Hemicraniectomy for Severe Ischemia Stroke
January 1, 2001 4 minutes read
Hemicraniectomy for Severe Ischemia Stroke
Abstracts & Commentary
Sources: Auer RN. Hemicraniectomy of ischemic stroke: Temerity or death cure? Can J Neurol Sci 2000;27:269; Wijdicks EF. Hemicraniotomy in massive hemispheric stroke: A stark perspective on a radical procedure. Can J Neurol Sci 2000;27:271-273; Demchuk AM. Hemicraniectomy is a promising treatment in ischemic stroke. Can J Neurol Sci 2000;27:274-277.
These three articles address the possible value of surgically removing the lateral-coronal skull (hemicraniectomy) so as to relieve compression from acute, grossly expanding, cerebral hemispheric strokes. Such circumstances usually have reflected a sudden occlusion at either the take-off of the middle cerebral artery (MCA) or the intracranial internal carotid artery to the MCA. Even more dangerous would be an additional major threat if the adjacent anterior cerebral artery also became occluded. The pathogenesis of the tissue lesions consists of progressive, expanding edema-necrosis tissues that usually reach a potentially lethal volume between 2-4 days. The process reflects the presence of ever increasing tissue osmols as cells die from anoxia; the ensuing swelling progressively compresses capillary flow and larger vessels in the enlarging penumbra of the primary lesion. The process, if not curtailed, leads to thalamic and possibly fatal brain stem compression. Wijdicks, however, notes that in his hospital-based stroke patients, mortality was 70% in those with large MCA lesions only if clinical deterioration has occurred beyond drowsiness and/or showed signs of diencephalic herniation.
Demchuk carries the flag to perform hemicraniectomy in large MCA strokes, citing several previous reports of the procedure. The first example he gives includes a study in which Rengachary and colleagues studied three persons with large, acute left hemisphere infarctions (Neurosurgery 1981;8:321-328). Ages were 51, 27, and 15 years; CT in all showed large areas of potential cerebral infarction. All became unconscious and had a dilated pupil ipsilateral to the side of the lesion. Craniectomy was conducted on each patient. Patients 1 and 2 became aware of self within 12 hours following surgery, but both permanently suffered "severe fixed neurological deficits." Patient 3, the boy, was alert and "seemed normal" two years afterwards.
In the second example, Carter and associates described hemicraniectomy in 14 patients suffering from acute, large infarcts affecting their nondominant hemispheres (Neurosurg 1997;40:1168-1176). One-year outcomes depended upon degree of regained function and were as followed: three died a cardiac death, two said "never again," and three said "maybe." Three became able to walk independently, five could walk with assistance, and nine could be at home. None regained self independence.
Demchuk’s final example is a study from Schwab and associates (Stroke 1998;29:1888-1893) directed at ap-plying hemicraniectomy following severe brain swelling caused by acute MCA stroke (Neurology Alert 1998;17:17-19). An earlier report from Schwab et al (Cerebrovasc Dis 1996;6:325-329) had indicated that if surgery was applied at an average of 39 hours after progressive symptoms, signs, and brain images all worsened. Of 32 patients, 11 (34%) died; but the survivors averaged a Bartle Index of 62.6. Schwab et al’s more recent Stroke article from 1998 described 31 additional new patients who suffered from similarly large, dynamically evolving MCA strokes. They differed from the previous group and received hemicraniectomy only at an average of 21 hours following large stroke onset. Only five patients in this last group died (16%) and the Bartle Index climbed to 68.8. The meaning of this change in time is unclear, but it implies that previous decisions to pursue hemicraniectomy later in time and after onset of stroke have less vigorous healing ability.
Demchuk, a neurosurgeon on the faculty of the University of Calgary, contributes a well-described history of the use of hemicraniectomy for decompressing brain swelling in patients suffering lobar-distributed, severe MCA strokes. As he emphasizes, the procedure unquestioningly can save the lives of patients of many ages. Nevertheless, most neurologists have found that almost no patients older than about 45 years of age can recapture a normal working life after such a devastating injury. Even in younger ages a certain fraction can be permanently disabled after decompression. Nevertheless, your editor’s guess is that it’s far more difficult to kill young nerve and vascular tissues than old ones. The younger the brain, the more it can overcome injury and effectively change its circuitry. Nevertheless, Demchuk removes age as a factor in trying the advantages of hemicraniectomy and seems to pay little attention to what life will be like in those patients.
Wijdicks sensibly clears the problem and reasons the functional neurological processes that can potentially stave off serious injuries to the brain. Furthermore, he possesses the understanding of which age-related physiological steps might have the capacity to preserve or protect certain injured neural systems that otherwise leave patients with life-long total invalidism.
Auer, a neuropathologist also at Calgary, wisely comments on the advantages of the hemicraniectomy trial. He points out that no functionally oxygenated capillaries lie at the deepest region of the infarct. Indeed, that’s where anoxic-injured and dying cells first increase their intracellular osmols, then explode. As these molecules and cells break down, they draw water into cellular and intercellular compartments. They are first generated for defense, but it also dangerously provides the source of progressive swelling. Swelling and breaking cells enlarge the critical penumbra that expands like a water ripple to continue the anoxogenic cellular breakdown. Ultimately, normally protected capillaries become destroyed from adjacent normal arterial beds. Removing the appropriate skull could take away approximately half the pathological pressure on the tissue, thereby decompressing a large part of the compressed infarct. Common sense says that the best time to protect the tissue by skull decompressions would be done shortly after the first serious symptoms, bodily signs, and major MRI diffusion signs appear. Unfortunately, this point cannot accurately be predicted until it has passed.
As Auer puts it, "Still, the concern that supercedes all others here is that we not convert the dead into the severely impaired living." —Fred Plum
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