• intracerebral hemorrhage accounts for 10-20% of all strokes
  • 30-day mortality is 40%, annual mortality ~50-60%, and the severe deficit is common in survivors  [Broderick, 1993]
    • bleeding on antithrombotic therapy is associated with higher mortality  (including DOACs and antiplatelet therapy) – HR 1.3 on antiplatelet therapy, 1.4 on anticoagulation  [Apostolaki-Hansson]
  • ICH is a heterogeneous group in terms of etiology, clinical presentation, and therapy
  • posterior fossa hematoma is always an acute, life-threatening condition
    • limited compliance in the posterior fossa can quickly lead to herniation upwards, transtentorially, or downward through the foramen magnum
Typical bleeding localization in patiens with hypertension


Classification according to the etiology
  • primary (80%)
    • hypertensive arteriolopathy (70%)
    • amyloid angiopathy (CAA)
    • eclampsia
  • secondary (20%)
    • bleeding into a pre-existing lesion (tumor, ischemia)
    • coagulopathies (incl. drug-induced disorders)
    • malformations etc.
Classification according to ICH localization
Supratentorial hemorrhage (85%)

  • cortical, lobar (30-35%)
  • deep hematomas – basal ganglia, internal capsule, and thalamus (55%)
Infratentorial hemorrhage (15%)

  • cerebellar (5-10%)
  • brainstem (5%)
Intraventricular hemorrhage (primary, secondary)
Intracerebral hemorrhage


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Clinical presentation

Reliable clinical differentiation of ischemia from hemorrhage is not possible
  • sudden, apoplectic onset
  • personal history
    • dementia? (amyloid angiopathy)
    • hematologic disorder, antiplatelet or anticoagulant therapy?
    • history of hypertension?
    • alcoholism, hepatopathy, renal disease?
    • history of bleeding or known malformations?
    • recent CEA or CAS? (hyperperfusion injury)
  • focal neurologic symptoms (hemiparesis, aphasia, hemianopsia, etc., depending on hematoma location)
  • altered level of consciousness (up to 50%) – more common in ICH compared to ischemic stroke
    • the patient is usually somnolent or even soporous
    • initial coma occurs with extensive thalamic or brainstem hemorrhage destructing the reticular formation
  • hypertension or hypertensive crisis (in up to 90%)
    • acutely decompensated chronic hypertension
    • stress-induced hypertension in otherwise normotensive patients
  • nausea and/or vomiting (24-50%)
  • headache (40%)
  • epileptic seizures (about 6%)
  • early improvement or fluctuation is not typical for ICH
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Bleeding progression

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Brain edema and intracranial hypertension

  • edema and intracranial hypertension develop soon after the onset of bleeding, with a peak between days 2-6
  • bleeding in the posterior fossa may lead to an acute obstructive hydrocephalus

→ see more here

Obstructive (non-communicating) hydrocephalus

  • the highest risk is present with:
    • extensive intraventricular hemorrhage (primary or secondary)  Obstructive hydrocephalus following IVH
    • extensive cerebellar or brainstem hematomas with direct compression of the cerebral aqueduct
  • ⇒ indication for acute surgery (EDV)

Extracranial (systemic) complications

  • extracranial complications are similar to those appearing in ischemic stroke → see here
  • some notes regarding blood pressure:
    • elevated blood pressure (BP) may be a consequence of decompensation of hypertension or a stress reaction in previously normotensive individuals
    • elevated BP on admission does not automatically imply a hypertensive etiology of the bleeding
    • normal BP on admission increases the likelihood of bleeding from any source  ⇒ perform vascular imaging (CTA, MRA, or DSA)


  • always make an initial rough estimate of the prognosis
  • ICH mortality ~ 50%, up to 70% for recurrent ICH
  • prognosis depends on the following:
    • age and general biological status
    • location and size of the hematoma (ICH score) and initial level of consciousness
      • GCS < 9 and ICH volume > 60ml ~ 90% mortality
      • GCS ≥ 9 and ICH volume < 30ml ~ 17% mortality
    • presence of spot sign, blend sign, and black hole sign
    • etiology of bleeding (SMASH-U)
  • risk of bleeding recurrence depends on the etiology
    • the estimated recurrence risk ranges from 1.2 to 3% per year across undifferentiated patients with ICH (with the highest event rate in the first year after bleeding)
    • ↑ risk:  lobar location of the initial ICH, older age, presence, number, and lobar location of microbleeds on MRI, presence of disseminated cortical superficial siderosis on MRI, poorly controlled hypertension, Asian or black race, presence of apolipoprotein E ε2 or ε4 alleles
ICH recurrence risk (annual)
Hypertonic bleeding (precise BP correction reduces RR by 50%) 1.1-2 %
Cerebral amyloid angiopathy (CAA)
7.5-10 %
AV malformation (AVM)
6-18 %
Cerebral cavernous malformation (CCM)
4.8 %
Dural AV fistula 0.15 %

ICH prevention

  • long-term blood pressure (BP) treatment is required in all ICH patients (AHA/ASA 2022 1/B-R)
  • start therapy ASAP
    • combine pharmacological and nonpharmacological approaches
  • long-term goal BP < 130/80 mmHg  (AHA/ASA 2022 2a/B-NR)

    • aim for BP below 120/80 mm Hg in younger patients without major comorbidities (Teo, 2022)
  • reduce salt intake
  • avoid smoking, alcohol, and drug abuse
  • treat sleep apnea if present
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  • there is not enough evidence to discontinue the hypolipidemic therapy  (AHA/ASA 2015 IIb/C)
  • the risks and benefits of statin therapy on ICH outcomes and recurrence are uncertain compared with the overall prevention of cardiovascular events  (AHA/ASA 2022 2b/B-NR)
  • in patients with spontaneous ICH, regular long-term use of nonsteroidal anti-inflammatory drugs (NSAIDs) is potentially harmful because of the increased risk of ICH (AHA/ASA 2022 3/B-NR)
  • the presence and extent of cerebral microbleeds and cortical superficial siderosis predict subsequent symptomatic ICH
  • incorporate available MRI results into decision-making regarding stroke prevention plans (avoid warfarin, apply strict BP management, etc.)  (AHA/ASA 2022 2b/C-LD)

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Etiology and clinical presentation of intracerebral hemorrhage
link: https://www.stroke-manual.com/intracerebral-hemorrhage-etiology-clinical-presentation/