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Stroke, Hemorrhagic

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Last Updated: November 18, 2005

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AUTHOR INFORMATION

Section 1 of 9

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Author: Denise Nassisi, MD, Clinical Assistant Professor, Department of

Emergency Medicine, Mount Sinai Medical Center
Denise Nassisi, MD, is a member of the following medical societies: American
College of Emergency Physicians, American Heart Association, and Society for
Academic Emergency Medicine
Editor(s): Richard S Krause, MD, Program Director, Clinical Assistant Professor,
Department of Emergency Medicine, State University of New York at Buffalo;
Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine; J
Stephen Huff, MD, Associate Professor of Emergency Medicine and Neurology,
Department of Emergency Medicine, University of Virginia Health System; John
Halamka, MD, Chief Information Officer, CareGroup Healthcare System, Assistant
Professor of Medicine, Department of Emergency Medicine, Beth Israel Deaconess
Medical Center; Assistant Professor of Medicine, Harvard Medical School; and
Charles V Pollack, Jr, MD, MA, FACEP, Associate Professor of Emergency
Medicine, University of Pennsylvania School of Medicine; Chairman, Department of
Emergency Medicine, Pennsylvania Hospital
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Encephalitis

INTRODUCTION

Section 2 of 9

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Background: The terms intracerebral hemorrhage (ICH) and hemorrhagic stroke are
used interchangeably in this discussion and are regarded as a separate entity from
hemorrhagic transformation of ischemic stroke. ICH accounts for 10-15% of all
strokes and is associated with higher mortality rates than cerebral infarctions.
Patients with hemorrhagic stroke present with similar focal neurologic deficits but
tend to be more ill than patients with ischemic stroke. Patients with intracerebral
bleeds are more likely to have headache, altered mental status, seizures, nausea
and vomiting, and/or marked hypertension; however, none of these findings
distinguish reliably between hemorrhagic and ischemic strokes.
Pathophysiology: In ICH, bleeding occurs directly into the brain parenchyma. The
usual mechanism is thought to be leakage from small intracerebral arteries damaged
by chronic hypertension. Other mechanisms include bleeding diatheses, iatrogenic
anticoagulation, cerebral amyloidosis, and cocaine abuse. ICH has a predilection for
certain sites in the brain, including the thalamus, putamen, cerebellum, and brain
stem. In addition to the area of the brain injured by the hemorrhage, the surrounding
brain can be damaged by pressure produced by the mass effect of the hematoma. A
general increase in intracranial pressure may occur.
Frequency:

In the US: ICH accounts for 10-15% of all strokes. Recent reports indicate an
incidence exceeding 500,000 new strokes of all types per year.

Headache,
Migraine

Hypernatremi

Hyperosmolar
Hyperglycemi
Nonketotic Co
Hypertensive
Emergencies

Hypoglycemia

Hyponatremia
Labyrinthitis
Meningitis

Neoplasms, B

Stroke, Ischem

Subarachnoid
Hemorrhage
Subdural
Hematoma

Transient Isch
Attack

Mortality/Morbidity:

Stroke is a leading killer and disabler. Combining all types of stroke, it is the
third leading cause of death and the first leading cause of disability.

Morbidity is more severe and mortality rates are higher for hemorrhagic stroke
than for ischemic stroke. Only 20% of patients regain functional
independence.

The 30-day mortality rate for hemorrhagic stroke is 40-80%. Approximately

50% of all deaths occur within the first 48 hours.

Race: African Americans have a higher incidence of hemorrhagic and ischemic

strokes than other races in the United States. The incidence of hemorrhagic stroke in

Continuin
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Patient Educ

Stroke Center

Stroke Overvi

the Japanese population is increased.

Stroke Cause

Age: The risk of stroke increases with age.

Stroke Sympt

Stroke Treatm

CLINICAL

Section 3 of 9

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

History:

Patients' symptoms vary depending on the area of the brain affected and the
extent of the bleeding.

Hemorrhagic strokes are more likely to exhibit symptoms of increased

intracranial pressure than other types of stroke.

Headache, often severe and sudden onset

Nausea and/or vomiting

Seizures are more common in hemorrhagic stroke than in ischemic stroke.

They occur in up to 28% of hemorrhagic strokes and generally occur at the
onset of the ICH or within the first 24 hours.

Physical:

Intracerebral hemorrhage (ICH) may be clinically indistinguishable from

ischemic stroke.

Hypertension commonly is a prominent finding.

