Stroke, Intracerebral Hemorrhage

For further information, see CMDT Part 24-08: Stroke

Essentials of Diagnosis

• Hypertension is the usual cause

• Hypertensive intracerebral hemorrhage occurs most frequently in the basal ganglia, pons, thalamus, cerebellum and less commonly in the cerebral white matter

• Hemorrhage may extend into the ventricular system or subarachnoid space, and signs of meningeal irritation are then found

General Considerations

Hypertensive intracerebral hemorrhage

• Spontaneous, nontraumatic intracerebral hemorrhage in patients with no angiographic evidence of an associated vascular anomaly (eg, aneurysm or angioma) is usually due to hypertension

• Likely pathologic basis is microaneurysms that develop on perforating vessels 100–300 mcm in diameter in hypertensive patients

• Occurs most frequently in the basal ganglia and less commonly in the pons, thalamus, cerebellum, and cerebral white matter

• Extension into the ventricular system or subarachnoid space may cause signs of meningeal irritation

• In the elderly, cerebral amyloid angiopathy is another important and frequent cause of hemorrhage

  • It is usually lobar in distribution and sometimes recurrent

  • It is associated with a better prognosis than hypertensive hemorrhage

Other causes

• May occur with

  • Hematologic and bleeding disorders (eg, leukemia, thrombocytopenia, hemophilia, or disseminated intravascular coagulation)

  • Anticoagulant therapy

  • Liver disease

  • High alcohol intake

  • Cocaine and methamphetamine abuse

  • Herpes simplex encephalitis

  • Vasculitis

  • Moyamoya disease

  • Reversible cerebral vasoconstriction syndrome

  • Primary or secondary brain tumors

• There is also an association with advancing age, male sex, and high alcohol intake

• Bleeding from an intracranial aneurysm or arteriovenous malformation is primarily into the subarachnoid space, but it may also be partly intraparenchymal

• Hemorrhage can also occur into arterial and venous cerebral infarcts

Symptoms and Signs

Hemorrhage into the cerebral hemisphere

• Consciousness is initially lost or impaired in about 50% of patients

• Vomiting is frequent at the onset, and headache is sometimes present

• Focal symptoms and signs follow, depending on the site of the bleed

• With hypertensive hemorrhage, there is generally a rapidly evolving neurologic deficit with hemiplegia or hemiparesis

• A hemisensory disturbance occurs with more deeply placed lesions

• With lesions of the putamen, loss of conjugate lateral gaze may be present

• With thalamic hemorrhage, there may be a loss of upward gaze, downward or skew deviation of the eyes, lateral gaze palsies, and pupillary inequalities

Cerebellar hemorrhage

• Sudden onset of nausea and vomiting; dysequilibrium; ataxia of gait, limbs, or trunk; headache; and loss of consciousness that may be fatal within 48 hours

• Less commonly, the onset is gradual and episodic or slowly progressive, suggesting an expanding cerebellar lesion

• Onset and course can be intermediate

  • Lateral conjugate gaze palsies to the side of the lesion

  • Small reactive pupils

  • Contralateral hemiplegia; peripheral facial weakness

  • Ataxia of gait, limbs, or trunk

  • Periodic respiration

  • Some combination of these findings

Differential Diagnosis

• Ischemic stroke

• Subarachnoid hemorrhage

• Space-occupying lesion, eg, brain tumor

• Subdural or epidural hemorrhage

Laboratory Tests

• A predisposing cause may be revealed by

  • Complete blood count

  • Platelet count

  • Bleeding time

  • Prothrombin and partial thromboplastin times

  • Liver biochemical and kidney function tests

• Lumbar puncture is contraindicated because it may cause herniation in patients with a large hematoma

Imaging Studies

• CT scanning (without contrast) is important in confirming hemorrhage and for determining the size and site of the hematoma

• CT is superior to MRI for detecting intracranial hemorrhage of less than 48 hours' duration

• If the patient's condition permits further intervention, CT angiography, magnetic resonance angiography, or cerebral angiography may reveal an aneurysm or arteriovenous malformation

Medications

• Intravenous labetalol or nicardipine

  • Should be used to lower systolic blood pressure below 140 mm Hg

  • Although randomized trials targeting systolic blood pressures of < 140 mm Hg and < 180 mm Hg have not shown a difference in outcomes

• Thrombocytopenia should be treated with platelet transfusion

• Coagulopathies should be reversed using

  • Fresh frozen plasma

  • Prothrombin complex concentrates

  • Vitamin K

  • Specific reversal agents, such as

    • Protamine for heparin

    • Idarucizumab for dabigatran

    • Andexanet alfa for apixaban, betrixaban, edoxaban, rivaroxaban

Surgery

• In cerebellar hemorrhage, prompt surgical evacuation of the hematoma is appropriate

• Decompression is helpful when a superficial hematoma in cerebral white matter is causing mass effect and herniation

• Ventricular drainage may be required in patients with intraventricular hemorrhage and acute hydrocephalus

Therapeutic Procedures

• Neurologic management is generally conservative and supportive, either in cases of profound deficit with associated brainstem compression or more localized deficits

• The treatment of underlying structural lesions or bleeding disorders depends on their nature

• Hemostatic therapy with recombinant activated factor VII has not improved survival or functional outcome

• There is no specific treatment for cerebral amyloid angiopathy

Prognosis

• Surgery for cerebellar hemorrhage may lead to complete resolution of the clinical deficit

• Untreated cerebellar hemorrhage can spontaneously deteriorate with a fatal outcome from brainstem herniation

• Follow-up imaging during the hospitalization may reveal hematoma expansion, a predictor of poor outcome

When to Refer

• All patients

When to Admit

• All patients