Bahan Stroke

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 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.
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.
Essential update: Inpatient statin use and maintenance may improve outcomes
post intracerebral hemorrhage
In a retrospective multicenter cohort study of 3481 patients with intracerebral
hemorrhage over a 10-year period, Flint et al found that inpatients who received a
statin (lovastatin, simvastatin, atorvastatin, pravastatin sodium) had better 30-day

survival rates following the bleeding event and were more likely to be discharged
home or to a rehabilitation center than those who didnt receive a statin while
hospitalizeddespite the fact that the statin users had significantly more severe
illness and more comorbidities than non statin users.[1, 2] Moreover, those whose
statins were discontinued during their hospitalization had worse outcomes than those
who remained on statins.
Inpatients treated with a statin had an 18.4% unadjusted 30-day mortality rate
compared to 38.7% for those not treated with a statin during their admission.[1, 2]
After adjustment for various factors (age, sex, race/ethnicity, comorbidities, number
of intracerebral hemorrhage cases by hospital, dysphagia), statin users were also more
likely to be alive at 30 days (odds ratio [OR], 4.25; 95% confidence interval [CI],
3.46-5.23; P < .001). Inpatients treated with statins had a 51.1% rate of discharge to
home or to a rehabilitation facility compared to 35.0% for patients not treated with
statins while hospitalized. Furthermore, patients who discontinued statin therapy after
hospital admission had an unadjusted mortality rate of 57.8% compared to 18.9% for
patients using a statin before and during hospitalization; they were also significantly
less likely to be alive at 30 days (OR, 0.16; 95% CI, 0.12-0.21; P < .001).[1, 2]
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 anticoagulantscoagulation studies (ie, prothrombin
time or international normalized ratio [INR] and an activated partial thromboplastin
time).[3]
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.
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
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. 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.[4] However, hemorrhagic stroke is associated with higher
mortality rates than is ischemic stroke. (See Epidemiology.)[5]
Patients with hemorrhagic stroke 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,
none of these findings reliably distinguishes between hemorrhagic and ischemic
stroke. (See Presentation.)[6]
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 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.
The treatment of patients with acute stroke 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. Surgical evacuation of the hematoma is a
potential therapeutic option, but it remains controversial. (See Treatment.)
For patient education information, see the Stroke Health Center, as well as Stroke.
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 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).
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.
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.[7] See the images below.
Noncontrast computed tomography (CT) scanning was performed emergently in a 71year-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.
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.[8, 9, 10, 11]
In 20-40% of patients with ischemic infarction, hemorrhagic transformation may
occur within 1 week after ictus.[12, 13]
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[11, 12, 14, 15, 16] :
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
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.[17]
Arteriovenous malformations
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 patients 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.
Hypertension
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.
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 predispositioninherited in an autosomal
dominant fashionto 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.[18]
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.[19]
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.[11, 12, 20] (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.[11, 13, 21] 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.[20, 22, 23] See the image below.
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.
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.[8, 24]
A 2010 retrospective review from a stroke center found that 40.9% of the 757 patients
in the study had suffered hemorrhagic strokes.[25] 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.[8]
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.[26]
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.[27]
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.[28]
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.[11, 29]
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%.[4, 29]
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 cm 3: 1 point
Intracerebral hemorrhage volume < 30 cm 3: 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.[30]
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.[3]
History
Obtaining an adequate history includes determining the onset and progression of
symptoms, as well as assessing for risk factors and possible causative events. Such
risk factors include the following:
Previous transient ischemic attack (TIA) and stroke

Hypertension
Diabetes
Smoking
Arrhythmia and valvular disease
Illicit drug use
Use of anticoagulants
Risk factors for thrombosis
A history of trauma, even if minor, may be important, as extracranial arterial
dissections can result in ischemic stroke.
Hemorrhagic versus ischemic stroke

Symptoms alone are not specific enough to distinguish ischemic from hemorrhagic
stroke. 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 and large ischemic strokes.
Seizures are more common in hemorrhagic stroke than in the ischemic kind. Seizures
occur in up to 28% of hemorrhagic strokes, generally at the onset of the intracerebral
hemorrhage or within the first 24 hours.
The neurologic deficits reflect the area of the brain typically involved, and stroke
syndromes for specific vascular lesions have been described. Focal symptoms of
stroke include the following:
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
Aphasia
Subarachnoid hemorrhage
Symptoms of subarachnoid hemorrhage may include the following:
Sudden onset of severe headache

Signs of meningismus with nuchal rigidity
Photophobia and pain with eye movements
Nausea and vomiting
Syncope - Prolonged or atypical
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 computed tomography
(NCCT) scans.
Physical Examination
The assessment in patients with possible hemorrhagic stroke includes vital signs; a
general physical examination that focuses on the head, heart, lungs, abdomen, and
extremities; and a thorough but expeditious neurologic examination.[3] However,
intracerebral hemorrhage may be clinically indistinguishable from ischemic stroke.
(Though stroke is less common in children, the clinical presentation is similar.)
Hypertension (particularly systolic blood pressure [BP] greater than 220 mm Hg) is
commonly a prominent finding in hemorrhagic stroke. Higher initial BP is associated
with early neurologic deterioration, as is fever.[3]
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 caused by increased intracranial pressure. Meningismus may result from blood in
the subarachnoid space.
Examination results can be quantified using various scoring systems. These include
the Glasgow Coma Scale (GCS), the Intracerebral Hemorrhage Score (which
incorporates the GCS; see Prognosis), and the National Institutes of Health Stroke
Scale.
The type of deficit depends upon the area of brain involved. If the dominant
hemisphere (usually the left) 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
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 for herniation and brainstem
compression. Herniation may cause a rapid decrease in the level of consciousness and
may result in apnea or death.
Specific brain sites and associated 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 Ipsilateral ataxia, facial weakness, 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, ranging
from mild headache to neurologic devastation. At times, a cerebral hemorrhage may
present as a new-onset seizure
iagnostic Considerations
Intracerebral hemorrhage may be clinically indistinguishable from ischemic stroke,
and a thorough history and physical examination are important. An acute onset of
neurologic deficit, altered level of consciousness/mental status, or coma is more
common with hemorrhagic stroke than with ischemic stroke. A history of trauma,
even if minor, may be important, as extracranial arterial dissections can result in
ischemic stroke.
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. Postictal (Todd) paralysis and
hyperosmolality should also be considered.
Other problems to consider are as follows:
Hyponatremia or hypernatremia
Migraine headache
Hyperosmolar hyperglycemic nonketotic coma
Differential Diagnoses
Acute Hypoglycemia
Brain Neoplasms
Encephalitis
Headache, Migraine
Hypernatremia in Emergency Medicine
Hyperosmolar Hyperglycemic Nonketotic Coma
Hypertensive Emergencies
Hyponatremia
Labyrinthitis Ossificans
Meningitis
Stroke, Ischemic
Subarachnoid Hemorrhage
Subdural Hematoma
Transient Ischemic Attack
Approach Considerations
Laboratory tests should include a complete blood count, a metabolic panel, and
particularly in patients taking anticoagulantscoagulation studies (ie, prothrombin
time or international normalized ratio [INR] and an activated partial thromboplastin
time).[3]
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.
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.[3]
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.[31]
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
Blood Pressure Control
No controlled studies have defined optimum BP levels for patients with acute
hemorrhagic stroke, but greatly elevated BP is thought to lead to rebleeding and
hematoma expansion. Stroke may result in loss of cerebral autoregulation of cerebral
perfusion pressure.
Intensive BP reduction (target BP < 140 mm Hg systolic) early in the treatment of
patients with intracerebral hemorrhage appears to lessen the absolute growth of
hematomas, particularly in patients who have received previous antithrombotic
therapy, according to a combined analysis of the Intensive Blood Pressure Reduction
in Acute Cerebral Hemorrhage Trials 1 and 2 (INTERACT).[32]
Suggested agents for use in the acute setting are beta blockers (eg, labetalol) and
angiotensin-converting enzyme inhibitors (ACEIs) (eg, enalapril). For more refractory
hypertension, agents such as nicardipine and hydralazine are used. Avoid
nitroprusside because it may raise intracranial pressure.
The 2010 AHA/ASA guidelines acknowledge that evidence for the efficacy of
managing BP in hemorrhagic stroke is currently incomplete. With that caveat, the
AHA/ASA recommendations for treating elevated BP are as follows[3] :
If systolic BP is over 200 mm Hg or mean arterial pressure (MAP) is over 150 mm