An altered level of consciousness or coma is more common with hemorrhagic

strokes than with ischemic strokes. Often, this is due to an increase in
intracranial pressure.
Meningismus may result from blood in the ventricles.

Focal neurologic deficits

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The type of deficit depends upon the area of brain involved.

If the dominant hemisphere (usually 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 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 also
may result in neglect when the patient has a 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.

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 ICH, ranging from
mild headache to neurologic devastation. At times, a cerebral
hemorrhage may present as a new-onset seizure.

Causes:

Hypertension (up to 60% of cases)

Advanced age (risk factor)

Cerebral amyloidosis (affects people who are elderly and may cause up to
10% of ICHs)

Coagulopathies (eg, due to underlying systemic disorders)

Anticoagulant therapy

Thrombolytic therapy for acute myocardial infarction (MI) and acute ischemic
stroke (can cause iatrogenic hemorrhagic stroke)

Abuse of cocaine and other sympathomimetic drugs

Arteriovenous malformation

Intracranial aneurysm

Vasculitis

Intracranial neoplasm

Bleeding due to a brain tumor

History of prior stroke (risk factor)

DIFFERENTIALS

Section 4 of 9

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Encephalitis
Headache, Migraine
Hypernatremia
Hyperosmolar Hyperglycemic Nonketotic Coma
Hypertensive Emergencies
Hypoglycemia
Hyponatremia
Labyrinthitis
Meningitis
Neoplasms, Brain
Stroke, Ischemic
Subarachnoid Hemorrhage
Subdural Hematoma
Transient Ischemic Attack
Other Problems to be Considered:
Postictal (Todd) paralysis
Hyperosmolality
WORKUP
Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Section 5 of 9

Lab Studies:

Complete blood count

Coagulation profile

Electrolytes

Serum glucose

Blood type and screen

Imaging Studies:

Noncontrast CT of the brain

o

Has been the modality of choice for imaging hemorrhagic stroke

Should be obtained on an emergent basis

Differentiates hemorrhagic stroke from ischemic strokes

Useful in distinguishing stroke from other intracranial pathology

Can identify virtually all intracerebral hematomas greater than 1 cm in diameter

MRI
o

Conventional MRI is not as sensitive for hemorrhage as CT scanning.

Recent progress has demonstrated that new MRI techniques are capable of accurately
diagnosing hemorrhagic stroke.

MRI, especially newer techniques such as diffusion-weighted imaging, has been shown
identify ischemic stroke earlier and more reliably than CT scanning. MRI is being utilized
increasing frequency in the evaluation of ischemic stroke.

Chest radiography

Other Tests:

Obtain an electrocardiogram (ECG) and begin cardiac monitoring. Cardiac dysrhythmias and
myocardial ischemia have a significant coincidence with stroke.

TREATMENT

Section 6 of 9

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Prehospital Care:

Identify and address, as clinically indicated, any compromise of ABCs.

Recognize signs and symptoms of stroke.

Notify the receiving hospital.

Rapid transport to the closest facility capable of providing appropriate stroke care (if applicable

In general, do not treat elevations of blood pressure (BP) in the field.

Emergency Department Care:

Assess ABCs. Address any compromise in patient's status as clinically indicated.

Establish intravenous (IV) access.

Obtain bedside glucose determination.

o

Hypoglycemia may mimic stroke.

Hyperglycemia has been associated with poorer outcomes in stroke patients.

Institute cardiac monitoring and obtain an ECG.

The use of prophylactic anticonvulsant therapy is controversial; some strongly believe that it sh
given to all patients. Phenytoin in conventional doses is commonly used.

Careful BP monitoring is important.

o
o
o
o
o

No controlled studies define optimum BP levels.

Greatly elevated BP is thought to lead to rebleeding and hematoma expansion.
Stroke patients may lose their cerebral autoregulation of cerebral perfusion pressure.
Although BP elevations may risk further hemorrhage, too rapid or aggressive BP lowerin
compromise cerebral perfusion.
The American Heart Association guidelines recommend intravenous antihypertensive tr
for patients with mean arterial pressure (MAP) > 130 mm Hg. MAP should be maintaine
90 mm Hg to ensure adequate cerebral perfusion.

Intubation should be performed for patients who demonstrate potential loss of airway protectiv

mechanisms or signs of brainstem dysfunction. If intubation is needed, rapid sequence intubat

should be performed with technique and medications aimed at limiting any increase in intracra
pressure.

Currently, no effective targeted therapy for hemorrhagic stroke exists. However, some prelimin
research indicates that treatment with hemostatic therapy may be effective. A recent preliminar
of treatment with recombinant factor 8 demonstrated reduced mortality and improved functiona
outcomes. Further studies are necessary to determine if this should be accepted as a clinical t
option.

