Perdarahan Sub Arachnoid

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.

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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
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.
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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, 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 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
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
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 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.
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.
History
The signs and symptoms of subarachnoid hemorrhage (SAH) range from subtle prodromal
events to the classic presentation. Prodromal events often are misdiagnosed, while the classic
presentation is one of the most pathognomonic pictures in all of clinical medicine.
Prodromal events
Signs and symptoms precede ruptured cerebral aneurysm in anywhere from 10-50% of cases.
Premonitory manifestations generally appear 10-20 days prior to rupture. The most common
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 one or more of the following:
Sentinel leaks
Mass effect of aneurysm expansion
Emboli
Sentinel leaks
Sentinel, or "warning," leaks with minor loss of blood from the aneurysm are reported to occur in
30-50% of aneurysmal SAHs. Sentinel leaks produce sudden focal or generalized head pain that
may be severe. Sentinel headaches precede aneurysm rupture by a few hours to a few months,
with a reported mean of 2 weeks prior to discovery of the SAH.
In addition to headaches, sentinel leaks may produce nausea, vomiting, photophobia, malaise, or,
less commonly, neck pain. These symptoms may be ignored by the physician. Therefore, a high
index of suspicion is necessary for accurate diagnosis. Sentinel leaks usually do not generate
symptoms suggestive of elevated intracranial pressure (ICP) or meningeal irritation. Sentinel
leaks usually do not occur in patients with arteriovenous malformations.
Mass effect
Prodromal presentations occasionally are caused by the mass effect of an expanding aneurysm
and have characteristic features based on aneurysm location, as follows:
Posterior communicating artery/internal carotid artery: focal, progressive retro-orbital
headaches and oculomotor nerve palsy
Middle cerebral artery: contralateral face or hand paresis, aphasia (left side), contralateral
visual neglect (right side)
Anterior communicating artery: bilateral leg paresis and bilateral Babinski sign
Basilar artery apex: vertical gaze, paresis, and coma
Intracranial vertebral artery/posterior inferior cerebellar artery: vertigo, components of

lateral medullary syndrome
Emboli
Emboli originating from intra-aneurysmal thrombus formation can cause transient ischemic
attacks.
Classic presentation
The central feature of classic SAH is sudden onset of severe headache (thunderclap headache),
often described as the "worst headache of my life." Less severe hemorrhages may cause
headache of moderate intensity, neck pain, and nonspecific symptoms. Absence of headache in
the setting of a ruptured intracranial aneurysm is rare and probably represents amnesia for the
event.
The headache may be accompanied by nausea and/or vomiting from increased ICP and
meningeal irritation. Symptoms of meningeal irritation, including nuchal rigidity and pain, back
pain, and bilateral leg pain, occur in as many as 80% of patients with SAH but may take several
hours to manifest. Photophobia and visual changes are common. Focal neurologic deficits may
also occur.
Sudden loss of consciousness (LOC) occurs at the ictus in as many as 45% of patients as
intracranial pressure (ICP) exceeds cerebral perfusion pressure. LOC often is transient; however,
approximately 10% of patients remain comatose for several days, depending on the location of
the aneurysm and the amount of bleeding.
Seizures during the acute phase of SAH occur in 10-25% of patients. Seizures result from the
sudden rise in ICP or direct cortical irritation by blood. No correlation exists between the seizure
focus and the anatomic site of aneurysm rupture.
A proposed decision rule for diagnosis of SAH focuses on the following 7 characteristics, which
are strongly associated with SAH:
Aged 40 years or older

Witnessed loss of consciousness
Complaint of neck pain or stiffness
Onset of manifestations with exertion
Arrival by ambulance
Vomiting
Diastolic blood pressure 100 mm Hg or systolic blood pressure 160 mm Hg
Should one or more of these be present in a patient with an acute nontraumatic headache
reaching maximum intensity within 1 hour, the possibility of SAH hemorrhage should be
investigated. [12] On the other hand, it may be possible to consider foregoing investigation in
patients with none of these characteristics. [12] This decision rule has not yet been validated.
Further study is needed before this approach can be recommended.
Approximately 30-40% of patients are at rest at the time of SAH. Physical or emotional strain,
defecation, coitus, and head trauma contribute to varying degrees in the remaining 60-70% of
cases.
Physical Examination
Physical examination findings may be normal. About half of patients have mild to moderate
blood pressure (BP) elevation. BP may become labile as ICP increases. Temperature elevation,
secondary to chemical meningitis from subarachnoid blood products, is common after the fourth
day following bleeding. Tachycardia may be present for several days after the occurrence of a
hemorrhage.
Funduscopy may reveal papilledema. Subhyaloid retinal hemorrhage (small round hemorrhage,
perhaps with visible meniscus, near the optic nerve head) is evident in 20-30% of patients. Other
retinal hemorrhages may be seen.
Global or focal neurologic abnormalities are found in more than 25% of patients. Global
depression of neurologic function may be noted, including altered level of consciousness and
confusional state. Motor neurologic deficits occur in 10-15% of patients, usually from middle
cerebral artery aneurysms. In 40% of patients, no localizing signs are evident. Seizures may
occur.
Focal neurologic findings
Cranial nerve palsies, along with memory loss, are present in 25% of patients. The most frequent
is oculomotor nerve palsy with or without ipsilateral mydriasis, which results from rupture of a
posterior communicating artery aneurysm. Abducens nerve palsy is usually due to increased ICP
rather than a true localizing sign. Monocular vision loss can be caused by an ophthalmic artery
aneurysm compressing the ipsilateral optic nerve.
Hemiparesis results from middle cerebral artery (MCA) aneurysm, ischemia or hypoperfusion in
the vascular territory, or intracerebral clot. Patients may also have aphasia, hemineglect, or both.
Leg monoparesis or paraparesis with or without akinetic mutism/abulia points to anterior
communicating aneurysm rupture.
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
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 neurological 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 1-3 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
Some complications of SAH include the following:
Hydrocephalus
Rebleeding
Vasospasm
Seizures
Cardiac dysfunction
Hydrocephalus
Hydrocephalus can be an acute or a delayed complication of SAH. Acute obstructive

hydrocephalus complicates 20% of SAH cases. Clinical risk factors for the development of
hydrocephalus include increased patient age, use of antifibrinolytic drugs, left ventricular
systolic dysfunction, and seizures.
Acute hydrocephalus usually occurs within the first 24 hours after hemorrhage but may occur as
late as 7 days afterward. It presents as a relatively abrupt mental status change, including
lethargy, stupor, or coma. CT scan differentiates hydrocephalus from rebleeding.
Acute hydrocephalus can precipitate life-threatening brainstem compression and occlusion of

