Published online before print August 28, 2003, doi: 10.1161/01.STR.0000089295.37380.A4
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(Stroke. 2003;34:2304.)
© 2003 American Heart Association, Inc.
Controversies in Stroke |
Surgical Decompression of Patients With Large Middle Cerebral Artery Infarcts Is Effective
From the Department of Neurology, University of Heidelberg, Germany.
Correspondence to Dr. Werner Hacke, Department of Neurology, University of Heidelberg, IM Neuenheimer Feld 400, 69120 Heidelberg, Germany. E-mail werner_hacke{at}med.uni-heidelberg.de
Key Words: critical care • decompression, surgical • infarction, middle cerebral artery
The Syndrome and Its "Natural" Course
Early mortality after acute ischemic stroke is most frequently caused by space-occupying ischemic brain edema. In case of complete middle cerebral artery territory (MCA) infarction, including the basal ganglia, a large space-occupying postischemic edema that finally leads to herniation and brain death may occur. These patients present with almost complete hemiplegia, head- and eye-turning progressive deterioration of consciousness over the first 24 to 48 hours, and a reduced ventilatory drive. Prognosis of large MCA or hemispheric infarctions is poor: in prospective case series, 80% died from herniation despite maximum conservative therapy.1
The Failure of Medical Intervention
General measures of treatment of increased intracranial pressure (ICP) after acute ischemic stroke include elevation of the head to a 30-degree angle to improve venous drainage and avoidance of both hyperthermia and hyperglycemia. As part of the specific anti-edematous pharmacological treatment, osmotherapy using glycerol, mannitol, or hyperosmolar saline solutions is used to reduce brain edema. All substances work by means of lowering ICP, but only for a limited time. The same is true for barbiturates, which may reduce critically elevated ICP reading massively, but only for a short period.2,3
Decompressive Surgery
Decompressive surgery for malignant MCA infarction is not a new invention. Actually, the first studies date back as early as 1935. Over the past decades, several case reports and smaller retrospective case series have suggested that decompressive surgery is a possible treatment option for massive hemispheric stroke. However, no controlled data were available to support its superiority. The rationale of decompressive surgery is to allow extracranial expansion of the edematous brain tissue to avoid ventricular compression and horizontal as well as vertical tissue shifts. This concept is supported by experimental studies indicating dramatic decrease in mortality and substantial tissue salvage with decompressive surgery.
However, it was not until 1995 that a large prospective case series was published. This series also included a concurrent control group, which, sadly enough, was not a randomized control group. Nevertheless, in this control group the well-known 80% mortality with maximum conservative treatment was demonstrated, while the mortality rate in the surgically treated group was only 34.4%. Among the survivors, the quality of survival was a surprisingly good modified Rankin score of 2.6 (range, 1 to 4).4
When to Operate?
This is probably the most important question for those who support this treatment. In the past, the treatment was frequently offered only in cases that were already herniating—it is no surprise that that outcome was not very good. In our first case series, we waited for first signs of reversible herniation and a major middle shift on CT, before surgery was considered.
Over the past 7 years, our prospective treatment protocol has been substantially changed in order to allow early recognition of candidates who maybe at risk for malignant MCA infarct and early intervention. We do not wait any more for the first signs of herniation or for elevated ICP readings to indicate the intervention. Early repeated CT scanning and, more recently, immediate diffusion and perfusion MRI studies allow very early identification of the size of the infarct, and, combined with the clinical syndrome of a complete MCA infarction, the diagnosis may be made long before the life-treating swelling occurs. Using the strategy of early identification of patients at risk for malignant MCA symptoms, a second series of 32 patients has been published, in which the intervention took place on average in the first 24 hours after stroke onset. Mortality in this cohort was down to 20%, and quality of survival was even better with a mean modified Rankin score of 2.4 (range, 2 to 4).5
The Drawbacks
Unfortunately, no study has a control group involved, yet.6 Therefore, comparison of mortality rates is difficult, because we are dealing with a historical control that was assembled 7 to 8 years ago. There may have also been shifts in our general ICU practice that would allow higher survival rate without decompressive surgery.
The Call for Randomized Trials
There are several randomized trials on the way both in the United States and in Europe. We are very supportive of the idea of performing a randomized trial. In hospitals, where at the present time no special treatment is offered to the victims of malignant MCA infarction, randomization would offer at least 50% of the patients a chance of receiving treatment; that allows decent survival. Of course, mortality is an important but not the only issue in such a randomized trial. Everyone is concerned about allowing survival in a completely dependent, noncommunicative state, although our experience does not support this concern.
We are aware of several randomized trials in planning stages to address this important issue.
What to Do in the Meantime?
What shall physicians do, meanwhile, now that we are waiting for controlled trials to start? If centers have not yet performed this type of treatment, they should send experienced neurologists and neurosurgeons to institutions to get trained. Centers in which 30 or more patients have been treated successfully, however, may continue with their treatment efforts and help the others to get the experience needed for a good study. This, by the way, is also true for another interesting option for the treatment of malignant MCA infarction, controlled moderate hypothermia of 33°C.7
Footnotes
Section Editors: Geoffry A. Donnan, MD, FRACP and Stephen M. Davis, MD, FRACP
The opinions expressed in this editorial are not necessarily those of the editors or of the American Stroke Association.
References
1. Hacke W, Schwab S, Horn M, Spranger M, De Georgia M, von Kummer R. "Malignant" middle cerebral artery territory infarction: clinical course and prognostic signs. Arch Neurol. 1996; 53: 309–315.
2. Schwab S, Spranger M, Schwarz S, Hacke W. Barbiturate coma in severe hemispheric stroke: useful or obsolete? Neurology. 1997; 48: 1608–1613.
3. Ropper AH, Shafran B. Brain edema after stroke: clinical syndrome and intracranial pressure. Arch Neurol. 1984; 41: 26–29.
4. Rieke K, Schwab S, Krieger D, von Kummer R, Aschoff A, Schuchardt V, Hacke W. Decompressive surgery in space-occupying hemispheric infarction: results of an open, prospective trial. Crit Care Med. 1995; 23: 1576–1587.[CrossRef][Medline] [Order article via Infotrieve]
5. Schwab S, Steiner T, Aschoff A, Schwarz S, Steiner HH, Jansen O, Hacke W. Early hemicraniectomy in patients with complete middle cerebral artery infarction. Stroke. 1998; 29: 1888–1893.
6. Morley NC, Berge E, Cruz-Flores S, Whittle IR. Surgical decompression for cerebral oedema in acute ischaemic stroke (Cochrane Review). In: The Cochrane Library, Issue 3, 2002. Oxford: Update Software; 2002.
7. Schwab S, Schwarz S, Spranger M, Keller E, Bertram M, Hacke W. Moderate hypothermia in the treatment of patients with severe middle cerebral artery infarction. Stroke. 1998; 29: 2461–2466.
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