Intracerebral Hemorrhage Symptoms and Treatment

Etiology

Intracerebral Hemorrhage usually results from rupture of an arteriosclerotic vessel long exposed to arterial hypertension. Less often, the cause is a congenital aneurysm or other vascular malformation, mycotic aneurysms, brain infarct, collagen diseases, blood dyscrasias or other systemic diseases. Most Intracerebral Hemorrhage, like infarct are located in the region of the internal capsule, basal ganglia and thalamus. Primary hemorrhages elsewhere in the cerebrum or in the cerebellum or brainstem. The hematoma compresses and displaces adjacent brain tissue and increases intracranial pressure. Pressure from hematoma and edema may cause transtentorial herniation, compressing the brainstem and causing secondary hemorrhage in the pons and midbrain.

Symptoms

Cerebral Hemorrhage characteristically begins abruptly with headache followed by steadily increasing neurologic deficits. Large hemorrhages produce hemiparesis when located in the hemispheres, and symptoms of cerebellar and brainstem dysfunction when located in the posterior fossa. Loss of consciousness is common and may occur at onset or develop gradually. Delirium, Nausea, Vomiting and focal or generalized seizures are also common. Large hemorrhages are fatal within a few days in more than 50% of patients. In those who survive, consciousness returns and neurologic deficits gradually recede as the extravasated blood is resorbed. Some degree of impairment usually remains, including some dysphasia if the dominant hemisphere was affected, but a reasonable degree of functional recovery most often occurs. Smaller hemorrhages cause focal deficits like those seen in ischemic stroke, as with infarcts, the deficits reflect the site of the damage.

Treatment

It is often difficult to distinguish small cerebral hemorrhages from ischemic stroke. Lumbar puncture must be done cautiously, if at all, when patients are unconscious or symptoms are worsening, since the consequent change in CSF pressure may precipitate transtentorial herniaton. With large hemorrhages, the CSF is almost always bloody (Hct > 1%) and under increased pressure. Treatment for Intracerebral Hemorrhage is similar to ischemic stroke treatment, except the anticoagulants and antiplatelet.

Anticoagulants and antiplatelet drugs are contraindicated in hemorrhage and should not be used in hemorrhage treatment. If patients have used anticoagulants, the effects are reversed when possible by giving fresh frozen plasma, vitamin K, or platelet transfusions as indicated. 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. (treatment source: http://www.merckmanuals.com/)