blood vessels. It is associated with lower preoperative Hunt and Hess grade and poorer
prognosis. Consequently, any change in the level of consciousness requires an emergent CT scan
to evaluate ventricular size. An obtunded patient with dilated ventricles deserves an immediate
ventriculostomy.
Late or chronic hydrocephalus, caused by scarring of the arachnoid granulations and alterations
in CSF absorption, occurs in 10-15% of patients with SAH. Typically, late hydrocephalus is of
the communicating type and develops 10 or more days after SAH. Patients may present with
incontinence, gait instability, and cognitive deterioration. It may be impossible to distinguish late
hydrocephalus from vasospasm clinically.
Rebleeding
The incidence of the complication of rebleeding 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. Clinical factors that increase the likelihood of rebleeding include the
following:
Hypertension
Anxiety [5]
Agitation
Seizures
Vasospasm
Currently, delayed ischemia from arterial smooth muscle contraction of the large capacitance
vessels at the base of the brain is the leading cause of death and disability following aneurysmal
SAH. Vasospasm is symptomatic in 36% of patients. The incidence of angiographic vasospasm is
30-70%; of these patients, 20-36% become symptomatic.
Risk factors for vasospasm include the following:
Larger volumes of blood in the subarachnoid space
Clinically severe SAH
Female sex
Young age
Smoking
Vasospasm may be clinically indistinguishable from rebleeding. Symptoms vary with the arterial
territory involved, but patients typically present with a new-onset general decrease in
consciousness or focal neurologic deficit. Lethargy, with or without focal neurologic deficit, is a
manifestation of vasospasm, until proven otherwise.
Overall, vasospasm typically has its onset on day 3 after SAH, is maximal at about days 6-8, and
usually resolves around day 12. However, the time of clinical onset differs according to whether
the patient has had a prior SAH. In patients with previous SAH, the incidence of vasospasm is
38.7% in the first 3 days and only 20% between days 10 and 17. In patients with no prior SAH,
most frequent time of onset is between days 10 and 17, with only a 4.2% incidence on day 3.
Overall, close to 50% of patients develop vasospasm in the peak period. Correlation between the
initial CT scan and the incidence of vasospasm is well established. When the CT scan fails to
demonstrate blood or shows only a thin layer, vasospasm is unlikely. If the CT scan shows a
significant blood clot of 5 X 3 mm or larger, severe angiographic spasm and clinical deficits
follow in nearly all cases.
Conventional angiography is the definitive imaging study for vasospasm. The diagnosis of
vasospasm can be made reliably at the bedside in a noninvasive fashion with transcranial
Doppler.
Other tests, such as single-photon emission computed tomography (SPECT), positron emission
tomography (PET), xenon CT scan, and radioactive xenon clearance, can be useful for evaluation
of regional cerebral blood flow in patients with vasospasm. However, these tests often are
difficult to perform on critically ill patients.
Seizures
Seizures occur in 13-24% of patients with SAH, commonly in the first 24 hours after the bleed.
[13]
They are most common after rupture of middle cerebral artery aneurysms. Generalized,
partial, and complex-partial seizures are observed after SAH. Seizures can lead to increased
cerebral blood flow, hypertension, and elevated ICP, thereby escalating the risk of rebleeding and
neurologic deterioration.
Cardiac dysfunction
Cardiac dysfunction occurs in a significant number of people with SAH. Neurogenic sympathetic
hyperactivity, as well as increased levels of systemic catecholamines, has been implicated in
SAH-associated cardiac dysfunction. Arrhythmias occur in as many as 90% of patients and most
commonly include the following:
Premature ventricular complexes (PVCs)
Bradyarrhythmias
Supraventricular tachycardia
Arrhythmias are most prevalent in the first 48 hours following SAH. Only a small percentage of
arrhythmias (usually those associated with hypokalemia) are life-threatening.
Diagnostic Considerations
Missing SAH obviously carries major medicolegal consequences. [14] In the emergency
department, clinicians should err on the side of "overtapping" patients.
A good history of the current headache is essential, even in known migraineurs, and if the
presentation has any unusual aspects (eg, worst ever headache, episode of loss of consciousness,
first ever episode of diplopia), obtain a CT scan of the head and perform a lumbar puncture even
if the CT scan is negative for blood. Do not forget to measure opening pressure and adequately
check for xanthochromia.
Differential Diagnoses
Aseptic Meningitis
Cluster Headache in Emergency Medicine
Encephalitis
First Adult Seizure
Hypertensive Emergencies in Emergency Medicine
Intracranial Hemorrhage
Ischemic Stroke in Emergency Medicine

Meningitis
Migraine Headache
Transient Ischemic Attack
Approach Considerations
The diagnosis of subarachnoid hemorrhage (SAH) usually depends on a high index of clinical
suspicion combined with radiologic confirmation via urgent computed tomography (CT) scan
without contrast. Traditionally, a negative CT scan is followed with lumbar puncture (LP).
However, noncontrast CT followed by CT angiography (CTA) of the brain can rule out SAH
with greater than 99% sensitivity. [2]
Compared with the traditional recommendation of CT followed by LP, CT/CTA may offer a less
invasive and more informative diagnostic approach for emergency department patients
complaining of acute-onset headache and with no significant risk factors for SAH. A
disadvantage of foregoing LP is that spinal fluid analysis may point toward an alternative
diagnosis.
After the diagnosis of SAH is established, further imaging should be performed to characterize
the source of the hemorrhage. This effort can include standard angiography, CT angiography, and
magnetic resonance (MR) angiography.
Laboratory studies for SAH should include the following:
Serum chemistry panel - To establish a baseline for detection of future complications
Complete blood count - For evaluation of possible infection or hematologic abnormality
Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - For evaluation
of possible coagulopathy
Blood typing/screening - To prepare for possible intraoperative transfusions
Cardiac enzymes - For evaluation of possible myocardial ischemia
Arterial blood gas (ABG) - Necessary in patients with pulmonary compromise
Serum cardiac troponin measurement is important in patients with subarachnoid hemorrhage,

even in those without underlying cardiac conditions. It was initially thought to be useful only as
a predictor for the occurrence of pulmonary and cardiac complications. [15] However, correlation
was subsequently found between troponin levels and neurologic complications and outcome. [16]
All patients with SAH should have a baseline chest radiograph to serve as a reference point for
evaluation of possible pulmonary complications. All patients with SAH should also have an
electrocardiogram (ECG) on admission. Patients with SAH can have myocardial ischemia due to
the increased level of circulating catecholamines or to autonomic stimulation from the brain.
Myocardial infarction is a rare complication. However, suspicion of SAH is a contraindication to
thrombolytic and anticoagulant therapy.
Because most of the ECG abnormalities that occur with SAH are benign and reversible,
differentiating true myocardial ischemia from benign changes is important. Two-dimensional
echocardiography often is more sensitive in detecting myocardial ischemia than is ECG and thus
is useful in the setting of SAH.
Other imaging studies may be indicated. MRI is performed if no lesion is found on angiography,
and transcranial Doppler studies are useful in the detection and monitoring of arterial vasospasm.
Computed Tomography
CT without contrast is the most sensitive imaging study in SAH (see the images below). When
carried out within 6 hours of headache onset, CT has 100% sensitivity and specificity. Sensitivity
is 93% within 24 hours of onset, [17] 80% at 3 days, and 50% at 1 week. [18] Sensitivity is less on
older second- or first-generation scanners, but most North American hospitals have been using
third-generation scanners since the mid 1980s. Thin (3 mm) cuts are necessary to properly
identify the presence of smaller hemorrhages.
CT scan reveals subarachnoid hemorrhage in the right sylvian fissure; no evidence of
hydrocephalus is apparent.
View Media Gallery
CT scan reveals subarachnoid hemorrhage in the sylvian fissure, right more than left.
View Media Gallery

A 47-year-old woman presented with headache and vomiting; her CT scan in the
emergency department revealed subarachnoid hemorrhage.