Hg, then consider aggressive reduction of BP with continuous IV infusion; check BP
every 5 minutes
If systolic BP is over 180 mm Hg or MAP is over 130 mm Hg and intracranial
pressure may be elevated, then consider monitoring intracranial pressure and reducing
BP using intermittent or continuous intravenous medications, while maintaining a
cerebral perfusion pressure of 60 mm Hg or higher
If systolic BP is over 180 or MAP is over 130 mm Hg and there is no evidence of
elevated intracranial pressure, then consider modest reduction of BP (target MAP of
110 mm Hg or target BP of 160/90 mm Hg) using intermittent or continuous
intravenous medications to control it, and perform clinical reexamination of the
patient every 15 minutes
In patients presenting with a systolic BP of 150 to 220 mm Hg, acute lowering of

systolic BP to 140 mm Hg is probably safe
For patients with aneurysmal subarachnoid hemorrhage, the 2012 AHA/ASA
guidelines recommend lowering BP below 160 mmHg acutely to reduce rebleeding.
[35]
The ongoing Antihypertensive Treatment in Acute Cerebral Hemorrhage-II (ATACHII) phase 3 randomized clinical trial is designed to determine whether the likelihood
of death or disability at 3 months after spontaneous supratentorial intracerebral
hemorrhage is lower when systolic BP has been reduced to 180 mm Hg or below or to
140 mm Hg or below. In ATACH-II, intravenous nicardipine is started within 3 hours
of stroke onset and continued for the next 24 hours.
Intracranial Pressure Control
Elevated intracranial pressure may result from the hematoma itself, from surrounding
edema, or from both. The frequency of increased intracranial pressure in patients with
intracerebral hemorrhage is not known.
Elevate the head of the bed to 30. This improves jugular venous outflow and lowers
intracranial pressure. The head should be midline and not turned to the side. Provide
analgesia and sedation as needed. Antacids are used to prevent gastric ulcers
associated with intracerebral hemorrhage.
More aggressive therapies, such as osmotic therapy (ie, mannitol, hypertonic saline),
barbiturate anesthesia, and neuromuscular blockage, generally require concomitant
monitoring of intracranial pressure and BP with an intracranial pressure monitor to
maintain adequate cerebral perfusion pressure of greater than 70 mm Hg. A
randomized, controlled study of mannitol in intracerebral hemorrhage failed to
demonstrate any difference in disability or death at 3 months.[36]
Hyperventilation (partial pressure of carbon dioxide [PaCO2] of 25 to 30-35 mm Hg)
is not recommended, because its effect is transient, it decreases cerebral blood flow,
and it may result in rebound elevated intracranial pressure.[5] Glucocorticoids are not
effective and result in higher rates of complications with poorer outcomes.
Treatment of Anticoagulation-associated Intracranial Hemorrhage
Patients on warfarin have an increased incidence of hemorrhagic stroke. Morbidity
and mortality for warfarin-associated bleeding is high, with over one half of patients
dying within 30 days. Most episodes occur with a therapeutic international normalized
ratio (INR), but overanticoagulation is associated with an even greater risk of
bleeding.
The need to reverse warfarin anticoagulation is a true medical emergency, and
reversal must be accomplished as quickly as possible to prevent further hematoma
expansion. Options for reversal therapy include the following:
Intravenous vitamin K
Fresh frozen plasma (FFP)
Prothrombin complex concentrates (PCC)
rFVIIa
FFP versus PCC
Because vitamin K requires more than 6 hours to normalize the INR, it should be
administered with either FFP or PCC. FFP is the standard of care in the United
States[42] ; however, FFP needs to be given in a dose of 15-20 mL/kg and therefore
requires a large-volume infusion. PCC contains high levels of vitamin K-dependent
cofactors and thus involves a smaller-volume infusion than FFP and more rapid
administration.[43, 44] However, PCC is associated with high rates of thrombotic
complications.
No randomized, controlled trial has studied the safety and efficacy of FFP versus PCC
for reversing the effects of warfarin in patients with intracranial hemorrhage. The
International Normalised ratio normalisation in patients with Coumarin-related
intracranial Haemorrhages (INCH) trial, a prospective, randomized, controlled,
multicenter trial comparing the 2 agents, began recruiting subjects in 2009.[45]
FVIIa
Based upon the available medical evidence, the use of FVIIa is currently not
recommended over other agents. The PCC available in the United States contains only
low levels of FVII, however, and Sarode et al have described successful, rapid
reversal of vitamin K antagonistrelated coagulopathy using a combination of lowdose FVIIa with PCC, although they note the need for caution in patients at high risk
for thrombosis.[42]
Patients on heparin (either unfractionated or low molecular weight heparin [LMWH])
who develop a hemorrhagic stroke should immediately have anticoagulation reversed
with protamine.[5] The dose of protamine is dependent upon the dose of heparin that
was given and the time elapsed since that dose.
Patients with severe deficiency of a specific coagulation factor who develop
spontaneous intracerebral hemorrhage should receive factor replacement therapy.[3]
Reversal of antiplatelet therapy and platelet dysfunction
There is controversy about whether patients on antiplatelet medications (eg, aspirin,
aspirin/dipyridamole [Aggrenox], clopidogrel) should be given desmopressin
(DDAVP) and/or platelet transfusions. Patients with renal failure and platelet
dysfunction may also benefit from the administration of desmopressin (DDAVP). The
2010 AHA/ASA guideline for management of spontaneous intracerebral hemorrhage
recommends platelet transfusions only when such hemorrhaging complicates severe
thrombocytopenia.[3]
SAH
Practice Essentials
The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the
subarachnoid space between the pial and arachnoid membranes (see the image
below). It occurs in various clinical contexts, the most common being head trauma.
However, the familiar use of the term SAH refers to nontraumatic (or spontaneous)
hemorrhage, which usually occurs in the setting of a ruptured cerebral aneurysm or
arteriovenous malformation (AVM).
A 47-year-old woman presented with headache and vomiting; her CT scan in the
emergency department revealed subarachnoid hemorrhage.
Signs and symptoms
Signs and symptoms of SAH range from subtle prodromal events to the classic
presentation. The most common premonitory symptoms are as follows:
Headache (48%)
Dizziness (10%)
Orbital pain (7%)
Diplopia (4%)
Visual loss (4%)
Signs present before SAH include the following:
Sensory or motor disturbance (6%)

