- Clinical science
Intracerebral hemorrhage
Summary
Intracerebral hemorrhage (ICH) refers to bleeding within the brain parenchyma. While the term "intracranial hemorrhage" is often used synonymously, it in fact describes a broader range of phenomena. The most important underlying cause of ICH is arterial hypertension. Symptoms are often nonspecific (e.g., headache) but, depending on the affected vessel and cerebral region, focal neurologic deficits (e.g., hemiparesis) may occur. Compared to ischemic stroke, patients with ICH typically present with more severe headache and symptoms usually worsen more rapidly. A noncontrast head CT is the most important diagnostic procedure, and shows a hyperdense lesion in acute ICH or a hypodense lesion in hyperacute ICH. Treatment involves management of the underlying and accompanying conditions (e.g., hypertension) and, in some cases, neurosurgery. Approximately half of patients with ICH die within 30 days.
Etiology
- Nontraumatic
- Hypertension: most common cause of spontaneous intracerebral hemorrhage
- Cerebral amyloid angiopathy
- Ruptured arteriovenous malformations
- Vasculitis (e.g., giant cell arteritis)
- CNS infections (e.g., herpes simplex virus) and septic embolisms
- Coagulation disorders (e.g., anticoagulant use)
- Neoplasms (e.g., meningioma)
- Stimulants (e.g., cocaine and amphetamines; possibly also caffeine)
- Infarctions (venous sinus thrombosis)
- Traumatic brain injury
References:[1][2][3][4][5]
Pathophysiology
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Nontraumatic mechanisms of hemorrhage
- Chronic arterial hypertension (→ lipohyalinosis of vessel walls) and/or cerebral amyloid angiopathy (→ deposition of β-amyloid in vessel walls) → focal damage with formation of microaneurysms with elevated risk of ruptures
- Structural abnormalities (e.g., vascular malformations) → parts of the abnormal vascular segment can be exposed to excessive strain → rupture
- Venous outflow obstruction and stimulant use (e.g., cocaine) → acute arterial hypertension
- Coagulopathies: impaired hemostasis → vascular microtrauma
- Inflammatory tissue necrosis → damage to vessels
- Traumatic: blunt or penetrating injury → damage to vessels
References:[6][3]
Clinical features
Diagnostics
- Noncontrast cCT (confirmatory test): solitary hyperdense lesion, surrounded by hypodense edema (most commonly within the basal ganglia or internal capsule; see: “CT and MRI findings in early ischemia and hemorrhage” for more details)
- Further diagnostics once hemorrhage is confirmed
- Laboratory studies: CBC , coagulation parameters, blood glucose levels
- Angiography → detection of vascular malformations and vasculitis
References:[3][7]
Treatment
-
Acute measures to stabilize patient and control ICP
- Fluid replacement
- Consider intubation with hyperventilation
- Head elevation (30°)
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Medical therapy
- Blood pressure
- Blood pressure goals
- > 180 mm Hg systolic (or > 130 mm Hg MAP) without elevated ICP → consider modest reduction to 160 mm Hg systolic (or 110 mm Hg MAP)
- > 180 mm Hg systolic (or > 130 mm Hg MAP) and elevated intracranial pressure (ICP) → monitor ICP, lower blood pressure cautiously (if needed )
- > 200 mm Hg systolic (or > 150 mm Hg mean arterial pressure, MAP) → lower to ∼ 140 mm Hg systolic
- Recommended medications: e.g., IV labetalol, nicardipine, enalapril, or hydralazine
- Blood pressure goals
- Maintain normal blood glucose and monitor anticoagulation parameters
- Blood pressure
-
Surgical intervention
- Patients with hemorrhage in the basal ganglia or the internal capsule should generally not undergo surgical clot removal.
- Indications for surgical treatment are signs of brain herniation (e.g., Cushing triad), obstructive hydrocephalus or hemorrhage extension > 3 cm
- Procedure: craniotomy and subsequent clot evacuation
Patients with signs of brain herniation should be operated on immediately!
References:[8][7][9][10]
Complications
- Repeat hemorrhage
- Vasospasms
- Deep vein thrombosis
- Dysphagia; : can lead to aspiration of food → pneumonia
- Seizures
- Elevated intracranial pressure and brain herniation
- Hydrocephalus
- Syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
References:[6][11]
We list the most important complications. The selection is not exhaustive.
Prognosis
Poor: ∼ 50% of patients die within 30 days.
References:[10]