View Media Gallery
Brain CT scan showing subtle finding of blood at the area of the circle of Willis
consistent with acute subarachnoid hemorrhage. Image courtesy of Dana Stearns, MD,
Massachusetts General Hospital.
View Media Gallery
Findings may be negative in 10-15% of patients with SAH. A falsely negative CT scan can result
from severe anemia or small-volume subarachnoid hemorrhage.
The location of blood within the subarachnoid space correlates directly with the location of the
aneurysm in 70% of cases. In general, blood localized to the basal cisterns, the sylvian fissure, or
the intrahemispheric fissure indicates rupture of a saccular aneurysm. Blood lying over the
convexities or within the superficial parenchyma of the brain often is indicative of arteriovenous
malformation (AVM) or mycotic aneurysm rupture.
Intraparenchymal hemorrhage may occur with middle communicating artery and posterior
communicating artery aneurysms. Interhemispheric and intraventricular hemorrhages may occur
with anterior communicating artery aneurysms.
A contrast-enhanced CT scan may reveal an AVM. However, this study should not be performed
before a noncontrast CT scan because the contrast may interfere with the visualization of
subarachnoid blood.
Degree and location of SAH are significant prognostic factors. The Fisher grading system is used
to classify SAH, as follows:
Grade 1 - No subarachnoid blood seen on CT scan
Grade 2 - Diffuse or vertical layers of SAH less than 1 mm thick
Grade 3 - Diffuse clot and/or vertical layer greater than 1 mm thick
Grade 4 - Intracerebral or intraventricular clot with diffuse or no subarachnoid blood
CT scan allows for the detection of ventricular size and, thus, evaluation and surveillance of
mass effect and hydrocephalus. On CT scan, hydrocephalus is evident as trapped temporal horns
and "Mickey Mouse" appearance of the ventricular system.
Infusion CT scan
Some centers have obtained good results with infusion CT scanning. This scan employs a
contrast dye and can be performed immediately after a noncontrast CT scan. Reformatted image
data can be viewed and rotated in 2-dimensional displays. Infusion CT scanning has been
reported to detect aneurysms larger than 3 mm with a sensitivity of 97%, which may provide
sufficient anatomic detail to allow for surgical management in the absence of angiography.
Lumbar Puncture
LP is traditionally performed as a follow-up test when a CT scan has shown no SAH and has
excluded possible contraindications to LP such as significant intracranial mass effect, elevated
ICP, obstructive hydrocephalus, or obvious intracranial bleed. LP should not be performed if the
CT scan demonstrates an SAH because of the (small) risk of further intracranial bleeding
associated with a drop in ICP.
An LP is performed to evaluate the cerebrospinal fluid for the presence of red blood cells (RBCs)
and xanthochromia. LP may be negative if performed less than 2 hours after an SAH occurs; LP
is most sensitive 12 hours after onset of symptoms. CSF samples taken within 24 hours of the
ictus usually show a WBC-to-RBC ratio that is consistent with the normal circulating WBC-to-
RBC ratio of approximately 1:1000. After 24 hours, CSF samples may demonstrate a
polymorphonuclear and mononuclear polycytosis secondary to chemical meningitis caused by
the degradation products of subarachnoid blood.
RBCs in the CSF can reflect a traumatic LP rather than SAH; however, SAH often can be
distinguished from traumatic LP by comparing the RBC count of the first and last tubes of CSF.
In traumatic LP, the RBC count in the last tube is usually lower, whereas in SAH the RBC
typically remains consistently elevated. Nevertheless, cases of SAH in which the RBC count is
lower have been reported.
No consensus is found in the literature on the lower limit of the RBC count in the CSF that
signifies a positive tap. However, most counts range from a few hundred to a million or more
cells per cubic millimeter. The most reliable method of differentiating SAH from a traumatic tap
is to spin down the CSF and examine the supernatant fluid for the presence of xanthochromia, a
pink or yellow coloration caused by the breakdown of RBCs and subsequent release of heme
pigments.
Xanthochromia typically will not appear until 2-4 hours after the ictus. In nearly 100% of
patients with an SAH, xanthochromia is present 12 hours after the bleed and remains for
approximately 2 weeks. Xanthochromia is present 3 weeks after the bleed in 70% of patients,
and it is still detectable at 4 weeks in 40% of patients. Spectrophotometry is much more sensitive
than the naked eye in detecting xanthochromia. Nevertheless, many laboratories rely on visual
inspection.
Some authors have suggested that the D-dimer assay can be used to discriminate SAH from
traumatic LP. Results have been conflicting, however, and further data are needed.
Patients with negative CT and LP findings have a favorable prognosis. However, LP findings can
be negative in approximately 10-15% of patients with SAH. In the past, LP findings were
thought to be positive in 5-15% of all SAH presentations that are not evident on the CT scan.
This number may be no longer valid with the advent of newer generations of CT scans. A small
retrospective review of patients who presented to the ED and underwent fifth-generation CT
scans and LP showed no cases of a positive LIP after a negative CT scan. [19
LP dilakukan untuk mengevaluasi cairan serebrospinal untuk kehadiran sel-sel darah merah (sel
darah merah) dan xanthochromia. LP mungkin negatif jika dilakukan kurang dari 2 jam setelah
SAH terjadi; LP adalah yang paling sensitif 12 jam setelah timbulnya gejala. sampel CSF
diambil dalam waktu 24 jam dari tekanan ritmik biasanya menunjukkan rasio WBC-to-RBC
yang konsisten dengan rasio yang normal beredar WBC-to-RBC sekitar 1: 1000. Setelah 24 jam,
sampel CSF mungkin menunjukkan polimorfonuklear dan polycytosis mononuklear sekunder
untuk meningitis kimia yang disebabkan oleh produk degradasi darah subarachnoid.
Sel darah merah dalam CSF dapat mencerminkan LP traumatis daripada SAH; Namun, SAH
sering dapat dibedakan dari LP traumatis dengan membandingkan jumlah RBC tabung pertama
dan terakhir dari CSF. Di LP traumatis, jumlah RBC dalam tabung terakhir biasanya lebih
rendah, sedangkan di SAH RBC biasanya tetap konsisten tinggi. Namun demikian, kasus SAH di
mana jumlah RBC yang lebih rendah telah dilaporkan.
Tidak ada konsensus ditemukan dalam literatur pada batas bawah dari jumlah RBC dalam CSF
yang menandakan keran positif. Namun, sebagian besar jumlah berkisar dari beberapa ratus
hingga satu juta atau lebih sel per milimeter kubik. Metode yang paling dapat diandalkan
membedakan SAH dari keran traumatis adalah untuk spin down CSF dan memeriksa cairan
supernatan untuk kehadiran xanthochromia, merah muda atau warna kuning yang disebabkan
oleh rusaknya sel darah merah dan rilis berikutnya dari pigmen heme.
Xanthochromia biasanya tidak akan muncul sampai 2-4 jam setelah tekanan ritmik tersebut.
Dalam hampir 100% dari pasien dengan SAH, xanthochromia hadir 12 jam setelah perdarahan
dan tetap selama kurang lebih 2 minggu. Xanthochromia hadir 3 minggu setelah perdarahan pada
70% pasien, dan masih terdeteksi pada 4 minggu di 40% dari pasien. Spektrofotometri jauh lebih
sensitif dibandingkan dengan mata telanjang dalam mendeteksi xanthochromia. Namun
demikian, banyak laboratorium mengandalkan inspeksi visual.
Beberapa penulis telah menyarankan bahwa uji D-dimer dapat digunakan untuk membedakan
SAH dari LP traumatis. Hasilnya bertentangan, namun, dan data lebih lanjut diperlukan.
Pasien dengan negatif CT dan LP temuan memiliki prognosis yang menguntungkan. Namun,
temuan LP bisa negatif di sekitar 10-15% dari pasien dengan SAH. Di masa lalu, temuan LP
yang dianggap positif dalam 5-15% dari semua presentasi SAH yang tidak jelas pada CT scan.
Jumlah ini mungkin sudah tidak berlaku lagi dengan munculnya generasi baru dari CT scan.
Sebuah tinjauan retrospektif kecil pasien yang disajikan kepada ED dan menjalani CT scan
generasi kelima dan LP menunjukkan tidak ada kasus dari LIP positif setelah CT scan negatif.
[19
Cerebral Angiography
Digital-subtraction cerebral angiography has been the criterion standard for the detection of
cerebral aneurysms (see the images below). It is particularly useful in cases of diagnostic
uncertainty (after CT scan and LP) and in patients with septic endocarditis and SAH to search for
the presence of mycotic aneurysms.
In cases where the diagnosis of SAH has been determined, the timing of cerebral angiography
will depend on surgical considerations. Cerebral angiography can provide the following
important surgical information in the setting of SAH:
Cerebrovascular anatomy
Aneurysm location and source of bleeding
Aneurysm size and shape, as well as orientation of the aneurysm dome and neck
Relation of the aneurysm to the parent artery and perforating arteries
Presence of multiple or mirror aneurysms (identically placed aneurysms in both the left
and right circulations)
A trial balloon occlusion of the parent artery can be performed and may help to guide
preoperative surgical planning.
Cerebral angiogram reveals a middle cerebral artery aneurysm.
View Media Gallery

Cerebral angiogram reveals a middle cerebral artery aneurysm.
View Media Gallery

Cerebral angiogram (lateral view) reveals a large aneurysm arising from the left anterior
choroidal artery.
View Media Gallery
Cerebral angiogram (anteroposterior view) reveals a large aneurysm arising from the left
anterior choroidal artery.

View Media Gallery
Negative angiographic findings do not rule out aneurysm. Approximately 10-20% of patients
with clinically diagnosed SAH (on CT and/or lumbar puncture) have negative angiographic
findings. A repeat angiogram is usually required in 10-21 days in such cases.
A negative study finding can result from aneurysm obliteration secondary to clotting.
Hemorrhage secondary to a ruptured AVM or spinal cord aneurysm may be present despite a
negative finding on cerebral angiogram. Perimesencephalic venous hemorrhage also should be
considered
Follow-up angiography is useful after surgical intervention. The postoperative study can confirm
aneurysmal obliteration and to evaluate for possible cerebral vasospasm. The management of
moribund patients with CT scan evidence of a large SAH and focal hematoma is controversial.
Performing angiography may result in a life-threatening delay in treatment.
CT Angiography
Although digital-subtraction cerebral angiography has been the criterion standard for the
detection of cerebral aneurysms, multidetector CT angiography (MD-CTA) of the intracranial
vessels is now routinely performed, and it is becoming fully integrated into the imaging and
treatment algorithm of patients presenting with acute subarachnoid hemorrhage in many centers
in the United Kingdom and Europe. [20]
The popularity of MD-CTA derives from its noninvasiveness and a sensitivity and specificity
comparable to that of cerebral angiography. [21, 22] This technique is beneficial in very unstable
patients who cannot undergo angiography or in emergent settings prior to operative intervention
for clot evacuation. [21
Magnetic Resonance Imaging
MRI is performed if no lesion is found on angiography. Its sensitivity in detecting blood is