Seizures (4%)
Ptosis (3%)
Bruits (3%)
Dysphasia (2%)
Prodromal signs and symptoms usually are the result of sentinel leaks, mass effect of
aneurysm expansion, emboli, or some combination thereof.
The classic presentation can include the following:
Sudden onset of severe headache (the classic feature)

Accompanying nausea or vomiting
Symptoms of meningeal irritation
Photophobia and visual changes
Sudden loss of consciousness at the ictus
Seizures during the acute phase
Physical examination findings may be normal or may include the following:
Mild to moderate BP elevation

Temperature elevation
Tachycardia
Papilledema
Retinal hemorrhage
Global or focal neurologic abnormalities
Complications of SAH include the following:
Hydrocephalus
Rebleeding
Vasospasm
Seizures
Cardiac dysfunction
See Clinical Presentation for more detail.
Diagnosis
Diagnosis of SAH usually depends on a high index of clinical suspicion combined
with radiologic confirmation via urgent noncontrast CT, followed by lumbar puncture
or CT angiography of the brain. After the diagnosis is established, further imaging
should be performed to characterize the source of the hemorrhage.
Laboratory studies should include the following:
Serum chemistry panel

Complete blood count
Prothrombin time (PT)/activated partial thromboplastin time (aPTT)
Blood typing/screening
Cardiac enzymes
Arterial blood gas (ABG) determination
Imaging studies that may be helpful include the following:
CT (noncontrast, contrast, or infusion)

Digital subtraction cerebral angiography
Multidetector CT angiography
MRI (if no lesion is found on angiography)
Magnetic resonance angiography (MRA; investigational for SAH)
Other diagnostic studies that may be warranted are as follows:
Baseline chest radiograph

ECG on admission
Lumbar puncture and CSF analysis
See Workup for more detail.
Management
Current treatment recommendations include the following:
Antihypertensive agents (eg, IV beta blockers) when mean arterial pressure exceeds
130 mm Hg
Avoidance of nitrates (which elevate ICP) when feasible
Hydralazine and calcium channel blockers
Angiotensin-converting enzyme (ACE) inhibitors (not first-line agents in acute SAH)
In patients with signs of increased ICP or herniation, intubation and hyperventilation
Other interventions for increased ICP are as follows:
Osmotic agents (eg, mannitol)

Loop diuretics (eg, furosemide)
IV steroids (controversial but recommended by some)
Additional medical management is directed toward the following common
complications:
Rebleeding
Vasospasm
Hydrocephalus
Hyponatremia
Seizures
Pulmonary complications
Cardiac complications
Surgical treatment to prevent rebleeding includes the following options:
Clipping the ruptured aneurysm

Endovascular treatment [1] (ie, coiling)
The choice between coiling and clipping usually depends on the location of the lesion,
the neck of the aneurysm, and the availability and experience of hospital staff.
Screening is not recommended in the general population. However, it can lower cost
and improve quality of life in patients at relatively high risk for aneurysm formation
and rupture.
See Treatment and Medication for more detail.
Background
The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the
subarachnoid space between the pial and arachnoid membranes. SAH constitutes half
of all spontaneous atraumatic intracranial hemorrhages; the other half consists of
bleeding that occurs within the brain parenchyma.
Subarachnoid hemorrhage (see the image below) occurs in various clinical contexts,
the most common being head trauma. However, the familiar use of the term SAH
refers to nontraumatic (or spontaneous) hemorrhage, which usually occurs in the
setting of a ruptured cerebral aneurysm or arteriovenous malformation (AVM).
CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of

hydrocephalus is apparent.
Intracranial saccular aneurysms (berry aneurysms) represent the most common
etiology of nontraumatic SAH; about 80% of cases of SAH result from ruptured
aneurysms. SAH is responsible for the death and/or disability of 18,000 persons each
year in North America alone. In the United States, it is associated with an annual cost
of $1.75 billion. Unfortunately, the difficulties in detecting unruptured aneurysms in
asymptomatic patients practically preclude the possibility of preventing most
instances of SAH.
About 6-8% of all strokes are caused by SAH from ruptured berry aneurysms. Over
the past several decades, the incidence of other types of strokes has decreased;
however, the incidence of SAH has not decreased.
The history and physical examination, especially the neurologic examination, are
essential components in the diagnosis and clinical staging of SAH (see Presentation).
The diagnosis is confirmed radiologically via urgent computed tomography (CT) scan
without contrast. Traditionally, a negative CT scan is followed with lumbar puncture.
However, noncontrast CT followed by CT angiography (CTA) of the brain can rule
out SAH with greater than 99% sensitivity.[2] (See Workup.)
Current treatment recommendations involve management in an intensive care unit
setting. The blood pressure is maintained with consideration of the patients
neurologic status, and additional medical management is directed toward the

