Intracranial Hemorrhage Workup

  • Author: David S Liebeskind, MD; Chief Editor: Helmi L Lutsep, MD   more...
 
Updated: Nov 17, 2011
 

Laboratory Studies

  • Complete blood count (CBC) with platelets: Monitor for infection and assess hematocrit and platelet count to identify hemorrhagic risk and complications.
  • Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy.
  • Serum chemistries including electrolytes and osmolarity: Assess for metabolic derangements, such as hyponatremia, and monitor osmolarity for guidance of osmotic diuresis.
  • Toxicology screen and serum alcohol level if illicit drug use or excessive alcohol intake is suspected: Identify exogenous toxins that can cause intracerebral hemorrhage.
  • Screening for hematologic, infectious, and vasculitic etiologies in select patients: Selective testing for more uncommon causes of intracerebral hemorrhage.
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Imaging Studies

Parenchymal imaging

  • CT scan
    • CT scan readily demonstrates acute hemorrhage as hyperdense signal intensity (see image below). Multifocal hemorrhages at the frontal, temporal, or occipital poles suggest a traumatic etiology. Intracranial hemorrhage. CT scan of right frontal Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
    • Hematoma volume in cubic centimeters can be approximated by a modified ellipsoid equation: (A x B x C)/2, where A, B, and C represent the longest linear dimensions in centimeters of the hematoma in each orthogonal plane.
    • Perihematomal edema and displacement of tissue with herniation also can be appreciated.
    • Iodinated contrast may be injected to increase screening yield for underlying tumor or vascular malformation.
    • CT angiography "spot sign" may be used to predict growth of intracerebral hematomas.[5]
  • MRI
    • The MRI appearance of hemorrhage on conventional T1 and T2 sequences evolves over time because of chemical and physical changes within and around the hematoma (see Table 1 below).
    • Conventional T1 and T2 sequences are not highly sensitive to hemorrhage in the first few hours, but newer gradient refocused echo sequences appear to be able to detect intracerebral hemorrhage reliably within the first 1-2 hours of onset (see following images). Intracranial hemorrhage. Fluid-attenuated inversioIntracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation. Intracranial hemorrhage. Fluid-attenuated inversioIntracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage due to sickle cell disease.
    • AVMs and cavernous angiomas may be identified by the presence of multiple flow voids adjacent to the hematoma.
    • Paramagnetic contrast may be injected to increase screening yield for underlying tumor or vascular malformation.
    • Gradient echo sequences may reveal multiple foci of hypointensity attributable to hemosiderin deposition from prior silent cerebral microbleeds. A multilobar distribution of hypointense foci on gradient echo imaging may provide supportive evidence of cerebral amyloid angiopathy, while multiple deep foci may suggest an underlying hypertensive arteriopathy.
    • MRI studies incorporating gradient echo or susceptibility-weighted sequences may be used as the sole imaging modality for patients with acute stroke, readily identifying intracranial hemorrhage.
    • Permeability techniques, including use of source perfusion imaging data, may be used to detect blood-brain derangements that precede hemorrhagic transformation after thrombolysis.[6] This MRI reveals petechial intracerebral hemorrhagThis MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis. This MRI reveals hemorrhagic transformation of an This MRI reveals hemorrhagic transformation of an ischemic infarct. This CT scan and MRI revealed midbrain intracerebrThis CT scan and MRI revealed midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated with a cavernous angioma.