considered equal or inferior to that of CT scan. The higher cost, lower availability, and longer
study time make it less optimal for detecting SAH. In addition, MRI is not sensitive for SAH
within the first 48 hours.
MRI is a useful tool to diagnose AVMs that are not detected by cerebral angiography or spinal
AVMs causing SAH. It can also be useful for diagnosing and monitoring unruptured cerebral
aneurysms. MRI can detect aneurysms 5 mm or larger with a high sensitivity and is useful for
monitoring the status of small, unruptured aneurysms. MRI can be used to evaluate the degree of
intramural thrombus in giant aneurysms.
One study found that cranial MRI including the brain and craniocervical region does not provide
additional benefit for the detection of bleeding sources in patients with perimesencephalic and
nonperimesencephalic SAH. However, MRI should be considered on a case-by-case basis
because rare bleeding sources are possible in cases of nonperimesencephalic SAH. [23]
Magnetic Resonance Angiography
The role of magnetic resonance angiography (MRA) in the detection of SAH currently is under
investigation; however, many authors believe that MRA eventually will replace conventional
transfemoral cerebral angiography. Given the current limitations of MRA, which include lower
sensitivity than cerebral angiography in the detection of small aneurysms and failure to detect
posterior inferior communicating artery and anterior communicating artery aneurysms in one
series, most authors feel that the risk/benefit ratio still favors conventional angiography.
Electrocardiography
All patients with SAH should have a baseline chest radiograph to serve as a reference point for
evaluation of possible pulmonary complications. All patients with SAH should have an
electrocardiogram (ECG) on admission. Patients with SAH can have myocardial ischemia due to
the increased level of circulating catecholamines or to autonomic stimulation from the brain.
Myocardial infarction is a rare complication.
ECG abnormalities frequently detected in patients with SAH include the following:
Nonspecific ST and T wave changes
Decreased PR intervals
Increased QRS intervals
Increased QT intervals
Presence of U waves
Dysrhythmias, including premature ventricular contractions (PVCs), supraventricular

tachycardia (SVT), and bradyarrhythmias
Meskipun digital-pengurangan angiography cerebral telah menjadi standar kriteria

untuk mendeteksi aneurisma otak, multidetector CT angiography (MD-CTA) dari
pembuluh intrakranial sekarang rutin dilakukan, dan itu menjadi sepenuhnya
terintegrasi ke dalam pencitraan dan pengobatan algoritma dari pasien yang
dengan perdarahan subarachnoid akut di banyak pusat di Inggris dan Eropa. [20]
Popularitas MD-CTA berasal dari noninvasiveness dan sensitivitas dan spesifisitas
sebanding dengan angiografi serebral. [21, 22] Teknik ini bermanfaat dalam pasien
sangat tidak stabil yang tidak dapat menjalani angiografi atau pengaturan muncul
sebelum intervensi operasi untuk evakuasi bekuan. [21
Magnetic Resonance Imaging
MRI dilakukan jika tidak ada lesi ditemukan pada angiografi. sensitivitas dalam
mendeteksi darah dianggap sama atau lebih rendah dengan yang CT scan. Biaya
yang lebih tinggi, ketersediaan rendah, dan waktu belajar lebih lama membuatnya
kurang optimal untuk mendeteksi SAH. Selain itu, MRI tidak sensitif untuk SAH
dalam 48 jam pertama.
MRI adalah alat yang berguna untuk mendiagnosa AVMs yang tidak terdeteksi
dengan angiografi serebral atau AVMs tulang belakang menyebabkan SAH. Hal ini
juga dapat berguna untuk mendiagnosis dan pemantauan aneurisma otak
unruptured. MRI dapat mendeteksi aneurisma 5 mm atau lebih besar dengan
sensitivitas yang tinggi dan berguna untuk memantau status kecil, aneurisma
ruptur. MRI dapat digunakan untuk menilai tingkat trombus intramural di aneurisma
raksasa.
Satu studi menemukan bahwa MRI kranial termasuk otak dan craniocervical daerah
tidak memberikan manfaat tambahan untuk deteksi perdarahan sumber pada
pasien dengan SAH perimesencephalic dan nonperimesencephalic. Namun, MRI
harus dipertimbangkan atas dasar kasus per kasus karena sumber perdarahan
langka yang mungkin dalam kasus SAH nonperimesencephalic. [23]
Magnetic Resonance Angiography
Peran magnetic resonance angiography (MRA) dalam mendeteksi SAH saat ini
sedang diselidiki; Namun, banyak penulis percaya bahwa MRA akhirnya akan
menggantikan angiografi serebral transfemoral konvensional. Mengingat
keterbatasan saat MRA, yang meliputi sensitivitas lebih rendah dari angiografi
serebral dalam mendeteksi aneurisma kecil dan kegagalan untuk mendeteksi
posterior rendah berkomunikasi arteri dan anterior berkomunikasi aneurisma arteri
dalam satu seri, sebagian besar penulis merasa bahwa rasio risiko / manfaat masih
nikmat angiografi konvensional .
elektrokardiografi
Semua pasien dengan SAH harus memiliki rontgen dada dasar untuk melayani
sebagai titik acuan untuk evaluasi komplikasi paru mungkin. Semua pasien dengan
SAH harus memiliki elektrokardiogram (EKG) pada masuk. Pasien dengan SAH dapat
memiliki iskemia miokard karena tingkat peningkatan sirkulasi katekolamin atau
stimulasi otonom dari otak. infark miokard merupakan komplikasi yang jarang.
Kelainan EKG sering terdeteksi pada pasien dengan SAH adalah sebagai berikut:
nonspesifik ST dan gelombang T perubahan
interval PR Penurunan
interval QRS Peningkatan
interval QT Peningkatan
Adanya gelombang U
Disritmia, termasuk kontraksi prematur ventrikel (PVC), supraventricular
tachycardia (SVT), dan bradiaritmia
Approach Considerations
The traditional treatment of subarachnoid hemorrhage (SAH) from a ruptured cerebral aneurysm
included strict blood pressure control, with fluid restriction and antihypertensive therapy. This
approach was associated with a high rate of morbidity and mortality from the ischemic
complications of hypovolemia and hypotension.
Current recommendations advocate the use of antihypertensive agents when the mean arterial
pressure (MAP) exceeds 130 mm Hg. Intravenous beta-blockers, which have a relatively short
half-life, can be titrated easily and do not increase intracranial pressure (ICP). Beta-blockers are
the agents of choice in patients without contraindications.
Most clinicians avoid the use of nitrates, such as nitroprusside or nitroglycerin, which elevate
ICP. Hydralazine and calcium channel blockers have a fast onset and lead to a relatively lower
increase in ICP than do nitrates. Angiotensin-converting enzyme inhibitors have a relatively slow
onset and are not first-line agents in the setting of acute SAH.
Patients with signs of increased ICP or herniation should be intubated and hyperventilated.
Minute ventilation should be titrated to achieve a PCO2 of 30-35 mm Hg. Avoid excessive
hyperventilation, which may potentiate vasospasm and ischemia.
Other interventions for increased ICP include the following:
Osmotic agents (eg, mannitol), which can decrease ICP dramatically (50% 30 minutes
post administration)
Loop diuretics (eg, furosemide) also can decrease ICP
The use of intravenous steroids (eg, dexamethasone [Decadron]) for decreasing ICP is
controversial but is recommended by some authors
Patients must be admitted to the intensive care unit (ICU) with strict bed rest until the etiology of
hemorrhage is determined. Patients should not be allowed out of bed for any reason. All patients
should receive frequent neurologic evaluation. Use sedatives and analgesics cautiously to avoid
masking the neurologic examination findings.
Additional medical management is directed to prevent and treat the following common
complications of SAH:
Rebleeding
Vasospasm
Hydrocephalus
Hyponatremia
Seizures
Pulmonary complications
Cardiac complications
Ideally, management of the complications of SAH should take place in a neurologic ICU or in an
ICU similarly equipped. To minimize stimuli that may lead to an elevation of ICP, have the
patient placed in a darkened, quiet, private room and given mild sedation if agitated. The head of
the bed should be kept elevated at 30 to ensure optimal venous drainage.
Blood pressure must be maintained with consideration of the patient's neurologic status.
Optimally, systolic blood pressure (SBP) of no more than 130-140 mm Hg should be the goal,
unless clinical evidence of vasospasm is noted.
Indwelling catheters include an arterial line, central venous access, and Foley catheter. Seizure
prophylaxis and calcium channel blockade are standard medical measures. Some centers favor
volume expansion to treat vasospasm that develops days after the initial bleeding episode.
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.
The neurosurgeon/neurointerventionalist must be involved early in the care of the patient with an
aneurysmal SAH.
Initial Management
The initial management of patients with SAH is directed at patient stabilization. Assess the level
of consciousness and airway, breathing, and circulation (ABCs).
Endotracheal intubation should be performed for patients presenting with coma, depressed level
of consciousness, inability to protect their airway, or increased intracranial pressure (ICP).
Rapid-sequence intubation should be employed, if possible, including the use of sedation,
defasciculation, short-acting neuromuscular blockade, and agents to blunt an increase in ICP.
Intravenous access should be obtained, including central and arterial lines. A short-acting
benzodiazepine, such as midazolam, should be administered prior to all procedures. Monitoring
should include the following:
Cardiac monitoring
Pulse oximetry
Automated and/or arterial blood pressure monitoring (arterial BP monitoring is indicated