prevention and treatment of complications. Surgical treatment to prevent rebleeding
consists of clipping the ruptured berry aneurysm. Endovascular treatment[1] (ie,
coiling) is an increasingly practiced alternative to surgical clipping (see Treatment).
Pathophysiology
Aneurysms are acquired lesions related to hemodynamic stress on the arterial walls at
bifurcation points and bends. Saccular or berry aneurysms are specific to the
intracranial arteries because their walls lack an external elastic lamina and contain a
very thin adventitiafactors that may predispose to the formation of aneurysms. An
additional feature is that they lie unsupported in the subarachnoid space.
Aneurysms usually occur in the terminal portion of the internal carotid artery and the
branching sites on the large cerebral arteries in the anterior portion of the circle of
Willis. The early precursors of aneurysms are small outpouchings through defects in
the media of the arteries.
These defects are thought to expand as a result of hydrostatic pressure from pulsatile
blood flow and blood turbulence, which is greatest at the arterial bifurcations. A
mature aneurysm has a paucity of media, replaced by connective tissue, and has
diminished or absent elastic lamina.
The probability of rupture is related to the tension on the aneurysm wall. The law of
La Place states that tension is determined by the radius of the aneurysm and the
pressure gradient across the wall of the aneurysm. Thus, the rate of rupture is directly
related to the size of the aneurysm. Aneurysms with a diameter of 5 mm or less have a
2% risk of rupture, whereas 40% of those with a diameter of 6-10 mm have already
ruptured upon diagnosis.
Although hypertension has been identified as a risk factor for aneurysm formation, the
data with respect to rupture are conflicting. However, certain hypertensive states, such
as those induced by use of cocaine and other stimulants, clearly promote aneurysm
growth and rupture earlier than would be predicted by the available data.
Brain injury from cerebral aneurysm formation can occur in the absence of rupture.
Compressive forces can cause injury to local tissues and/or compromise of distal
blood supply (mass effect).
When an aneurysm ruptures, blood extravasates under arterial pressure into the
subarachnoid space and quickly spreads through the cerebrospinal fluid around the
brain and spinal cord. Blood released under high pressure may directly cause damage
to local tissues. Blood extravasation causes a global increase in intracranial pressure
(ICP). Meningeal irritation occurs.
Rupture of AVMs can result in both intracerebral hemorrhage and SAH. Currently, no
explanation can be provided for the observation that small AVMs (< 2.5 cm) rupture
more frequently than large AVMs (>5 cm).
In a 25-year autopsy study of 125 patients with ruptured or unruptured aneurysms
conducted at Johns Hopkins, the following conditions correlated positively with the
formation of saccular aneurysms:
Hypertension
Cerebral atherosclerosis
Vascular asymmetry in the circle of Willis
Persistent headache
Pregnancy-induced hypertension
Long-term analgesic use
Family history of stroke
The occurrence of aneurysms in children indicates the role of intrinsic vascular
factors. A number of disease states resulting in weakness of the arterial wall are
associated with an increased incidence of berry aneurysms.
Mechanisms and disease states associated with higher incidence of berry aneurysms
include the following:
Increased blood pressure: Fibromuscular dysplasia, polycystic kidney disease, aortic

coarctation
Increased blood flow: Cerebral arteriovenous malformation (AVM); persistent
carotid-basilar anastomosis; ligated, aplastic, or hypoplastic contralateral vessel
Blood vessel disorders: Systemic lupus erythematosus (SLE), Moyamoya disease, [3]
granulomatous angiitis
Genetic disorders: Marfan syndrome, Ehlers-Danlos syndrome, Osler-Weber-Rendu
syndrome, pseudoxanthoma elasticum, Klippel-Trenaunay-Weber syndrome
Congenital conditions: Persistent fetal circulation, hypoplastic/absent arterial
circulation
Metastatic tumors to cerebral arteries: Atrial myxoma, choriocarcinoma,
undifferentiated carcinoma
Infections: Bacterial, fungal
Complications
Hydrocephalus
Rebleeding
Delayed cerebral ischemia from vasospasm
Intracerebral hemorrhage
Intraventricular hemorrhage
Left ventricular systolic dysfunction
Subdural hematoma
Seizures
Increased intracranial pressure
Myocardial infarction [4]
Hydrocephalus
SAH can cause hydrocephalus by 2 mechanisms: obstruction of CSF pathways (ie,
acute, obstructive, noncommunicating type) and blockage of arachnoid granulations
by scarring (ie, delayed, nonobstructive, communicating type). Acute hydrocephalus
is caused by compromise of CSF circulation pathways by interfering with CSF
outflow through the sylvian aqueduct, fourth ventricular outlet, basal cisterns, and
subarachnoid space. CSF production and absorption rates are unaltered.
Intraventricular blood is the strongest determinant for the development of acute

hydrocephalus. Other risk factors include the following:
Bilateral ambient cisternal blood

Increased age
Vasospasm
Use of antifibrinolytic drugs
Subdural hematoma
Seizures
Rebleeding
Rebleeding of SAH occurs in 20% of patients in the first 2 weeks. The rebleeds in the
first days ("blow out" hemorrhages) are thought to be related to the unstable nature of
the aneurysmal thrombus, as opposed to lysis of the clot sitting over the rupture site.
Clinical factors that increase the likelihood of rebleeding include hypertension,
anxiety,[5] agitation, and seizures.
Cerebral ischemia
Delayed cerebral ischemia from arterial smooth muscle contraction is the most
common cause of death and disability following aneurysmal SAH. Vasospasm can
lead to impaired cerebral autoregulation and may progress to cerebral ischemia and
infarction.[6] Most often, the terminal internal carotid artery or the proximal portions
of the anterior and middle cerebral arteries are involved. The arterial territory
involved is not related to the location of the ruptured aneurysm.
Vasospasm is believed to be induced in areas of thick subarachnoid clot. The putative
agent responsible for vasospasm is oxyhemoglobin, but its true etiology and
pathogenesis remain to be elucidated.
The mechanism of intracerebal hemorrhage (ICH) is direct rupture of aneurysm into
the brain. ICH commonly results from internal cerebral artery (ICA), pericallosal, and
anterior cerebral artery (ACA) aneurysms. Secondary rupture of a subarachnoid
hematoma into the brain parenchyma most commonly arises from middle cerebral
artery aneurysms.
Found in 13-28% of clinical cases of ruptured aneurysms and in 37-54% of autopsy
cases, intraventricular hemorrhage (IVH) is a significant predictor of poor neurologic
grade and outcome. Sources of IVH include the following:
Anterior cerebral artery (40%)

