Intracerebral Hemorrhage Management (Review for Experts 1/06)

By David Alway, MD

Spontaneous intracerebral hemorrhage (ICH) accounts for only about 10 percent of all strokes, but it carries about a 50 percent risk of mortality. Even in the best treatment facilities the management guidelines are plagued with uncertainty, largely due to the paucity of randomized controlled trials. As a result, many physicians find themselves relying on less scientific data when planning a treatment strategy.

Fortunately, some recent discoveries may go a long way towards helping us make the best decisions for our patients. In this review I’ll look at some of the latest research on ICH that could carry over to clinical practice.

Picturing the Problem

Brain imaging is the only reliable way to diagnose ICH, since the presenting symptoms are often very similar to an ischemic stroke. The most commonly used method is CT due to its speed, widespread availability and reliability in detecting a hematoma.  MRI may also be used to detect ICH, but is generally unnecessary for this purpose acutely.

There are many ways an ICH can cause brain damage. Most often, the hematoma causes an immediate damage to surrounding tissues. Interestingly, even though the hemotoma’s compression of adjacent brain tissue may lead to reduced blood flow, recent PET and MRI data find no evidence of significant perihematomal ischemia in small or moderate sized hematomas.^2,3  Whether this observation applies to individuals with large hematomas remains unknown, hence concern remains over the best blood pressure management of these patients.  While blood pressure reduction is considered appropriate, the optimal amount of blood pressure reduction remains a matter of contention, even among experts.

Some recent studies suggest that there is also hematoma induced neurotoxicity which may lead to cerebral edema.⁴ Within a week this tissue edema may result in a volume twice as large as the hematoma itself.¹ The mass effect of the hematoma alone, or later with associated edema and further bleeding, may lead to increased ICP, with the possibility of global ischemia due to decreased brain perfusion pressure. Concomitant hydrocephalus may also develop, further increasing ICP.

Surgery vs. Medical Management

There are few firm data regarding surgical intervention for supratentorial hemorrhages.  Many surgeons avoid surgical evacuation of small, deep hematomas in patients without signs of increased ICP or clinical worsening, preferring to operate on patients who are clinically worsening or who have more superficial/accessible hematomas and significant neurological disability.

However, a recent large randomized study⁵ compared the best medical management techniques to early (within 24 hours of randomization) surgical evacuation for supratentorial hemorrhages. Surgeons were allowed to use whatever techniques they felt were indicated, including craniotomy or minimally invasive techniques for clot aspiration and lysis.  Of note, surgery was allowed in any patient who worsened, even if he/she was originally in the medical arm. Using an intention-to-treat analysis, there was no significant difference found in neurological outcomes after six months. In light of these results, we must consider surgery for supratentorial intracerebral hemorrhages of unproven benefit. However, surgical management will require continual reappraisal since newer surgical techniques are continually being developed and may prove beneficial.⁶

In contrast to supratentorial hemorrhages, surgery for cerebellar hemorrhages is often indicated.  The American Heart Association study group recommends that patients with cerebellar hematomas larger than 3 cm who are either neurologically worsening or who appear to be headed towards hydrocephalus or early brainstem compression, undergo emergent surgical evacuation.

Elevated ICP can cause a decreased level of consciousness, nausea, vomiting, and herniation. Physicians have varying opinions about how to manage elevated ICP, but measures such as IV mannitol infusion, hyperventilation, induction of barbituate coma and placement of a ventriculostomy in patients who develop hydrocephalus are all considered reasonable. Steroids have no proven benefit in the management of ICH and may damage patients due to a higher number of infections and elevated glucose.