in high-grade SAH or when blood pressure is labile)
End-tidal carbon dioxide, if applicable
Urine output via placement of a Foley catheter
For more information, see the Medscape Reference article Emergent Management of
Subarachnoid Hemorrhage.
Rebleeding and Clipping/Coiling Aneurysms
Rebleeding is the most dreaded early complication of SAH. The greatest risk of rebleeding
occurs within the first 24 hours of rupture (4.1%). The cumulative risk of rebleeding is 19% at 14
days. The overall mortality rate from rebleeding is reported to be as high as 78%. Measures to
prevent rebleeding include bed rest in a quiet room, analgesia, and sedation. Stool softeners are
given to prevent Valsalva maneuvers with resultant peaks in SBP and ICP. Clipping or coiling
aneurysms is the surgical approach to prevent rebleeding (see below).
Pain is associated with a transient elevation in blood pressure and increased risk of rebleeding.
Analgesia is preferably achieved with a short-acting and reversible agent such as fentanyl.
Sedation is used with caution to avoid distorting subsequent neurologic evaluation. The preferred
agent is a short-acting benzodiazepine such as midazolam. Antifibrinolytics have been shown to
reduce the occurrence of rebleeding. However, outcome likely does not improve because of a
concurrent increase in the incidence of cerebral ischemia.
Clipping or coiling of aneurysms
Surgical treatment to prevent rebleeding is by clipping the ruptured berry aneurysm.

Endovascular treatment [1] (ie, coiling) is an increasingly practiced alternative to surgical clipping.
For more information, see the Medscape Reference article Subarachnoid Hemorrhage Surgery.
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. At many institutions,
higher-grade patients and those with significant medical comorbidities tend to be treated by
coiling rather than clipping. Posterior circulation aneurysms are preferentially treated by coiling
because of the significant morbidity and mortality associated with surgical clipping.
Koivisto et al did not show any difference between the 2 techniques at 1 year. [24] In contrast, the
randomized prospective International Subarachnoid Aneurysm Trial (ISAT) found coiling to be
significantly safer for the treatment of ruptured aneurysms that were deemed equally suitable
candidates for either surgical or endovascular treatment. [25, 26, 27] The incidence of rebleeding was
slightly higher in the coiled group, but the endovascularly treated group did so much better
overall that the study was stopped after reviewing the 1-year outcome data.
Partially because of the ISAT study, endovascular treatment is becoming the first-line treatment
for many aneurysms. However, a 2009 study expresses concerns regarding the generalizability of
the ISAT and suggests that further analyses are needed. [28]
The data to establish long-term results of endovascular treatment are insufficient. In general, the
incidence of recanalization is higher with coiling. Significant advances have been made with the
introduction of new coated coils that either swell within the aneurysm or promote fibrous tissue
formation and organization of the intra-arterial clot.
Other advances include the use of intracranial stents to promote coiling (especially in aneurysms
with wide necks) and decrease inflow into the aneurysm in certain instances. The stents have also
provided a novel approach to treating certain types of aneurysms that have historically been
untreatable. At the moment, no long-term follow-up data exist to assess the efficacy of these new
treatment modalities.
In a retrospective study, Chitale et al compared the safety and efficacy of stent-assisted coiling
(SAC) and balloon-assisted coiling (BAC) in 84 patients with ruptured complex and wide-
necked aneurysms in the setting of acute SAH. They concluded from their findings that SAC
may be an acceptable alternative to BAC for the management of these types of aneurysms in the
acute phase of SAH. According to the authors, the rates of hemorrhagic, thromboembolic, and
overall procedural complications were not significantly different in the SAC and BAC groups:
6.8% vs 2.5% (P = .5), 11.4% vs 7.5% (P = .6), and 18.2% vs 10% (P = .3), respectively. In
addition, they found that the rate of favorable outcomes did not differ significantly: 61% vs 77%
(P = .1). [29]
Manajemen awal
Manajemen awal pasien dengan SAH diarahkan pada stabilisasi pasien. Menilai tingkat
kesadaran dan saluran napas, pernapasan, dan sirkulasi (ABC).
Intubasi endotrakeal harus dilakukan untuk pasien dengan koma, tingkat depresi kesadaran,
ketidakmampuan untuk melindungi jalan nafas mereka, atau peningkatan tekanan intrakranial
(ICP). Cepat-urutan intubasi harus digunakan, jika memungkinkan, termasuk penggunaan sedasi,
defasciculation, short-acting neuromuskular blokade, dan agen untuk menumpulkan peningkatan
ICP.
Akses intravena harus diperoleh, termasuk garis tengah dan arteri. Sebuah benzodiazepine short-
acting, seperti midazolam, harus diberikan sebelum semua prosedur. Pemantauan harus
mencakup sebagai berikut:
monitoring jantung
oksimetri Pulse
Otomatis dan / atau tekanan darah arteri pemantauan (arteri BP monitoring ditunjukkan dalam
bermutu tinggi SAH atau ketika tekanan darah labil)
End-tidal karbon dioksida, jika berlaku
Output urine melalui penempatan kateter Foley
Untuk informasi lebih lanjut, lihat artikel Medscape Referensi Emergent Pengelolaan
subarachnoid Perdarahan.
Perdarahan ulang dan Kliping / melingkar Aneurisma
Perdarahan ulang adalah komplikasi awal yang paling ditakuti SAH. Risiko terbesar perdarahan
ulang terjadi dalam 24 jam pertama pecah (4,1%). Risiko kumulatif perdarahan ulang adalah
19% pada 14 hari. Tingkat kematian secara keseluruhan dari perdarahan ulang dilaporkan
setinggi 78%. Langkah-langkah untuk mencegah perdarahan ulang termasuk istirahat di ruang
tenang, analgesia, dan sedasi. pelunak tinja diberikan untuk mencegah manuver Valsalva dengan
puncak yang dihasilkan di SBP dan ICP. Kliping atau melingkar aneurisma adalah pendekatan
bedah untuk mencegah perdarahan ulang (lihat di bawah).
Nyeri berhubungan dengan elevasi transien tekanan darah dan meningkatkan risiko perdarahan
ulang. Analgesia lebih disukai dicapai dengan short-acting dan agen reversibel seperti fentanil.
Sedasi digunakan dengan hati-hati untuk menghindari distorsi evaluasi neurologis berikutnya.
Agen disukai adalah benzodiazepin short-acting seperti midazolam. Antifibrinolitik telah terbukti
mengurangi terjadinya perdarahan ulang. Namun, hasil yang mungkin tidak meningkatkan
karena peningkatan bersamaan dalam kejadian iskemia serebral.
Kliping atau melingkar dari aneurisma
Bedah pengobatan untuk mencegah perdarahan ulang adalah dengan menjepit pecah berry
aneurisma. pengobatan endovascular [1] (yaitu, coiling) merupakan alternatif semakin
dipraktekkan untuk kliping bedah. Untuk informasi lebih lanjut, lihat artikel Medscape Referensi
subarachnoid Perdarahan Bedah.
Pilihan antara melingkar dan kliping biasanya tergantung pada lokasi lesi, leher aneurisma, dan
ketersediaan dan pengalaman staf rumah sakit. Pada banyak lembaga, pasien kelas yang lebih
tinggi dan mereka dengan komorbiditas medis yang signifikan cenderung diperlakukan dengan
melingkar bukan kliping. Posterior aneurisma sirkulasi yang istimewa diperlakukan dengan
melingkar karena morbiditas dan kematian yang terkait dengan kliping bedah.
Koivisto et al tidak menunjukkan perbedaan antara 2 teknik pada 1 tahun. [24] Sebaliknya,
prospektif acak Internasional subarachnoid Aneurysm Trial (ISAT) ditemukan melingkar secara
signifikan lebih aman untuk pengobatan aneurisma pecah yang dianggap kandidat sama-sama
cocok baik untuk perawatan bedah atau endovascular. [25, 26, 27] Insiden perdarahan ulang
sedikit lebih tinggi pada kelompok melingkar, tetapi kelompok endovascularly diperlakukan
melakukan jauh lebih baik secara keseluruhan bahwa penelitian dihentikan setelah meninjau data
hasil 1 tahun.
Sebagian karena studi ISAT, pengobatan endovascular menjadi pengobatan lini pertama bagi
banyak aneurisma. Namun, sebuah studi 2009 mengungkapkan kekhawatiran mengenai
generalisasi dari ISAT dan menunjukkan bahwa analisis lebih lanjut diperlukan. [28]
Data untuk membangun hasil jangka panjang pengobatan endovascular tidak mencukupi. Secara
umum, kejadian rekanalisasi lebih tinggi dengan coiling. kemajuan signifikan telah dibuat
dengan pengenalan kumparan dilapisi baru yang baik membengkak dalam aneurisma atau
mempromosikan pembentukan jaringan fibrosa dan organisasi dari bekuan intra-arteri.
Kemajuan lain termasuk penggunaan stent intrakranial untuk mempromosikan melingkar
(terutama di aneurisma dengan leher lebar) dan menurunkan aliran ke dalam aneurisma dalam
kasus tertentu. Stent juga telah menyediakan pendekatan baru untuk mengobati beberapa jenis
aneurisma yang secara historis tidak dapat diobati. Pada saat ini, tidak ada data tindak lanjut
jangka panjang ada untuk menilai efikasi modalitas pengobatan baru.
Dalam sebuah penelitian retrospektif, Chitale et al membandingkan keamanan dan kemanjuran
stent yang dibantu melingkar (SAC) dan balon-dibantu melingkar (BAC) di 84 pasien dengan
kompleks dan lebar berleher pecah aneurisma dalam pengaturan SAH akut. Mereka
menyimpulkan dari temuan mereka bahwa SAC mungkin menjadi alternatif yang dapat diterima
untuk BAC untuk pengelolaan jenis aneurisma di
Timing of intervention
The timing of surgery has been the subject of controversy for more than 40 years. Initially, the
high complication rate related to early clipping of the aneurysm was thought to outweigh the risk
of rebleeding, and a philosophy of delayed surgery was generally accepted. With the
improvement of surgical technique, especially the routine adoption of microneurosurgical
techniques, a major shift has occurred in favor of early surgery for patients with aneurysms of
favorable grade.
Early surgery or coiling is generally recommended in patients with straightforward aneurysms of