Internal cerebral artery (25%)
Middle cerebral artery (21%)
Vertebrobasilar artery (14%)
LV systolic dysfunction in humans with SAH is associated with normal myocardial

perfusion and abnormal sympathetic innervation. These findings may be explained by
excessive release of norepinephrine from myocardial sympathetic nerves, which could
damage both myocytes and nerve terminals.[7]
Subdural hematoma
Subdural hematoma (SDH) is rare following aneurysmal SAH, with reported
incidence of 1.3-2.8% in clinical series and as high as 20% in autopsy series. The
mechanisms of SDH involve tearing of arachnoid adherent to the dome of the
aneurysm at the time of rupture, direct tearing of arachnoid by a jet of blood, and
disruption of arachnoid by ICH, with secondary decompression of ICH into the
subdural space.
Elevations in ICP are due to mass effect of blood (subarachnoid, intracranial,
intraventricular, or subdural hemorrhage) or acute hydrocephalus. Once ICP reaches
mean arterial pressure (MAP), cerebral perfusion pressure becomes zero and cerebral
blood flow stops, resulting in loss of consciousness and death.
Etiology
Of nontraumatic subarachnoid hemorrhages, approximately 80% are due to a ruptured
berry aneurysm. Rupture of arteriovenous malformations (AVMs) is the second most
identifiable cause of SAH, accounting for 10% of cases of SAH. Most of the
remaining cases result from rupture of the following types of pathologic entities:
Mycotic aneurysm
Angioma
Neoplasm
Cortical thrombosis
SAH may reflect a secondary dissection of blood from an intraparenchymal
hematoma (eg, bleeding from hypertension or neoplasm).
Both congenital and acquired factors are thought to play a role in SAH. Evidence
supporting the role of congenital causes in aneurysm formation includes the
following:
Clusters of familial occurrence, such as in Finland, where the incidence of familial

cerebral aneurysm is 10%
Significant incidence of multiple aneurysms in patients with SAH (15%)
The association of aneurysms with specific congenital diseases (eg, coarctation of the
aorta, Marfan syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia,
polycystic kidney disease)
Familial cases of AVM are rare, and the problem may result from sporadic
abnormalities in embryologic development. AVMs are thought to occur in
approximately 4-5% of the general population, of which 10-15% are symptomatic.
Congenital defects in the muscle and elastic tissue of the arterial media in the vessels
of the circle of Willis are found in approximately 80% of normal vessels at autopsy.
These defects lead to microaneurysmal dilation (< 2 mm) in 20% of the population
and larger dilation (>5 mm) and aneurysms in 5% of the population.

Acquired factors thought to be associated with aneurysmal formation include the
following:
Atherosclerosis
Hypertension
Advancing age
Smoking
Hemodynamic stress
Less common causes of SAH include the following:
Fusiform and mycotic aneurysms

Fibromuscular dysplasia
Blood dyscrasias
Moyamoya disease
Infection
Neoplasm
Trauma (fracture at the base of the skull leading to internal carotid aneurysm)
Amyloid angiopathy (especially in elderly people)
Vasculitis
Reversible cerebral vasoconstriction syndrome (RCVS) is characterized by recurrent
thunderclap headaches and reversible segmental multifocal cerebral artery narrowing,
and it results in SAH in more than 30% of cases. Muehlschlegel and colleagues found
that clinical and imaging findings can differentiate RCVS with SAH from other
causes of SAH.[8, 9]
After analyzing clinical and imaging features of 38 patients with RCVS-SAH, 515
patients with aneurysmal SAH, and 93 patients with cryptogenic (angiogram
negative) SAH, Muehlschlegel et al identified clinical characteristics and radiological
findings that can differentiate RCVS-SAH from aneurysmal SAH or cryptogenic
SAH. These researchers concluded that these differences may be useful for improving
diagnostic accuracy, clinical management, and resource utilization.[8, 9]
Risk factors
Although risk factors for SAH have been evaluated extensively, little conclusive
evidence has been derived. Smoking appears to be a significant risk factor, as does
heavy alcohol consumption. The risk of AVM rupture is greater during pregnancy.
Data regarding the relationship between hypertension and SAH are conflicting.
Previously documented acute severe hypertension with diastolic pressure over 110
mm Hg has been linked to SAH.
The following do not appear to be significant risk factors for SAH:
Use of oral contraceptives

Hormone replacement therapy
Hypercholesterolemia
Vigorous physical activity
Epidemiology
United States statistics

The frequency of ruptured and unruptured aneurysms has been estimated at 1-9% in
different autopsy series, with a prevalence of unruptured aneurysms of 0.3-5%.
Retrospective arteriographic studies show a prevalence of less than 1% with the
limitation that some cases did not receive adequate evaluation and thus some
aneurysms may have been missed. Annual incidence increases with age and probably
is underestimated because death is attributed to other reasons that are not confirmed
by autopsies.
The annual incidence of aneurysmal SAH in the United States is 6-16 cases per
100,000 population, with approximately 30,000 episodes occurring each year. Unlike
other subcategories of stroke, the incidence of SAH has not decreased over time.
However, since 1970, population-based survival rates have improved.
International statistics
The reported incidence of subarachnoid hemorrhage is high in the United States,
Finland, and Japan, while it is low in New Zealand and the Middle East. In Finland,
the estimated incidence based on different studies is 14.4-19.6 cases per 100,000
population, although numbers as high as 29.7 have been reported.
In Japan, the reported rates vary between 11 and 18.3 cases per 100,000 population,
with one study showing an incidence of 96.1 cases per 100,000 population (this study
included only patients aged 40 and older in the data collection, and results were not
adjusted for sex and age to the same reference population). In New Zealand, ageadjusted incidence was reported as 14.3 cases per 100,000 population.
An Australian study reported an incidence of 26.4 cases per 100,000 population but
only for patients older than 35 years, as age was not adjusted in the reference
population. In the Netherlands, the age-specific incidence was reported as 7.8 cases
per 100,000 population (this is believed to be an underestimate).
Iceland reported 8 cases per 100,000 population, but a significant portion of the
affected rural population was believed to be missed. Greenland Eskimos had 9.3 cases
per 100,000 population; ethnic Danes there had an incidence of 3.1 cases per 100,000
population. This latter figure is consistent with the figures in Denmarkmarked
differences are postulated to be related to genetic factors. On the Faeroe Islands (part
of Denmark with an isolated population of the same genetic ancestry), the reported
incidence is 7.4 cases per 100,000 population.
In China, the reported incidence is low, but no good studies have been published to
support this statement. The incidence among Indians and Rhodesian Africans is
significantly lower than in those from European nations; this can be explained partly
by the low incidence of atherosclerosis in these populations. In the Middle East, the
numbers are very low as well; the best available estimate is 5.1 cases per 100,000
population in Qatar.
Race-, sex-, and age-related demographics
The risk is higher in blacks than in whites; however, people of all ethnic groups
develop intracranial aneurysms. The disparity in frequency of rupture has been
attributed to population variance with respect to prevalence of risk factors and age
distribution.
The incidence of SAH in women is higher than in men (ratio of 3 to 2). The risk of
SAH is significantly higher in the third trimester of pregnancy, and SAH from
aneurysmal rupture is a leading cause of maternal mortality, accounting for 6-25% of
maternal deaths during pregnancy. A higher incidence of AVM rupture also has been
reported during pregnancy.
Incidence increases with age and peaks at age 50 years. Approximately 80% of cases
of SAH occur in people aged 40-65 years, with 15% occurring in people aged 20-40
years. Only 5% of cases of SAH occur in people younger than 20 years. SAH is rare
in children younger than 10 years, accounting for only 0.5% of all cases.
Prognosis
Although mortality rates of SAH have decreased in the past 3 decades, it remains a
devastating neurologic problem. An estimated 10-15% of patients die before reaching
the hospital. Approximately 25% of patients die within 24 hours, with or without
medical attention. Hospitalized patients have an average mortality rate of 40% in the
first month. About half of affected individuals die in the first 6 months. Rebleeding, a
major complication, carries a mortality rate of 51-80%.
Age-adjusted mortality rates are 62% greater in females than in males and 57%
greater in blacks than in whites. Morbidity and mortality increase with age and are
related to the overall health status of the patient.
More than one third of survivors have major neurologic deficits. Cognitive deficits are
present even in many patients considered to have a good outcome.
Al-Khindi et al found that survivors of aneurysmal SAH commonly experience
deficits in memory, executive function, and language that affect their day-to-day
functioning, including activities of daily living, instrumental activities of daily living,
return to work, and quality of life. Deficits in cognition and day-to-day functioning
are further compounded by depression, anxiety, fatigue, and sleep disturbances.[10]
Factors that affect morbidity and mortality rates are as follows:
Severity of hemorrhage
Degree of cerebral vasospasm
Occurrence of rebleeding
Presence of comorbid conditions and the hospital course (eg, infections, myocardial
infarction)
Other factors that affect the prognosis of patients who have suffered an SAH include
age, Hunt and Hess grade (see below), smoking history, and location of the aneurysm.
Younger patients do better. Patients with a history of cigarette smoking have a poorer
prognosis. Anterior circulation aneurysms carry a more favorable prognosis.
Acute cocaine use was associated with higher rates of in-hospital death and a
significantly increased risk for aneurysm rerepture in a retrospective study of 1134
patients with aneurysmal SAH. Compared with patients who had not used cocaine in
the 72 hours preceding their event, those who had used cocaine had a nearly 3-fold
increased risk for in-hospital mortality. Mortality remained higher among cocaine
users after patients with rerupture were excluded from the analysis, suggesting that
rerupture was not entirely responsible for the higher mortality rate in these patients.
[11]
Clinical grading scales
Clinical assessment of SAH severity commonly utilizes grading scales. The 2 clinical
scales most often employed are the Hunt and Hess and the World Federation of
Neurological Surgeons (WFNS) grading systems. A third, the Fisher scale, classifies
SAH based on CT scan appearance and quantification of subarachnoid blood.
The WFNS scale is as follows:
Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent

