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

Classification

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)
    • 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

Etiology

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Clinical presentation

Reliable clinical differentiation of ischemia from hemorrhage is not possible
  • sudden, apoplectic onset
  • personal history
    • dementia? (amyloid angiopathy)
    • hematological disorder, antiplatelet or anticoagulant therapy?
    • hypertension?
    • alcoholism, hepatopathy, renal disease?
    • previous bleeding or known malformation?
    • recent CEA or PTA? (hyperperfusion injury)
  • focal neurological symptoms (hemiparesis, aphasia, hemianopsia, etc. – depending on hematoma localization)
  • 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 in extensive thalamic or brainstem hemorrhage destructing reticular formation
  • hypertension or hypertensive crisis (in up to 90%)
    • acutely decompensated chronic hypertension
    • stress reaction in otherwise normotensive patients
  • nausea and/or vomiting (24-50%)
  • headaches (40%)
  • epileptic seizures (about 6%)
  • early improvement or fluctuations are not typical for ICH
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Complications

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 in:
    • extensive intraventricular hemorrhages (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 consequence of decompensation of hypertension or stress reaction in so far normotensive individuals
    • elevated BP on admission does not automatically imply a hypertensive etiology of bleeding
    • normal BP on admission increases the likelihood of bleeding from some source  ⇒ perform vessel imaging (CTA, MRA, or DSA)

Prognosis

  • always perform an initial rough estimate of the prognosis
  • ICH mortality ~ 50%, up to 70% in recurrent ICH
  • prognosis depends on:
    • age and overall biological status
    • location and size of the hematoma (ICH score) and initial impairment 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 the hemorrhage)
    • ↑ 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
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 non-pharmacological approaches
  • long-term target BP < 130/80 mmHg  (AHA/ASA 2022 2a/B-NR)
  • reduce salt uptake
  • avoid smoking, alcohol and drug abuse
  • treat sleep apnea if present
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  • there is not enough evidence to discontinue the hypolipidemic medication  (AHA/ASA 2015 IIb/C)
  • the risks and benefits of statin therapy on ICH outcomes and recurrence relative to overall prevention of cardiovascular events are uncertain (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 extension of cerebral microbleeds and cortical superficial siderosis predicted subsequent symptomatic ICH
  • incorporate available MRI results in decision-making about stroke prevention plans (avoid warfarin, apply strict BP management, etc.)  (AHA/ASA 2022 2b/C-LD)
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