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Drugs & Diseases > Emergency Medicine

Hemorrhagic Stroke

Updated: Apr 22, 2019

Author: David S Liebeskind, MD, FAAN, FAHA, FANA; Chief Editor: Andrew K Chang, MD, MS more...

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Practice Essentials

In hemorrhagic stroke, bleeding occurs directly into the brain parenchyma. The usual mechanism is
thought to be leakage from small intracerebral arteries damaged by chronic hypertension. The terms
intracerebral hemorrhage and hemorrhagic stroke are used interchangeably in this article and are
regarded as separate entities from hemorrhagic transformation of ischemic stroke. See the image
below.

Axial noncontrast computed tomography scan of the

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.

View Media Gallery

See Acute Stroke, a Critical Images slideshow, for more information on incidence, presentation,
intervention, and additional resources.

Also, see the Vertigo: 5 Case-Based Diagnostic Puzzles slideshow to help recognize diagnostic clues in
vertigo cases.

Signs and symptoms

Patients with intracerebral bleeds are more likely than those with ischemic stroke to have headache,
altered mental status, seizures, nausea and vomiting, and/or marked hypertension. Even so, none of
these findings reliably distinguishes between hemorrhagic and ischemic stroke.
Focal neurologic deficits

The type of deficit depends on the area of brain involved. If the dominant (usually the left)
hemisphere is involved, a syndrome consisting of the following may result:

Right hemiparesis

Right hemisensory loss

Left gaze preference

Right visual field cut

Aphasia

Neglect (atypical)

If the nondominant (usually the right) hemisphere is involved, a syndrome consisting of the following
may result:

Left hemiparesis

Left hemisensory loss

Right gaze preference

Left visual field cut

See Clinical Presentation for more detail.

Diagnosis
Laboratory tests should include a complete blood count (CBC), 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]

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.

See Workup for more detail.

CONTINUE READING BELOW

Management

The treatment and management of patients with acute intracerebral hemorrhage depends on the
cause and severity of the bleeding. Basic life support, as well as control of bleeding, seizures, blood
pressure (BP), and intracranial pressure, are critical. Medications used in the treatment of acute
stroke include the following:

Anticonvulsants – To prevent seizure recurrence

Antihypertensive agents – To reduce BP and other risk factors of heart disease

Osmotic diuretics – To decrease intracranial pressure in the subarachnoid space

A potential treatment for hemorrhagic stroke is surgical evacuation of the hematoma. However, the
role of surgical treatment for supratentorial intracranial hemorrhage remains controversial.
Outcomes in published studies are conflicting.

Endovascular therapy using coil embolization, as an alternative to surgical clipping, has been
increasingly employed with great success, although controversy still exists over which treatment is
ultimately superior.

See Treatment and Medication for more detail.

Background
Hemorrhagic stroke is less common than ischemic stroke (ie, stroke caused by thrombosis or
embolism); epidemiologic studies indicate that only 8-18% of strokes are hemorrhagic. [2] However,
hemorrhagic stroke is associated with higher mortality rates than is ischemic stroke. (See
Epidemiology.) [3]

CONTINUE READING BELOW

Patients with hemorrhagic stroke may present with focal neurologic deficits similar to those of
ischemic stroke but tend to be more ill than are patients with ischemic stroke. However, though
patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures,
nausea and vomiting, and/or marked hypertension.

Brain imaging is a crucial step in the evaluation of suspected hemorrhagic stroke and must be
obtained on an emergent basis (see the image below). Brain imaging aids in excluding ischemic
stroke, and it may identify complications of hemorrhagic stroke such as intraventricular hemorrhage,
brain edema, and hydrocephalus. Either noncontrast computed tomography (NCCT) scanning or
magnetic resonance imaging (MRI) is the modality of choice. For more information, see Ischemic
Stroke in Emergency Medicine. (See Workup.)

Axial noncontrast computed tomography scan of the

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.

View Media Gallery

CONTINUE READING BELOW

Anatomy

Knowledge of cerebrovascular arterial anatomy and the brain regions supplied by the arteries is
useful in determining which vessels are involved in acute stroke. Atypical patterns that do not
conform to a vascular distribution may indicate another diagnosis, such as venous infarction.

The cerebral hemispheres are supplied by 3 paired major arteries: the anterior, middle, and
posterior cerebral arteries. The anterior and middle cerebral arteries are responsible for the anterior
circulation and arise from the supraclinoid internal carotid arteries. The posterior cerebral arteries
arise from the basilar artery and form the posterior circulation, which also supplies the thalami,
brainstem, and cerebellum. The angiograms in the images below demonstrate some portions of the
circulation involved in hemorrhagic strokes.
Frontal view of a cerebral angiogram with selectiv

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).

