• intracerebral hemorrhage (ICH) is characterized by spontaneous rupture of blood vessels within the cerebral parenchyma, leading to focal hematoma formation and subsequent mass effect
  • ICH accounts for approx. 10-20% of all strokes
  • the 30-day mortality is up to 40%, the annual mortality is ~50-60%, and severe deficits are common in survivors  [Broderick, 1993]
    • bleeding during antithrombotic therapy is associated with increased mortality (including DOACs and antiplatelets) – 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
  • a hematoma in the posterior fossa is always an acute, life-threatening condition
    • limited compliance can quickly lead to herniation upwards, transtentorially, or downward through the foramen magnum
Typical locations of bleeding in hypertensive patients

Intracranial vs. intracerebral hemorrhage

Intracranial hemorrhage refers to any bleeding within the skull, including the brain, its surrounding structures, and spaces. Intracerebral hemorrhage (ICH), a subset of intracranial hemorrhage, specifically denotes bleeding directly into the brain parenchyma.


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 location
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


  • hypertensive arteriolopathy is the most common cause of intracerebral hemorrhage (ICH)
  • the relative risk of ICH in a patient with arterial hypertension compared to a person without hypertension is approximately 4
  • hypertension leads to bleeding by two mechanisms:
    • rupture of an artery affected by chronic hypertension
    • acute or subacute severe hypertension leading to rupture of a previously unaffected artery (malignant hypertension)
  • typical localization: basal ganglia, thalamus, cerebellum, pons   Typical localisations of hypertonic bleeding  Lenticulo-striate arteries
    • a secondary extension of the hematoma into the ventricles (hemocephalus) or subarachnoid space is possible
  • hypertension leads to hypertrophy and degeneration of the media of small arteries (lipohyalinosis, fibrinoid necrosis)
  • the findings that suggest hypertensive etiology:
    • history of hypertension
    • typical ICH localization
    • absence of any other apparent cause of bleeding
    • left ventricular hypertrophy
    • leukoaraiosis on CT/MRI   Hypertensive small vessel disease (microangiopathy)
    • hypertensive retinopathy
    • high blood pressure on admission is not a conclusive indicator of hypertensive disease; it may be a result of stress reaction and intracranial hypertension
  • aneurysm
    • 20-40% of SAHs have an IC hematoma component   Combination of SAH and ICH
    • rarely, rupture manifests as isolated ICH  [Li, 2016]
  • vascular malformations
MRI 0.25-0.7%
rebleeding 4.5%
MRI, DSA 0.2-0.4%
DSA, CTA 2-4 %
rebleeding 6-18%
MRI very low
type I – very low
type II, III – up to 8%
Carotido-cavernous fistula (CCF) DSA, MRA very low
Vascular malformations
  • anticoagulants (LMWHs, UFH, warfarin, DOACs)
    • the risk of ICH with long-term anticoagulant therapy is ~2% (risk is lower with DOACs)
    • risk of major bleeding with warfarin is 1.7% in those aged < 75 years, ~4.2% in those aged > 75 years; the risk of ICH is 0.6 vs. 1.8 (according to SPAF II)
    • hematomas are often non-homogeneous and multilobar (with a positive black hole and blend sign)
  • antiplatelet therapy
    • bleeding is more common with dual antiplatelet therapy (DAPT) and in combination with other risk factors
  • fibrinolytics
    • risk of symptomatic ICH (sICH) in acute stroke treated with tPA is ~ 6%
  • other coagulation disorders
    • leukemia, liver disease (related to alcoholism)
    • thrombocytopenia or thrombocytopathy
  • cerebral amyloid angiopathy (CAA)     Cerebral amyloid angiopathy
    • age >60 years or a positive family history
    • cognitive deterioration
    • β-amyloid deposits in small and medium-sized cerebral arteries
    • lobar hematomas, repeated/multiple hemorrhages (including microscopic ones)
    • leukoaraiosis on MRI and/or microbleeds on GRE    Cortical and subcortical CMBs
    • risk of recurrence ~10%/year (higher in individuals with APOE E2 and E4 positivity)
  • intracranial artery dissection (which is more likely to cause SAH or a combination of SAH+ICH)
  • vasculitis (polyarteritis nodosa, Wegener’s granulomatosis, SLE, Henoch-Schönlein, syphilis, primary CNS granulomatosis, etc.)
    • usually, hemorrhagic transformation of ischemia that must be distinguished from a primary hematoma
  • occasionally, it may be difficult to distinguish between a traumatic hematoma and a spontaneous hematoma that was the cause of the fall
  • signs of a traumatic etiology:
    • history of significant head trauma
    • CT scan with hemorrhagic contusions in the frontal and temporal lobes +/- concomitant SDH, EDH, or a traumatic SAH   Post-traumatic hemorrhagic contusions 
    • hemosinus Post-traumatic hemosinus on the CT scan
    • skull fracture visible in the bone window Bone fracture (the CT scan in the bone window)
  • cocaine, pseudoephedrine, amphetamine
  • drugs often cause lobar hematomas
Etiologic Classification of Intracerebral Hemorrhage – SMASH-U [Meretoja, 2012]
incidence mortality at 3 months
Structural lesions (cavernous malformation, AVM) 5% 4 %
Medication (warfarin, DOAC, antiplatelet therapy) 14% 54 %
Cerebral Amyloid Angiopathy (CAA)
20% 22 %
Systemic disease (liver, kidney disease, thrombocytopenia/thrombocytopathies) 5% 44 %
Hypertension 35% 33 %
Undetermined 21% 30%

