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(Stroke. 2003;34:2305.)
© 2003 American Heart Association, Inc.

Controversies in Stroke

Surgical Decompression of Patients With Large Middle Cerebral Artery Infarcts Is Effective: Not Proven

Martin M. Brown, MD, FRCP

From the Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, London, UK.

Correspondence to Dr Martin M. Brown, Institute of Neurology, University College London, National Hospital for Neurology and Neurosurgery, Queen Square, London WC1N 3BG. E-mail m.brown{at}ion.ucl.ac.uk

Key Words: brain edema • craniectomy • decompression • infarction, middle cerebral artery • intracranial pressure

Middle cerebral artery territory infarction is an important cause of disability and death after stroke. Mortality associated with middle cerebral artery infarcts is usually caused by the complications of severe stroke, eg, pneumonia or pulmonary embolism. Death in a small proportion of cases is caused by coning secondary to malignant cerebral edema. Initially, ischemic cytotoxic edema causes only limited cell swelling, but the subsequent development of vasogenic edema can result in significant enlargement of the volume of infarcted tissue. Typically, patients destined to develop malignant edema present with symptoms of ischemia in the middle cerebral artery but initially remain alert. After a delay of 24 to 48 hours, as the infarct swells there is a rapid decline of consciousness from herniation leading to unresponsiveness and often death. It is logical to consider surgical decompression by craniectomy in these cases. Removal of a large portion of the skull vault allows the edematous hemisphere to expand out through the defect in the skull, relieving the mass effect. There is no doubt that this treatment appears to be life-saving in some cases. However, the syndrome of malignant cerebral artery edema is seen only in large infarcts, often resulting from internal carotid artery occlusion associated with poor collateral supply. Usually, the patients are young, presumably because cerebral atrophy with aging provides space for expansion of the brain and protects against a rise in intracranial pressure. Generally, most centers have limited treatment to younger patients with nondominant hemisphere infarction because of the assumption that residual aphasia would not be an acceptable outcome. This means that the proportion of patients currently thought suitable for decompressive surgery is small, and the exact indications have not been established.

One rationale for decompressive surgery argues that edema compresses adjacent tissues, causing secondary damage and extension of the infarction into the ischemic penumbra, and it has therefore been suggested that susceptible patients should be treated as early as possible.^1,2 It is logical that the earlier patients are decompressed, the less likely secondary damage, but it is not clear that malignant cerebral artery edema can be reliably predicted. Better outcomes reported in patients treated early could simply reflect the selection of patients who were destined to do well. Moreover, the experience from thrombolysis suggests that penumbral tissue remains viable for only a few hours. One can argue that it is therefore unlikely that decompression will have an effect on the eventual size of cerebral infarction. Hence, even if decompressive surgery prevents death, it may not prevent disability, except in the rare patient otherwise destined to develop additional nonfatal infarction in the territories of the anterior or posterior cerebral arteries or brain stem perforators, secondary to herniation.

Reducing mortality may seem an obvious benefit of craniectomy, but this is likely to be acceptable only if the rate of disability is also reduced. Patients with malignant middle cerebral artery edema invariably have large infarcts, and the patient is therefore bound to be left with some impairment. In particular, recovery of arm function is unlikely and a degree of cognitive impairment is inevitable.³ Depression and poor integration into society are common.⁴ One of the early and influential randomized trials of acute stroke treatment studied dextran infusions and concluded that reduction of cerebral swelling reduced mortality in patients with severe stroke, but as more survivors were severely disabled, this was considered a negative outcome.⁵ Other treatments that reduce mass effect, including glycerol, mannitol, dexamethasone, and surgical evacuation of hematomas, have also failed to show convincing benefit on functional outcome in clinical trials.^6–9 These trials argue that treating cerebral edema is treating dead tissue to little avail. Even the impression from case series that craniectomy is beneficial in terms of mortality may be misleading. Randomized trials have often shown that logical surgical treatments, eg, extracranial-intracranial bypass surgery, fail to deliver significant benefit when properly tested, because the risks outweigh the benefits.

Although some previous case series of decompressive surgery have reported encouraging results, these must be treated with caution.^2,10 Other series have reported disappointing results with high mortality rates and poor functional outcome.^3,11 Moreover, surgery has risks, including intracranial hemorrhage,¹² intracranial infection, wound infection, and bone flap infection. Overall, there are only a small number of patients reported in the literature and the results have been compared with poorly matched or historical controls.¹⁰ The problem with comparing any case series with historical controls is that the routine care of stroke improved in the intervening period. Only randomization provides a cohort of patients in whom decompressive surgery can be compared with best medical management alone, in patients matched for baseline characteristics, severity of stroke, and other treatments. There were no completed randomized trials of decompressive surgery for middle cerebral artery infarction identified in a recent Cochrane review, although there were 2 ongoing trials.¹⁰

In summary, craniectomy looks like a hopeful treatment, but one should conclude that its benefits have not been proven. We need the results of prospective randomized studies to establish the magnitude of benefit, optimum time for surgery, and the factors predicting severe residual disability despite surgery. Finally, economic studies are needed to establish the cost effectiveness of the treatment, with quality-of-life measures to establish the acceptability to patients of various degrees of long-term disability. For an expensive and invasive treatment, the number needed to treat to obtain benefit will need to be relatively small to be cost effective and to avoid exposing substantial numbers of patients to unnecessary surgery.

Footnotes

The opinions expressed in this editorial are not necessarily those of the editors or of the American Stroke Association.

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This Article Full Text (PDF) All Versions of this Article: 34/9/2305    most recent 01.STR.0000089298.19012.9Bv1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Brown, M. M. Search for Related Content PubMed PubMed Citation Articles by Brown, M. M.