eMedicine Specialties > Neurology > Neurological Emergencies

Intracranial Hemorrhage: Differential Diagnoses & Workup

Author: David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center
Contributor Information and Disclosures

Updated: Apr 27, 2009

Differential Diagnoses

Acute Stroke Management
Lumbar Puncture (CSF Examination)
Amyloid Angiopathy
Magnetic Resonance Imaging in Acute Stroke
Anisocoria
Moyamoya Disease
Arteriovenous Malformations
Neonatal Injuries in Child Abuse
Blood Dyscrasias and Stroke
Neurological Sequelae of Infectious Endocarditis
Cardioembolic Stroke
Posttraumatic Epilepsy
Cerebellar Hemorrhage
Reperfusion Injury in Stroke
Cerebral Aneurysms
Status Epilepticus
Cerebral Venous Thrombosis
Stroke Anticoagulation and Prophylaxis
CNS Melanoma
Subarachnoid Hemorrhage
Cocaine
Subdural Empyema
Dissection Syndromes
Subdural Hematoma
Epidural Hematoma
Thrombolytic Therapy in Stroke
Head Injury
Vein of Galen Malformation
Herpes Simplex Encephalitis
Hydrocephalus

Other Problems to Be Considered

Vasculitis

Workup

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.

Imaging Studies

Parenchymal imaging

  • CT scan
    • CT scan readily demonstrates acute hemorrhage as hyperdense signal intensity (see Media file 1). 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.

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      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).
    • 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 Media files 2-3).

      Intracranial hemorrhage. Fluid-attenuated inversi...

      Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI illustration of intracerebral hemorrhage associated with a right frontal arteriovenous malformation.

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      Intracranial hemorrhage. Fluid-attenuated inversi...

      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 inversi...

      Intracranial hemorrhage. Fluid-attenuated inversion-recovery, T2-weighted, and gradient echo MRI depiction of left temporal intracranial hemorrhage due to sickle cell disease.

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      Intracranial hemorrhage. Fluid-attenuated inversi...

      Intracranial 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

[#Table1]Table 1. MRI Appearance of Intracerebral Hemorrhage

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Table
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
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.

Other Tests

ECG frequently identifies cerebrum-induced dysrhythmia or cardiac injury.

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

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.

Staging

Table 2. Grading of Subependymal Hemorrhage

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Table
GradeHemorrhage Location
ISubependymal hemorrhage
IIIntraventricular hemorrhage without ventriculomegaly
IIIIntraventricular hemorrhage with ventriculomegaly
IVIntraventricular hemorrhage with parenchymal hemorrhage
GradeHemorrhage Location
ISubependymal hemorrhage
IIIntraventricular hemorrhage without ventriculomegaly
IIIIntraventricular hemorrhage with ventriculomegaly
IVIntraventricular hemorrhage with parenchymal hemorrhage

More on Intracranial Hemorrhage

Overview: Intracranial Hemorrhage
Differential Diagnoses & Workup: Intracranial Hemorrhage
Treatment & Medication: Intracranial Hemorrhage
Follow-up: Intracranial Hemorrhage
Multimedia: Intracranial Hemorrhage
References
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Further Reading

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Keywords

intracranial hemorrhage, intracerebral hemorrhage, intraparenchymal hemorrhage, intracranial hematoma, intracerebral hematoma, intraparenchymal hematoma, epidural hematoma, subdural hematoma, subarachnoid hemorrhage, intraventricular hemorrhage, intracranial pressure

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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 at Los Angeles; 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.

Medical Editor

Jeffrey L Saver, MD, Director, Stroke Center, Professor, Department of Neurology, University of California at Los Angeles Medical Center
Jeffrey L Saver, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, and National Stroke Association
Disclosure: Boehringer-Ingelheim - Secondary Prevention Consulting fee Consulting; Talacris Consulting fee Consulting; ImaRx Consulting fee Consulting

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

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: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
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: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; 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; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

 
 
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