Clinical presentation

Reliable clinical differentiation of cerebral ischemia from hemorrhage is not possible
  • sudden, apoplectic onset
  • personal medical history
    • dementia? (potential 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? (risk of hyperperfusion injury)
  • focal neurologic symptoms (such as hemiparesis, aphasia, hemianopsia, etc., depending on hematoma location) →  Signs and symptoms of cerebral lesions
  • 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


Bleeding progression

  • about 1/3 of patients with ICH experience a 1/3 increase in hematoma within 3 hours of onset (2/3 of them within 1 hour) Asi u 1/3 pacientů s ICH dojde k nárůstu hematomu o 1/3 do 3 hodin (Kazui,1996)  [Kazui,1996]
    • perform a follow-up CT scan within 24 hours or immediately if the neurological status worsens
    • some protocols suggest performing a CT scan every 12 hours until the hematoma volume has stabilized
    • progression is most common in hematologic disorders but can also occur in typical hypertensive bleeding
  • progression of bleeding is associated with early neurological deterioration and poorer prognosis
  • radiologic predictors of progression:
  • hematoma progression in the following days is less typical and may indicate recurrent bleeding
    • particularly with hematologic disorders or vascular malformations (most commonly in aneurysms or AVMs)

Brain edema and intracranial hypertension

  • edema and intracranial hypertension develop shortly after the onset of bleeding, peaking between days 2 and 6
  • bleeding in the posterior fossa may lead to acute obstructive hydrocephalus

→ intracranial hypertension

Obstructive (non-communicating) hydrocephalus

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

Epileptic seizures

Extracranial (systemic) complications

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


  • always make an initial rough estimation of the prognosis
    • 30-day mortality 35-50%, up to 70% for recurrent ICH
  • prognosis depends on the following:
    • age and general biological status (incl. comorbidities)
    • initial level of consciousness (LOC)
    • ICH location
    • hematoma size (ICH score)
      • GCS < 9 and ICH volume > 60ml ~ 90% mortality
      • GCS ≥ 9 and ICH volume < 30ml ~ 17% mortality
      • poor outcome is associated with an ICH score of 4-6
    • presence of spot sign, blend sign, and black hole sign
    • etiology of bleeding (SMASH-U)
    • acute phase complications (sepsis, ischemic stroke, prolonged mechanical ventilation, etc.)
  • functional recovery after ICH is highest in the first few weeks to months (greatest within 30 days)
    • early and long-term rehabilitation and ergotherapy are essential
    • for assessing the functional outcome, the Modified Rankin Scale (mRS) is frequently used
  • assess cognitive functions, as impairment is frequently observed among patients after ICH

Risk of recurrence

  • risk of ICH recurrence depends on etiology and risk factors
  • the estimated recurrence risk  is  1.2-7% per year across undifferentiated patients with ICH (with the highest event rate occurring in the first year after bleeding)
  • risk factors for the recurrence of ICH
    • advanced age
    • race (Black, Asian)
    • poorly controlled hypertension
    • history of prior ICH and ischemic stroke
    • ICH location (nonlobar<lobar)
    • etiology (increased risk with coagulation disorders, CCA, brainstem cavernous malformations, Moyamoya disease, AVM, tumors)
    • imaging features (lobar microbleeds, leukoencephalopathy, cortical superficial siderosis)
    • CHKD (can be a marker of atherosclerotic disease)
    • genetic features (carriers of apolipoprotein-E e2 or e4 genotypes)
ICH recurrence risk (annual)
Hypertonic bleeding (precise BP correction reduces RR by 50%) 1.1-4 %
Cerebral amyloid angiopathy (CAA)
7.5-20 %
AV malformation (AVM)
6-18 %
Cerebral cavernous malformation (CCM)
Dural AV fistula 0.15 %