View Media Gallery

CONTINUE READING BELOW

Lateral view of a cerebral angiogram illustrates t

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.

View Media Gallery

Frontal projection from a right vertebral artery a

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.

View Media Gallery

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Pathophysiology

In intracerebral hemorrhage, 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.

Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus,
putamen, cerebellum, and brainstem. 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.
Subarachnoid hemorrhage

The pathologic effects of subarachnoid hemorrhage (SAH) on the brain are multifocal. SAH results in
elevated intracranial pressure and impairs cerebral autoregulation. These effects can occur in
combination with acute vasoconstriction, microvascular platelet aggregation, and loss of
microvascular perfusion, resulting in profound reduction in blood flow and cerebral ischemia. [4] See
the images below.

CONTINUE READING BELOW

Noncontrast computed tomography (CT) scanning was

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.

View Media Gallery

Computed tomographic angiography examination and s

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.

View Media Gallery

CONTINUE READING BELOW

Lateral view of a selective injection of the left

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.

View Media Gallery

Etiology

The etiologies of stroke are varied, but they can be broadly categorized into ischemic or
hemorrhagic. Approximately 80–87% of strokes are from ischemic infarction caused by thrombotic
or embolic cerebrovascular occlusion. Intracerebral hemorrhages account for most of the remainder
of strokes, with a smaller number resulting from aneurysmal subarachnoid hemorrhage. [5, 6, 7, 8]
In 20–40% of patients with ischemic infarction, hemorrhagic transformation may occur within 1
week after ictus. [9, 10]

CONTINUE READING BELOW

Differentiating between the different types of stroke is an essential part of the initial workup of
patients with stroke, as the subsequent management of each disorder will be vastly different.

Risk factors

The risk of hemorrhagic stroke is increased with the following factors:

Advanced age

Hypertension (up to 60% of cases)

Previous history of stroke

Alcohol abuse

Use of illicit drugs (eg, cocaine, other sympathomimetic drugs)

Causes of hemorrhagic stroke include the following [8, 9, 11, 12, 13] :

Hypertension

Cerebral amyloidosis

Coagulopathies

Anticoagulant therapy
Thrombolytic therapy for acute myocardial infarction (MI) or acute ischemic stroke (can cause
iatrogenic hemorrhagic transformation)

Arteriovenous malformation (AVM), aneurysms, and other vascular malformations (venous and
cavernous angiomas)

Vasculitis

Intracranial neoplasm

Hypertension

CONTINUE READING BELOW

The most common etiology of primary hemorrhagic stroke (intracerebral hemorrhage) is

hypertension. At least two thirds of patients with primary intraparenchymal hemorrhage are
reported to have preexisting or newly diagnosed hypertension. Hypertensive small-vessel disease
results from tiny lipohyalinotic aneurysms that subsequently rupture and result in intraparenchymal
hemorrhage. Typical locations include the basal ganglia, thalami, cerebellum, and pons.

Amyloidosis

Cerebral amyloidosis affects people who are elderly and may cause up to 10% of intracerebral
hemorrhages. Rarely, cerebral amyloid angiopathy can be caused by mutations in the amyloid
precursor protein and is inherited in an autosomal dominant fashion.

Coagulopathies

Coagulopathies may be acquired or inherited. Liver disease can result in a bleeding diathesis.
Inherited disorders of coagulation such as factor VII, VIII, IX, X, and XIII deficiency can predispose to
excessive bleeding, and intracranial hemorrhage has been seen in all of these disorders.

Anticoagulant therapy

Anticoagulant therapy is especially likely to increase hemorrhage risk in patients who metabolize
warfarin inefficiently. Warfarin metabolism is influenced by polymorphism in the CYP2C9 genes.
Three known variants have been described. CYP2C9*1 is the normal variant and is associated with
typical response to dosage of warfarin. Variations *2 and *3 are relatively common polymorphisms
that reduce the efficiency of warfarin metabolism. [14]

Arteriovenous malformations

CONTINUE READING BELOW

Numerous genetic causes may predispose to AVMs in the brain, although AVMs are generally
sporadic. Polymorphisms in the IL6 gene increase susceptibility to a number of disorders, including
AVM. Hereditary hemorrhagic telangiectasia (HHT), previously known as Osler-Weber-Rendu
syndrome, is an autosomal dominant disorder that causes dysplasia of the vasculature. HHT is
caused by mutations in ENG, ACVRL1, or SMAD4 genes. Mutations in SMAD4 are also associated
with juvenile polyposis, so this must be considered when obtaining the patient’s history.

HHT is most frequently diagnosed when patients present with telangiectasias on the skin and
mucosa or with chronic epistaxis from AVMs in the nasal mucosa. Additionally, HHT can result in
AVMs in any organ system or vascular bed. AVM in the gastrointestinal tract, lungs, and brain are the
most worrisome, and their detection is the mainstay of surveillance for this disease.