Grade 2 - GCS of 13-14, motor deficit absent
Grade 3 - GCS of 13-14, motor deficit present
Grade 4 - GCS of 7-12, motor deficit absent or present
Grade 5 - GCS of 3-6, motor deficit absent or present
The Fisher scale (CT scan appearance) is as follows:
Group 1 - No blood detected

Group 2 - Diffuse deposition of subarachnoid blood, no clots, and no layers of blood
greater than 1 mm
Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in thickness
Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots
are present
The Hunt and Hess grading system is as follows:
Grade 0 - Unruptured aneurysm

Grade I - Asymptomatic or mild headache and slight nuchal rigidity
Grade Ia - Fixed neurologic deficit without acute meningeal/brain reaction
Grade II - Cranial nerve palsy, moderate to severe headache, nuchal rigidity
Grade III - Mild focal deficit, lethargy, or confusion
Grade IV - Stupor, moderate to severe hemiparesis, early decerebrate rigidity
Grade V - Deep coma, decerebrate rigidity, moribund appearance
In the Hunt and Hess system, the lower the grade, the better the prognosis. Grades IIII generally are associated with favorable outcome; these patients are candidates for
early surgery. Grades IV and V carry a poor prognosis; these patients need
stabilization and improvement to grade III before surgery is undertaken. Some
recommend more aggressive management for patients with poor clinical grade.
Survival correlates with the grade of subarachnoid hemorrhage upon presentation.
Reported figures include a 70% survival rate for Hunt and Hess grade I, 60% for
grade II, 50% for grade III, 40% for grade IV, and 10% for grade V.
The Hunt and Hess and the WFNS grading systems have been shown to correlate well
with patient outcome. The Fisher classification has been used successfully to predict
the likelihood of symptomatic cerebral vasospasm, one of the most feared
complications of SAH. All 3 grading systems are useful in determining the indications
for and timing of surgical management. For an accurate assessment of SAH severity,
these grading systems must be used in concert with the patient's overall general
medical condition and the location and size of the ruptured aneurysm.
Complications
Hydrocephalus
Rebleeding
Delayed ischemia
Intraventricular hemorrhage (IVH)
Subdural hematoma
Seizures
Myocardial infarction [4]
The incidence of rebleeding complication is greatest in the first 2 weeks. The peak is
within 24-48 hours following initial SAH (approximately 6%), with a rate of 1.5% per
day for the next 12-13 days. The cumulative 2-week incidence is 20-30% in
unoperated patients. After the first 30 days, rebleed rate decreases to 1.5% per year for
the first 10 years. In another study, rebleeding was reported at a rate of 3% per year
after 6 months, with a 67% mortality rate at 20 years.
Delayed ischemia
Delayed ischemia from cerebral vasospasm is currently the most common cause of
death and disability following aneurysmal SAH. It has to some degree cancelled out
the improvement in morbidity and mortality from the lower rebleed rate related to
early surgical clipping.
An estimated 10-20% of patients with aneurysmal SAH suffer delayed cerebral
ischemia, resulting in permanent disability or death. This complication alone accounts
for 14-32% of deaths and permanent disability in large studies, while the direct effect
of aneurysm rupture accounts for 25% and rebleeding for 17.6%. Approximately 1520% of patients with symptomatic vasospasm will have a poor outcome despite
maximal medical therapy, including mortality in 7-10% of patients and severe
morbidity in 7-10% of patients.
Found in 13-28% of clinical cases of ruptured aneurysms and in 37-54% of autopsy
cases, intraventricular hemorrhage (IVH) is a significant predictor of poor neurologic
grade and outcome. Patients with IVH are at higher risk of developing hydrocephalus.
In one study of 91 patients, IVH was associated with an overall mortality rate of 64%.
The key prognostic indicator is the degree of ventricular dilatation.
ICH
ntracerebral hemorrhage (ICH)
A+ | Reset | AOverview
Intracerebral hemorrhage (ICH) is a type of stroke caused by bleeding within the brain tissue itself a very life-threatening situation. A stroke occurs when the brain is depriv
arteriovenous malformations, or head trauma. Treatment focuses on stopping the bleeding, removing the blood clot (hematoma), and relieving the pressure on the brain.
What is an intracerebral hemorrhage (ICH)?
Tiny arteries bring blood to areas deep inside the brain (see Anatomy of the Brain). High blood pressure (hypertension) can cause these thin-walled arteries to rupture, releasing b
pressure on surrounding brain tissue (Fig. 1). Increased intracranial pressure (ICP) makes a person confused and lethargic. As blood spills into the brain, the area that artery supp
released that further damage brain cells in the area surrounding the hematoma.
Figure 1. An intracerebral hemorrhage (ICH) is usually caused by rupture of tiny arteries within the brain tissue (left). As blood collects, a hematoma or blood clot form
cause bleeding into brain tissue (right).
An ICH can occur close to the surface or in deep areas of the brain. Sometimes deep hemorrhages can expand into the ventricles the fluid filled spaces in the center of the brain.
What are the symptoms?
If you experience the symptoms of an ICH, call 911 immediately! Symptoms usually come on suddenly and can vary depending on the location of the bleed. Common symptoms inc
headache, nausea, and vomiting
lethargy or confusion
sudden weakness or numbness of the face, arm or leg, usually on one side
loss of consciousness
temporary loss of vision
seizures
What are the causes?
Hypertension: an elevation of blood pressure that may cause tiny arteries to burst inside the brain.
Blood thinner therapy: drugs such as coumadin, heparin, and warfarin used to treat heart and stroke conditions.
AVM: a tangle of abnormal arteries and veins with no capillaries in between.
Aneurysm: a bulge or weakening of an arterial wall.
Head trauma: fractures to the skull and penetrating wounds (gunshot) can damage an artery and cause bleeding.
Bleeding disorders: hemophilia, sickle cell anemia, DIC, thrombocytopenia.
Tumors: highly vascular tumors such as angiomas and metastatic tumors can bleed into the brain tissue.
Amyloid angiopathy: a degenerative disease of the arteries.
Drug usage: cocaine and other illicit drugs can cause ICH.
Spontaneous: ICH by unknown causes.

