Intracerebral Hemorrhage

Intracerebral hemorrhage (ICH) refers to a spontaneous or traumatic bleed into the brain parenchyma and is the 2nd-most common cause of cerebrovascular accidents (CVAs), commonly known as stroke, after ischemic CVAs. Trauma, hypertension, vasculopathy, vascular malformations, tumors, coagulopathy, and hemorrhagic conversion of ischemic stroke may all be causative factors. Clinical presentation may vary depending on the size and location of the hemorrhage and may range from headache, neurologic signs and symptoms, and altered level of consciousness to coma. Treatment includes stabilization, stopping or reversing of anticoagulation, blood pressure control, monitoring in a neurologic ICU, and possible neurosurgical intervention. Intracerebral hemorrhage is associated with significant morbidity and mortality.

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Definition and Epidemiology


Intracerebral hemorrhage (ICH) refers to a spontaneous or traumatic bleed into the brain parenchyma and is the 2nd-most common cause of cerebrovascular accidents (CVAs).

Deep ICH:

  • Accounts for ⅔ of the cases of ICH
  • Affects the deeper structures within the cranial vault:
    • Basal ganglia
    • Internal capsule
    • Brain stem
    • Cerebellum

Lobar ICH:

  • Accounts for ⅓ of the cases of ICH
  • Affects structures of the cerebral cortex and the superficial subcortical structures
  • Involves 1 or more lobes of the brain


  • Spontaneous (atraumatic) ICH accounts for approximately 10% of CVAs.
  • Incidence:
    • Approximately 12–20 per 100,000 individuals
    • Doubles every 10 years in individuals 35 years and older
    • In the US, the incidence varies by ethnicity (highest to lowest):
      • Chinese and Japanese Americans
      • African Americans
      • Mexican Americans
      • Non-Hispanic White Americans
  • Slightly more common in men than in women


Risk factors

  • Hypertension:
    • Most important risk factor
    • More than doubles the risk for ICH
  • Vasculopathy
  • Advanced age
  • Prior CVA
  • Coagulopathy:
    • Anticoagulant therapy
    • Antiplatelet therapy (minor increase in risk)
    • Thrombolytics
    • Inherited bleeding disorders
    • Chronic liver disease
  • CKD
  • History of falls
  • Obesity
  • Low cholesterol levels (especially LDL)
  • Lifestyle factors:
    • Sedentary lifestyle
    • Heavy dependence on alcohol
    • Tobacco use
    • Use of stimulant drugs:
      • Cocaine
      • Amphetamines
      • Sympathomimetics

Leading causes

  • Hypertensive vasculopathy:
    • Most common cause
    • Association with deep ICH is greater than that with lobar ICH.
    • Affected vessels include branches of:
      • Basilar artery
      • Posterior vertebral arteries
      • Middle cerebral artery
    • Affected vessels largely supply:
      • Pons
      • Midbrain
      • Thalamus
      • Globus pallidus
      • Putamen
      • Caudate nucleus
      • Cerebellar nuclei
    • Accelerates degenerative changes in the cerebral arterial/arteriolar branch points
    • Increased risk in the setting of comorbid vasculitis and/or coagulopathy
  • Cerebral amyloid angiopathy:
    • 2nd-most common cause
    • Association with lobar ICH is greater than that with deep ICH.
    • More common in the elderly
    • Amyloid accumulation in the arterioles of the cortex is causative.
    • Affected individuals are prone to recurrent ICH.