a favorable clinical grade. Evidence from clinical trials suggests that patients who undergo
surgery within 72 hours have a lower rate of rebleeding and tend to fare better than those treated
later. [30]
Poor-grade patients who fail to improve after stabilizing measures (including ventriculostomy
placement) may not get treated in the acute period or may be preferentially treated by coiling.
Delayed intervention is also recommended in patients with giant or complicated aneurysms.
A cost-utility analysis from the Netherlands reports that at age 80 years, the risks and benefits of
aneurysm occlusion sway toward not performing the procedure. The authors suggest that in
patients 80 years or older, aneurysm occlusion should be performed only if the predicted life
expectancy of the patient leaves a margin for benefit. [31]
Vasospasm
For prevention of vasospasm, maintenance of normovolemia, normothermia, and normal

oxygenation are paramount. Volume status should be monitored closely, with avoidance of
volume contraction, which can predispose to vasospasm.
Nimodipine
Oral nimodipine is the most studied calcium channel blocker for prevention of vasospasm after
SAH. An American Heart Association/American Stroke Association guideline recommends its
use for this purpose (class I, level of evidence A). [32] Calcium channel blockers have been shown
to reduce the incidence of ischemic neurologic deficits, and nimodipine has been shown to
improve overall outcome within 3 months of aneurysmal SAH. Calcium channel blockers and
other antihypertensives should be used cautiously to avoid the deleterious effects of hypotension.
[33, 34]
The mechanisms of nimodipines protective effect in vasospasm is unproved. However, it

appears that nimodipine may prevent the ischemic complications of vasospasm by the
neuroprotective effect of blockading the influx of calcium into damaged neurons.
In May 2013, the US Food and Drug Administration (FDA) approved a new oral nimodipine
solution (Nymalize) for the treatment of patients with SAH. Nimodipine had been available
previously only as a liquid-filled gel capsule. Intravenous (IV) administration of nimodipine
meant for oral use has been reported to cause death, cardiac arrest, severe decreases in blood
pressure, and other heart-related complications. The oral formulation has the potential to
decrease or eliminate inadvertent IV administration of the drug. [35]
Thrombolytic therapy
Some evidence indicates that subarachnoid clot removal achieved via intracisternal injections of
recombinant tissue plasminogen activator (rTPA) may dramatically reduce the risk of vasospasm.
This is performed after the clipping of the aneurysm.
Thrombolytic therapy is associated with the theoretical risk of intracranial bleeding, and
although the results of preliminary studies are favorable, rigorous clinical trials are needed to
establish the safety and efficacy of this approach. Intracisternal antioxidants and anti-
inflammatory agents are of uncertain value.
Aspiration and irrigation
Aspiration and irrigation of the subarachnoid clot at the time of aneurysmal clipping usually
results in suboptimal removal of the clot and is associated with a significant risk of iatrogenic
trauma to pial surfaces and small vessels.
Intraoperative sodium chloride lavage to clear blood products from the subarachnoid space may
be of some benefit, but its effectiveness remains unproved.
CSF drainage
Some authors suggest that early CSF drainage via a ventricular drain may decrease the incidence
of vasospasm. This intervention is performed after the aneurysm has been secured.
Use caution to prevent rapid or overly aggressive drainage of CSF, which may precipitate
aneurysmal rebleeding. One author suggests draining the CSF if the intracranial pressure exceeds
20 mm Hg. The drain should be set at a height to drain at 20 mm Hg to avoid an excessive
reduction in ICP.
Statins
Statin therapy has been proposed as a means of preventing vasospasm and delayed cerebral
ischemia. Statins may improve cerebral vasomotor reactivity through cholesterol-dependent and
cholesterol-independent mechanisms. [36, 37] The use of statins in SAH is controversial. Several
small studies have shown promise. Two meta-analyses have shown contradicting results. Sillberg
et al concluded that statin therapy reduces vasospasm and cerebral ischemia, [38] while Vergouwen
et al found no benefit of statin therapy. [39] Until more data are available, the use of statins cannot
be routinely recommended. [40]
The Simvastatin in Aneurysmal Subarachnoid Hemorrhage (STASH) study, a multicenter
randomized controlled clinical trial, will be investigating the effects of 40 mg of simvastatin in
patients with SAH. The trial is currently recruiting participants. The planned sample size is 1600
patients, which should be powerful enough to answer the controversy surrounding statin therapy
in SAH.
Triple H therapy
Treatment for symptomatic vasospasm has traditionally involved the induction of hypertension,
hypervolemia, and hemodilution, or triple H therapy. This therapy should be reserved for patients
with aneurysms secured by surgical clipping or endovascular techniques in order to reduce the
risk of rebleeding.
The efficacy of triple H therapy remains subject to debate. A review of controlled studies showed
no positive effect of triple H therapy or its components on increasing cerebral blood flow. [41]
Aggressive hypertensive therapy with inotropes and vasopressors (eg, dobutamine) can be
initiated, if warranted. Hypervolemia may be achieved by using packed erythrocytes, isotonic
crystalloid, and colloid and albumin infusions in conjunction with vasopressin injection.
Corticosteroids may be of some benefit; however, such treatment remains controversial.
Hemodilution or transfusion is used to maintain the hematocrit at 30-35% in order to optimize
blood viscosity and oxygen delivery.
Initiation of triple H therapy requires placement of a pulmonary artery catheter in order to guide
volume expansion and inotropic or vasopressor therapy. Central venous pressure (CVP) should
be maintained at 10-12 mm Hg. Pulmonary artery wedge pressure (PAWP) should be maintained
at 14-20 mm Hg.
Transluminal balloon angioplasty
Transluminal balloon angioplasty is recommended for treatment of vasospasm after failure of

conventional therapy. One study reported improved neurologic outcome in 70% of patients with
symptomatic vasospasm after transluminal angioplasty. Case series reports have indicated that
angioplasty appears to be effective in treating vasospasm of large proximal vessels. [42]
Angioplasty is not effective in direct treatment of vasospasm of more distal vessels; however,
distal blood flow may be increased as a result of increased proximal vessel diameter. The
potential complications of angioplasty include vessel rupture, dissection, or occlusion, as well as
intracerebral hemorrhage.
Papaverine, magnesium, and investigational agents

