SYMPOSIUM ON CEREBROVASCULAR DISEASES
SUBARACHNOID HEMORRHAGE
Subarachnoid Hemorrhage:
Neurointensive Care and Aneurysm Repair
EELCO F. M. WIJDICKS, MD; DAVID F. KALLMES, MD; EDWARD M. MANNO, MD; JIMMY R. FULGHAM, MD;
AND DAVID G. PIEPGRAS, MD
Aneurysmal subarachnoid hemorrhage (SAH) is often a neurologic
catastrophe. Diagnosing SAH can be challenging, and treatment
is complex, sophisticated, multidisciplinary, and rarely routine.
This review emphasizes treatment in the intensive care unit,
surgical and endovascular therapeutic options, and the current
state of treatment of major complications such as cerebral vaso-
spasm, acute hydrocephalus, and rebleeding. Outcome assess-
ment in survivors of SAH and controversies in screening of family
members are discussed.
Mayo Clin Proc. 2005;80(4):550-559
CSF = cerebrospinal fluid; CT = computed tomography; MCA = middle
cerebral artery; SAH = subarachnoid hemorrhage
R upture of an intracranial aneurysm into the subarach-
noid compartment immediately leaves patients in
critical condition. Some patients do not receive care in
time. Sudden death from a massive increase in intracranial
pressure occurs in approximately 1 of 10 patients (with
40% in a posterior circulation aneurysm), and another 10%
to 20% of patients who arrive at the emergency department
are comatose and need immediate respiratory support.1,2 At
the other end of the clinical spectrum—and certainly more
commonly—patients present with acute excruciating head-
ache, confusion, or abnormal behavior. Because of the
comparatively infrequent presentation of subarachnoid
hemorrhage (SAH) (approximately 1 in 10,000 Americans
annually), physicians who encounter patients with SAH are
not attuned to its severity and may find recognizing its key
components difficult.3
The care of a patient with aneurysmal SAH involves early
repair of the recently ruptured aneurysm. In most larger
institutions, patients are admitted to a neurologic-neurosur-
gical intensive care unit and receive aggressive care to pre-
vent further deterioration, which can substantially affect out-
come. We describe aspects of initial evaluation, neurologic
intensive care, and methods of definitive repair. This care
involves a multidisciplinary team with immediate availabil-
ity that can be provided only in tertiary care medical centers.
From the Department of Neurology (E.F.M.W., E.M.M., J.R.F.), Department of
Radiology (D.F.K.), and Department of Neurologic Surgery (D.G.P.), Mayo
Clinic College of Medicine, Rochester, Minn.
Individual reprints of this article are not available. The entire Symposium on
Cerebrovascular Diseases will be available for purchase as a bound booklet
from the Proceedings Editorial Office at a later date.
© 2005 Mayo Foundation for Medical Education and Research
550 Mayo Clin Proc. • April 2005;80(4):550-559
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CHALLENGES IN DIAGNOSIS
A ruptured cerebral aneurysm causes an unexpected, sud-
den headache and may lead to loss of consciousness. Pa-
tients describe a “thunderclap headache” (an unfortunate
term because no sound is heard). The patient reports the
worst headache of his or her life, more precisely, a split-
second, extremely intense, and overwhelming headache
that fails to subside. Many patients report feeling as if “the
top of my head is blown off” or as though “someone hit me
in the head with a hammer,” but these key elements in the
medical history may be difficult to elicit in confused pa-
tients. Rarely, there are other nonaneurysmal causes of
thunderclap headache present. These disorders include pi-
tuitary apoplexy, arterial dissection, cerebral venous throm-
bosis, and hypertensive encephalopathy. Also, thunderclap
headache may be idiopathic.4 In these conditions (other
than SAH), computed tomography (CT) or results of ce-
rebrospinal fluid (CSF) examination may be normal, in
which case magnetic resonance imaging is indicated.
When the patient is seen hours after onset of symptoms,
neurologic examination may reveal nuchal rigidity, cranial
neuropathy (third or sixth cranial nerve most commonly),
or other localized neurologic deficit (aphasia, hemipare-
sis); however, major neurologic signs generally are absent.
Seizures may occur in a small percentage of surviving pa-
tients, and epilepsy may develop in less than 10%, particu-
larly in those who had a subdural hematoma or cerebral
infarction during their hospital course.5 Subarachnoid hem-
orrhage usually is graded by using the World Federation of
Neurosurgical Societies grading scale, which is based on
the Glasgow Coma Scale (Table 1). Poor-grade SAH is de-
fined arbitrarily as grade IV and V; when caused by rupture
alone, immediate definitive treatment may be deferred, with
many neurosurgeons awaiting patient improvement.6
Computed tomography is the first-line diagnostic proce-
dure in patients with suspected SAH (Figure 1). Histori-
cally, CT has 90% to 95% sensitivity for recent SAH; with
modern CT equipment, sensitivity is closer to 98%.7,8
On CT, an aneurysm is rarely seen but when present
indicates large size (>10 cm) (Figure 1). Examination of
CSF is necessary when CT is normal and has been reviewed
for subtle areas of subarachnoid blood (posterior horns,
sylvian fissure, and sulci). Prompt ascertainment of a diag-
nosis of SAH is warranted because a ruptured aneurysm has
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 SUBARACHNOID HEMORRHAGE

