Sections

Intracranial Hemorrhage

Sections Intracranial Hemorrhage
Overview
Presentation
- History
- Physical
- Causes
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DDx
Workup
Treatment
Medication
Follow-up
Questions & Answers
Media Gallery
Tables
References

Workup

Laboratory Studies

See the list below:

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.

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 intracerebral hemorrhage complicating thrombolysis of an ischemic stroke.

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Patients with mild blunt head trauma and preinjury anticoagulant or antiplatelet use are at increased risk of intracranial hemorrhage and should undergo urgent and liberal CT scanning.^[6]

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.^[7]

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

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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.^[8]

This MRI reveals petechial intracerebral hemorrhage (ICH) due to cerebral venous thrombosis.

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This MRI reveals hemorrhagic transformation of an ischemic infarct.

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This CT scan and MRI revealed midbrain intracerebral hemorrhage (ICH) and intraventricular hemorrhage (IVH) associated with a cavernous angioma.

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

Phase	Time	Hemoglobin	T1	T2
Hyperacute	< 24 hours	Oxyhemoglobin (intracellular)	Iso or hypo	Hyper
Acute	1-3 days	Deoxyhemoglobin (intracellular)	Iso or hypo	Hypo
Early subacute	>3 days	Methemoglobin	Hyper	Hypo
Late subacute	>7 days	Methemoglobin (extracellular)	Hyper	Hyper
Chronic	>14 days	Hemosiderin (extracellular)	Iso or hypo	Hypo

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

See the list below:

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.^[9]

Histologic Findings

See the list below:

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 (Open Table in a new window)

Grade	Hemorrhage Location
I	Subependymal hemorrhage
II	Intraventricular hemorrhage without ventriculomegaly
III	Intraventricular hemorrhage with ventriculomegaly
IV	Intraventricular hemorrhage with parenchymal hemorrhage

Treatment & Management

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Media Gallery

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.

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Author

David S Liebeskind, MD, FAAN, FAHA, FANA Professor of Neurology and Director, Neurovascular Imaging Research Core, Director, Vascular Neurology Residency Program, Department of Neurology, University of California, Los Angeles, David Geffen School of Medicine; Director, UCLA Outpatient Stroke and Neurovascular Programs; Director, UCLA Cerebral Blood Flow Laboratory; Associate Neurology Director, UCLA Stroke Center

David S Liebeskind, MD, FAAN, FAHA, FANA 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, Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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 Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

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

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

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2; Physician Advisory Board for Coherex Medical; National Leader and Steering Committee Clinical Trial, Bristol Myers Squibb; Abbott Laboratories, advisory group.

Additional Contributors

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, National Stroke Association

Disclosure: Received the university of california regents receive funds for consulting services on clinical trial design provided to covidien, stryker, and lundbeck. from University of California for consulting.