Subarachnoid Hemorrhage

INTRODUCTION

The term subarachnoid hemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the
pial and arachnoid membranes. SAH comprises half of spontaneous atraumatic intracranial hemorrhages, the other
half consist of bleeding that occurs within the brain parenchyma. Intracranial hemorrhage as a whole comprises 20%
of all strokes.

SAH is a devastating condition with high morbidity and mortality, and, in the United States, it is associated with an
annual cost of $1.75 billion. SAH occurs in various clinical contexts, the most common being head trauma. However,
the familiar medical 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). The scope of this chapter is
confined to nontraumatic SAH.

History of the Procedure: Ancient Greek, Egyptian, and Arabic literature all have references to intracranial
aneurysms. The first successful treatment of an intracranial aneurysm was reported in the early 19th century; however,
such outcomes did not become routine until the Dandy era and the advent of modern neurosurgical techniques.

Dandy performed the first successful clipping of an aneurysm in 1937, using a vascular clip designed by Harvey
Cushing. In the following years, advancements in microneurosurgical techniques, including the operating microscope,
microsurgical instruments, better anesthesia, and improved management of SAH complications, have led to significant
improvements in surgical outcomes.

Endovascular therapy for the treatment of intracranial aneurysms was pioneered in the mid 1970s by Serbinenko at the
Moscow Institute of Neurosurgery. This initial approach, which attempted to achieve parent vessel occlusion using
latex balloons, was moderately successful in a limited subset of cases. However, it never gained widespread
applicability.

Other balloon devices, including detachable silicon and latex balloons, subsequently were developed in the United
States, Europe, and Japan. The success of balloon embolization has been tempered by the associated complications of
deflation and aneurysmal rupture.

Arguably, the most significant recent development in endovascular therapy occurred in 1990, when Guglielmi and
colleagues at the University of California Los Angeles (UCLA) Medical Center developed the Guglielmi detachable
coil system (GDC).

The GDC is a radiopaque platinum coil that is delivered through a microcatheter into an aneurysm, which then is
detached by electrolysis. GDCs gained approval by the Food and Drug Administration (FDA) in 1995 for treatment of
aneurysms that have the potential for high surgical morbidity and mortality. In Europe, GDCs are used as a first-line
intervention in lieu of surgical treatment for patients without contraindications to endovascular therapy.

Other endovascular techniques under investigation include liquid embolic agents, intravascular laser treatments, and
intravascular stents. As endovascular occlusive techniques evolve, it seems likely that they will play a larger role in
the management of SAH.
Problem: Nontraumatic SAH usually is the result of a ruptured cerebral aneurysm or AVM. Blood extravasation into
the subarachnoid space has a detrimental effect on both local and global brain function and leads to high morbidity
and mortality rates.

Although mortality rates of SAH have decreased since 1979, it remains a devastating neurological problem. An
estimated 15% of patients die before reaching the hospital. Approximately 25% of patients die within 24 hours, with
or without medical attention. The mortality rate at the end of 1 week approaches 40%. Half of all patients die in the
first 6 months.

Age-adjusted mortality rates are 62% greater in females than in males and 57% greater in blacks than in whites. While
advances in the management of SAH have led to an overall decrease in mortality rates, approximately 40% of all
survivors have major neurologic deficits. Morbidity and mortality increase with age and are related to the overall
health status of the patient.

Frequency: SAH is a major clinical problem worldwide.

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. The incidence of SAH
worldwide varies widely (2-49 cases per 100,000 population), with the highest rates occurring in Japan and Finland.

Age: 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. The prevalence of SAH is rare in children younger than 10 years; SAH in children younger than 10
years accounts for only 0.5% of all cases.

Sex: Incidence of SAH in women is higher than in men (3:2). 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.

Race: 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.

Etiology: Nontraumatic cases of SAH usually are caused by extravasation of blood from abnormal blood vessels onto
the surface of the brain. Usually, this is the result of aneurysmal or AVM leakage or rupture. Rupture of “berry,” or
saccular, aneurysms of the basal vessels of the brain comprises 77% of nontraumatic SAH cases.

The etiology of cerebral aneurysms is unknown, but both congenital and acquired factors are thought to play a role.
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%)
 Aneurysms have been associated with specific congenital diseases (eg, coarctation of the aorta, Marfan
syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia, polycystic kidney disease).
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 dilatation in 20% of the
population (<2 mm) 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
 Hemodynamic stress

AVMs are the second most identifiable cause of SAH, accounting for 10% of cases of SAH. 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.
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
 Idiopathic SAH

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. Data regarding the relationship between
hypertension and SAH are conflicting. The following do not appear to be significant risk factors for SAH:
 Use of oral contraceptives
 Hormone replacement therapy
 Hypercholesterolemia
 Vigorous physical activity

The risk of AVM rupture is greater during pregnancy.

