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Excerpt
Large middle cerebral artery (MCA) infarctions may cause space occupying hemispheric oedema that finally leads to brainstem compression within 2-3 days. Initially these patients already present with severe contralateral hemiparesis. Owing to the progressing intracerebral oedema, most patients become unconscious and develop respiratory insufficiency within 24-48 hours. Some 70-80% of these patients die within 3-5 days despite full-range anti-oedematous treatment. Therefore, this syndrome has been called 'malignant' MCA infarction [1].
Decompressive surgery has been shown to lower mortality from 80% to 32%, resulting in a moderate functional disability measured by Barthel Index (BI) of 62.5 [2]. Mortality can be lowered to less than 20% if hemicraniectomy is initiated within 24 hours, with a BI of 69 [3].
The stepwise escalating therapy consists of three parts: first, a basic treatment aiming for normoglycaemia, normothermia, normotension; second, conservative antioedematose treatment (including glycerol, mannitol or sorbitol, Hyper-HAES, THAM-buffer and ultimately barbiturates); third, hemicraniectomy or moderate hypothermia.
Clinical assessment and monitoring is difficult since at a certain time point all patients are sedated and ventilated. Early computed tomography (CT) can help to predict fatal brain swelling: Early infarct signs can be seen on the initial CT in 68% of patients at 2 hours after onset of stroke and in 89% at the third hour [4]. Major infarct signs will become visible during the first 12 hours after onset of symptoms, including severe brain swelling with midline shift. The positive predictive value for fatal outcome is 85% if CT hypodensity covers more than 50% of the MCA territory. The risk of fatal outcome is 70% if local brain swelling occurs in patients with angiographically proven MCA trunk occlusion [5]. Poor collateral blood supply and absence of recanalization within 8-24 hours after onset of symptoms induce further increase of ischaemic oedema and midline shift [4]. With spiral CT-angiography, information on the site of the occlusion and presence of collateral vessels can be obtained. Multimodal magnetic resonance imaging (MRI) techniques may in future help to recognize patients who are at risk of developing malignant MCA infarction at a very early stage by differentiating between irreversibly and reversibly damaged tissue. Information on thrombus location and quality of collateral blood supply can be depicted from the same examination [6].
Brain stem acoustic evoked potentials (BAEP) were shown to have predictive value within the first 24 hours before surgery [7]. Continuous intracranial pressure (ICP) and cerebral perfusion pressure (CPP), continuous partial tissue oxygen pressure (pbrO2) [8] and serial B-mode transcranial ultrasound examinations further support therapy.
The rational of hemicraniectomy is based on the decompression of brain tissue and collateral blood vessels. To reach this goal a large craniectomy of at least 13-14 cm in diameter is essential (Fig. 1)[9]. The operation technique consists of our neurosurgeons removal of a large bone flap, including the frontal, parietal, temporal, and parts of the occipital squama, in combination with consecutive large dural graft. Complication rate of the procedure is low. We mainly observed minor epidural and subdural bleedings.