Other causes

  • Vascular malformations:
    • Arteriovenous malformations
    • Cavernous malformations
  • Thrombosis of the cerebral vein:
    • Most common in individuals with thrombophilia
    • Thrombosis increases venous pressure and leads to venous capillary rupture.
  • Hemorrhagic transformation of ischemic CVAs:
    • Common in large ischemic infarcts with significant associated cerebral edema
    • Common in ischemic infarcts of embolic origin
  • Primary tumors:
    • Glioma
    • Glioblastoma
    • Primary CNS lymphoma
    • Pineal tumors
    • Pituitary tumors
    • Meningioma
    • Acoustic neuroma
  • Metastatic tumors:
    • Melanoma
    • Lung carcinoma
    • Choriocarcinoma
    • Renal cell carcinoma
    • Thyroid carcinoma
  • Infection of CNS structures:
    • Meningitis
    • Encephalitis
    • Brain abscess
  • Mycotic aneurysms:
    • Originate from the emboli from infective endocarditis
    • May seed and infect the arterial wall causing weakening and aneurysm formation
  • Cerebral vasculitis: from the primary CNS or systemic vasculitis
  • Cerebral hypoperfusion syndrome:
    • May occur in chronic carotid artery disease after revascularization
    • Previously hypoperfused tissue accommodates poorly to the increased cerebral perfusion pressure.
  • Reversible vertebral vasoconstriction syndrome (RVCS):
    • Rare
    • Transient arterial narrowing that leads to thunderclap headache presentation
    • Vasoconstriction may cause hemorrhagic and/or ischemic parenchymal insults.


In the absence of trauma, cerebral parenchymal bleed generally results from the rupture of small penetrating arteries.

Vascular rupture

Vascular rupture often occurs at or near the bifurcation of the affected arterioles and is attributed to degenerative vascular changes associated with:

  • Common vascular risk factors:
    • Advancing age
    • Hypertension
    • Diabetes
    • Smoking
  • Hypertensive vasculopathy:
    • Cumulative effect of aging and vascular shear forces
    • Hyperplasia of the intimal layer
    • Hyaline deposition in the vessel wall
    • Focal vessel wall necrosis
  • Cerebrovascular amyloid deposition:
    • Deposition of amyloid proteins between the media and adventitia
    • Subsequent extension into and degradation of the smooth muscle layer
    • Affects small arteries, arterioles, and capillaries
    • Manifestations include perivascular inflammation, microaneurysms, and fibrinoid necrosis.

Hematoma expansion

Causes a mass effect leading to:

  • Increased intracranial pressure (ICP)
  • Neurologic deterioration
  • Possible herniation

Perilesional edema

  • Multiple contributing factors:
    • Mass effect
    • Perilesional neuronal ischemia
    • Release or accumulation of:
      • Vasoactive mediators (i.e., inflammatory vasodilators)
      • Cytotoxic mediators (i.e., cytokines)
  • May persist for days to weeks after the initial bleeding insult
  • Decreased perfusion to the perilesional cerebral parenchyma causes a secondary ischemic insult.

Vasogenic and cytotoxic mediator accumulation

  • Promotes edema adjacent to the hematoma
  • Disrupts the blood–brain barrier
  • Causes neuronal sodium pump failure leading to neuronal death

Cessation of bleeding

  • Occurs via the intrinsic homeostatic pathways
  • Vascular tamponade is imposed by the cranial vault.
  • Impaired/delayed by the presence of coagulopathy (iatrogenic or pathologic)
  • Impaired/delayed by the presence of severely elevated blood pressure

Clinical Presentation

The signs and symptoms of ICH depend on the anatomical location and size of the hemorrhage.

General symptoms and signs

  • Symptoms:
    • Higher likelihood of occurrence and in presenting severely in larger hemorrhages compared with smaller hemorrhages:
      • Headache
      • Nausea/vomiting
      • Altered level of consciousness
      • Neck pain/stiffness
    • Onset is most common at routine levels of exertion.
    • Hypertensive bleed: emotional or physical stress/exertion
    • Smaller/slower bleed: insidious onset of symptoms over minutes
    • Larger bleed: rapid progression of symptoms
  • Signs:
    • Severe blood pressure elevation
    • Meningismus
    • Altered level of consciousness
    • Seizure
    • Focal neurologic deficit
    • Progressive neurologic deterioration

Specific neurological findings

The following findings suggest rapidly progressive neurological impairment due to elevated ICP:

  • Pupillary palsy
  • Extraocular movement palsy
  • Progressive drowsiness
  • Cushing triad:
    • Bradycardia
    • Respiratory depression
    • Hypertension