Pathophysiology: Aneurysms usually occur at the branching sites on the large cerebral arteries 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 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 via compressive forces that 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 (CSF) 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).
Clinical: The signs and symptoms of SAH range from subtle prodromal events, which often are misdiagnosed, to the
classic presentation of catastrophic headache. The history and physical examination, especially the neurologic
examination, are essential components in the diagnosis and clinical staging of SAH.
Prodromal signs and symptoms usually are the result of one or more of the following: sentinel leaks, mass effect of
aneurysm expansion, or emboli.
 Sentinel, or "warning," leaks that produce minor blood leakage 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 symptomatology
suggestive of elevated ICP. Sentinel leaks usually do not occur in the setting of AVM.
 Mass effect: Prodromal presentations occasionally are caused by the mass effect of an expanding aneurysm
and have characteristic features based upon aneurysm location.
o Posterior communicating artery/internal carotid artery - Focal, progressive retro-orbital headaches and
oculomotor nerve palsy
o Middle cerebral artery - Contralateral face or hand paresis, aphasia (left side), contralateral visual
neglect (right side)
o Anterior communicating artery - Bilateral leg paresis and bilateral Babinski sign
o Basilar artery apex - Vertical gaze, paresis, and coma
o Intracranial vertebral artery/posterior inferior cerebellar artery - Vertigo, components of lateral
medullary syndrome
 Emboli: Transient ischemic attacks can occur from emboli originating from intra-aneurysmal thrombus
formation. The classic symptoms and signs of aneurysmal rupture into the subarachnoid space comprise one of
the most pathognomonic presentations in all of clinical medicine. Symptomatology is as follows:
o A sudden onset of severe headache, often described as the “worst headache of my life” (Absence of
headache in the setting of a ruptured intracranial aneurysm is rare, and probably represents amnesia for
the event.)
o Nausea and/or vomiting
o 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).
o Photophobia and visual changes are common.
o A sudden loss of consciousness (LOC) occurs at the ictus in as many as 45% of patients as ICP exceeds
cerebral perfusion pressure.
o LOC often is transient; however, approximately 10% of patients are comatose for several days,
depending on the location of the aneurysm and the amount of bleeding.
o Seizures during the acute phase of SAH occur in 10-25% of patients.
o No correlation exists between seizure focus and the anatomical site of aneurysm rupture.
 o Less severe hemorrhages may present with headache of moderate intensity, neck pain, and nonspecific
symptoms.
 Findings on physical examination of the patient with SAH may be normal or consistent with one or more of
the following:
o Focal neurologic abnormalities, including hemiparesis, aphasia, hemineglect, cranial nerve palsies, and
memory loss, are present in 25% of patients.
o Motor neurologic deficits occur in 10-15% of patients, usually from middle cerebral artery aneurysms.
o Ophthalmologic examination may reveal subhyaloid retinal hemorrhages (20-30%) and papilledema.
o Blood pressure elevation is observed in about 50% of patients. Blood pressure often becomes labile as
ICP increases.
o Temperature elevation, secondary to chemical meningitis from subarachnoid blood products, is
common after the fourth day following bleeding.
o Tachycardia often is present for several days after SAH.

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 Fischer
scale, classifies SAH based on CT scan appearance and quantification of subarachnoid blood.
 Hunt and Hess grading system
o Grade 1 - Asymptomatic or mild headache
o Grade 2 - Moderate-to-severe headache, nuchal rigidity, and no neurological deficit other than possible
cranial nerve palsy
o Grade 3 - Mild alteration in mental status (confusion, lethargy), mild focal neurological deficit
o Grade 4 - Stupor and/or hemiparesis
o Grade 5 - Comatose and/or decerebrate rigidity
 WFNS scale
o Grade 1 - Glasgow Coma Score (GCS) of 15, motor deficit absent
o Grade 2 - GCS of 13-14, motor deficit absent
o Grade 3 - GCS of 13-14, motor deficit present
o Grade 4 - GCS of 7-12, motor deficit absent or present
o Grade 5 - GCS of 3-6, motor deficit absent or present
 Fischer scale (CT scan appearance)
o Group 1 - No blood detected
o Group 2 - Diffuse deposition of subarachnoid blood, no clots, and no layers of blood greater than 1 mm
o Group 3 - Localized clots and/or vertical layers of blood 1 mm or greater in thickness
o Group 4 - Diffuse or no subarachnoid blood, but intracerebral or intraventricular clots are present

The Hunt and Hess and the WFNS grading systems have been shown to correlate well with patient outcome. The
Fischer 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.
INDICATIONS

The indications for surgery in patients with SAH can be stratified based on clinical grade. Other factors, such as
overall medical condition of the patient, aneurysm size and location, accessibility of the aneurysm for surgical repair,
and presence or absence of thrombus, also are important.

For patients with a mild- or intermediate-grade SAH (Hunt and Hess/WFNS grades 1-3), surgical treatment is strongly
recommended because the risks of SAH complications greatly exceed the risk of surgical complications.

For patients with a poor grade of SAH (Hunt and Hess/WFNS grades 4-5), the decision whether to operate is
controversial and largely institution-dependent. The overall outcome is poor, with or without surgical intervention.

