1.

INTRODUCTION
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.

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 the Japanese population is increased.
Age: The risk of stroke increases with age.

2. CLINICAL
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 hemiinattention 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)

3. DIFFERENTIAL DIAGNOSIS
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
4. WORK UP
Lab Studies:

Complete blood count

Coagulation profile

Electrolytes

Serum glucose

Blood type and screen

Imaging Studies:

Noncontrast CT of the brain

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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
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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 to identify ischemic stroke earlier and more
reliably than CT scanning. MRI is being utilized with 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.

5. TREATMENT
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.

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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 should be given to all patients. Phenytoin in
conventional doses is commonly used.

Careful BP monitoring is important.

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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 lowering may compromise cerebral perfusion.
The American Heart Association guidelines recommend intravenous
antihypertensive treatment for patients with mean arterial pressure
(MAP) > 130 mm Hg. MAP should be maintained above 90 mm Hg to
ensure adequate cerebral perfusion.

Intubation should be performed for patients who demonstrate potential loss

of airway protective mechanisms or signs of brainstem dysfunction. If
intubation is needed, rapid sequence intubation should be performed with
technique and medications aimed at limiting any increase in intracranial
pressure.

Currently, no effective targeted therapy for hemorrhagic stroke exists.

However, some preliminary research indicates that treatment with
hemostatic therapy may be effective. A recent preliminary study of treatment
with recombinant factor 8 demonstrated reduced mortality and improved
functional outcomes. Further studies are necessary to determine if this
should be accepted as a clinical treatment option.

Consultations:

Emergent neurosurgical or neurological consultation often is indicated; local

referral patterns may vary.
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A potential treatment of hemorrhagic stroke is surgical evacuation of

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

Surgical intervention for cerebellar hematoma has been shown to

improve outcome. It can be lifesaving in the prevention of brainstem
compression.

Need for invasive intracranial pressure monitoring should be

assessed by the neurosurgeon.

Need for emergent cerebral angiography should be assessed by the

neurosurgeon. Patients with no clear cause of the hemorrhage and
who would otherwise be candidates for surgery should be considered
for angiographic evaluation.

6. FOLLOW UP
Further Inpatient Care:

ICU admission is mandatory.

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Monitor for airway compromise.

Monitor and carefully address the patient's BP.

Reassess neurologic status frequently.

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 cerebral edema is often implicated in neurologic
deterioration in the first 24-48 hours.

Early hemorrhage growth is associated with neurologic deterioration.

Expansion of the hematoma is 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 hours.

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 mortality. A larger volume of
blood is associated with a poorer prognosis. The presence of blood in the
ventricles is associated with a higher mortality rate. Other complicating
medical comorbidities also affect the prognosis.

Patient Education:

For excellent patient education resources, visit eMedicine's Stroke Center.

Also, see eMedicine's patient education article Stroke.