Sections

Workup

Laboratory Studies

Laboratory tests should include a complete blood count, a metabolic panel, and—particularly in patients taking anticoagulants—coagulation studies (ie, prothrombin time or international normalized ratio [INR] and an activated partial thromboplastin time).^[1]

Imaging Studies

Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be obtained on an emergent basis. Brain imaging aids diagnosing hemorrhage, and it may identify complications such as intraventricular hemorrhage, brain edema, or hydrocephalus. Either noncontrast computed tomography (NCCT) scanning or magnetic resonance imaging (MRI) is the modality of choice.

Computed tomography (CT)-scan studies can also be performed in patients who are unable to tolerate a magnetic resonance examination or who have contraindications to MRI, including pacemakers, aneurysm clips, or other ferromagnetic materials in their bodies. Additionally, CT-scan examination is more easily accessible for patients who require special equipment for life support. See the image below.

Noncontrast computed tomography scan of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region, with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial magnetic resonance imaging scan (middle image) again demonstrates the hemorrhage, with surrounding high-signal edema. The coronal gradient-echo image (right) demonstrates susceptibility related to the hematoma, with markedly low signal adjacent the left caudate head. Gradient-echo images are highly sensitive for blood products.

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CT angiography and contrast-enhanced CT scanning may be considered for helping identify patients at risk for hematoma expansion. Extravasation of contrast within the hematoma indicates high risk.

When clinical or radiologic findings suggest an underlying structural lesion, useful techniques include CT angiography, CT venography, contrast-enhanced CT scanning, contrast-enhanced MRI, magnetic resonance angiography (MRA), or magnetic resonance venography.^[1]

Conventional angiography is the gold standard in evaluating for cerebrovascular disease and for providing less-invasive endovascular interventions. This modality can be performed to clarify equivocal findings or to confirm and treat disease seen on MRA, CTA, transcranial Doppler, or neck ultrasonograms. However, Zhu et al found that in patients with spontaneous intracranial hemorrhage, angiographic yield was significantly lower in patients older than 45 years and those who had preexisting hypertension.^[29]

Although the traditional approach to excluding underlying vascular abnormalities in patients with spontaneous intracerebral hemorrhage is to use digital subtraction angiography (DSA) in the acute and subacute phases, Wong et al found that MRA was able to detect most structural vascular abnormalities in the subacute phase in most patients. Consequently, they recommend MRA as the screening test.

Treatment & Management

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Media Gallery

Axial noncontrast computed tomography scan of the brain of a 60-year-old man with a history of acute onset of left-sided weakness. Two areas of intracerebral hemorrhage are seen in the right lentiform nucleus, with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle, with intraventricular extension of the hemorrhage.
Noncontrast computed tomography scan of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region, with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial magnetic resonance imaging scan (middle image) again demonstrates the hemorrhage, with surrounding high-signal edema. The coronal gradient-echo image (right) demonstrates susceptibility related to the hematoma, with markedly low signal adjacent the left caudate head. Gradient-echo images are highly sensitive for blood products.
Noncontrast computed tomography scan (left) obtained in a 75-year-old man who was admitted for stroke demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right), with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted, with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.
Noncontrast computed tomography (CT) scanning was performed emergently in a 71-year-old man who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT scan (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. There is diffuse loss of gray-white differentiation. The fluid-attenuated inversion-recovery (FLAIR) image (right) demonstrates high signal throughout the cortical sulci and in the basilar cisterns, as well as in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage; the suppression of high cerebrospinal fluid signal aids in making subarachnoid hemorrhage more conspicuous than do conventional magnetic resonance imaging sequences.
Computed tomographic angiography examination and subsequent cerebral angiography were performed in 71-year-old man who presented with acute onset of severe headache and underwent rapid neurologic deterioration. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery injection. Balloon-assisted coil embolization was performed.
Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.
Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and sylvian triangle. The pericallosal artery has been described as arising distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: (1) the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery, (2) A2 extends to the junction of the rostrum and genu of the corpus callosum, (3) A3 extends into the bend of the genu of the corpus callosum, and (4) A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The sylvian triangle overlies the opercular branches of the middle cerebral artery, with the apex representing the sylvian point.
Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SCA) arise distally from the basilar artery before its bifurcation into the posterior cerebral arteries.
Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The middle cerebral artery can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities).
Frontal view from a cerebral angiogram in a 41-year-man who presented 7 days earlier with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm (which was treated with surgical clipping). There is significant narrowing of the proximal left ACA, left M1 segment, and left supraclinoid internal carotid artery, indicating vasospasm.
Angiographic view in a 41-year-man who presented 7 days earlier with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm (which was treated with surgical clipping). Superimposed road map image demonstrates placement of a wire across the left M1 segment and balloon angioplasty. The left proximal ACA and supraclinoid internal carotid artery (ICA) were also angioplastied, and intra-arterial verapamil was administered. Follow-up image on the right after treatment demonstrates resolution of the left M1 segment and distal ICA, which are now widely patent. Residual narrowing is seen in the left proximal ACA.
A cerebral angiogram was performed in a 57-year-old man with a family history of subarachnoid hemorrhage and who was found on previous imaging to have a left distal internal carotid artery (ICA) aneurysm. The lateral projection from this angiogram demonstrates a narrow-necked aneurysm arising off the posterior aspect of the distal supraclinoid left ICA, with an additional nipplelike projection off the inferior aspect of the dome of the aneurysm. There is also a mild, lobulated dilatation of the cavernous left ICA.
Follow-up cerebral angiogram after coil embolization in a 57-year-old man with a left distal internal carotid artery aneurysm. Multiple coils were placed with sequential occlusion of the aneurysm, including the nipple at its inferior aspect. A small amount of residual filling is noted at the proximal neck of the aneurysm, which may thrombose over time.

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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

Erik D Schraga, MD Staff Physician, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates

Disclosure: Nothing to disclose.

Chief Editor

Andrew K Chang, MD, MS Vincent P Verdile, MD, Endowed Chair in Emergency Medicine, Professor of Emergency Medicine, Vice Chair of Research and Academic Affairs, Albany Medical College; Associate Professor of Clinical Emergency Medicine, Albert Einstein College of Medicine; Attending Physician, Department of Emergency Medicine, Montefiore Medical Center

Andrew K Chang, MD, MS is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American Academy of Pain Medicine, American College of Emergency Physicians, American Geriatrics Society, American Pain Society, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Acknowledgements

J Stephen Huff, MD Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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.

Richard S Krause, MD Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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

Denise Nassisi, MD Assistant Professor, Department of Emergency Medicine, Mount Sinai Medical Center

Denise Nassisi, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Heart Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

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

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