Several alternatives are available when cerebral hemorrhage is the result of an anticoagulant. In addition to vitamin K, which may not act immediately, warfarin related hemorrhages can be treated with fresh frozen plasma, although 6 to 8 units may be required and this is a large volume to handle for elderly patients or those with congestive heart failure. Protein complex concentrates containing varying amounts of vitamin K dependent factors (II, VII, IX, X) and particularly VII have been used but their superiority over other approaches has been difficult to demonstrate. Orally administered factor Xa inhibitors and direct thrombin inhibitors now have specific antidotes. Cerebral hemorrhage associated with severe thrombocytopenia is generally treated with platelet infusions but the results are variable since the underlying disease that caused thrombocytopenia is often the determining factor. There has been controversy regarding the administration of platelets to patients who were on antiplatelet therapy; we often will administer several units if a patient has been on dual antiplatelet therapy and particularly, there is evidence of expansion of the hematoma. Tissue plasminogen activator related cerebral hemorrhage is generally treated with fibrinogen concentrate. Mayer and coworkers studied the promising approach of administering clotting factor VII within 4 h of spontaneous cerebral hemorrhage. In a preliminary study, survival was improved and there was a reduction in enlargement of the hematoma, but a subsequent trial failed to confirm the benefit on survival.
If acute hydrocephalus has resulted from a centrally placed hemorrhage or rupture into the ventricular system, a extraventricular drain may be needed. These blood-filled drains frequently become clotted and in a study of the infused tissue plasminogen activator through the ventricular catheter no difference was found in overall functional outcome (Hanley et al) but often, there are limited alternatives besides this to keep the apparatus open to drain bloody cerebrospinal fluid. It has been appreciated for some time that intraventricular extension of cerebral hemorrhage generally denotes a poor outcome. An exception may be small thalamic hemorrhages.
Once the patient with a supratentorial hemorrhage becomes deeply comatose with dilated fixed pupils, the chance of recovery is negligible. Even in retrospective studies in which clinical worsening was the reason for surgery, such as the one by Rabinstein and colleagues, only 25 percent of patients attained a state of functional independence and all of their patients who lost their brainstem reflexes and had extensor posturing died despite surgery; there have been a few exceptions to this observation. Some of the mortality in series of cerebral hemorrhage patients is undoubtedly due to the self-fulfilling aspect of withdrawal of care in seemingly hopeless circumstances.
In comatose patients with large hemorrhages, the placement of a device for monitoring of intracranial pressure enables the clinician to use medical measures with greater precision, as outlined in Chap. 16, but there is no evidence that outcome is significantly improved (Ropper and King). Whether hemicraniectomy is of value, as it is with large hemispheral strokes, is not known but it seems unlikely. Cerebellar hemorrhage represents a special case regarding neurosurgery, as commented below.
The issue often arises of the appropriate timing of restarting anticoagulation in patients whose hemorrhage occurred on warfarin. In some instances, such as a prosthetic heart valve requires warfarin, medication is often reintroduced after a week or two. However, for the more common indication of this drug, namely atrial fibrillation, there have been diverging suggestions from different surveys. In an often-cited study by Majeed and colleagues, a retrospective review of almost 3,000 patients over 6 years suggested that the risk of creating another hemorrhage by restarting warfarin earlier than 10 to 30 weeks after the initial stroke was quite high.