care, Department of Neurology and the Department of Neurosurgery, College of Physicians and Surgeons (SAM), Columbia University, New York, NY 10032, USA
                Article
                cc7092
                10.1186/cc7092
                2646334
                19108704
                0c90572c-d54b-493b-85cb-d0135c492166
                Copyright © 2008 BioMed Central Ltd
                History
                Categories
                Review

                Emergency medicine & Trauma
                Emergency medicine & Trauma

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