The management of patients with large intracerebral hemorrhages and coma includes the maintenance of adequate ventilation, selective acute use of controlled hyperventilation to a Pco2 of 25 to 30 mm Hg, monitoring of intracranial pressure in some cases and its control by the use of tissue-dehydrating agents such as mannitol (osmolality kept at 295 to 305 mOsm/L and Na at 145 to 150 mEq), and limiting intravenous infusions to normal saline. Qureshi’s group offered data suggesting that aggressive measures to reduce intracranial pressure may be lifesaving and result in good outcome even in patients who have signs of transtentorial herniation. In our experience, this type of recovery is exceptional, but medical treatment of raised intracranial pressure may be justified in patients whose medical condition allows it.
As mentioned, most patients with intracerebral hemorrhage are hypertensive immediately after the stroke because of a generalized sympathoadrenal response. The natural trend is for the blood pressure to diminish over several days; therefore active treatment in the acute stages has been a matter of controversy. Rapid reduction of moderately elevated blood pressure (between 140 and 160 mm Hg systolic), in the hope of reducing further bleeding, is not recommended, because it risks compromising cerebral perfusion in cases of raised intracranial pressure. On the other hand, sustained mean blood pressures of greater than 110 mm Hg (generally above 160 mm Hg systolic) may exaggerate cerebral edema and perhaps enhance the risk extension of the clot. It is at approximately this level of acute hypertension that the use of beta-blocking drugs (esmolol, labetalol) or angiotensin-converting enzyme (ACE) inhibitors is recommended. The major calcium channel-blocking drugs are used less often for this purpose because of reports of adverse effects on intracranial pressure, although this information derives mainly from patients with brain tumors. Hayashi and associates have shown that although blood pressure is lowered with nifedipine after cerebral hemorrhage, intracranial pressure is raised, resulting in an unfavorable net reduction in cerebral perfusion pressure.
In a randomized trial of rapid reduction in blood pressure in patients with acute cerebral hemorrhage, Anderson and colleagues (2013) found that targeting a level of systolic blood pressure below 140 mm Hg within an hour resulted in similar overall clinical outcomes and mortality to guideline-recommended treatment that targets a systolic blood pressure of less than 180 mm Hg. More rapidly acting and titratable agents such as nitroprusside may be used in extreme situations, recognizing that they may further raise intracranial pressure.
Although it would appear intuitively that evacuation of a hematoma might be beneficial, surgical results have not been found to be superior to medical measures alone (Waga and Yamamoto; Batjer et al; Juvela et al; Rabinstein et al). A multicenter, randomized study involving 1,033 patients with supratentorial hemorrhage, under the auspices of the Surgical Trial in Intracerebral Haemorrhage (STICH) study reported by Mendelow and colleagues, has failed to show a benefit from early surgery on survival or neurologic functioning at 6 months. This negative result extended to almost all levels of neurologic deficit and all age groups. In a post hoc analysis, clots that were small and close to the surface of the brain may have benefited from evacuation. As a result, a direct surgical approach has been used less frequently than in the past, but we acknowledge that in a few instances with ongoing deterioration in young patients with hematomas that were easily accessible from the cortical surface, we have asked our neurosurgical colleagues to undertake evacuation of the clot.