Key Clinical Questions
What are the types of intracranial hemorrhage, and how are they identified?
How is anticoagulation reversed and when can it be reinstituted?
What is the appropriate management of blood pressure after cerebral hemorrhage?
What medical treatments bear on the management of intracranial hemorrhage?
How is raised intracranial pressure managed?
Is anticoagulation safe after an intracranial hemorrhage?
What tests should be obtained in patients with ventriculoperitoneal shunts and fever?
Intracranial hemorrhages, increasingly frequent in practice as a result of anticoagulation, are of three main types. They are categorized as spontaneous intracerebral hemorrhage (bleeding within the brain parenchyma), subarachnoid hemorrhage from aneurysm rupture, and intracranial bleeding from cranial trauma. Intracerebral hemorrhage accounts for 10% of strokes, with rates in the United States of approximately 10 cases per 100,000 persons yearly, and a higher incidence in African Americans and Hispanics than in whites. The highest incidence globally is found in Japan, where rates approach 60 cases per 100,000.
SPONTANEOUS INTRACEREBRAL HEMORRHAGE
The most common underlying causes of intracerebral hemorrhage are hypertension and therapeutic anticoagulation. Other associated conditions include acquired coagulopathy, bleeding into a cerebral tumor, cerebral venous thrombosis, vascular malformations, hemorrhagic transformation of ischemic stroke, and amyloid angiopathy. The frequency of chronic hypertension in patients with cerebral hemorrhage had been ~75% in population studies, but the proportion of bleeds related to anticoagulant and antiplatelet medications has been increasing. Hypertensive patients at high risk for intracranial hemorrhage are those with poorly controlled disease, those younger than 55 years, smokers, and especially those who have recently stopped taking chronically administered antihypertensive medications. Spontaneous intracerebral bleeding with the use of adrenergically active medications and toxins such as cocaine should be suspected in young individuals. Acquired coagulopathy from underlying systemic disease is a well-known cause of primary intracerebral hemorrhage, particularly when caused by cancer or chemotherapy-related bone marrow suppression, uremia, or liver failure.
The clinical features that distinguish cerebral hemorrhage from other forms of stroke are headache, nausea, vomiting, confusion, acute and severe hypertension, and with large clots, decreased level of consciousness, hemiplegia, and enlargement of the pupils. The most common location for spontaneous intracerebral hemorrhage is the basal ganglia, accounting for ~65% of cases. Thalamic hemorrhage manifests similarly, usually with hemiplegia and hemianesthesia. Pontine hemorrhage causes rapid coma, quadriplegia, pinpoint pupils, and loss of extraocular movements. Cerebellar hemorrhage has special significance because of the benefits from surgical evacuation; vomiting, vertigo, dizziness, gait ataxia, and progressive coma from hydrocephalus are typical. Lobar hemorrhages confined to one subcortical region cause signs referable to the area affected and simulate ischemic stroke.
Computed tomography (CT) scan without contrast is the primary diagnostic tool. Conventional or CT angiogram or magnetic resonance imaging (MRI) may be required in special cases to establish the diagnosis of an underlying aneurysm, vascular malformations, ...