Patients with a higher grade of SAH or poor medical status that do not qualify for early surgery may be candidates for
delayed surgery or endovascular obliteration of the aneurysm.

Other indications for surgical management have been described recently and include the following:

 Large and giant aneurysm

 Wide-necked aneurysms
 Vessels emanating from the aneurysm dome
 Mass effect or hematoma associated with the aneurysm
 Recurrent aneurysm after coil embolization

Indications for endovascular treatment

Endovascular therapy (eg, coil embolization) has been used increasingly in recent years in lieu of surgical clipping,
with promising results. More definitive data are required comparing the traditional treatment modality (aneurysmal
clipping) with newer endovascular techniques before conclusive recommendations can be made. In general,
endovascular treatment of aneurysms is favored over surgery in the following situations:
 Patients with poor clinical grade
 Patients who are medically unstable
 In situations where aneurysm location imparts an increased surgical risk, such as cavernous sinus and many
basilar tip aneurysms
 Small-neck aneurysms in the posterior fossa
 Patients with early vasospasm
 Cases where the aneurysm lacks a defined surgical neck (although these are also difficult to "coil")
 Patients with multiple aneurysms in different arterial territories if surgical risk is high

Surgery remains the standard reference for therapy and is favored over endovascular treatment when surgical risk is
low or equal to that of endovascular therapy. However, many patients may be treated adequately with either method,
and the ultimate choice of intervention often is guided by physician and institution preference.
A combined approach may benefit a particular subset of patients, eg, those with a poor clinical grade and an aneurysm
that cannot be occluded completely by endovascular therapy.
Surgical indications for unruptured symptomatic aneurysms
Surgery usually is indicated in patients with unruptured symptomatic aneurysms because the rate of subsequent
rupture is high. Most symptomatic aneurysms are giant (large) aneurysms rather than saccular aneurysms. Patients
with giant aneurysms face an increased surgical risk; however, this risk usually is much less than the morbidity and
mortality associated with aneurysm rupture.
Surgical indications for asymptomatic aneurysms
The risk of aneurysmal rupture increases relative to the size of the aneurysm; however, the critical size with respect to
increased risk of rupture is unknown.
Unruptured aneurysms are reported to rupture at a rate of 1-1.4% per year. Most authors propose that surgical risks are
eclipsed by the risks of mass effect and aneurysm rupture in patients younger than 65 years who have aneurysms
larger than 1 cm in size. The impact of the size of the aneurysm is controversial.

RELEVANT ANATOMY AND CONTRAINDICATIONS

Relevant Anatomy:

Circle of Willis

Most saccular aneurysms occur at bifurcations of the vessels that comprise the circle of Willis. The circle of Willis is
in close proximity to the ventral surface of the diencephalon and is adjacent to the optic nerves and tracts. It extends
from the superior border of the pons to the longitudinal fissure between the cerebral hemispheres. The circle of Willis
is an important anastomosis for the 4 arteries that supply the brain—the 2 vertebral and the 2 internal carotid arteries.
It can be divided into anterior and posterior sections.
Anterior portion of the circle of Willis
The anterior section of the circle of Willis consists of the internal carotid arteries, the anterior cerebral artery, and the
anterior communicating artery.
 The right internal carotid artery, along with the right external carotid artery, branches from the common
carotid artery most often at C3 or C4, with a range of C1-T2.
 The right common carotid artery originates from the brachiocephalic trunk, the first branch of the aorta.
 The left common carotid artery, the second branch of the aorta, branches into the right internal and right
external carotid arteries at about the same level as the right common carotid bifurcation.
 The cerebral portions of the internal carotid arteries branch into the anterior and middle cerebral arteries at the
medial end of the lateral sulcus.
 The anterior communicating artery is a short segment that connects the 2 anterior cerebral arteries and forms
the anterior border of the circle.

Posterior portion of the circle of Willis

The posterior segment of the circle of Willis consists of the proximal portions of the posterior cerebral arteries and the
paired posterior communicating arteries.
 The 2 posterior cerebral arteries arise from the terminal bifurcation of the basilar artery.
 The basilar artery is formed by the union of the 2 vertebral arteries, each of which begins as a branch of the
first part of the subclavian artery.
 The posterior communicating arteries connect the internal carotid and the posterior cerebral arteries and form
the posterior-lateral borders of the circle of Willis.
Location of aneurysm rupture

Approximately 85% of saccular aneurysms occur in the anterior circulation. The most common sites of rupture are as
follows:
 The internal carotid artery, including the posterior communicating junction (41%)
 The anterior communicating artery/anterior cerebral artery (34%)
 The middle cerebral artery (20%)
 The vertebral-basilar arteries (4%)
 Other arteries (1%)

Contraindications: No strict contraindications to surgery for aneurysmal SAH exist other than unstable medical
status or a lesion not amenable to surgical therapy. Patient stratification with respect to endovascular therapy versus
surgery is discussed in Treatment

