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Intracerebral hemorrhage is focal bleeding from a blood vessel in the brain parenchyma. The cause is usually hypertension. Typical symptoms include focal neurologic deficits, often with abrupt onset of headache, nausea, and impairment of consciousness. Diagnosis is by CT or MRI. Treatment includes BP control, supportive measures, and, for some patients, surgical evacuation.
Most intracerebral hemorrhages occur in the basal ganglia, cerebral lobes, cerebellum, or pons. Intracerebral hemorrhage may also occur in other parts of the brain stem or in the midbrain.
Intracerebral hemorrhage usually results from rupture of an arteriosclerotic small artery that has been weakened, primarily by chronic arterial hypertension. Such hemorrhages are usually large, single, and catastrophic. Other modifiable risk factors that contribute to arteriosclerotic hypertensive intracerebral hemorrhages include cigarette smoking, obesity, and a high-risk diet (eg, high in saturated fats, trans fats, and calories). Use of cocaine or, occasionally, other sympathomimetic drugs can cause transient severe hypertension leading to hemorrhage.
Less often, intracerebral hemorrhage results from congenital aneurysm, arteriovenous or other vascular malformation (see Vascular Lesions in the Brain), trauma (see Traumatic Brain Injury (TBI)), mycotic aneurysm, brain infarct (hemorrhagic infarction), primary or metastatic brain tumor, excessive anticoagulation, blood dyscrasia, intracranial arterial dissection, moyamoya disease, or a bleeding or vasculitic disorder.
Lobar intracerebral hemorrhages (hematomas in the cerebral lobes, outside the basal ganglia) usually result from angiopathy due to amyloid deposition in cerebral arteries (cerebral amyloid angiopathy), which affects primarily the elderly. Lobar hemorrhages may be multiple and recurrent.
Blood from an intracerebral hemorrhage accumulates as a mass that can dissect through and compress adjacent brain tissues, causing neuronal dysfunction. Large hematomas increase intracranial pressure. Pressure from supratentorial hematomas and the accompanying edema may cause transtentorial brain herniation (see Figure: Brain herniation.), compressing the brain stem and often causing secondary hemorrhages in the midbrain and pons. If the hemorrhage ruptures into the ventricular system (intraventricular hemorrhage), blood may cause acute hydrocephalus. Cerebellar hematomas can expand to block the 4th ventricle, also causing acute hydrocephalus, or they can dissect into the brain stem. Cerebellar hematomas that are > 3 cm in diameter may cause midline shift or herniation. Herniation, midbrain or pontine hemorrhage, intraventricular hemorrhage, acute hydrocephalus, or dissection into the brain stem can impair consciousness and cause coma and death.
Symptoms typically begin with sudden headache, often during activity. However, headache may be mild or absent in the elderly. Loss of consciousness is common, often within seconds or a few minutes. Nausea, vomiting, delirium, and focal or generalized seizures are also common. Neurologic deficits are usually sudden and progressive. Large hemorrhages, when located in the hemispheres, cause hemiparesis; when located in the posterior fossa, they cause cerebellar or brain stem deficits (eg, conjugate eye deviation or ophthalmoplegia, stertorous breathing, pinpoint pupils, coma). Large hemorrhages are fatal within a few days in about half of patients. In survivors, consciousness returns and neurologic deficits gradually diminish to various degrees as the extravasated blood is resorbed. Some patients have surprisingly few neurologic deficits because hemorrhage is less destructive to brain tissue than infarction.
Small hemorrhages may cause focal deficits without impairment of consciousness and with minimal or no headache and nausea. Small hemorrhages may mimic ischemic stroke.
Diagnosis is suggested by sudden onset of headache, focal neurologic deficits, and impaired consciousness, particularly in patients with risk factors. Intracerebral hemorrhage must be distinguished from ischemic stroke, subarachnoid hemorrhage, and other causes of acute neurologic deficits (eg, seizure, hypoglycemia); blood glucose level should be measured at the bedside immediately.
Immediate CT or MRI is necessary. Neuroimaging is usually diagnostic. If neuroimaging shows no hemorrhage but subarachnoid hemorrhage is suspected clinically, lumbar puncture is necessary (see Lumbar puncture (spinal tap)). CT angiography, done within hours of bleeding onset, may show areas where contrast extravasates into the clot (spot sign); this finding indicates that bleeding is continuing and suggests that the hematoma will expand and the outcome will be poor .
Treatment includes supportive measures and control of modifiable risk factors. Anticoagulants and antiplatelet drugs are contraindicated. If patients have used anticoagulants, the effects are reversed when possible by giving fresh frozen plasma, prothrombin complex concentrate, vitamin K, or platelet transfusions as indicated. Hemodialysis can remove about 60% of dabigatran.
Hypertension should be treated only if mean arterial pressure is > 130 mm Hg or systolic BP is > 185 mm Hg. Nicardipine 2.5 mg/h IV is given initially; dose is increased by 2.5 mg/h q 5 min to a maximum of 15 mg/h as needed to decrease systolic BP by 10 to 15%.
Cerebellar hemisphere hematomas that are > 3 cm in diameter may cause midline shift or herniation, so surgical evacuation is often lifesaving. Early evacuation of large lobar cerebral hematomas may also be lifesaving, but rebleeding occurs frequently, sometimes increasing neurologic deficits. Early evacuation of deep cerebral hematomas is seldom indicated because surgical mortality is high and neurologic deficits are usually severe. Anticonvulsants are not typically used prophylactically; they are used only if patients have had a seizure.
With intracerebral hemorrhage, sudden, severe symptoms (eg, sudden headache, loss of consciousness, vomiting) are common, but headache may be absent (particularly in the elderly), and small hemorrhages may mimic ischemic stroke.
Do CT or MRI and a bedside glucose test immediately.
Essential supportive care may include reversing anticoagulation and decreasing BP if mean arterial pressure is > 130 mm Hg or systolic BP is > 185 mm Hg.
Consider surgical evacuation for large lobar cerebral hematomas and hematomas > 3 cm in a cerebellar hemisphere.
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