Cardiac manifestations

  • ECG abnormalities:
    • ST-T wave inversions
    • QT interval prolongation
    • Ventricular dysrhythmia
  • Echocardiographic findings:
    • Reduced left ventricular ejection fraction
    • Focal or global wall motion abnormalities
  • Elevated cardiac biomarkers (generally, mild elevation):
    • Cardiac enzymes:
      • Creatine kinase-MB (CKMB)
      • Troponin-I
      • Troponin-T
      • Troponin-C


Intracerebral hemorrhage should be suspected in any individual presenting with neurologic signs or symptoms suggestive of a CVA. Prompt diagnosis is critical, as ICH is associated with significant morbidity and mortality.


Noncontrast head CT:

  • Should be performed emergently
  • To distinguish between ischemic CVAs and ICH
  • Findings suggesting rapidly progressive neurological impairment due to elevated ICP:
    • Cerebellar hemorrhage:
      • > 3 cm in diameter
      • With neurologic deterioration
      • Compression of the brainstem
      • Ventricular obstruction leading to hydrocephalus
    • Intraventricular hemorrhage:
      • Ventricular enlargement indicating hydrocephalus
      • Neurologic deterioration
    • Supratentorial (hemispheric) hemorrhage:
      • Neurological deterioration
      • Brain compression
      • Hydrocephalus

Follow-up imaging:

  • Repeat CT/MRI appropriate for:
    • Evaluation of neurologic deterioration
    • Confirmation of hematoma stabilization
  • Brain MRI with contrast is the modality of choice to evaluate the underlying cause of ICH.
  • CT with contrast may be an option if MRI is contraindicated.
  • CTA or MRA to evaluate for vascular abnormalities

Laboratory evaluation

  • CBC
  • Comprehensive metabolic panel:
    • Electrolytes
    • BUN/creatinine
    • Hepatic transaminases
    • Glucose
  • Coagulation studies:
    • PT and INR
    • PTT
  • Urinalysis
  • Urine toxicology screen

Cardiac evaluation

  • Baseline ECG
  • Cardiac enzymes to evaluate for myocardial ischemia
  • Echocardiogram


Electroencephalography is indicated to evaluate seizures and unexplained encephalopathy.


Acute ICH is an emergent neurologic situation that may sometimes require surgical intervention. Failure of prompt treatment could result in hemorrhagic expansion, parenchymal brain injury, elevated ICP, brain herniation, and ultimately death.


  • Evaluate and stabilize the affected individual using advanced trauma life support (ATLS) or advanced cardiac life support (ACLS) protocols.
  • Airway management and respiratory support, if indicated
  • Stop/reverse all anticoagulants/antiplatelet agents.
  • Line placement (peripheral IV, central venous catheter, arterial line)
  • Emergent neurosurgical consultation:
    • Surgical clinical decision-making
    • Placement of an ICP-monitoring device
    • Emergent CSF drainage for:
      • Severely elevated ICP
      • Obstructive hydrocephalus

General management

  • Noncontrast head CT as soon as possible
  • Assessment:
    • Baseline and serial neurologic examination
    • Repeat noncontrast CT immediately if deterioration is detected.
  • Cessation of bleeding:
    • Stop/reverse anticoagulants/antiplatelet agents.
    • Order baseline coagulation studies.
  • Prophylactic measures:
    • Elevate the head of the bed.
    • Sedate agitated individuals.
    • Treat fever.
  • Maintain eunatremia.
  • Prophylactic osmotic therapy:
    • Administration of hypertonic saline and/or mannitol
    • Administer prophylactic osmotic therapy:
      • If severe neurologic impairment on presentation
      • If rapid neurologic deterioration is detected
      • If there is a delay in imaging
      • If neurosurgical evaluation is delayed
  • Hyperventilation:
    • Induced by manipulation of ventilator settings
    • Induces cerebral vasoconstriction → reduced cerebral blood volume
    • Hyperventilation is a temporizing measure reserved for:
      • Individuals with acute brain herniation (until better definitive therapy is available)
      • Individuals with neurologic deterioration awaiting either urgent surgery or central venous access for osmotherapy