An intracranial pressure monitor may help the physician balance the desire to avoid hypertension, which theoretically increases the tendency toward hematoma enlargement, with the need to maintain adequate cerebral perfusion. AHA guidelines recommend that the cerebral perfusion pressure (MAP–ICP) be kept at >70 mm Hg.⁷

Early Treatment Option

Hematoma growth is common within the first few hours of an ICH and uncommon after 24 hours. With this in mind, a recent clinical trial⁸ involved treating patients who were diagnosed with acute intracerebral hemorrhage with recombinant activated factor VII (NovoSeven). Within four hours of symptom onset, 399 patients received either placebo or one of three doses of rFVIIa (40mcg, 80mcg, or 160mcg per kg). After three months mortality was significantly lower in the treated groups compared with the placebo group (18-19 percent vs. 29 percent p<0.01). Neurological outcomes were also better in the treated groups, although there was no clear dose/response relationship. While there was a statistically significant increase in the percentage of thrombotic complications in the treated groups, the clinical effect of these tended to be mild.  Although this intervention appears promising, we should await further trials (now in progress) to determine the optimal dose and range of side effects of this treatment.

Prevention After Hospitalization

Follow-up is essential after patients are  discharged. Before they go back home or to their assisted care facility, they should be educated on the risk factors for recurrent ICH. 

Patients who suffered from a spontaneous ICH thought to be due to hypertension should have their blood pressure maintained in the normal range (120/80mmHg) or below and they should avoid both legal and illegal stimulants. Antiplatelet medications should be avoided for at least the first few months after an ICH and, in cases of cerebral amyloid angiopathy, lobar hemorrhage, residual tumor, or residual vascular malformation, they should never be restarted. In other cases, the risk of ischemic events must be weighed against the potential for further intracerebral hemorrhages, it being reasonable to restart antiplatelet medications in patients who also suffer from coronary artery disease.⁹

David Alway, MD, is a physician at The Neurology & Headache Center in Alexandria, VA (www.neurologychannel.com/neuro-headache/). He writes about stroke treatment and prevention at Stroke Doc (http://strokedoc.typepad.com/) and he has recently published a stroke prevention book targeted at those who have had a stroke or TIA called Stop Your Next Stroke.

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1. Kidwell, KS et al.Comparison of MRI and CT for Detection of Acute Intracerebral Hemorrhage. JAMA 2004;292:1823-1830.

2. Rosand J, Eskey C, Chang Y, Gonzalez RG, Greenberg SM, Koroshetz WJ. Dynamic single-section CT demonstrates reduced cerebral blood flow in acute intracerebral hemorrhage. Cerebrovasc Dis. 2002;14(3-4):214-20

3. Zazulia AR, Diringer MN, Videen TO, Adams RE, Yundt K, Aiyagari V, Grubb RL Jr, Powers WJ. Hypoperfusion without ischemia surrounding acute intracerebral hemorrhage. J Cereb Blood Flow Metab. 2001 Jul;21(7):804-10

4. Lampl Y, Shmuilovich O, Lockman J, Sadeh M, Lorberboym M. Prognostic Significance of Blood Brain Barrier Permeability in Acute Hemorrhagic Stroke. Cerebrovasc Dis. 2005;20(6):433-7.

5. Mendelow AD, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. 2005 Jan 29-Feb 4;365(9457):387-97.

6. Nishihara T et al. Newly developed endoscopic instruments for the removal of intracerebral hematoma. Neurocrit Care. 2005;2(1):67-74.

7. Guidelines for the Management of Spontaneous Intracerebral Hemorrhage. A Statement for Healthcare Professionals From a Special Writing Group of the Stroke Council, American Heart Association. Broderick JP et. al. Stroke 1999;30:905-915

8. Mayer, SA et al. Recombinant Activated Factor VII for Acute Intracerebral Hemorrhage. NEJM 352:8 Feb 24,2005.

9. Kissela BM et al. Subarachnoid hemorrhage: a preventable disease with a heritable component. Stroke 2002 May;33(5):1321-6.)

10. Report from the Priorities for Clinical Research in the Treatment of Acute, non-Traumatic Intracerebral hemorrhage Workshop, Nov 2003.

11. Carvi y Nievas, MN. Why, when, and how spontaneous intracerebral hematomas should be operated. Med Sci Monit. 2005 11(1):RA24-31.

12. Bernstein, RA. Recent advances in the management of acute intracerebral hemorrhage Curr Neurol Neurosci Rep. 2005;5(6):483-7.

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