INTRACEREBRAL HEMORRHAGE

Diagnosis of intracerebral hemorrhage

Created 27/04/2021, last revision 20/11/2023

  • for patients presenting with stroke-like symptoms, rapid neuroimaging using CT or MRI is recommended to confirm the diagnosis of spontaneous intracerebral hemorrhage (ICH)
  • the detection of intracerebral bleeding itself by imaging methods is easy; the diagnostic evaluation is focused on determining the underlying etiology

Physical Examination and focused history

Focused personal history

  • time of symptoms onset (or time patient was last seen normal)
  • symptoms
    • headache
      • thunderclap: aneurysm, RCVS, rarely CVST
      • slower onset: mass lesion, CVST, ischemic stroke with hemorrhagic transformation
    • focal neurologic deficits
    • seizures
    • decreased level of consciousness
  • vascular risk factors
    • prior ICH or SAH
    • hypertension
    • hyperlipidemia
    • diabetes
    • metabolic syndrome
    • imaging biomarkers (e.g., cerebral microbleeds)
  • medications
    • anticoagulant drugs
    • thrombolytic drugs
    • antiplatelet agents
    • NSAIDs
    • vasoconstrictors (associated with RCVS): triptans, SSRIs, decongestants, stimulants, phentermine, sympathomimetics
    • 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, , it is likely to be calcification, foreign body, etc. Densities of acute hematoma and calcification in plexus
    • resorption of the hematoma occurs within days to weeks; accompanied by a decrease in its density
    • hematoma becomes isodense within 1-6 weeks
    • in the chronic stage, a hypodense pseudocyst with atrophy of the surrounding brain tissue is usually found at the site of the resorbed hematoma (indistinguishable 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 location of bleeding:
    • typical “hypertensive” bleeding   Typical bleeding localisation in patiens with hypertension 
      • putamen, thalamus, internal capsule (lenticulostriate arteries)   Lenticulostriatal arteries
      • brainstem, cerebellum
      • concomitant hypertension + age > 55 (65) years almost rule out other etiologies
    • atypical bleeding → search for structural cause (CTA/MRI+MRA/DSA)
      • 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 AComA with perforation of the terminal lamina and bleeding into the third ventricle   Primary intraventricular hemorrhage (IVH)
      • age < 50 years in the absence of hypertension despite typical ICH location
      • large and early vasogenic edema
Thalamic hemorrhage

Hemorrhage in the basal ganglia

Cerebellar hemorrhage

Pontine hemorrhage

Intraventricular hemorrhage (hemocephalus)

Lobar hematoma with the island sign

DDx of a primary ICH and arterial hemorrhagic (HI) infarction

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DDx of a primary ICH and venous hemorrhagic infarction

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CT angiography (CTA)

  • CTA (+/- venography) is useful for the identification of the potential source of bleeding (vascular malformations) or cerebral venous thrombosis
  • it can be performed as part of the baseline CT scan in patients with:
    • age < 50 years
    • atypical hematoma location/appearance
    • hematoma in typical location without history of hypertension
    • isolated intraventricular hemorrhage
  • in atypical parenchymal hematomas, add MRI+MRA or DSA if baseline CTA is negative
    • it may be reasonable to start with MRI and MRA to establish a non-macrovascular cause of ICH (such as CAA, deep perforating vasculopathy, cavernous malformation, or malignancy)
    • MRI may help to rule out the hemorrhagic transformation of ischemia
  • search for markers of hemorrhage expansion
    • spot sign on source CTA images or post-contrast CT images Spot sign on CTA Spot sign on CTA (top), progression of IC hematoma in the same patient (bottom) Spot sign on CTA
    • “leakage sign” may also serve as a predictor of continued bleeding   Leakage sign on CTA  [Orito, 2016]
      • initial CTA + delayed phase (5 min interval)
      • a 10% increase in HU density indicates ongoing bleeding

Magnetic resonance imaging (MRI)

  • MRI of the brain is highly sensitive for detecting intracerebral hemorrhage
  • the appearance of hemorrhage 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 (GRE) can detect early bleeding with similar sensitivity to NCCT ⇒  MRI can be used as the initial imaging method in stroke programs (Kidwell, 2004)     → see here
    • hyperacute hematoma:
      • T1 isointense
      • T2/FLAIR – isointense or slightly 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 location 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 workup
  • DSA should be performed if CTA/MRA suggests a macrovascular cause of bleeding  (AHA/ASA 2022 1/C-LD)
    • DSA confirms the diagnosis of a malformation 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 features (stenosis of a draining vein,  intranidal or perinidal aneurysm, etc.)
  • DSA is performed when CTA/MRA is negative or equivocal, and there is a reasonable suspicion of a bleeding source  Cerebral arteriovenous malformation (DSA)
    • age < 50 years in the absence of hypertension
    • atypical location or appearance of the hematoma
    • typical location with no 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 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 outcome
    • 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) 
    • specific anti-Xa (xabans)
  • 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 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 potential (exclude peripartum angiopathy, eclampsia, HELLP syndrome, and cerebral sinus thrombosis)

Others

  • 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/