the highest rate of rerupture within the initial 48 hours. TABLE 1. Grading System Proposed by the World Federation of
Neurosurgical Societies (WFNS) for the Classification of
However, no evidence suggests that lumbar puncture in- Subarachnoid Hemorrhage
creases the risk of aneurysmal rehemorrhage. Testing CSF
WFNS Glasgow Coma Scale
for the presence of xanthochromia, the yellow tinge in CSF grade score Motor deficit
caused by the breakdown products of hemoglobin, is the
I 15 Absent
gold standard for diagnosis of SAH, with a sensitivity greater II 14-13 Absent
than 99%. Xanthochromia is present as early as 6 hours after III 14-13 Present
SAH and along with bilirubin remains detectable until about IV 12-7 Present or absent
V 6-3 Present or absent
2 to 3 weeks after SAH.9,10 When gross blood is present in the
initial CSF specimen tube, a decrease in the quantity of red
blood cells in successive specimen tubes is a frequently used
(albeit unreliable) marker for the absence of SAH. (The ric data acquisition during conventional catheter angiogra-
medicolegal implications can be substantial if cerebral an- phy (Figure 3). The technique is used routinely in many
giography is deferred on the basis of this loose criterion.) medical centers. Its primary advantage over 2-dimensional
Determining the presence of xanthochromia is the best angiography is that it allows a better understanding of the
method to document disintegrated erythrocytes, but vials complex relationships between aneurysm necks and adja-
should be held against a bright light and white back- cent arteries. In some circumstances, angiography should
ground to appreciate the discoloration (Figure 211). Visual be repeated several weeks later to detect abnormalities not
inspection is far from perfect, and, although used rarely in visualized on earlier studies. One important entity that
the United States, spectrophotometry of CSF may docu- needs to be recognized is nonaneurysmal pretruncal (or
ment oxyhemoglobin or bilirubin if visual assessments of perimesencephalic) SAH.12-17 This type of hemorrhage has
the vial with centrifuged CSF are conflicting. Bilirubin certain CT characteristics (Figure 4), mainly with a focal
absorbance at 473 λ is diagnostic (note that iodine used clot in the front of the brainstem. The major concern is the
during the procedure may lead to a false-positive effect).9 presence of a posterior circulation aneurysm that may pro-
Once a diagnosis of SAH is confirmed, 4-vessel cerebral duce—at least in 1 study—similar CT patterns in up to 17%
angiography is needed to identify and characterize the of cases.18
source of hemorrhage. Noninvasive imaging techniques
such as magnetic resonance angiography and CT angiogra-
INITIAL TREATMENT
phy continue to improve and are being used for making
fundamental treatment decisions for intracranial aneurysm. Although surgical and endovascular therapeutic options
Three-dimensional rotational angiography allows volumet- have substantially changed the approach to SAH, medical

FIGURE 1. Computed tomograms show blood in basal cisterns, sulci, and visible giant
aneurysm of the anterior communicating artery (left) and basilar artery (right).

