• in patients presenting with stroke-like symptoms, rapid neuroimaging with CT or MRI is recommended to confirm the diagnosis of spontaneous ICH
  • detection of intracerebral bleeding is easy on imaging methods, and the diagnostic evaluation is focused on the determination of etiology

Physical Examination and focused history

  • focused personal history (see tab below)
  • quick physical examination →  Early management of patients with suspected stroke
    • vital signs – assessment of airway, breathing, circulation
    • a general physical examination focusing on the head, heart, lungs, abdomen, and extremities
    • a focused neurological examination + NIHSS
    • assess GCS in patients with impaired LOC
  • time of symptoms onset (or time patient was last seen normal)
  • symptoms
    • headache
      • Thunderclap: Aneurysm, RCVS, some instances of CVST
      • Slower onset: Mass lesion, some instances of CVST, ischemic stroke with hemorrhagic transformation
    • Focal neurologic deficits
    • Seizures
    • Decreased level of consciousness
  • vascular risk factors Ischemic stroke
    • prior ICH or SAH
    • hypertension
    • hyperlipidemia
    • diabetes
    • metabolic syndrome
    • imaging biomarkers (e.g., cerebral microbleeds)
  • medications
    • anticoagulant drugs
    • thrombolytic drugs
    • antiplatelet agents
    • NSAIDs
    • vasoconstrictive agents (associated with RCVS): triptans, SSRIs, decongestants, stimulants, phentermine, sympathomimetic drugs
    • antihypertensives (as a marker of chronic hypertension)
    • estrogen-containing oral contraceptives (risk of CVST)
  • cognitive impairment or dementia (possible amyloid angiopathy)
  • substance use
    • smoking
    • alcohol use
    • marijuana (associated with RCVS)
    • sympathomimetic drugs (amphetamines, methamphetamines, cocaine)
  • liver disease, uremia, malignancy, and hematologic disorders (→ secondary coagulopathy)

Computed tomography (CT)

Non-contrast CT scan (NCCT)

  • baseline examination objectives:
    • detect and localize the hematoma
    • assess its type, volume, probable etiology, risk of complications
    • assess the prognosis (→ ICH scales)
  • fresh blood is hyperdense on NCCT   Density of an acute hematoma on NCCT
    • increased density is caused by the high hemoglobin content of retracted clot or sedimented blood
    • the density of the hematoma in the acute stage is typically around 70-80HU; if the lesion has a density > 100-120HU, probable calcification, foreign body, etc. are depicted  Densities of acute hematoma and calcification in plexus
    • resorption of the hematoma occurs within days to weeks; it is accompanied by a decrease in its density
    • within 1-6 weeks, hematoma becomes isodense
    • in the chronic stage, we usually find a hypodense pseudocyst with atrophy of the surrounding brain tissue at the site of the absorbed hematoma (it cannot be distinguished from old ischemia)  Chronic intracerebral hemorrhage on NCCT
  • vasogenic edema gradually appears around the subacute hematoma as a hypodense area  ICH with collateral edema on NCCT Edema surrounding hemorrhage
  • type and localization of bleeding:
    • typical “hypertonic” bleeding   Typical bleeding localisation in patiens with hypertension 
      • putaminal and thalamic, internal capsule (lenticulostriate artery)   Lenticulostriatal arteries
      • brainstem, cerebellum
      • concomitant hypertension + age > 55 years almost rule out other etiologies
    • atypical bleeding
      • lobar hematomas  Repeated lobar hematomas in patient with CAA
      • primary intraventricular hemorrhage (IVH) – exclude AVM or small aneurysm in the ventricular wall or SAH from ACoA with perforation of the terminal lamina and blood propagation into the third ventricle   Primary intraventricular hemorrhage (IVH)
      • age < 50 years in the absence of hypertension despite localization
      • → search for the cause (CTA/MRI+MRA/DSA)
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CT angiography (CTA)

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Magnetic resonance imaging (MRI)

  • MRI of the brain is highly sensitive for detecting intracerebral hemorrhage
  • hemorrhage appearance depends on the stage of hemoglobin breakdown (see table below)
    • oxy-Hb is weakly diamagnetic, deoxy-Hb has 4 unpaired electrons per iron atom and is strongly paramagnetic
  • gradient recalled echo sequence (GRE) can detect early bleeding with similar sensitivity to NCCT ⇒  MRI can be used as an initial imaging method in stroke program  (Kidwell, 2004)     → see here
    • hyperacute hematoma:
      • T1 isointense
      • T2/FLAIR – isointense or mildly hyperintense
      • GRE hypointense (initially only hypointense rim + core of heterogenous signal intensity (due to the diamagnetic oxyhemoglobin)
      • DWI hyperintense, ADC hypointense
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Digital subtraction angiography (DSA)

  • indicated in search for the source of bleeding (consider patients’ age, clinical condition, comorbidities, prognosis, the localization and extent of bleeding)
  • DSA is often replaced by CTA/MRA, which can be performed quickly and without significant risk as part of the initial diagnostic evaluation
  • DSA should be performed if CTA/MRA suggests a macrovascular cause of bleeding  (AHA/ASA 2022 1/C-LD)
    • DSA confirms the diagnosis and provides additional information about the main tributaries, presence, type, and extent of the nidus, type of flow (high or low flow), venous drainage, and other pathologies (stenosis of a draining vein,  intranidal or perinidal aneurysm, etc.)
  • DSA is performed when CTA/MRA is negative or unclear, and there is a reasonable suspicion of a bleeding source  Cerebral arteriovenous malformation (DSA)
    • age < 50 years, with the absence of hypertension
    • atypical localization or appearance of the hematoma
    • typical localization without a history of hypertension
    • isolated intraventricular hemorrhage  (AHA/ASA 2022 1/BNR)
  • in patients with spontaneous ICH and a negative DSA and no clear microvascular diagnosis or other structural lesions, it may be reasonable to perform a repeat DSA 3-6 months after ICH to identify a previously obscured vascular lesion

Other examinations and tests

Blood tests

  • complete blood count (check platelets)
    • admission anemia is associated with hemorrhagic expansion and poor outcomes
    • thrombocytopenia is associated with increased mortality
  • coagulation tests  (to exclude anticoagulant-related hemorrhage and coagulopathy from other causes)
    • APTT, Quick, INR, TT, fibrinogen (especially after thrombolysis)
    • ECT and Hemoclot (dabigatran) → see here
    • specific anti-Xa (xabans) → see here
  • glucose
    • admission hyperglycemia is associated with unfavorable short- and long-term outcome
  • urea nitrogen, osmolality
  • liver tests (coagulopathy secondary to liver failure)
  • ionogram including Ca2+, Mg2+
  • creatinine/estimated glomerular filtration rate (GFR)
    • renal failure on admission also is associated with poor functional outcome
    • possible altered clearance of DOACs
  • D-dimers
  • cardiac enzymes + troponin
  • inflammatory markers (ESR, CRP) – infective endocarditis?
  • urine toxicology screen (sympathomimetic drugs are associated with ICH)
  • pregnancy test in a woman of childbearing age (exclude peripartum angiopathy, eclampsia, HELLP syndrome, and cerebral sinus thrombosis)


  • 12-lead ECG on admission, followed by continuous ECG monitoring
  • pulse oximetry
  • blood pressure monitoring (invasive/noninvasive)
  • chest x-ray

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Diagnosis of intracerebral hemorrhage
link: https://www.stroke-manual.com/intracerebral-hemorrhage-diagnosis/