WORKUP

Lab Studies:

 CBC count - For evaluation of possible infection or hematologic abnormality

 Prothrombin time (PT) and activated partial thromboplastin time (aPTT) - For evaluation of possible
coagulopathy

 Serum electrolytes - To establish a baseline for detection of future complications

 Blood type and screen - In case intraoperative transfusion is required or in the setting of massive hemorrhage

 Cardiac enzymes - For evaluation of possible myocardial ischemia

 Arterial blood gas (ABG) - Assessment is necessary in cases with pulmonary compromise

Imaging Studies:
 CT scan: The diagnosis of SAH usually depends on a high index of clinical suspicion combined with
radiographic confirmation via CT scan without contrast. The sensitivity decreases with respect to increased
time from ictus and decreased scanner resolution (older CT scanners). CT scan has a sensitivity of 98% within
the first 12 hours of the ictus and 93% within 24 hours; sensitivity decreases to approximately 80% at 72 hours
and 50% at 1 week. CT scan findings are positive in 92% of patients who have SAH. Sensitivity is less on
older second- or first-generation scanners. Most North American hospitals have been using third-generation
scanners since the mid 1980s.

o Thin (3 mm) cuts are necessary to properly identify the presence of smaller hemorrhages.

o CT scan findings may be falsely negative in patients with small hemorrhages and in patients with
severe anemia.
 o 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 found lying over the
convexities or within the superficial parenchyma of the brain often is indicative of AVM or mycotic
aneurysm rupture.

o Anterior communicating artery aneurysms often are associated with interhemispheric and
intraventricular hemorrhages. Middle communicating artery and posterior communicating artery
aneurysms are associated with intraparenchymal hemorrhages.

o CT scan allows for the detection of ventricular size and, thus, evaluation and surveillance of mass
effect and hydrocephalus.

o 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.

 After the diagnosis of SAH, 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. If
the diagnosis of SAH is yet unclear, lumbar puncture (LP) should be performed (see Diagnostic Procedures).

 Cerebral angiography 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.

o 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)

o A trial balloon occlusion of the parent artery can be performed and may help to guide preoperative
surgical planning. If cerebral angiography findings are negative (10-20%) a repeat test should be
performed 3-4 weeks later. Patients with SAH and a negative finding on cerebral angiography may
have an improved prognosis. 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.

o Follow-up angiogram also is useful postsurgically to detect the presence of aneurysmal obliteration and
to evaluate for possible cerebral vasospasm.

o The management of moribund patients with CT scan evidence of a large SAH and focal hematoma is
controversial.
 o Performing angiography may result in a life-threatening delay in treatment.

 Infusion CT scan and CT angiography: 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.

 MRI: This 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 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.

 Magnetic resonance angiography (MRA): The role of 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 (eg, 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.

 Transcranial Doppler studies are useful in the detection and monitoring of arterial vasospasm.

 Chest radiograph: All patients with SAH should have a baseline chest radiograph to serve as a reference point
for evaluation of possible pulmonary complications.

 Evaluation of ventricular wall motion via echocardiogram may be necessary in cases with suspected
myocardial ischemia.

Other Tests:
 All patients with SAH should have an ECG on admission. Changes noted on ECG are attributed to myocardial
ischemia and/or infarction caused by high levels of circulating catecholamines. Myocardial ischemia/infarction
is present in 20% of SAH cases. Electrocardiogram abnormalities frequently detected in patients with SAH
include the following:

o Nonspecific ST and T wave changes

o Decreased PR intervals

o Increased QRS intervals

o Increased QT intervals

o Presence of U waves

o Dysrhythmias, including premature ventricular contractions (PVCs), supraventricular tachycardia

(SVT), and bradyarrhythmias
  Anticoagulation and thrombolytic therapy are contraindicated in cases of suspected SAH.

Diagnostic Procedures:
 LP should be performed when strong clinical suspicion of SAH exists with a negative finding on CT scan or
when a CT scan is not available.

o If possible, a CT scan should be performed before LP to exclude significant intracranial mass effect,
elevated ICP, obstructive hydrocephalus, or obvious intracranial bleed. LP findings often are negative
within 2 hours of the ictus, and LP is most sensitive 12 hours after the bleed.

o No consensus is found in the literature on the lower limit of RBCs in the CSF, which signifies a
positive tap. However, most counts range from a few hundred to a million or more cells per cubic
millimeter.

o 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.

o SAH often can be distinguished from traumatic LP by comparing the red blood cell count of the first
and last tubes of CSF. The RBC count usually will not decrease between the first and last tubes in the
setting of SAH; however, case reports of this phenomenon do exist.

o 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 of the
CSF supernatant caused by the breakdown of RBCs and subsequent release of heme pigments.

o Spectrophotometry is much more sensitive than the naked eye in detecting xanthochromia.
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.

 D-dimer assay: Some authors have suggested that the D-dimer assay can be used to discriminate SAH from
traumatic LP; however, results have been conflicting, and further data are needed. Spinal fluid 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.