Cholesterol

A study of almost 28,000 women over a period of approximately 20 years found that women with
very low levels of low-density lipoprotein cholesterol (LDL-C) (< 70 mg/dL) may be more than twice
as likely to have a hemorrhagic stroke than women with higher levels (100–130 mg/dL). [15]

Aneurysms and subarachnoid hemorrhage

The most common cause of atraumatic hemorrhage into the subarachnoid space is rupture of an
intracranial aneurysm. Aneurysms are focal dilatations of arteries, with the most frequently
encountered intracranial type being the berry (saccular) aneurysm. Aneurysms may less commonly
be related to altered hemodynamics associated with AVMs, collagen vascular disease, polycystic
kidney disease, septic emboli, and neoplasms.

Nonaneurysmal perimesencephalic subarachnoid hemorrhage may also be seen. This phenomenon

is thought to arise from capillary or venous rupture. It has a less severe clinical course and, in
general, a better prognosis.

Berry aneurysms are most often isolated lesions whose formation results from a combination of
hemodynamic stresses and acquired or congenital weakness in the vessel wall. Saccular aneurysms
typically occur at vascular bifurcations, with more than 90% occurring in the anterior circulation.
Common sites include the following:

The junction of the anterior communicating arteries and anterior cerebral arteries—most commonly,
the middle cerebral artery (MCA) bifurcation

The supraclinoid internal carotid artery at the origin of the posterior communicating artery

The bifurcation of the internal carotid artery (ICA)

Genetic causes of aneurysms

Intracranial aneurysms may result from genetic disorders. Although rare, several families have been
described that have a predisposition—inherited in an autosomal dominant fashion—to intracranial
berry aneurysms. A number of genes, all categorized as ANIB genes, are associated with this
predisposition. Presently, ANIB1 through ANIB11 are known.

Autosomal dominant polycystic kidney disease (ADPKD) is another cause of intracranial aneurysm.
Families with ADPKD tend to show phenotypic similarity with regard to intracranial hemorrhage or
asymptomatic berry aneurysms. [16]

Loeys-Dietz syndrome (LDS) consists of craniofacial abnormalities, craniosynostosis, marked arterial

tortuosity, and aneurysms and is inherited in an autosomal dominant manner. Although intracranial
aneurysms occur in LDS of all types, saccular intracranial aneurysms are a prominent feature of LDS
type IC, which is caused by mutations in the SMAD3 gene. [17]

Ehlers-Danlos syndrome is a group of inherited disorders of the connective tissue that feature
hyperextensibility of the joints and changes to the skin, including poor wound healing, fragility, and
hyperextensibility. However, Ehlers-Danlos vascular type (type IV) also is known to cause
spontaneous rupture of hollow viscera and large arteries, including arteries in the intracranial
circulation.

Patients with Ehlers-Danlos syndrome may also have mild facial findings, including lobeless ears, a
thin upper lip, and a thin, sharp nose. The distal fingers may appear prematurely aged (acrogeria). In
the absence of a suggestive family history, it is difficult to separate Ehlers-Danlos vascular type from
other forms of Ehlers-Danlos. Ehlers-Danlos vascular type is caused by mutations in the COL3A1
gene; it is inherited in an autosomal dominant manner.
See Genetic and Inflammatory Mechanisms in Stroke, as well as Blood Dyscrasias and Stroke.
Information on metabolic diseases and stroke can be found in the following articles:

Methylmalonic Acidemia

Homocystinuria/Homocysteinemia

Fabry Disease

MELAS – Mitochondrial Encephalomyopathy, Lactic Acidosis, Strokelike Episodes

Hyperglycemia/Hypoglycemia

Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an area of

hemorrhage. Proposed mechanisms for hemorrhagic transformation include reperfusion of
ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood
supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the
blood-brain barrier, red blood cells extravasate from the weakened capillary bed, producing
petechial hemorrhage or frank intraparenchymal hematoma. [8, 9, 18] (For more information, see
Reperfusion Injury in Stroke.)

Hemorrhagic transformation of an ischemic infarct occurs within 2–14 days postictus, usually within
the first week. It is more commonly seen following cardioembolic strokes and is more likely with
larger infarct size. [8, 10, 19] Hemorrhagic transformation is also more likely following
administration of tissue plasminogen activator (tPA) in patients whose noncontrast computed
tomography (CT) scans demonstrate areas of hypodensity. [18, 20, 21] See the image below.

Noncontrast computed tomography scan (left) obtain

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.

