Intracerebral hemorrhage (ICH…)

Intracerebral hemorrhage (ICH) refers to bleeding within the brain parenchyma. The term should not be confused with “intracranial hemorrhage,” which encompasses any type of bleeding within the skull, i.e., extradural, subdural, subarachnoid, and intracerebral. The most significant risk factor for spontaneous 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 progress more rapidly. A noncontrast head CT, the most important diagnostic procedure, shows a hyperdense lesion in acute ICH and a hypodense lesion in hyperacute ICH. Treatment involves management of the underlying and accompanying conditions (e.g., controlling hypertension, reversing coagulopathy) and, in severe cases, neurosurgical intervention. Approximately half of patients with ICH die within 30 days.

See also overview of stroke, ischemic stroke, and subarachnoid hemorrhage for more information.

• Intracranial hemorrhage: a broad term used to describe any bleeding within the skull (including intracerebral hemorrhage, subarachnoid hemorrhage, subdural hemorrhage, and epidural hemorrhage) due to traumatic brain injury or nontraumatic causes (e.g., hemorrhagic stroke, ruptured aneurysm, hypertensive vasculopathy)
• Hemorrhagic stroke
  • Rupture of a blood vessel within the brain or the cerebrospinal fluid
  • Subtypes
    • Intracerebral hemorrhage (intraparenchymal hemorrhage): bleeding within the brain parenchyma
    • Subarachnoid hemorrhage: bleeding into the subarachnoid space
    • Intraventricular hemorrhage: bleeding within the ventricles

• ICH is responsible for approx. 10% of all strokes. ^[1][2]
• Most commonly affects the deep structures of the brain ^[3]
• Intraventricular extension occurs in approx. 30% of patients with ICH. ^[4]

Epidemiological data refers to the US, unless otherwise specified.

• Nontraumatic (spontaneous)
  • Hypertension: most common cause of spontaneous ICH
  • Cerebral amyloid angiopathy: most common cause of spontaneous ICH in individuals > 60 years of age
  • Arteriovenous malformations: most common cause of spontaneous intracerebral hemorrhage in children
  • Vasculitis (e.g., giant cell arteritis)
  • Neoplasms (e.g., meningioma)
  • Ischemic stroke (due to reperfusion injury)
  • CNS infections (e.g., HSV encephalitis)
  • Septic emboli
  • Coagulopathy (e.g., hemophilia, anticoagulant use)
  • Stimulant use (e.g., cocaine and amphetamines; possibly also caffeine)
• Traumatic: : see traumatic brain injury

References:^{[5][2][4][6][7]}

• Nontraumatic mechanisms of hemorrhage
  • Chronic arterial hypertension → lipohyalinosis of lenticulostriate vessels, which supply the basal ganglia → formation and rupture of Charcot-Bouchard microaneurysms → lacunar strokes (ischemia) of the basal ganglia
    • Putamen most commonly affected
    • Other locations: thalamus (second most common) and infratentorial parts of the brain (e.g., pons, cerebellum)
  • Cerebral amyloid angiopathy: deposition of β-amyloid peptides in vessel walls → focal damage with formation of microaneurysms → rupture → recurrent lobar intracerebral hemorrhage
  • Structural abnormalities (e.g., vascular malformations) → exposure of parts of the abnormal vascular segment 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:^[8][4]

• Headache
  • Absent in small hemorrhages
  • Most common in cerebellar and lobar hemorrhages ^[9]
• Focal neurologic signs and symptoms may occur, depending on the location and size of the hemorrhage (see stroke symptoms by affected vessel and stroke symptoms by affected region in stroke)
  • Putaminal hemorrhage: contralateral hemiparesis or hemiplegia with less severe contralateral hemisensory loss; eyes deviate toward the side of the hematoma
  • Thalamic hemorrhage: contralateral hemiparesis, contralateral hemisensory loss, decreased consciousness, wrong way eyes
• Course
  • Symptoms typically progress gradually over minutes to a few hours
  • Focal deficits worsen with expansion of the hematoma
  • Late: symptoms of increased intracranial pressure
    • Nausea and vomiting
    • Confusion and loss of consciousness
    • Bradycardia
    • Fixed pupils

References:^[4][9]

Initial evaluation

• Immediate noncontrast head CT
  • Best initial test
  • Expected findings
    • Hyperacute: hypodense lesion
    • Acute: hyperdense lesion with hypodense perifocal edema
    • Chronic: hemorrhage may appear as a hypodense lesion
    • Midline shift and/or mass effect may suggest impending herniation
• Diffusion-weighted MRI
  • More sensitive than head CT
  • Expected findings
    • Hyperacute
      • T1: hypointense
      • T2: hyperintense
    • Acute: hypointense

Subsequent evaluation

• Laboratory studies
  • CBC
  • Coagulation parameters (PTT and INR)
  • Blood glucose level
  • Troponin
  • Toxicology screen
• Angiography (e.g., CTA and/or MRA): to identify the source of the bleeding if the patient does not have any risk factors
• EEG

References:^[4][10]

Medical therapy ^[11]

• Reverse anticoagulation
• Blood pressure management ^[11]
  • Systolic BP > 220 mm Hg → rapidly lower to 140–160 mm Hg
  • Systolic BP 150-220 mm Hg → rapidly lower to 140 mm Hg
  • Recommended agents: IV labetalol, nicardipine, enalapril, and/or hydralazine
• Maintain euvolemia
• Avoid/treat hyponatremia
• Maintain normoglycemia
• If there are signs of elevated ICP (e.g., Cushing triad)
  • Consider intubation with hyperventilation
  • Head elevation (30°)
  • IV mannitol
  • Removal of CSF (e.g., via lumbar puncture)
  • See ICP management
• Antiepileptic drugs: for seizures

Surgical therapy ^[11]

• Craniotomy and clot evacuation
  • Indications
    • Signs of brain herniation (e.g., Cushing triad)
    • Brainstem compression
    • Obstructive hydrocephalus
    • Cerebellar hemorrhage with progressive neurological deterioration
    • Cerebellar hemorrhage extension > 3 cm ^[11]
  • Patients with hemorrhage in the basal ganglia or the internal capsule should generally not undergo surgical clot removal. ^[10]
• If hydrocephalus is present: ventricular drain, serial LPs, or permanent ventriculoperitoneal shunt may be indicated

Patients with signs of brain herniation should be operated on immediately!

References:^{[12][10][11][13]}

• Elevated intracranial pressure and brain herniation
• Intraventricular hemorrhage → hydrocephalus
• Recurrent hemorrhage
• Vasospasm and cerebral ischemia
• Dysphagia; : can lead to aspiration of food and pneumonia
• Seizures
• Hydrocephalus
• SIADH
• Deep vein thrombosis
• See complications of stroke

References:^{[8][10][11][21]}

We list the most important complications. The selection is not exhaustive.