Emergent neurosurgical interventions

  • Placement of an invasive ICP monitor:
    • Intraventricular monitor (gold standard)
    • Intraparenchymal device
    • Subarachnoid bolts
  • CSF drainage in case of:
    • Severely elevated ICP
    • Obstructive hydrocephalus

Blood pressure control

  • Blood pressure elevation may be the cause of hemorrhage.
  • Conversely, increased ICP may cause blood pressure elevation.
  • Elevated blood pressure may be necessary to maintain cerebral perfusion in the setting of cerebral edema.
  • Pain due to ICH may also contribute to blood pressure elevation.
  • Choice of medication:
    • Systolic blood pressure > 160 mm Hg: nicardipine
    • Systolic blood pressure < 160 mm Hg: labetalol

Surgical intervention

  • CSF drainage:
    • Generally performed for obstructive hydrocephalus
    • Obstructive hydrocephalus may be seen in:
      • Thalamic hemorrhage → compression of the 3rd ventricle
      • Cerebellar hemorrhage → compression of the 4th ventricle
      • Extension of ICH into the ventricular space(s)
  • Craniectomy with hematoma evacuation
  • Other potential interventions:
    • Craniotomy with endoscopic hemorrhage aspiration
    • CT-guided stereotactic aspiration

Seizure management

  • Individuals with ICH often experience seizures:
    • Early seizures in the course of management:
      • Usually self-limiting
      • Attributed to acute neurochemical changes associated with ICH
    • Status epilepticus during the course of management
    • Late seizures after ICH stabilization:
      • Usually recurrent and also known as “post-stroke epilepsy”
      • Attributed to scarring/gliosis after ICH
  • Seizure prophylaxis is not recommended.
  • Acute (early) ICH-related seizures: immediate IV administration of antiepileptics
  • Post-stroke (late) seizures: long-term antiepileptic therapy


  • Mortality:
    • 30-day mortality rate: 30%–50%
    • 10-year survival rate: < 20%
  • Morbidity:
    • Residual neurologic impairment and associated disability
    • Cognitive impairment
  • Risk factors for poor outcomes:
    • Advanced age
    • Severe baseline neurologic impairment
    • Early neurologic deterioration
    • Premature or early withdrawal of support
    • Use of anticoagulants/antiplatelet agents
    • Hematoma characteristics:
      • Large volume
      • Cerebellar location
      • Infratentorial location
      • Intraventricular extension
      • Early rebleeding

Differential Diagnosis

  • Ischemic stroke: an ischemic infarct of the cerebral parenchyma caused by the occlusion of a cerebral artery by atherosclerotic lesions or cardioembolic emboli. Ischemic stroke presents with neurologic deficits and/or altered mental status/altered level of consciousness that depends on the size and location of the infarct. Diagnosis is clinical and confirmed by neuroimaging. Management includes initial stabilization, possible cerebrovascular intervention, and addressing identifiable underlying etiologies (severe hypertension, embolus), and cardiovascular risk factors.
  • Other hemorrhagic cerebral conditions: Carotid/cerebral artery dissection, epidural hemorrhage, intraparenchymal hemorrhage, and subdural hemorrhage are other hemorrhagic manifestations of the cerebral vasculature that can present with neurologic deficits and/or altered mental status/altered level of consciousness. Diagnosis is clinical and confirmed by neuroimaging. Management depends on the hemorrhagic etiology and includes initial stabilization, neurosurgical/endovascular consultation, management of ICP, and monitoring in a neurologic ICU.
  • Hypertensive encephalopathy: neurologic deficits and/or altered mental status/altered level of consciousness that present in the setting of severe hypertension. Diagnosis is based on the presence of elevated blood pressure and neurologic signs and symptoms. Neuroimaging is useful to rule out ischemic or hemorrhagic CVAs.


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