TREATMENT

Medical therapy: The initial management of patients with SAH is directed at patient stabilization. Assess the level of
consciousness and airway, as well as 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 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 (IV) 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

The traditional treatment of ruptured cerebral aneurysms 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.
The 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 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 relatively less 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% after 30 min postadministration)
 Loop diuretics (eg, furosemide) also can decrease ICP
 The use of IV steroids (eg, Decadron) is controversial but is recommended by some authors.

All patients should receive frequent neurological evaluation.

Use sedatives and analgesics cautiously to avoid masking the neurological examination. Emergent neurosurgical
consultation should be obtained in all cases of suspected SAH.
Prophylaxis and treatment of complications
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 intensive care unit or in an
intensive care unit similarly equipped.
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 the following:
 Bedrest in a quiet room
 Analgesia, preferably with a short-acting and reversible agent such as fentanyl: Pain is associated with a
transient elevation in blood pressure and increased risk of rebleeding.
 Sedation (used with caution to avoid distorting subsequent neurologic evaluation) with a short-acting
benzodiazepine such as midazolam
 Stool softeners
 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.

Cerebral vasospasm, the delayed narrowing of the large capacitance vessels at the base of the brain, is a leading cause
of morbidity and mortality in survivors of nontraumatic SAH. Vasospasm is reported to occur in as many as 70% of
patients with SAH and is clinically symptomatic in as many as 30% of patients. Most commonly, this occurs 4-14
days after the hemorrhage. Vasospasm can lead to impaired cerebral autoregulation and may progress to cerebral
ischemia and infarction. 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. Risk factors for vasospasm include the following:
 Larger volumes of blood in the subarachnoid space
 Clinically severe SAH
 Female sex
 Young age
 Smoking

Symptoms vary with the arterial territory involved, but patients typically present with a new-onset general decrease in
consciousness or focal neurological deficit. Vasospasm may be clinically indistinguishable from rebleeding; imaging
studies are required to exclude the latter. 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 but often are difficult to perform on critically ill patients. 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. Measures used for prevention of vasospasm include the
following:
 Maintenance of normovolemia, normothermia, and normal oxygenation are paramount to vasospasm
prophylaxis. Volume status should be monitored closely, with avoidance of volume contraction, which can
predispose to vasospasm.
 Prophylaxis with oral nimodipine: Calcium channel blockers have been shown to reduce the incidence of
ischemic neurological deficits, and nimodipine has been shown to improve overall outcome within 3 months of
aneurysmal SAH. Although the mechanism is unproved, it appears that nimodipine may prevent the ischemic
complications of vasospasm by the neuroprotective effect of blockading the influx of calcium into damaged
neurons. Calcium channel blockers and other antihypertensives should be used cautiously to avoid the
deleterious effects of hypotension.
 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 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.
 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 ICP 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.

If vasospasm becomes symptomatic, most authors advocate the use of hypertensive, hypervolemic, and
hemodilutional (HHH) therapy. While the efficacy of HHH therapy still is subject to debate, a number of studies have
demonstrated improved cerebral blood flow and resolution of the ischemic effects of vasospasm.
Initiation of HHH therapy requires placement of a pulmonary artery catheter in order to guide volume expansion and
inotropic or vasopressor 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.
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. The hematocrit should be maintained at 30-35% via hemodilution or transfusion in order to optimize
blood viscosity and oxygen delivery. Central venous pressure (CVP) should be maintained at 10-12 mm Hg.
Pulmonary artery wedge pressure (PAWP) should be maintained at 19-20 mm Hg. Aggressive hypertensive therapy
with inotropes and vasopressors (eg, dobutamine) can be initiated, if warranted.
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. It 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.
Intra-arterial injection of papaverine has been reported to improve outcome, but more data are needed before routine
use can be recommended. The beneficial effects of papaverine infusion appear to be short-lived compared to those of
angioplasty.
Acute obstructive hydrocephalus complicates 20% of SAH cases and usually occurs within the first 24 hours after
hemorrhage. This condition can precipitate life-threatening brainstem compression and occlusion of blood vessels.
Hydrocephalus presents as a relatively abrupt mental status change, including lethargy, stupor, or coma. CT scan
differentiates hydrocephalus from rebleeding.
Treatment for acute hydrocephalus includes external ventricular drainage, depending on the severity of clinical
neurologic dysfunction or CT scan findings. Rapid lowering of ICP 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.
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.
Symptomatic cases of hydrocephalus may be managed by temporary lumbar CSF drainage, serial LPs, or placement
of a permanent ventricular shunt. Shunt placement may not be necessary in mild cases.
Hyponatremia following SAH 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 in recent studies of post-
SAH hyponatremia. 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 occur in as many as 25% of patients following SAH and are most common after rupture of middle cerebral
artery aneurysms. Seizures can lead to increased cerebral blood flow, hypertension, and elevated ICP, thereby
escalating the risk of rebleeding and neurologic deterioration. Generalized, partial, and complex-partial seizures are
observed after SAH. 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 neurological evaluation; phenobarbital is used
less frequently than phenytoin.
 Chronic anticonvulsants are not recommended in patients without prior seizure activity or risk factors such as
hematoma, infarct, or middle cerebral artery aneurysm.