Table 1. MRI Appearance of Intracerebral Hemorrhage (Open Table in a new window)

PhaseTimeHemoglobinT1T2
Hyperacute< 24 hoursOxyhemoglobin (intracellular)Iso or hypoHyper
Acute1-3 daysDeoxyhemoglobin (intracellular)Iso or hypoHypo
Early subacute>3 daysMethemoglobinHyperHypo
Late subacute>7 daysMethemoglobin (extracellular)HyperHyper
Chronic>14 daysHemosiderin (extracellular)Iso or hypoHypo
  • Vessel imaging
    • CT angiography permits screening of large and medium-sized vessels for AVMs, vasculitis, and other arteriopathies.
    • MR angiography permits screening of large and medium-sized vessels for AVMs, vasculitis, and other arteriopathies.
    • Conventional catheter angiography definitively assesses large, medium-sized, and sizable small vessels for AVMs, vasculitis, and other arteriopathies.
    • Consider catheter angiography for young patients, patients with lobar hemorrhage, patients without a history of hypertension, and patients without a clear cause of hemorrhage who are surgical candidates. Angiography may be deferred for older patients with suspected hypertensive intracerebral hemorrhage and patients who do not have any structural abnormalities on CT scan or MRI.
    • Timing of angiography depends on clinical status and neurosurgical considerations.
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Other Tests

ECG frequently identifies cerebrum-induced dysrhythmia or cardiac injury.

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Procedures

  • Lumbar puncture in the setting of IVH may reveal xanthochromia and a biochemical profile similar to that observed in subarachnoid hemorrhage.
  • Ventriculostomy allows for external ventricular drainage in patients with intraventricular extension of blood products. Intraventricular administration of thrombolytics may assist clot removal.
  • Endoscopic hematoma evacuation may be a promising ultra-early stage treatment for intracerebral hemorrhage that improves long-term prognosis.[7]
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Histologic Findings

  • Gross examination reveals focal accumulation of blood with adjacent destruction of parenchyma.
  • Microscopically, bleeding sites appear as round collections of platelets surrounded by fibrin.
  • Charcot-Bouchard microaneurysms may be seen at bifurcations of distal lateral lenticulostriate vessels in hypertensive intracerebral hemorrhage.
  • Lobar hemorrhages of cerebral amyloid angiopathy may reveal pathological deposition of beta-amyloid protein within the media of small cortical and meningeal vessels.
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Staging

Table 2. Grading of Subependymal Hemorrhage (Open Table in a new window)

GradeHemorrhage Location
ISubependymal hemorrhage
IIIntraventricular hemorrhage without ventriculomegaly
IIIIntraventricular hemorrhage with ventriculomegaly
IVIntraventricular hemorrhage with parenchymal hemorrhage
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Contributor Information and Disclosures
Author

David S Liebeskind, MD  Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California, Los Angeles, David Geffen School of Medicine; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center

David S Liebeskind, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Jeffrey L Saver, MD, FAHA, FAAN  Professor of Neurology, Director, UCLA Stroke Center, University of California, Los Angeles, David Geffen School of Medicine

Jeffrey L Saver, MD, FAHA, FAAN is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, and National Stroke Association

Disclosure: University of California The University of California Regents receive funds for consulting services on clinical trial design provided to Telecris, Ev3, and CoAxia. Consulting

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Howard S Kirshner, MD  Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Selim R Benbadis, MD  Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Pfizer Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting

Chief Editor

Helmi L Lutsep, MD  Professor, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

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Intracranial hemorrhage. CT scan of right frontal intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.
Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.
Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage due to sickle cell disease.
This MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.
This CT scan and MRI revealed midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated with a cavernous angioma.
This MRI reveals hemorrhagic transformation of an ischemic infarct.
Table 1. MRI Appearance of Intracerebral Hemorrhage
PhaseTimeHemoglobinT1T2
Hyperacute< 24 hoursOxyhemoglobin (intracellular)Iso or hypoHyper
Acute1-3 daysDeoxyhemoglobin (intracellular)Iso or hypoHypo
Early subacute>3 daysMethemoglobinHyperHypo
Late subacute>7 daysMethemoglobin (extracellular)HyperHyper
Chronic>14 daysHemosiderin (extracellular)Iso or hypoHypo
Table 2. Grading of Subependymal Hemorrhage
GradeHemorrhage Location
ISubependymal hemorrhage
IIIntraventricular hemorrhage without ventriculomegaly
IIIIntraventricular hemorrhage with ventriculomegaly
IVIntraventricular hemorrhage with parenchymal hemorrhage
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