Intra-arterial injection of papaverine has been reported to improve outcome, but more data are
needed before its routine use can be recommended. The beneficial effects of papaverine infusion
appear to be short-lived compared with those of angioplasty.
Magnesium is a neuroprotective agent that acts as an N-methyl-D-aspartate (NMDA) receptor

antagonist and a calcium channel blocker. It has been used to reduce cerebral ischemic events in
SAH patients. Magnesium levels should be carefully monitored. Studies of magnesium treatment
in SAH have yielded disparate results. A small, randomized, placebo-controlled pilot study by
Westermaier et al found that maintaining serum magnesium concentrations of 2-2.5 mmol/L
reduced the occurrence of cerebral ischemic events following aneurysmal SAH. [43]
A meta-analysis showed that magnesium reduced the risk of delayed cerebral ischemia and poor
outcome in aneurysmal SAH. [44] However, a larger multicenter phase III trial by Wong et al
found no significant difference at 6 months between patients treated with magnesium IV or
placebo. [45]
Several new agents have been investigated for the use in SAH, especially to ameliorate
vasospasm. In a randomized, double-blind, placebo-controlled, pilot trial, methylprednisolone
did not decrease vasospasm but improved functional outcomes. [46] Tirilazad, a nonglucocorticoid
21-aminosteroid, has not shown consistent benefit. [47] Intra-arterial colforsin is under
investigation to improve vasospasm. [48]
Hydrocephalus
Treatment for acute hydrocephalus includes external ventricular drainage, depending on the
severity of clinical neurologic dysfunction or CT scan findings. Rapid lowering of intracranial
pressure during intraventricular catheter placement is associated with a higher risk of rebleeding
and should be avoided. Resolution of hydrocephalus may be assessed periodically by blocking
CSF drainage while monitoring ICP.
Symptomatic cases of hydrocephalus may be managed by temporary lumbar CSF drainage, serial
LPs, or placement of a permanent ventricular shunt. Ventriculostomy placement is associated
with an increased risk for rebleeding, along with known infectious risk; therefore, patients with
dilated ventricles but no compromise of level of consciousness should be treated conservatively,
with close monitoring of mental status and prompt intervention in case their clinical status
declines.
Nevertheless, ventriculostomy, when done correctly, is a relatively low-risk procedure that can
result in dramatic and immediate clinical improvement in about two thirds of patients. If the
patient's grade improves enough as a result of ventriculostomy, the patient may become a
candidate for early surgery.
When grading patients clinically, great care must be taken to note possibly reversible deficits
related to hydrocephalus, which may be contributing to the patients' poor condition. According to
a study of 47 patients with poor-grade aneurysm without CT evidence of irreversible brain
destruction who underwent ventriculostomy, early control of the ICP and aggressive management
appeared to be the appropriate treatment in this subset of patients.
Other Complications
Hyponatremia
Hyponatremia following subarachnoid hemorrhage occurs in 10-34% of cases. Elevated levels of

atrial natriuretic factor (ANF) and syndrome of inappropriate secretion of antidiuretic hormone
(SIADH) have been implicated.
Administration of isotonic fluid can prevent volume contraction but not hyponatremia. Use of
slightly hypertonic sodium chloride (1.5% sodium chloride) at rates above maintenance
requirements usually is efficacious for SAH-induced hyponatremia. Avoid fluid restriction in
patients with SAH.
Seizures
Agents used for seizure prophylaxis include the following:
Phenytoin, the agent of choice, can achieve rapid therapeutic concentrations when loaded
intravenously, and it does not cause alterations in consciousness
Phenobarbital produces a sedative effect, which may mask the neurologic evaluation;
phenobarbital is used less frequently than phenytoin
Long-term anticonvulsants are not recommended in patients without prior seizure activity
or risk factors such as hematoma, infarct, or middle cerebral artery aneurysm
Some studies argue that anticonvulsant therapy can be limited safely to the immediate
perioperative period in patients with no parenchymal clot, ischemic infarct, or postoperative
hematoma.
Acute pulmonary edema and hypoxemia
Acute pulmonary edema and hypoxia are almost universal in severe subarachnoid hemorrhage.
The pulmonary edema in SAH is believed to be neurogenic in origin and unrelated to triple H
therapy; however, the latter is associated with an increased risk of fluid overload.
SAH-induced hypoxemia likewise is believed to be partially neurogenic in origin because it is

out of proportion to what would be expected from cardiac insufficiency or fluid overload.
Treatment of acute pulmonary edema may include the use of gentle diuresis, dobutamine, and
positive end-expiratory pressure.
Cardiac dysfunction
Cardiac dysfunction is common in subarachnoid hemorrhage, particularly in the first 48 hours,

but it is typically benign. The perioperative therapy to prevent secondary cerebral ischemia
(hypervolemia, hypertension) may exacerbate myocardial ischemia.
Conversely, therapy for myocardial ischemia, such as nitrates, may increase intracranial pressure,
lower cerebral perfusion pressure, and exacerbate cerebral ischemia.
Screening
Screening is generally not recommended in the general population. Even in special populations,
such as patients with polycystic kidney disease, studies have failed to show any benefit to
screening. [49] In patients who have had 2 or more first-degree relatives with radiographically
proven intracranial aneurysms, screening with CT or MR angiography may be considered on an
individual basis. [50]
In general, the screening of patients with previous SAH cannot be recommended. However,
screening can save costs and increase quality-adjusted life-years (QALYs) in the subset of
patients who are at relatively high risk of both aneurysm formation and rupture. In addition, in
patients with fear of recurrence, screening may increase QALYs at acceptable costs. [51]
Nevertheless, more data are needed to help identify patients who can benefit from screening.
Medication Summary
The goals of treatment in patients with subarachnoid hemorrhage (SAH) are as follows:
Blood pressure control
Prevention of seizures
Treatment of nausea
Management of intracranial pressure
Prevention of vasospasm
Control of pain
Maintenance of cerebral perfusion

Medications used for these purposes include analgesics, calcium channel blockers, antiepileptic
drugs, stool softeners, antihypertensive agents, antiemetics, osmotic agents, diuretics, and
general anesthetics. The use of aminocaproic acid for hemostasis is controversial.
Opioid Analgesics
Class Summary
Pain control is essential to quality patient care. It ensures patient comfort and promotes
pulmonary toilet. Most analgesics have sedating properties that benefit patients who experience
pain.
Fentanyl citrate (Actiq, Abstral, Onsolis, Fentora, Duragesic)
View full drug information
Fentanyl is a synthetic opioid that is 75-200 times more potent than morphine sulfate and has a
much shorter half-life. It has less of a hypotensive effect and is safer in patients with hyperactive
airway disease than morphine because of minimal to no associated histamine release. By itself,
fentanyl causes little cardiovascular compromise, although the addition of benzodiazepines or
other sedatives may result in decreased cardiac output and blood pressure.
Consider giving fentanyl by continuous infusion because of its short half-life. The parenteral
form is the drug of choice for conscious sedation analgesia. It is ideal for analgesic action of
short duration during anesthesia and the immediate postoperative period. It is also an excellent
choice for pain management and sedation, with its short duration (30-60 min) and easy titration.
After the initial parenteral dose, subsequent parenteral doses should not be titrated more
frequently than every 3 or 6 hours.
The transdermal form of fentanyl is used only for chronic pain conditions in opioid-tolerant
patients. When using the transdermal dosage form, most patients are controlled with 72-hour
dosing intervals; however, some patients require dosing intervals of 48 hours.
The effects of fentanyl are easily and quickly reversed by naloxone. Fentanyl is highly lipophilic
and protein bound. Prolonged exposure leads to accumulation in fat and delays the weaning
process.
Calcium Channel Blockers