Who is affected?
Ten percent of strokes are caused by ICH (approximately 70,000 new cases each year). ICH is twice as common as subarachnoid hemorrhage (SAH) and has a 40% risk of death. IC
aged African Americans and Japanese. Advancing age and hypertension are the most important risk factors for ICH. Approximately 70% of patients experience long-term deficits aft
How is a diagnosis made?
When you or a loved one is brought to the emergency room with an ICH, the doctor will learn as much about your symptoms, current and previous medical problems, current medic
location of the bleeding.
Computed Tomography Angiography (CTA) scan is a noninvasive X-ray to review the anatomical structures within the brain to see if there is any blood in the brain (Fig. 2). A
arteries of the brain.
Figure 2. CT scan showing a large ICH.

Angiogram is an invasive procedure, where a catheter is inserted into an artery and passed through the blood vessels to the brain. Once the catheter is in place, a contrast dye is injec
Magnetic resonance imaging (MRI) scan is a noninvasive test, which uses a magnetic field and radio-frequency waves to give a detailed view of the soft tissues of your brain. A
which means it examines the blood vessels as well as the structures of the brain.
What treatments are available?
Once the cause and location of the bleeding is identified, medical or surgical treatment is performed to stop the bleeding, remove the clot, and relieve the pressure on the brain. If lef
caused by ICP and blood toxins may be irreversible.
Generally, patients with small hemorrhages (<10 cm3) and minimal deficits are treated medically. Patients with cerebellar hemorrhages (>3 cm3) who are deteriorating or who h
possible. Patients with large lobar hemorrhages (50 cm3) who are deteriorating usually undergo surgical removal of the hematoma.
Medical treatmentBlood pressure is managed to decrease the risk of more bleeding yet provide enough blood flow (perfusion) to the brain.
Controlling intracranial pressure is the biggest factor in the outcome of ICH. A device called an ICP monitor is placed directly into the ventricles or within the brain to measure press
Removing cerebrospinal fluid (CSF) from the ventricles is a common method to control ICP. A ventricular catheter (VP shunt) may be placed in the ventricles to drain CSF fluid t
ICP. In some cases, coma may be induced with drugs to bring down ICP.
Surgical treatment The goal of surgery is to remove as much of the blood clot as possible and stop the source of bleeding if it is from an identifiable cause such as an AVM or tumor
Craniotomy involves cutting a hole in the skull with a drill to expose the brain and remove the clot. Because of the increased risk to the brain, this technique is usually u
that must also be removed.
Stereotactic aspiration is a less invasive technique preferred for large hematomas located deep inside the brain. The procedure requires attaching a stereotactic fram
discomfort. A metal cage, which looks like a birdcage, is placed on the frame. Next, you undergo a CT scan to help the surgeon pinpoint the exact coordinates of the he
stereotactic frame, a hollow needle is passed through the hole, through the brain tissue, directly into the clot. The hollow needle is attached to a large syringe, which the su
Recovery & prevention
Immediately after an ICH, the patient will stay in the intensive care unit (ICU) for several weeks where doctors and nurses watch them closely for signs of rebleeding, hydrocephalus
ICH patients may suffer short-term and/or long-term deficits as a result of the bleed or the treatment. Some of these deficits may disappear over time with healing and therapy. Th
function.
Clinical trials
Clinical trials are research studies in which new treatmentsdrugs, diagnostics, procedures, and other therapiesare tested in people to see if they are safe and effective. Research
including eligibility, protocol, and locations, are found on the Web. Studies can be sponsored by the National Institutes of Health (see clinicaltrials.gov) as well as private industry an
Lobar Intracerebral Hemorrhage

An intracerebral hemorrhage (ICH) occurs when blood suddenly bursts into
brain tissue, causing damage to the brain, which may present symptoms
similar to that of a stroke. Lobar intracerebral hemorrhages occur in the
cerebral lobes outside of the basal ganglia. The basal ganglia are a structure
located in the cerebrum (the largest part of the brain) that aids in motor
control, procedural learning, eye movement, and cognitive function.
Stroke-like symptoms usually appear suddenly during ICH, causing symptoms

that include headache, weakness, confusion, and paralysis, particularly on
one side of the body. The buildup of blood puts pressure on the brain and
interferes with its oxygen supply. This can quickly cause brain and nerve
damage.
This is a medical emergency requiring immediate treatment. ICH is not as

common as ischemic stroke (when a blood vessel is blocked by a clot), but is
more serious.
Treatment generally involves surgery to repair damaged blood vessels.

