Hemorrhagic Stroke in Emergency Medicine Clinical Presentation

  • Author: David S Liebeskind, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Aug 17, 2011
 

History

Obtaining an adequate history includes the onset and progression of symptoms as well as an assessment for risk factors and possible causative events. These include previous transient ischemic attack (TIA) and stroke, hypertension, diabetes, smoking, arrhythmia and valvular disease, illicit drug use, and risk factors for thrombosis. History of trauma, even if minor, may be important, as extracranial arterial dissections can result in ischemic stroke.

Symptoms alone are not specific enough to distinguish ischemic from hemorrhagic infarction. However, generalized symptoms, including nausea, vomiting, and headache as well as an altered level of consciousness may indicate increased intracranial pressure and are more common with hemorrhagic strokes or large ischemic strokes. Seizures are more common in hemorrhagic stroke than in ischemic stroke and occur in up to 28% of hemorrhagic strokes, generally at the onset of the intracerebral hemorrhage or within the first 24 hours.

Other, more focal, symptoms of stroke include weakness or paresis that may affect a single extremity, one half of the body, or all 4 extremities; facial droop; monocular or binocular blindness; blurred vision or visual field deficits; dysarthria and trouble understanding speech; vertigo or ataxia; and aphasia. The neurologic deficits reflect the area of the brain typically involved, and stroke syndromes for specific vascular lesions have been described.

Symptoms of subarachnoid hemorrhage may include sudden onset of headache, signs of meningismus with nuchal rigidity, photophobia and pain with eye movements, nausea, and vomiting. The most common clinical scoring systems for grading aneurysmal subarachnoid hemorrhage are the Hunt and Hess grading scheme and the World Federation of Neurosurgeons (WFNS) grading scheme, which incorporates the Glasgow Coma Scale. The Fisher Scale incorporates findings from noncontrast CT (NCCT) scans.

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Physical Examination

Intracerebral hemorrhage may be clinically indistinguishable from ischemic stroke. Hypertension is commonly a prominent finding. An acute onset of neurologic deficit, altered level of consciousness/mental status, or coma is more common with hemorrhagic stroke than with ischemic stroke. Often, this is due to an increase in intracranial pressure. Meningismus may result from blood in the ventricles.

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Focal neurologic deficits

The type of deficit depends upon the area of brain involved. If the dominant hemisphere (usually the left) is involved, a syndrome consisting of right hemiparesis, right hemisensory loss, left gaze preference, right visual field cut, and aphasia may result. If the nondominant (usually the right) hemisphere is involved, a syndrome of left hemiparesis, left hemisensory loss, right gaze preference, and left visual field cut may result. Nondominant hemisphere syndrome may also result in neglect when the patient has left-sided hemi-inattention and ignores the left side. If the cerebellum is involved, the patient is at high risk of herniation and brainstem compression. Herniation may cause a rapid decrease in the level of consciousness, apnea, and death.

Specific brain sites and deficits involved in hemorrhagic stroke include the following:

  • Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, aphasia, neglect, or apraxia
  • Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion
  • Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia
  • Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion
  • Brainstem - Quadriparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability
  • Cerebellum - Ataxia (usually beginning in the trunk), ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness

Other signs of cerebellar or brainstem involvement include the following:

  • Gait or limb ataxia
  • Vertigo or tinnitus
  • Nausea and vomiting
  • Hemiparesis or quadriparesis
  • Hemisensory loss or sensory loss of all 4 limbs
  • Eye movement abnormalities resulting in diplopia or nystagmus
  • Oropharyngeal weakness or dysphagia
  • Crossed signs (ipsilateral face and contralateral body)

Many other stroke syndromes are associated with intracerebral hemorrhage and range from mild headache to neurologic devastation. At times, a cerebral hemorrhage may present as a new-onset seizure.

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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.

Coauthor(s)

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.

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

Specialty Editor Board

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.

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

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.

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

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

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Axial noncontrast computed tomography scan of the brain in a 60-year-old male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage 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 image (middle image) redemonstrates 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 after a 75-year-old male was admitted for cerebrovascular accident 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 male 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, basilar cisterns and in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage, owing to the suppression of high cerebrospinal fluid signal lending to greater conspicuity of subarachnoid hemorrhage compared with conventional magnetic resonance image sequences.
The patient above subsequently underwent a computed tomographic angiography examination and subsequent cerebral angiography. 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 to arise 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: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; 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-male who presented 7 days before with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm 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 the same patient as above (image on left) with superimposed road map image to demonstrate placement of a wire across the left M1 segment and balloon angioplasty. The left proximal anterior communicating artery (ACA) and supraclinoid internal carotid artery (ICA) were also angioplastied and intraarterial 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 male 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 in the same patient as above following coil embolization. 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.
The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes, insula, and basal ganglia. The anterior cerebral artery (blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
 
 
 
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