Acute pulmonary edema and hypoxia are almost universal in severe SAH. The pulmonary edema in SAH is believed
to be neurogenic in origin and unrelated to HHH 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 (PEEP).
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.
Because most ECG abnormalities that occur with SAH are benign and reversible, differentiating true myocardial
ischemia from these benign changes is important. The perioperative therapy to prevent secondary cerebral ischemia
(hypervolemia, hypertension) may exacerbate myocardial ischemia. Conversely, therapy for myocardial ischemia,
such as nitrates, may increase ICP, lower cerebral perfusion pressure, and exacerbate cerebral ischemia. Two-
dimensional echocardiography often is more sensitive in detecting myocardial ischemia than is ECG, and 2-
dimensional echocardiography is useful in the setting of SAH.
Surgical therapy: Surgical methods for treatment of SAH have improved dramatically with the advent of modern
microsurgical techniques and, more recently, with the success of endovascular therapy. See Indications for discussion
of the specific indications for treating an aneurysm surgically, endovascularly, or both. Current surgical options
include the following:
Direct aneurysmal clipping is still considered first-line treatment in the United States. The aneurysmal neck is
obliterated via application of a clip that occludes blood flow to the aneurysmal dome without compromising flow to
the parent artery. Clips are available in various sizes and shapes. Giant aneurysms or aneurysms with a calcified neck
require specialized clips with added strength (tandem or booster clips).
Of the various endovascular options currently available, most authors believe that GDCs will have the largest
influence with respect to treatment of SAH. GDCs are first-line therapy in Europe. They are soft, flexible, and can be
contoured to the configuration of the aneurysm. Sizes range from 2-20 mm in diameter and 2-30 cm in length. In
limited clinical trials, GDCs have been reported to achieve excellent rates of aneurysmal occlusion combined with a
low complication rate in appropriate patients. Two experimental coils, the bidimensional GDC and the 3-dimensional
GDC may have even better potential for aneurysm occlusion than the current generation of GDCs, but further study is
needed.
Balloon embolization is efficacious in selected patients, but it has a higher incidence of complications than coil
embolization.
Other surgical options include the following:
Proximal ligation of the parent artery or trapping of aneurysms with or without bypass: Proximal ligation is effective
for giant aneurysms. Trial balloon occlusion can be used to assess which cases necessitate a bypass graft during the
trapping procedure.
Wrapping or coating of aneurysms may be the only option in rare cases of dissecting or fusiform aneurysms
Preoperative details: The presurgical examination should consist of a general assessment, a neurologic assessment,
and a radiologic assessment.
General assessment
Cardiac and pulmonary function can decline with SAH; therefore, all patients should undergo ECG and ABG
monitoring. Hemodynamic status should be monitored with a pulmonary artery catheter in patients that show evidence
of compromise. A funduscopic examination should be performed. As many as 10% of patients with SAH have
subretinal hemorrhage, which can lead to loss of vision.
Neurologic assessment
Serial neurologic examinations should be performed until the time of surgery for early detection of complications.
Minor changes in mood, mentation, or focal neurologic function can be an early indicator of an impending
complication, such as arterial vasospasm.
Radiologic assessment
Transfemoral cerebral angiography can provide important information about the size, shape, and configuration of the
aneurysmal dome and neck, as well as the relationship of the parent vessel and perforators. Multiple views should be
obtained to best delineate the anatomy of the aneurysmal neck. During diagnostic angiography, a trial balloon
occlusion of the parent artery can be performed. This can be important in giant and fusiform aneurysms that may need
to be “trapped” because they lack a defined neck for surgical clipping. A trial balloon occlusion also may provide
important information about collateral blood flow.
Transcranial Doppler studies are useful in detecting and following the course of arterial vasospasm.
CT scan may detect calcification of the aneurysmal dome and neck, as well as the presence of thrombus. This
information can have important surgical implications. CT angiography may be helpful in demonstrating the anatomy
and relationships to other vessels.
An MRI can help delineate the degree of intramural thrombus in giant aneurysms.

