In the special case of large cerebellar infarctions, usually from occlusion of a vertebral artery, swelling may compress the lower brainstem within hours or days. This complication carries the risk of sudden respiratory arrest. Cerebellar swelling may occur with or without an associated lateral medullary stroke and the situation is comparable to medullary compression caused by cerebellar hemorrhage. Hydrocephalus usually develops as a prelude to deterioration and is manifest as drowsiness and stupor, increased tone in the legs, and Babinski signs; other sentinel signs of compression of the brainstem are gaze paresis, sixth nerve palsy, or hemiparesis ipsilateral to the ataxia (Kanis and Ropper). It is at times difficult to differentiate the effects of increasing hydrocephalus from those of brainstem infarction from thrombus propagation in the basilar artery (Lehrich et al). Surgical decompression of the infarcted and swollen tissue should be undertaken almost as soon as cerebellar edema becomes clinically apparent by the emergence of hydrocephalus or brainstem signs, as further swelling can be anticipated. A brief period of observation before committing to surgery is not unreasonable if the fourth ventricle and peribrainstem cisterns are open and the patient is awake. Mannitol may be used to prepare the patient for surgery or if a period of observation is anticipated but its value is not clear. As in the case of cerebellar hemorrhage, ventricular drainage alone is usually inadequate and, in any case, is unnecessary if the pressure is relieved by hemicraniectomy and resection of infarcted tissue.
The relative advantages of placing the seriously ill acute stroke patient in a special stroke unit have been the subject of much study. The outcome in these patients in terms of morbidity and mortality is improved, although the differences have been small and difficult to document. However, this organizational plan has not been widely implemented and instead protocols for rapid evaluation of stroke and the emergence of a specialty of stroke neurology have proliferated. If nothing else, this is the result of a general recognition that stroke, like myocardial infarction, requires special expertise and focus. Protocols to prevent excessive hypertension after thrombolytic treatment are best instituted in units that have staffing patterns that create familiarity with these and other protocols. As already emphasized, the prevention of aspiration and pneumonia is paramount by identifying those patients at risk. The patients at risk also benefit from systematic application of protocols. Also deserving attention is the prevention of venous thrombosis in the legs, pulmonary embolism, and coronary syndromes. Some units find it advisable to keep patients supine for the first hours or day after an ischemic stroke, mainly to prevent hypotension and cerebral hypoperfusion; this approach has not been studied systematically. When sitting and walking begin, special attention should be given to the maintenance of normal blood pressure. The rigid control of glucose after stoke has fallen in and out of favor based on various trials but it generally prudent to keep glucose within reasonably normal levels.
Despite conflicting evidence, current practice has encouraged the maintenance of euglycemia. Experimental models of ischemic stroke certainly support the avoidance of hyperglycemia. This is complicated by the high frequency of diabetes as a risk factor for stroke and the need to make decisions regarding glycemic control. Excessively tight control of glucose may not confer a benefit in the acute phase.
Several studies have confirmed the high prevalence of new or enhanced levels of hypertension immediately following an ischemic stroke and its tendency to decline over subsequent days even without medications. The treatment of previously unappreciated hypertension is preferably deferred until the neurologic deficit has stabilized. As suggested by Britton and colleagues, it is prudent to avoid antihypertensive drugs in the first few days unless there is active myocardial ischemia or the blood pressure is high enough to pose a risk to other organs, particularly the kidneys, or there is a special risk of cerebral hemorrhage as a result of the use of thrombolytic drugs.