Consultations:

Emergent neurosurgical or neurological consultation often is indicated; local referral patterns m

o

A potential treatment of hemorrhagic stroke is surgical evacuation of the hematoma. The

surgical treatment for supratentorial intracranial hemorrhage remains controversial. Out
in published studies are conflicting. A published meta-analysis of studies suggested som
promise for early surgical intervention. However, a recent study comparing early surgery
initial conservative treatment failed to demonstrate a benefit with surgery.

Surgical intervention for cerebellar hematoma has been shown to improve outcome. It c
lifesaving in the prevention of brainstem compression.

Need for invasive intracranial pressure monitoring should be assessed by the neurosurg

Need for emergent cerebral angiography should be assessed by the neurosurgeon. Pat
with no clear cause of the hemorrhage and who would otherwise be candidates for surg
should be considered for angiographic evaluation.

FOLLOW-UP
Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Further Inpatient Care:

ICU admission is mandatory.

o

Monitor for airway compromise.

Monitor and carefully address the patient's BP.

Reassess neurologic status frequently.

Section 7 of 9

Monitor cardiovascular status continuously.

Select patients may require intracranial pressure monitoring.

Select patients may require intraventricular catheterization for hydrocephalus.

Transfer:

Patients with ICH should be considered for transfer to a facility with neurosurgical capabilities.

Complications:

Increased intracranial pressure and herniation are the dreaded complications. Worsening cere
edema is often implicated in neurologic deterioration in the first 24-48 hours.

Early hemorrhage growth is associated with neurologic deterioration. Expansion of the hemato
the most common cause of neurologic deterioration in the first 3 hours.

In patients who are initially alert, 25% will have a decrease in consciousness within the first 24

Post-stroke seizures may develop.

Stroke is the leading cause of permanent disability.

Prognosis:

The prognosis varies depending on the severity of stroke and the location and the size of the
hemorrhage. Lower Glasgow coma scores are associated with poorer prognosis and higher m
A larger volume of blood is associated with a poorer prognosis. The presence of blood in the v
is associated with a higher mortality rate. Other complicating medical comorbidities also affect
prognosis.

Patient Education:

For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicin
patient education article Stroke.
PICTURES

Section 8 of 9

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Caption: Picture 1. Large intracerebral hemorrhage with midline shift.

View Full Size Image

eMedicine Zoom View (Interactive!)

Picture Type: CT
BIBLIOGRAPHY

Section 9 of 9

Author Information Introduction Clinical Differentials Workup Treatment Follow-up Pictures Bibliography

Broderick JP, Adams HP, Barsan W, et al: Guidelines for the management of spontaneous intra
hemorrhage: A statement for healthcare professionals from a special writing group of the Strok
Council, American Heart Association. Stroke 1999 Apr; 30(4): 905-15[Medline].
Brott T, Broderick J, Kothari R, et al: Early hemorrhage growth in patients with intracerebral
hemorrhage. Stroke 1997 Jan; 28(1): 1-5[Medline].
Brott T, Thalinger K, Hertzberg V: Hypertension as a risk factor for spontaneous intracerebral
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Brown DL, Morgenstern LB: Stopping the bleeding in intracerebral hemorrhage. N Engl J Med
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Program. JAMA 1986 May 2; 255(17): 2311-4[Medline].
Fiebach JB, Schellinger PD, Gass A, et al: Stroke magnetic resonance imaging is accurate in
hyperacute intracerebral hemorrhage: a multicenter study on the validity of stroke imaging. Str
2004 Feb; 35(2): 502-6[Medline].
Kaneko M, Tanaka K, Shimada T, et al: Long-term evaluation of ultra-early operation for hypert
intracerebral hemorrhage in 100 cases. J Neurosurg 1983 Jun; 58(6): 838-42[Medline].
Kanno T, Sano H, Shinomiya Y, et al: Role of surgery in hypertensive intracerebral hematoma.
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Kidwell CS, Chalela JA, Saver JL, et al: Comparison of MRI and CT for detection of acute intra
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Kopitnik TA Jr, Kaufman HH: The future. Prospects of innovative treatment of intracerebral
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Mendelow AD, Gregson BA, Fernandes HM, et al: Early surgery versus initial conservative trea
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NOTE:

Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, e
and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards
time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party
with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the articl
the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indicatio
contraindications should be confirmed in the package insert. FULL DISCLAIMER
Stroke, Hemorrhagic excerpt

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