Timing of surgical intervention

The timing of surgery for SAH has been a controversial topic for over 3 decades. Early surgery (0-3 d) has the
following advantages:
  Prevention of rebleeding, which is associated with a high mortality rate
 Possible prophylaxis against vasospasm by removal of subarachnoid clot
 Prevention and treatment of ischemic complications
 Prevention of medical complications
 Decreased duration of hospitalization

Disadvantages of early surgery for SAH include the following:

 Technical problems associated with edematous brain tissue
 High risk of intraoperative rupture of fragile aneurysm
 Higher surgical morbidity and mortality rates

Delayed surgery for SAH (>10 d posthemorrhage) has the following advantages:
 Brain tissue is less edematous.
 Lower risk of intraoperative aneurysm rupture
 Lower surgical morbidity and mortality rates
 Flexibility of scheduling

The disadvantages of delayed surgery are as follows:

 Increased rate of morbidity and mortality due to rebleeding
 Technical difficulties due to adhesions around the aneurysm

The International Cooperative Study on Timing of Aneurysm Surgery findings are as follows:
 Surgical outcomes usually are superior with delayed surgery; however, the increased morbidity and mortality
rate associated with delay (as high as 30% in some studies for patients with low-grade SAH) negated these
results.
 Overall results were comparable for early and delayed surgery with the exception that patients with low-grade
SAH (Hunt and Hess/WFNS grades 1-2) had a better outcome with early surgery.
 Subsequently, many centers have published favorable results with early surgery for low-grade SAH, and it
now is a common treatment decision.

For patients with an intermediate grade of SAH (Hunt and Hess/WFNS grade 3), the published results are less
conclusive.
 Several studies show no difference in morbidity and mortality rates between early and delayed surgery.
 A 1995 study in Japan suggests that early surgery is beneficial in this group of patients.
 Greater microsurgical experience and advances in neuroanesthesia and neurointensive management are likely
to improve the outcomes for early surgery in this group of patients.

The timing of surgical management for patients with high-grade SAH (Hunt and Hess/WFNS grades 4-5) must be
individualized depending on the following criteria:
 Admission clinical examination findings and GCS
 CT scan evidence of brain destruction
 ICP
 Concurrent medical problems
 Presence of absence of cerebral vasospasm

Data suggest that some patients with an initial GCS less than 5 can have good outcomes if the following occur:
  A ventricular drain is placed emergently.
 ICP does not exceed 30 mm Hg.
 Angiography shows normal intracranial filling.

Patients with significant evidence of brain destruction, increased ICP, and angiogram revealing poor intracranial
filling have a universally poor outcome regardless of treatment.
The overall outcome in patients with high-grade SAH is poor with or without surgical intervention; however; because
surgical treatment seems to benefit some patients, many authors suggest an aggressive approach to management.
Intraoperative details:

Surgical clipping
Most anterior circulation aneurysms can be approached from the pterion. Exceptions include (1) aneurysms arising
from the division of the anterior cerebral artery into the pericallosal and callosal marginal branches and (2) small
mycotic aneurysms on distal branches of the middle cerebral artery.
Posterior circulation aneurysms are less accessible, and a number of modified approaches have been developed.
 The modified pterional approach can be employed for aneurysms arising from the head of the basilar artery
where the head is above the dorsum sellae.
 The subtemporal approach is used for aneurysms that initiate at the head of the basilar artery in which the
bifurcation of the basilar artery is below the dorsum sellae.
 A posterior subtemporal approach can be used for most aneurysms arising from the trunk of the basilar artery.
 A far lateral inferior approach can be used for certain lower basilar trunk and midline vertebral artery
aneurysms. A midline suboccipital approach can be utilized for aneurysms extending from the vertebral artery
where it pierces the dura. The midline suboccipital approach also may be used for a group of aneurysms that
arise from the distal posterior inferior communicating artery.

Skillful brain retraction is paramount in aneurysm surgery, with care taken to minimize tissue and vessel damage. Use
of one blade only of a self-retaining retractor (eg, Yasargil, Greenburg, Sugita) usually is sufficient for adequate
exposure of most saccular aneurysms and allows for the compensatory expansion and displacement of nonretracted
areas of the brain, thus minimizing tissue trauma.
The general approach to surgical clipping of saccular aneurysms is as follows:
 Dissection is undertaken to identify the parent artery for possible temporary clipping in the event of
aneurysmal rupture.
 Incision of the arachnoid overlying the aneurysm is accomplished with the tip of a #11 blade scalpel.
 The walls of the aneurysm are dissected away from the perforating vessels with a small aneurysm dissector or
spatula. Aneurysmal sac volume can be decreased, under hypotension, by compression with a suction device
placed over a cotton pad.
 Mobilization of the aneurysm in all directions is necessary for visualization of any perforating vessels that
might inadvertently be incorporated by clip misplacement.
 Occlusion of the aneurysm is accomplished with an appropriately sized clip placed across the base. Use of a
clip that is as small as possible helps facilitate the visualization of perforating vessels after aneurysm repair.
o Avoid placing the clip too close to the parent artery, which may cause a tear in the aneurysmal sac.
o If a tear does occur, a clip graft is used for repair. Use of a clip graft is associated with the risk of
damage to perforating vessels, so it should be employed only when necessary.
o Suturing in close proximity to an aneurysm can result in damage to the parent artery and should be
avoided.
  An attempt should be made to gently open the basal cisterns and to carefully remove as much of the
subarachnoid blood as possible with suction, lavage, and, possibly, intracisternal infusion of antifibrinolytics,
when appropriate.

