Intracerebral hemorrhage

Last updated: September 11, 2023

Summarytoggle arrow icon

Intracerebral hemorrhage (ICH) refers to bleeding within the brain parenchyma. The term should not be confused with intracranial hemorrhage, which is a broader term that encompasses bleeding within any part of the skull, i.e., extradural, subdural, subarachnoid, or intracerebral bleeding. The most significant risk factor for spontaneous ICH is arterial hypertension. Symptoms are often nonspecific (e.g., headache); however, depending on the affected vessel and cerebral region, focal neurological deficits (e.g., hemiparesis) may occur. Compared with ischemic stroke, patients with ICH are more likely to present with severe headache and have rapidly progressing symptoms. The initial imaging investigation of choice is CT head without contrast, which typically shows a hyperdense mass lesion. Treatment involves management of the underlying and associated conditions (e.g., controlling hypertension, reversing coagulopathy) in order to limit hematoma expansion and prevent secondary brain injury. In severe cases, neurosurgical intervention may be required. Approximately half of patients with spontaneous ICH die within 30 days of symptom onset. Traumatic ICH may result from traumatic brain injury (TBI) and is managed similarly to spontaneous ICH.

See also “Overview of intracranial hemorrhage” and “Overview of stroke” for more information.

Definitiontoggle arrow icon

Epidemiologytoggle arrow icon

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

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon


Pathophysiologytoggle arrow icon

Clinical featurestoggle arrow icon

Managementtoggle arrow icon

For the approach to patients with suspected traumatic ICH, see “Management of traumatic ICH.”

Initial evaluation [7][8][9]

Consider the sudden onset of focal neurological deficits a vascular event until proven otherwise and evaluate patients as promptly as possible (preferably within the so-called “golden hour”). [10][11][12]

Patients with signs of brain herniation should be evaluated immediately for neurosurgical intervention!


Acute stabilizationtoggle arrow icon

Acute stabilization should begin immediately after symptom onset, in parallel with diagnostic measures, with the goal of reducing hematoma expansion and limiting secondary brain injury. [7]

Remember to stop all anticoagulants and antiplatelet medication, including aspirin, in patients with ICH.

Platelet transfusion is not routinely indicated in patients with normal platelet counts taking antiplatelet agents (e.g., aspirin, clopidogrel). [7][20][21]

Diagnosticstoggle arrow icon

Approach to ICH diagnostics [7][9][13]
Time interval from initial presentation Laboratory studies Imaging
Within the first hour
  • CT head without contrast
  • MRI head (alternative)
Hours to days

Characteristic neuroimaging findings [24]

Variation in ICH density on imaging over time [25][26]
Time since ICH Hematoma density

CT without contrast

MRI (T2 weighted)
Hyperacute (< 24 hours)



Acute (1–3 days)

Hyperdense with fluid level and hypodense perifocal edema

Hypointense with a hyperintense border

Early subacute (> 3 days to 1 week)

Hyperdense becoming isodense


Late subacute (weeks to months)

Isodense or hypodense


Chronic (> months)



  • Additional possible features
    • Midline shift and/or mass effect; (if significant, this should raise suspicion for impending herniation)
    • Intraventricular extension [9]

Angiography findings

Angiography may be performed to assess for signs of further bleeding and structural abnormalities in patients with suspected underlying pathology (e.g., patients aged < 55 years and those without risk factors for ICH). [7]

  • CTA spot sign [27]
    • Definition: localized area of enhancement visible within an intracerebral hemorrhage only after administration of IV contrast
    • Implication: indicates active hemorrhage; is a predictor of hematoma expansion [7][27][28]
  • Aneurysms or other vascular lesions

Treatmenttoggle arrow icon


Detection and management of complications

Common complications following spontaneous ICH [7]
Complication Screening and management
Dysphagia [29]


Cardiac abnormalities
Electrolyte abnormalities

Venous thromboembolism (VTE)

Hematoma expansion

Prophylactic anticonvulsants are not recommended in patients with ICH. [7]

Surgical management [7]

Neurosurgical consultation is advised for acute ICP management (see “Acute stabilization”) and definitive management. Evacuation of the hematoma may be appropriate depending on the size, location, and associated clinical features of the ICH.

Hematoma evacuation

Decompressive craniotomy

Acute management checklisttoggle arrow icon

Management of traumatic ICHtoggle arrow icon

The management of traumatic ICH is similar to the management of spontaneous ICH, with some modifications.

Differential diagnosestoggle arrow icon

See “Differential diagnoses of stroke.”

The differential diagnoses listed here are not exhaustive.

Complicationstoggle arrow icon

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

Prognosistoggle arrow icon

  • 30-day mortality ranges from 25% to 50%. [41][42]
  • Patients aged > 65 years and those with large hematomas and low GCS scores (≤ 11) typically have poor outcomes. [41][42]
  • The ICH score is used to assess the severity of bleeds, and, in conjunction with other features, to estimate the patient's prognosis. [7]
ICH score [43][44]
Variable Findings Points
GCS score 3–4 2
5–12 1
13–15 0
ICH volume ≥ 30 cm3 1
< 30 cm3 0
Intraventricular hematoma Yes 1
No 0
ICH of infratentorial origin Yes 1
No 0
Patient age ≥ 80 years 1
< 80 years 0

Total ICH score: 0–6

Predicted 30-day mortality

  • Score = 0: 0%
  • Score = 1: 13%
  • Score = 2: 26%
  • Score = 3: 72%
  • Score = 4: 97%
  • Score = 5: 100%
  • Score = 6: estimated to be 100%

The ICH score was designed to assess ICH severity and aid clinical communication; it should not be used in isolation to determine prognosis!

Referencestoggle arrow icon

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