Patients with intracerebral hemorrhage (ICH) have a high risk of neurologic deterioration, particularly early after presentation. Close neurologic monitoring is thus important. Intubation and mechanical ventilation are necessary in some patients due to obtundation or coma. Aggressive blood pressure control may reduce the risk of hemorrhage expansion in the acute period; an initial target of < 160/90 mmHg is reasonable. Easily titratable intravenous antihypertensives with a short duration of action, such as labetalol or nicardipine, are preferred. Neurosurgical consultation is indicated for patients with mass effect or intraventricular hemorrhage potentially causing increased intracranial pressure as hemorrhage evacuation or external ventricular drainage may be needed. Head of bed should be positioned at 30 degrees or greater to reduce intracranial pressure. Patients with witnessed or suspected seizures should receive antiepileptic drugs, but prophylactic treatment is generally not indicated.
Urgent laboratory workup to evaluate for coagulopathy (complete blood count, prothrombin, and partial thromboplastin time) is important, and a urine toxicology screen should be sent to evaluate for potential sympathomimetic drugs (cocaine, amphetamines) that might contribute to ICH. Importantly, the presence of such drugs does not preclude another underlying ICH mechanism, so even if present a thorough evaluation should still be performed.
In addition to laboratory testing for coagulopathy, focused history to identify recent anticoagulant or thrombolytic use is essential. Reversal of any identified coagulopathy should be immediately undertaken (see Chapter 52 ). The presence of coagulopathy does not necessarily exclude another contributing cause of ICH (e.g., anticoagulant use may increase risk of bleeding into a brain metastasis), so additional evaluation may still be needed and should be based on clinical suspicion.
Common etiologies of hemorrhage vary based on the hemorrhage location. Deep, subcortical hemorrhages, for example in the thalamus or basal ganglia, are typically due to chronic hypertension. In contrast, superficial, lobar hemorrhages (i.e., cortical) are less commonly due to hypertension; in the elderly, amyloid angiopathy is a common cause. Look for finger-like projections of lobar ICH, which supports the diagnosis of amyloid angiopathy.
While most deep hemorrhages are hypertensive in etiology, in the absence of a history of hypertension or evidence of end-organ damage attributable to chronic hypertension, further diagnostic evaluation is warranted. Brain magnetic resonance imaging (MRI) showing severe microvascular disease or chronic deep microhemorrhages (see section G) strongly suggests a hypertensive etiology. The presence of elevated blood pressure in the acute period should not be considered to indicate chronic hypertension; this is a common physiologic response to the brain hemorrhage itself.
Simultaneous multifocal acute ICHs are rare and suggest an atypical hemorrhage etiology. Most of these specific causes will be identified with a contrast enhanced brain MRI. Venous sinus thrombosis sufficient to cause multifocal ICH is almost always visible on standard enhanced brain MRI; however, MR venography may be necessary to confirm the diagnosis and assess the degree of compromise to venous drainage. In some cases, it may be necessary to repeat imaging in 4–8 weeks after acute hemorrhage has cleared to better evaluate underlying lesions.
It is important to ensure brain MRI is performed with gradient echo (GRE) or susceptibility weighted imaging (SWI) sequences. These sequences identify chronic, often asymptomatic, areas of hemorrhage within the brain typically not visualized with standard MRI sequences. When multiple microhemorrhages are present in a cortical distribution in an elderly patient with lobar hemorrhage, amyloid angiopathy is usually the cause. Amyloid angiopathy is associated with a substantial risk of ICH recurrence, and thus antithrombotic therapy must be scrupulously avoided. While a superficial or lobar ICH location is atypical for hypertensive hemorrhages, long-term blood pressure control remains important and may reduce the risk of recurrent ICH. Other important causes of superficial or lobar hemorrhage include arteriovenous malformations, cavernomas, hemorrhagic metastasis, and venous sinus thrombosis. The latter diagnosis must always be carefully considered as management requires acute parenteral anticoagulation, completely different than that for all other causes of ICH. MR venography or computed tomography (CT) venography are used to confirm the diagnosis. Occasionally, hemorrhagic conversion of ischemic stroke may be confused with a primary ICH. A good rule of thumb is that if the initial CT scan is done within 6 hours of symptom onset and shows ICH, hemorrhagic conversion of ischemic stroke is highly unlikely.
A small subset of patients with arteriovenous malformation or dural arteriovenous fistulas will have normal CT or MR angiography. If there is high suspicion for vascular malformation and no other identified cause, catheter angiography should be pursued. Repeat MRI brain and vessel imaging should be considered 4–8 weeks after initial presentation if the etiology of ICH remains unknown. This allows time for resolution of the hematoma and surrounding edema that may mask underlying pathology.
Acute Spontaneous Intracerebral Hemorrhage
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