Endovascular treatment with the Guglielmi detachable coil system

Adequate airway protection, oxygenation, sedation, blood pressure management, and ICP management are paramount
during the procedure. Ideally, endovascular treatment for patients with SAH should be performed under general
anesthesia. Complete immobilization of the patient during catheterization and embolization is mandatory.
 After the femoral artery puncture and initial angiogram, anticoagulation is initiated with heparin. The risk of
thromboembolic events during the procedure in patients with acute SAH eclipses the risk of hemorrhage.
 A guide catheter (6F) is placed in the internal carotid or vertebral artery. This allows for the passage of the
microcatheter and facilitates contrast injection for angiograms and road mapping. Road mapping is a
computer-generated technique that allows for real-time visualization of endovascular equipment superimposed
over a map of the intracranial arteries.
 The size of the aneurysm must be approximated before embolization by estimation based on the size of the
adjacent intracranial arteries, by using objects such as coins for reference, or by use of a guiding catheter with
a known size.
 The clinician should find the projection that allows for optimal visualization of the parent artery in relation to
the aneurysm; this usually requires views in multiple planes.
 The plastic microcatheter tip and the Micro-Guide wire are shaped according to the configuration of the
aneurysm.
 The aneurysm is catheterized with the microcatheter and guide wire using road mapping. The microcatheter
should not touch the walls of the aneurysm.
 When the microcatheter is in the desired position within the aneurysm, the first GDC can be delivered. The
first coil should be slightly smaller than the diameter of the aneurysm, and it should cross the neck of the
aneurysm several times to form a receptacle. Delivery of the GDC typically takes 1-4 minutes; however, newer
GDC systems can detach in 20-30 seconds.
 After placement of the first coil has been achieved, the aneurysm is filled with coils of decreasing size until
densely packed. Complete packing of the aneurysmal sac and neck usually is possible with small aneurysms.
In some larger aneurysms, the neck cannot be occluded completely. These aneurysms have a higher risk of
recurrence. Often, aneurysms with larger necks can be treated successfully with a balloon-assisted GDC
technique.
 The microcatheter is withdrawn cautiously from the aneurysm, and a final angiogram is obtained.
 Heparinization is reversed with protamine, the femoral sheath is removed, and the patient is transferred to the
neurologic intensive care unit.

Postoperative details: The postoperative management of SAH is directed at prophylaxis and treatment of the
complications of SAH (see Prophylaxis and treatment of complications).
Follow-up care: Patients with neurologic deficits may require outpatient rehabilitation. Cognitive and psychological
rehabilitation often is needed.
SAH often causes nonspecific symptoms similar to postconcussion syndrome and include the following:
 Headache
 Dizziness
 Blurred vision
 Poor concentration
 Poor short-term memory
  Emotional lability
 Insomnia
 Fatigue

Specific postsurgical problems include the following:

 Jaw pain and stiffness due to temporalis muscle scarring
 Paralysis of the frontalis muscle
 Deranged or absent sense of smell due to intraoperative traction on the olfactory tract
 Local neuralgias
 Wound infection

Some patients may require steroid and/or anticonvulsant therapy as outpatients. Oral nimodipine therapy often is
continued for 3-4 weeks after SAH.
COMPLICATIONS

Complications of surgical clipping include the following:

 Hemorrhagic complications
 Ischemic complications
 Damage to parent artery or perforating arteries
 Acute or delayed neurological deficits from iatrogenic trauma
 Meningitis
 Cellulitis and wound infection
 Nonspecific postsurgical syndrome similar to postconcussive syndrome

Common complications of endovascular therapy include the following:

 Aneurysm rupture (GDCs, balloons)
 Thromboembolism (GDCs) with acute or delayed neurologic deficit
 Balloon rupture or deflation

OUTCOME AND PROGNOSIS

Despite advances in medical and surgical therapy, the mortality rate for aneurysmal SAH remains 50% at 1 year.

Survival is inversely proportional to SAH grade upon presentation. Reported data demonstrate an approximate 70%
survival rate for Hunt and Hess grade 1, 60% for grade 2, 50% for grade 3, 20% for grade 4, and 10% for grade 5.

Approximately 25% of survivors have persistent neurologic deficits.

Most survivors have either a transient or a permanent cognitive deficit.

Mortality and morbidity are influenced by the magnitude of the bleed, the age of the patient, the presence or absence
of comorbid conditions, and the occurrence of medical complications.

For excellent patient education resources, visit eMedicine's Headache Center. Also, see eMedicine's patient education
article, Aneurysm, Brain.
FUTURE AND CONTROVERSIES

The future of SAH management most likely will revolve around the continuing development and refinement of
minimally invasive endovascular techniques.

Currently, controversy remains regarding the question of which aneurysms are appropriate for surgical or
endovascular treatment; rigorous studies coupled with additional clinical experience will help with the formation of
guidelines. Some aneurysms may require a combined approach.

While GDC therapy is, to date, the most promising development in the realm of endovascular methodologies for SAH,
the future almost certainly will provide materials that are even safer and more efficacious in occluding aneurysms