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SUBARACHNOID HEMORRHAGE

clipping of ruptured aneurysm, and nitroprusside and other

FIGURE 2. Xanthochromia from a patient with recent subarachnoid
hemorrhage. Vial with cerebrospinal fluid is compared with water.
Note that xanthochromia is hardly recognizable when vial is held
against blue sky (left) vs a light box (right). Adapted from Catastrophic
Neurologic Disorders in the Emergency Department, 2nd ed, by Eelco
F. M. Wijdicks.11 Copyright 2004 by Oxford University Press, Inc. Used
by permission of Oxford University Press, Inc.
treatment also has shifted considerably. On the basis of
evidence from randomized trials, several therapies have
been discarded because of a serious concern of doing more
harm than good, including antifibrinolytic agents, sublin-
gual nifedipine, fluid restriction for hyponatremia, delayed
vasodilators.19-22
Close neurologic monitoring in the neurologic-neuro-
surgical intensive care unit should lead to prompt identifi-
cation and treatment of new neurologic deterioration due to
aneurysmal rebleeding, acute hydrocephalus, early cere-
bral vasospasm, or other medical complications. Before an
aneurysm has been treated definitively, blood pressure gen-
erally is controlled, with a target systolic pressure of less
than 180 mm Hg and a target mean arterial pressure be-
tween 100 and 120 mm Hg. Use of antifibrinolytic agents
typically is avoided. Although long-term (21 day) anti-
fibrinolytic agents decrease the risk of rehemorrhage, they
increase the incidence of ischemic neurologic deficit due to
cerebral vasospasm and do not improve overall out-
come.19,20 A large pilot study of short-term antifibrinolytic
use did not suggest reduced rebleeding.20
Our approach to initial treatment is shown in Table 2.23
The guiding principles by organ systems are aimed at
preservation of homeostasis, use of prophylactic drugs,
and preparation for definitive aneurysm treatment. Nor-
mal CSF circulation may become obstructed secondary to
intraventricular blood due to a thick clot in the basal cis-
terns or a clot at the level of the arachnoid villi. Certain
clinical and radiographic features may predict the occur-
rence of acute hydrocephalus: intracerebral extension of
hemorrhage, posterior circulation aneurysm, and reduced
Glasgow Coma Scale score on admission.24 Acute hydro-
cephalus after SAH is a necessary consideration in pa-
tients presenting with altered consciousness; by CT crite-
ria, it is present in 20% of patients. Acute neurologic
deterioration in the setting of progressive ventricular en-

FIGURE 3. Left, Lateral view of a conventional digital subtraction angiogram from which a diagnosis of anterior
choroidal artery infundibulum was made because a vessel appeared to emanate from the dome. LT ICA = left
internal carotid artery. Right, Three-dimensional rotational angiography shows that an aneurysm is present
rather than an infundibulum because the anterior choroidal artery originated separately from the dome.

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 SUBARACHNOID HEMORRHAGE

largement on CT is a clear indication for external ven-

tricular drainage.25,26 However, the treatment of patients
who arrive at the hospital in a comatose state with ven-
tricular enlargement on CT is more controversial because
the neurologic impairment may be a result of the effect of
the initial hemorrhage rather than due to hydrocephalus.
Such patients can be observed initially for 24 hours, and
some will improve clinically without intervention. If se-
rial CT scans reveal progressive ventricular enlargement
or if the neurologic condition deteriorates, external ven-
tricular drainage is indicated. Other clinicians may advo-
cate early placement of external ventricular drains and
then observation for possible improvement. The most
recent data suggest that external ventricular drainage does
not increase the likelihood of aneurysmal rehemorrhage
when drainage is performed at moderate pressures (<10
cm H2O).
The risks of ventriculostomy are small but not inconse-
FIGURE 4. Nonaneurysmal pretruncal subarachnoid hemorrhage.
quential. Infection can occur, particularly if the drain is in
place for extended periods. Aseptic technique during place-
ment is crucial, as is meticulous sterile technique when and directionally sensitive, which allows for insonation
caring for the wound site, tubing, and fluid collection sys- of the cerebral vessels at varying depths and direc-
tem. The use of prophylactic antibiotics is not established, tions.27,28 Elevated flow velocities in the middle cerebral
but we administer antibiotics (cefazolin or vancomycin) artery (MCA) are correlated with angiographic narrow-
while the drain is present and perform CSF culture every 2 ing of this vessel, although the correlation of angiograph-
to 3 days or if laboratory and/or clinical signs of infection ic vessel narrowing with other cerebral vessels is less
emerge such as fever and leukocytosis. reliable.27,28
A prompt clinical response such as an improved level However, the ability of transcranial Doppler ultrasonog-
of consciousness is often seen after CSF diversion. If raphy to predict which patients will develop ischemic defi-
no improvement occurs within 36 to 48 hours, the clin- cits secondary to cerebral vasospasm is problematic. Early
ical state of the patient is likely due to the effects of studies suggested that increasing flow velocities in the MCA
the SAH.25 In patients who show improvement, weaning could precede neurologic deficits.29,30 However, later studies
from the ventriculostomy can start after intracranial pres-
sure is controlled for 48 hours. This is done in steps and TABLE 2. Initial Treatment of Subarachnoid Hemorrhage*
involves elevating the height of the drain to 20 cm above
Type Treatment
the tragus and eventually clamping the drain. While
monitoring intracranial pressure, clamping and reopening Airway Intubation and mechanical ventilation if patient has
aspiration, neurogenic pulmonary edema, Glasgow
of the drain may need to be done several times during the Coma Scale motor score of withdrawal, or worse
course of a day if the patient develops symptoms of in- Fluid 2-3 L of 0.9% NaCl per 24 hours
creased intracranial pressure or the intracranial pressure Fludrocortisone acetate, 0.3 mg/d if patient has
increases. Failure to wean the patient from the ventricu- hyponatremia
lostomy and persistent drainage of high CSF volumes Blood Accept MAP of ≤130 mm Hg. If MAP is >130 mm Hg,
pressure esmolol bolus, 500 µg/kg in 1 min; or labetalol, 20 mg
indicate the need for a permanent shunt. IV in 2 min; or enalaprilat, 0.625 mg IV in 5 min
Another major complication is cerebral vasospasm. The
Nutrition Enteric nutrition with continuous infusion on day 2
foundation for prevention and treatment of vasospasm is
Additional Nimodipine, 60 mg 6 times a day for 21 days
maintaining euvolemia or mild hypervolemia and normo- measures Stool softener
tension or moderate hypertension. Pneumatic compression devices
Transcranial Doppler ultrasonography is a noninva- Acetaminophen with codeine or morphine, 1-2 mg, or
tramadol (if no seizures), 50-100 mg, orally every
sive method for monitoring development of cerebral va- 4 hours for pain management
sospasm. A handheld probe is used to transmit and re- Phenytoin, 20 mg/kg if seizures have occurred
ceive a low-frequency pulsed wave through the temporal *b.i.d. = twice daily; IV = intravenously; MAP = mean arterial pressure.
bone of the skull. This ultrasonic wave is both range gated Adapted from Wijdicks.23

