Surgical Decompression for Malignant Middle Cerebral Artery Infarction: A Challenge to Conventional Thinking
Early mortality after large middle cerebral artery (MCA) infarcts is most often due to acute brain swelling, with midline shift and transtentorial herniation. This is particularly relevant in younger stroke patients, with the syndrome of “malignant MCA infarction.”1 Conversely, neurological recovery may be better after a life-saving intervention. Medical management of ischemic brain edema is limited and at best may result in only temporary reduction in intracranial pressure. Hence, the logic of craniectomy with surgical decompression is appealing, although the concern has always been that a reduction in mortality might be outweighed by major disability in survivors. It seems likely that a driving force in early anecdotal reports of hemicraniectomy was the more obvious benefit seen in posterior fossa decompression with acute cerebellar infarction, although this is also an unproven management strategy.
One barrier to clinicians’ willingness to embrace the procedure is the daunting prospect of what appears to be major surgery in patients with a perceived poor prognosis. In fact, this type of surgery is commonly performed in trauma centers in cases with malignant cerebral edema and is technically relatively simple. Another issue relates to the inclusion of patients with dominant hemisphere infarction. We are not convinced that these should be excluded from clinical trials, since improvement may be just as dramatic in either hemisphere.
Both protagonists have pointed out that there are no definitive trials, although a number are fortunately in progress.2 In the HEADDFIRST study, patients are randomized to hemicraniectomy with durotomy versus control with death and disability measured at 21 days, 3 months, and 6 months. In the HAMLET study, Hoffmeijer et al plan to randomize about 100 patients under the age of 60 years to hemicraniectomy and duraplasty, with outcomes measured at 6 months. Obviously, more trials may be needed to refine patient selection, timing of intervention, and surgical approach, even if these initial trials are positive.
One of the most puzzling aspects of the management of patients who develop acute middle cerebral artery infarction is the development of malignant edema in only a subset. Clearly, better clinical and imaging selection criteria need to be defined. Some attempts have been made to identify those with a poor prognosis using strategies such as sonographic monitoring of midline shift,3 and SPECT.4 Possibly, as Schwab and Hacke mentioned, newer techniques such as perfusion and diffusion MRI may be more reliable, given their greater sensitivity in imaging acutely ischemic tissue.
What should the practicing clinician do in the meantime? While Brown is a little more cautious than Schwab and Hacke, all agree that more data are required from prospective randomized trials. We suggest that in younger patients with large MCA infarcts who are developing obvious edema with clinical deterioration, decompressive surgery should be considered earlier rather than later based on the limited information available to date. It would seem pointless to us to suggest surgery in patients with established signs of transtentorial herniation where the likelihood of recovery is remote. For stroke clinicians able to be involved in a prospective trial, we would encourage use of the uncertainty principle to randomize patients to surgical or medical management. Once we considered thrombolysis a radical possibility for stroke therapy. We should continue to challenge conventional thinking.
Morley NCD, Berge E, Cruz-Flores S, Whittle IR. Surgical decompression for cerebral oedema in acute ischaemic stroke (Cochrane Review). In: The Cochrane Library, Issue 1, 2003. Oxford: Update Software; 2003.
Gerriets T, Stolz E, Konig S, Babacan S, Fiss I, Jauss M, Kaps M. Sonographic monitoring of midline shift in space-occupying stroke: an early outcome predictor. Stroke. 2001; 32: 422–427.
Berrouschot J, Barthel H, von Kummer R, Knapp WH, Hesse S, Schneider D. Stroke. 1998; 29: 2556–2562.