Follow up imaging

  • patients who fail to improve or deteriorate during the recovery phase need imaging to rule out recurrent bleeding
  • stabilized patients with hypertensive ICH don´t require additional imaging
    • features indicative of hypertensive bleeding: history of hypertension (HTN), subcortical microbleeds, no atypical imaging features, age ≥65 years
  • no definitively established etiology or baseline imaging features suggestive of an underlying cause require follow-up imaging performed after bleeding and edema have resolved
    • perform brain MRI  4-16 weeks after the ICH (incl. GRE/SWI and contrast-enhanced images);  if an underlying vascular cause is suspected, add noninvasive vascular imaging, such as CTA or MRA
    • MRI is optimal for detecting cerebral venous sinus thrombosis, vascular malformations, hemorrhagic transformation of an ischemic infarct, or neoplasms
    • contrast-enhanced CT of the brain is a reasonable alternative for those who are unable to undergo an MRI
  • stabilized CAA patients may not require additional imaging

Clinical features raising suspicion for an underlying cause

  • age <65 years
  • no history or new diagnosis of HTN
  • history of new-onset headaches
  • history of new-onset neurologic symptoms preceding ICH
  • thunderclap headache at the onset of hemorrhage
  • history of prior ICH (unless attributed to uncontrolled HTN or CAA)

Imaging features on baseline imaging raising suspicion for secondary cause of ICH

  • early perihematomal edema disproportional to the size of the hematoma
  • nonconfluent hemorrhage in the arterial vascular territory (probable ischemic infarction)
  • enhancement of intracranial vessels around ICH
  • multifocal hemorrhage
  • isolated intraventricular hemorrhage

ICH prevention

  • long-term precise blood pressure (BP) control is required in all ICH patients (AHA/ASA 2022 1/B-R)
    • this approach is supported by evidence from ischemic stroke prevention trials  (SPS3, RESPECT)
  • start therapy ASAP, combining pharmacological and nonpharmacological approaches
    • the first-choice drug is usually an ACE inhibitor; if not tolerated, use an angiotensin receptor blocker, thiazide diuretic, or calcium channel blocker
    • usually, a combination of drugs is necessary
  • acute BP management is discussed elsewhere (target 140-160 mmHg)
  • long-term BP should be maintained < 130/80 mmHg (AHA/ASA 2022 2a/B-NR)
  • aim for a BP < 120/80 mmHg in younger patients without major comorbidities (Teo, 2022)
  • a stepwise correction to achieve target values is suggested in the subacute phase (within 2 weeks)
  • outpatient monitoring is essential to ensure long-term proper BP control
  • reduced salt intake, healthy diet
  • cessation of smoking and excessive alcohol intake
  • treatment of sleep apnea, if present
  • regular physical activity
  • maintenance of a healthy body weight
  • avoidance of sympathomimetics
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  • epidemiological studies and clinical trials provide conflicting data
    • in patients with spontaneous ICH and an established indication for statin pharmacotherapy, the risks and benefits of statin therapy are uncertain (AHA/ASA guidelines 2022
    • the decision to use statins in patients with ICH depends on the individual assessment of the risk of ischemic events versus recurrent ICH
  • there is no strong evidence to discontinue the hypolipidemic therapy after ICH

    • a large 10-year nationwide cohort study from Taiwan found no association between statin dose and risk of recurrent ICH  (Tai, 201)
    • statins are associated with improved functional outcome and reduced mortality in patients with prior ICH  (Ziff, 2018)
    • data from the Danish registry show, that exposure to statins is not associated with an increased risk of recurrent ICH but was associated with a lower risk of any stroke (Gaist, 2023)
  • in patients with a high risk of hemorrhage (typically after recurrent parenchymal hematoma), a more cautious approach may be warranted, potentially involving alternative lipid-lowering drugs
  • 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)
  • prefer nonacetylated salicylates
  • 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
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