Class Summary
In specialized conducting and automatic cells in the heart, calcium is involved in the generation
of the action potential. The calcium channel blockers inhibit movement of calcium ions across
the cell membrane, depressing both impulse formation (automaticity) and conduction velocity.
These agents may attenuate deleterious effects of calcium influx in patients with acute
neurotrauma.
Nimodipine (Nymalize)
Nimodipine is indicated to reduce poor outcome related to aneurysmal subarachnoid

hemorrhage. [32] While studies have shown benefit regarding severity of neurologic deficits
caused by cerebral vasospasm following SAH, no evidence exists that nimodipine either prevents
or relieves spasms of cerebral arteries. Thus, the actual mechanism of action is unknown.
Begin therapy within 96 hours of SAH. Nimodipine is given orally. If the patient cannot swallow
the gel capsule because he or she is undergoing surgery or is unconscious, administer the oral
solution (Nymalize, 60 mg/20 mL) via nasogastric or gastric tube and flush tubing before and
after with normal saline. If the oral solution is not available, make holes at both ends of the gel
capsule with an 18-gauge needle and extract the contents into a syringe, empty the contents into
the patient's in situ nasogastric tube, and flush the tube with 30 mL of isotonic saline.
Anticonvulsants, Other
Class Summary
These agents prevent seizure recurrence and terminate clinical and electrical seizure activity. The
use of antiepileptic drugs in patients with SAH who have not had seizures is controversial and
depends on the individual preference of the neurosurgeon; they usually are used only in patients
who have had seizures. Conventional loading doses may be used.
Phenytoin (Dilantin, Phenytek)
Phenytoin may act in the motor cortex, where it may inhibit spread of seizure activity. The
activity of brainstem centers responsible for the tonic phase of grand mal seizures also may be
inhibited. The dose should be individualized. If the daily dose cannot be divided equally,
administer the larger portion at bedtime.
Phenobarbital
Phenobarbital elevates the seizure threshold and limits the spread of seizure activity; it also has
sedative properties.
Fosphenytoin (Cerebyx)
Fosphenytoin is a diphosphate ester salt of phenytoin that acts as a water-soluble prodrug of

phenytoin; plasma esterases convert fosphenytoin to phosphate, formaldehyde, and phenytoin;
phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.
The dose of fosphenytoin is expressed as phenytoin equivalents (PE), to avoid the need to
perform molecular weightbased adjustments when converting between fosphenytoin and
phenytoin sodium doses.
Fosphenytoin is intended for parenteral administration. Intravenous use is the route of choice and
should be used in emergency situations.
Stool Softeners
Class Summary
These agents prevent elevation of intracranial pressure from the Valsalva maneuver.
Docusate sodium (Colace, Correctol, Dok)
Docusate is an anionic surfactant used for patients who should avoid straining during defecation.
This agent allows incorporation of water and fat into stool, causing stool to soften. It has minimal
laxative effect.
Senna (Senokot, Ex-Lax, Senexon, SennaGen)
Senna is an anthraquinone stimulant hydrolyzed by colonic bacteria into an active compound. It

is more potent than cascara sagrada and produces considerably more abdominal pain. Senna
usually produces action 8-12 hours after administration.
Beta-Blockers, Alpha Activity

Class Summary
In patients who have suffered SAH from a ruptured aneurysm, these agents are used to maintain
blood pressure in a range that allows for sufficient cerebral perfusion yet limits the risk of
rebleeding from elevated ICP.
Labetalol (Trandate)
Labetalol blocks alpha-, beta1-, and beta2-adrenergic receptor sites, decreasing blood pressure.
Antiemetic Agents
Class Summary
These agents are used for the treatment of nausea or vomiting.
Promethazine (Phenergan, Phenadoz, Promethegan)
Promethazine is an antidopaminergic agent effective in the treatment of emesis. It blocks

postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to the
brainstem reticular system.
Diuretics, Osmotic Agents

Class Summary
These agents are used in an attempt to lower ICP and cerebral edema by creating an osmotic
gradient across an intact blood-brain barrier; as water diffuses from the brain into the
intravascular compartment, ICP decreases.
Mannitol (Osmitrol, Aridol)
Mannitol may reduce pressure within the subarachnoid space by creating an osmotic gradient
between the CSF in the arachnoid space and the plasma. This agent is not for long-term use.
Diuretics, Loop
Class Summary
These agents are used to decrease plasma volume and edema by causing diuresis.
Furosemide (Lasix)

Furosemide is used in the acute setting for reduction of increased ICP. Doses must be
individualized. The proposed mechanisms in lowering ICP include the following:
Suppression of cerebral sodium uptake
Inhibition of carbonic anhydrase, resulting in decreased CSF production
Inhibition of the cellular membrane cation-chloride pump, thereby affecting transport of water
into astroglial cells
Hemostatics
Class Summary
These agents are potent inhibitors of fibrinolysis and can reverse states that are associated with
excessive fibrinolysis. Their use is controversial; consultation with admitting physicians is urged
prior to use.
Aminocaproic acid (Amicar)
Aminocaproic acid inhibits fibrinolysis via inhibition of plasminogen activator substances and, to
a lesser degree, through antiplasmin activity. The main problems with its use are that thrombi
that form during treatment are not lysed and its effectiveness is uncertain. This agent has been
used to prevent recurrence of SAH.
General Anesthetics, Systemic

Class Summary
These agents provide sedation when neuromuscular blocking agents are used for intubation.
Thiopental
Thiopental is a short-acting barbiturate sedative-hypnotic with rapid onset and a duration of

action of 5-20 minutes. Like methohexital, it is most commonly used as an induction agent for
intubation.
Thiopental depresses consciousness and diminishes or terminates seizure effects; it facilitates

transmission or impulses from the thalamus to the cortex of the brain, resulting in an imbalance
in central inhibitory and facilitating mechanisms. To use thiopental as a sedative, titrate in dosage
increments of 25 mg (adjust to lower dose in children).
Etomidate (Amidate)
Amidate is a nonbarbiturate imidazole compound with sedative properties. It is short-acting and

has a rapid onset of action; the duration of action is dose dependent (15-30 minutes). Its most
useful feature as an induction agent is that it produces deep sedation while causing minimal
cardiovascular effects.
The major application of amidate is induction for endotracheal intubation, particularly in patients
with, or at risk for, hemodynamic compromise. Amidate has been shown to depress adrenal
cortical function; however, this effect is not significant clinically during short-term
administration. Since the drug is mixed in propylene glycol, continuous infusion not
recommended.
Anxiolytics, Benzodiazepines
Class Summary
By binding to specific receptor sites, these agents appear to potentiate the effects of gamma-
aminobutyrate (GABA) and to facilitate inhibitory GABA neurotransmission, as well as other
inhibitory transmitters.
Midazolam
Midazolam is a shorter-acting benzodiazepine sedative-hypnotic that is useful in patients

requiring acute or short-term sedation. It is also useful for its amnestic effects.

Perdarahan Sub Arachnoid

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Practice Essentials

emergency department revealed subarachnoid hemorrhage.

Signs and symptoms

Orbital pain (7%)

Visual loss (4%)

Signs present before SAH include the following:

Sensory or motor disturbance (6%)

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

Seizures during the acute phase

Physical examination findings may be normal or may include the following:

Mild to moderate BP elevation

Global or focal neurologic abnormalities

Complications of SAH include the following:

See Clinical Presentation for more detail.

Laboratory studies should include the following:

Serum chemistry panel

Complete blood count

Prothrombin time (PT)/activated partial thromboplastin time (aPTT)

Arterial blood gas (ABG) determination

Imaging studies that may be helpful include the following:

CT (noncontrast, contrast, or infusion)

Digital subtraction cerebral 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

Lumbar puncture and CSF analysis

See Workup for more detail.

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:

Surgical treatment to prevent rebleeding includes the following options:

Clipping the ruptured aneurysm

Endovascular treatment [1] (ie, coiling)

See Treatment and Medication for more detail.

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

Vascular asymmetry in the circle of Willis

Long-term analgesic use

Family history of stroke

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

Increased blood flow: Cerebral arteriovenous malformation (AVM); persistent carotid-

Genetic disorders: Marfan syndrome, Ehlers-Danlos syndrome, Osler-Weber-Rendu

Congenital conditions: Persistent fetal circulation, hypoplastic/absent arterial circulation

Metastatic tumors to cerebral arteries: Atrial myxoma, choriocarcinoma, undifferentiated

Infections: Bacterial, fungal

Complications of SAH include the following:

Delayed cerebral ischemia from vasospasm

Left ventricular systolic dysfunction

Increased intracranial pressure

Myocardial infarction [4]

Bilateral ambient cisternal blood

Use of antifibrinolytic drugs