View Media Gallery

Epidemiology

Occurrence in the United States

Each year in the United States, approximately 795,000 people experience new or recurrent stroke.
Of these, approximately 610,000 represent initial attacks, and 185,000 represent recurrent strokes.
Epidemiologic studies indicate that approximately 87% of strokes in the United States are ischemic,
10% are secondary to intracerebral hemorrhage, and another 3% may be secondary to subarachnoid
hemorrhage. [5, 22]

A 2010 retrospective review from a stroke center found that 40.9% of the 757 patients in the study
had suffered hemorrhagic strokes. [23] The researchers speculate that improved availability and
implementation of computed tomography (CT) scanning may have unmasked a previous
underestimation of the actual percentage of hemorrhagic strokes, or increased use of antiplatelet
agents and warfarin may have led to a higher incidence of hemorrhage. Alternatively, this higher
rate may represent referral bias of patients with intracerebral hemorrhages to medical centers with
neurosurgical capabilities.

The incidence of stroke varies with age, sex, ethnicity, and socioeconomic status. For example,
American Heart Association (AHA) researchers found that rates of intracerebral hemorrhage are
higher in Mexican Americans, Latin Americans, blacks, Native Americans, Japanese people, and
Chinese people than they are in whites. [5]

Flaherty et al found that excess risk of intracranial hemorrhage in African Americans is largely
attributable to higher hemorrhage rates in young and middle-aged persons, particularly for deep
cerebral and brainstem locations. Hypertension is the predominant risk factor. [24]

International occurrence

According to the World Health Organization (WHO), 15 million people suffer stroke worldwide each
year. Of these, 5 million die and another 5 million are left permanently disabled. [25]

The global incidence of stroke has at least a modest variation from nation to nation, suggesting the
importance of genetics and environmental factors, such as disparities in access to health care in
developing countries. The age-adjusted incidence of total strokes per 1000 person-years for people
55 years or older has been reported in the range of 4.2 to 6.5. The highest incidences have been
reported in Russia, Ukraine, and Japan.
In a prospective, population-based registry study from Italy, the crude annual incidence rate of
intracerebral hemorrhage was 36.9 per 100,000 population. When standardized to the 2006
European population, the rate was 32.9 per 100,000 population; standardized to the world
population, the rate was 15.9 per 100,000 population. [26]

Overall, the incidence of acute stroke has demonstrated a constant decline over the past several
decades, most notably during the 1970s-1990s, although in recent years the rate trend has begun to
plateau. However, the increased survival among stroke victims will place an increased demand on
health-care systems globally. [8, 27]

Stroke subtypes also vary greatly in different parts of the world and between different races. For
example, the proportion of hemorrhagic strokes may be higher in certain populations, such as the
Chinese population, in which it has been reported to be up to 39.4%, and the Japanese, in which it is
reportedly up to 38.7%. [2, 27]

Prognosis

The prognosis in patients with hemorrhagic stroke varies depending on the severity of stroke and
the location and the size of the hemorrhage. Lower Glasgow Coma Scale (GCS) scores are associated
with poorer prognosis and higher mortality rates. A larger volume of blood at presentation is also
associated with a poorer prognosis. Growth of the hematoma volume is associated with a poorer
functional outcome and increased mortality rate.

The intracerebral hemorrhage score is the most commonly used instrument for predicting outcome
in hemorrhagic stroke. The score is calculated as follows:

GCS score 3–4: 2 points

GCS score 5–12: 1 point

GCS score 13–15: 0 points

Age ≥80 years: Yes, 1 point; no, 0 points

Infratentorial origin: Yes, 1 point; no, 0 points

Intracerebral hemorrhage volume ≥30 cm3: 1 point

Intracerebral hemorrhage volume < 30 cm3: 0 points

Intraventricular hemorrhage: Yes, 1 point; no, 0 points

In a study by Hemphill et al, all patients with an Intracerebral Hemorrhage Score of 0 survived, and
all of those with a score of 5 died; 30-day mortality increased steadily with the Score. [28]

Other prognostic factors include the following:

Nonaneurysmal perimesencephalic stroke has a less severe clinical course and, in general, a better
prognosis

The presence of blood in the ventricles is associated with a higher mortality rate; in one study, the
presence of intraventricular blood at presentation was associated with a mortality increase of more
than 2-fold

Patients with oral anticoagulation-associated intracerebral hemorrhage have higher mortality rates
and poorer functional outcomes

In studies, withdrawal of medical support or issuance of Do Not Resuscitate (DNR) orders within the
first day of hospitalization predict poor outcome independent of clinical factors. Because limiting
care may adversely impact outcome, American Heart Association/American Stroke Association
(AHA/ASA) guidelines suggest that new DNR orders should probably be postponed until at least the
second full day of hospitalization. Patients with DNRs should be given all other medical and surgical
treatment, unless the DNR explicitly says otherwise. [1]

For more information, see Motor Recovery in Stroke.

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Clinical Presentation

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Hemorrhagic Stroke

Overview
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Background

Anatomy

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Etiology

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