Subarachnoid Hemorrhage: Practice Essentials, Background, Pathophysiology 5/2/16, 6:42 PM

Subarachnoid Hemorrhage
Author: Tibor Becske, MD; Chief Editor: Helmi L Lutsep, MD more...

Updated: Oct 30, 2015

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
Focal neurologic deficits
Sudden loss of consciousness at the ictus

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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)

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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

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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

Complications of SAH include the following:

Hydrocephalus
Rebleeding
Delayed cerebral ischemia from vasospasm
Intracerebral hemorrhage
Intraventricular hemorrhage
Left ventricular systolic dysfunction
Subdural hematoma
Seizures
Increased intracranial pressure

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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
Intraventricular hemorrhage
Left ventricular systolic dysfunction
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.

Intracerebral hemorrhage

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.

Intraventricular hemorrhage

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%)

Left ventricular systolic dysfunction

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.

Increased intracranial pressure

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

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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

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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, age-adjusted 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 Denmark
marked 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

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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 I-III 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

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Complications of SAH include the following:

Hydrocephalus
Rebleeding
Delayed ischemia
Intracerebral hemorrhage
Intraventricular hemorrhage (IVH)
Left ventricular systolic dysfunction
Subdural hematoma
Seizures
Increased intracranial pressure
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 15-20% 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.

Intraventricular hemorrhage

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.

Clinical Presentation

Contributor Information and Disclosures

Author
Tibor Becske, MD Clinical Assistant Professor, Departments of Radiology and Neurology, Langone Medical
Center, New York University School of Medicine; Assistant Attending Physician, Departments of Radiology and
Neurology, Bellevue Hospital Center

Tibor Becske, MD is a member of the following medical societies: Society of NeuroInterventional Surgery,
Society of Vascular and Interventional Neurology

Disclosure: Received reimbursement of expenses and proctoring honoraria from ev3 for independent contractor.

Coauthor(s)
George I Jallo, MD Professor of Neurosurgery, Pediatrics, and Oncology, Director, Clinical Pediatric
Neurosurgery, Department of Neurosurgery, Johns Hopkins University School of Medicine

George I Jallo, MD is a member of the following medical societies: American Association of Neurological
Surgeons, American Medical Association, American Society of Pediatric Neurosurgeons

Disclosure: Received grant/research funds from Codman (Johnson & Johnson) for consulting; Received
grant/research funds from Medtronic for consulting.

Chief Editor
Helmi L Lutsep, MD Professor and Vice Chair, Department of Neurology, Oregon Health and Science
University School of Medicine; Associate Director, OHSU Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology, American
Stroke Association

Disclosure: Medscape Neurology Editorial Advisory Board for: Stroke Adjudication Committee, CREST2.

Acknowledgements
Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha,
American Academy of Neurology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice
Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke
Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff,

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Subarachnoid Hemorrhage: Practice Essentials, Background, Pathophysiology 5/2/16, 6:42 PM

Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American
Academy of Neurology, American Heart Association, American Medical Association, American Neurological
Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and
Tennessee Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center
College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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