Depending on the location of the hemorrhage and the amount of damage,
long-term treatment may include physical, speech, and occupational therapy.
Most people have some level of permanent disability.
Part 2 of 8: Symptoms
Symptoms of Intracerebral Hemorrhage

Symptoms of ICH include:
sudden weakness, tingling, or paralysis in the face, arm, or leg, especially if it

occurs on only one side of the body
sudden onset of severe headache
trouble swallowing
trouble with vision in one or both eyes
loss of balance and coordination, dizziness
trouble with language skills (reading, writing, speaking, understanding)
nausea, vomiting
apathy, sleepiness, lethargy, loss of consciousness
confusion, delirium
This is a serious medical condition. If you or someone near you is having
symptoms of stroke, call 911 immediately.
Part 3 of 8: Causes
Causes of Intracerebral Hemorrhage
High blood pressure is the most common cause of intracerebral hemorrhage.
In younger people, another common cause is abnormally formed blood
vessels in the brain. Other causes include:
head injury or trauma

blood clot that blocks an artery in the brain
ruptured cerebral aneurysm (weak spot in a blood vessel that bursts)
arteriovenous malformation (a grouping of malformed blood vessels in the
brain that disrupts normal blood flow)
use of blood thinners
bleeding tumors
cocaine use, which can cause severe hypertension and lead to hemorrhage
bleeding disorders such as hemophilia and sickle cell anemia
Anyone can have an intracerebral hemorrhage, but your risk increases with
age. According to the Mayfield Clinic, men are at higher risk than women, as
are middle-aged people of Japanese or African-American descent (Mayfield
Clinic, 2009).
Part 4 of 8: Diagnosis
Diagnosing Intracerebral Hemorrhage
If you have some symptoms of ICH, a neurological exam will be performed.
Imaging tests are used to determine if you are having an ischemic stroke
(blockage) or a hemorrhagic (bleeding) stroke. Diagnostic testing for ICH may
include:
Computed tomography (CT scan): This type of test creates images of the
brain, which can detect skull fractures or confirm bleeding.
Magnetic resonance imaging (MRI): This type of imaging test may help your
doctor see the brain more clearly to better identify the cause of the bleeding.
Angiogram: This test uses X-ray technology to take pictures of blood flow
within an artery.
Blood tests may also be used to identify immune system disorders,

inflammation, and blood clotting problems that can cause bleeding in the
brain.
Part 5 of 8: Treatment
Treatment for Intracerebral Hemorrhage
Treatment within the first three hours of the onset of symptoms generally
results in a better outcome.
Surgery can relieve pressure on the brain and repair torn arteries. In addition,
certain medications may be prescribed to manage symptoms, such as
painkillers to ease severe headaches. Antianxiety drugs may be necessary to
control blood pressure. If your doctor determines that you are at risk for
seizures, antiepileptic drugs may be prescribed.
Long-term treatment will be needed to overcome symptoms caused by

damage to the brain. Depending on your symptoms, treatment may include
physical and speech therapy to help restore muscle function or improve
communication. Occupational therapy may help a person regain certain skills
and independence by practicing and modifying everyday activities.
Part 6 of 8: Complications
Complications from Intracerebral Hemorrhage
Depending on the location of the hemorrhage and how long your brain was
deprived of oxygen, complications may include:
impaired language skills

fatigue
problems with swallowing
vision loss
difficulty with sensations or movements on one side of the body
pneumonia
cognitive dysfunction (memory loss, difficulty reasoning), confusion
swelling on the brain
seizures
depression, emotional problems
Part 7 of 8: Outlook
Long-Term Outlook for Intracerebral Hemorrhage
Recovery following ICH differs greatly from person to person, and will depend
on a variety of factors, including your age and overall health, the location of
the hemorrhage, and the extent of the damage.
Some people may take months or years to recover. Most ICH patients have
some long-term disability. In some cases, around-the-clock or nursing home
care may be needed. According to The University of Washington Medical
Center (UWM), about 40 percent of ICH patients die within the first month
(UWM).
Stroke support groups can help people and families cope with long-term care.
Your doctor or hospital can provide information about support groups that
meet in your area.
Part 8 of 8: Prevention
Preventing Intracerebral Hemorrhage
You can decrease your chances of ICH by:
not smoking
treating heart disease
treating high blood pressure
keeping diabetes under control
maintaining a healthy lifestyle

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Practice Essentials

statin (lovastatin, simvastatin, atorvastatin, pravastatin sodium) had better 30-day

Anticonvulsants - To prevent seizure recurrence

microvascular platelet aggregation, and loss of microvascular perfusion, resulting in

Computed tomographic angiography examination and subsequent cerebral

deficiency can predispose to excessive bleeding, and intracranial hemorrhage has

reperfusion of ischemically injured tissue, either from recanalization of an occluded

GCS score 3-4: 2 points

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

Previous transient ischemic attack (TIA) and stroke

Hemorrhagic versus ischemic stroke

Sudden onset of severe headache

Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral

Gait or limb ataxia

Hypernatremia in Emergency Medicine

Hyperosmolar Hyperglycemic Nonketotic Coma

Noncontrast computed tomography scan of the brain (left) demonstrates an acute

Conventional angiography is the gold standard in evaluating for cerebrovascular

If systolic BP is over 200 mm Hg or mean arterial pressure (MAP) is over 150 mm

In patients presenting with a systolic BP of 150 to 220 mm Hg, acute lowering of

Sensory or motor disturbance (6%)

Sudden onset of severe headache (the classic feature)

Mild to moderate BP elevation

Serum chemistry panel

CT (noncontrast, contrast, or infusion)

Baseline chest radiograph

Osmotic agents (eg, mannitol)

Clipping the ruptured aneurysm

CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of

neurologic status, and additional medical management is directed toward the

formation of saccular aneurysms:

Increased blood pressure: Fibromuscular dysplasia, polycystic kidney disease, aortic

Intraventricular blood is the strongest determinant for the development of acute

Bilateral ambient cisternal blood

Anterior cerebral artery (40%)

LV systolic dysfunction in humans with SAH is associated with normal myocardial

Clusters of familial occurrence, such as in Finland, where the incidence of familial

and larger dilation (>5 mm) and aneurysms in 5% of the population.

Fusiform and mycotic aneurysms

Use of oral contraceptives

United States statistics

Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent

Group 1 - No blood detected

Grade 0 - Unruptured aneurysm

headache, nausea, and vomiting

temporary loss of vision

AVM: a tangle of abnormal arteries and veins with no capillaries in between.

Aneurysm: a bulge or weakening of an arterial wall.

Bleeding disorders: hemophilia, sickle cell anemia, DIC, thrombocytopenia.

Amyloid angiopathy: a degenerative disease of the arteries.

Spontaneous: ICH by unknown causes.

Figure 2. CT scan showing a large ICH.

Lobar Intracerebral Hemorrhage

Stroke-like symptoms usually appear suddenly during ICH, causing symptoms

This is a medical emergency requiring immediate treatment. ICH is not as

Treatment generally involves surgery to repair damaged blood vessels.

Symptoms of Intracerebral Hemorrhage

sudden weakness, tingling, or paralysis in the face, arm, or leg, especially if it

head injury or trauma

Blood tests may also be used to identify immune system disorders,

Long-term treatment will be needed to overcome symptoms caused by

impaired language skills

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