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SUBARACHNOID HEMORRHAGE
TABLE 3. Mayo Clinic Protocol for Hemodynamic Augmentation
in the Treatment of Cerebral Vasospasm
in Aneurysmal SAH*
SAH, clinically asymptomatic but TCD or CT evidence of diffuse cerebral
vasospasm
Place central venous catheter
Obtain hourly readings of fluid balance and body weight
Accomplish volume repletion with crystalloids
Note end points of volume resuscitation: CVP ≥8 mm Hg, urine
output >250 mL/h
Avoid antihypertensive and diuretic agents
SAH, secured aneurysm, clinical evidence of cerebral vasospasm†
Notify interventional neuroradiologist for possible cerebral
angiography
Place pulmonary artery catheter
Give crystalloid bolus or albumin 5% until increase in stroke volume
index is <10% for every 2 mm Hg increase in pulmonary capillary
wedge pressure
Match fluid input with urine output
When urine output is >250 mL/h, start administration of
fludrocortisone acetate, 0.2 mg b.i.d.
Wait 1 hour for clinical improvement
If no improvement, start administration of phenylephrine,
10-30 µg/min with increase in MAP 25% above baseline or
>120 mm Hg
Start administration of dobutamine, 5-15 µg/kg/min to increase cardiac
index >3.5 L/min/m2
Consider replacing phenylephrine with norepinephrine if desired
effect is not attained
If no effect, perform cerebral angiography for angioplasty or
papaverine infusion
*b.i.d. = twice daily; CT = computed tomography; CVP = central venous
pressure; MAP = mean arterial pressure; SAH = subarachnoid hemor-
rhage; TCD = transcranial Doppler ultrasonography.
†See “Treatment of Symptomatic Cerebral Vasospasm” in text. Typically,
fluctuation in level of consciousness or a localizing sign such as aphasia,
hemiparesis, paraparesis, or apraxia.
From Wijdicks.23
noted that multiple systemic and operator-dependent factors
could influence these flow velocities, limiting their useful-
ness as a prognostic tool.31,32 More recently, 1 study claimed
that MCA flow velocities slower than 120 cm/s and faster
than 200 cm/s, respectively, have strong negative and posi-
tive predictive powers for determining which patients will
develop ischemic deficits.33
TREATMENT OF SYMPTOMATIC
CEREBRAL VASOSPASM
For patients who become symptomatic with delayed is-
chemic deficit due to vasospasm, more aggressive intravas-
cular volume expansion and induced hypertension are
used. To ensure appropriate intravascular volume and car-
diac output in symptomatic patients, invasive monitoring in
the form of right atrial or pulmonary artery catheterization
is recommended. Nimodipine, a calcium channel blocker
administered orally, improves overall patient outcome after
SAH. Of note, the drug does not increase the caliber of
narrowed cerebral arteries on cerebral angiography. Rather,
554 Mayo Clin Proc. • April 2005;80(4):550-559
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the calcium channel blockade seems to have a neuro-
protective effect mediated through an uncharacterized
mechanism.34,35
Our approach to cerebral vasospasm is stepwise, hemo-
dynamic augmentation with improvement of volume status
followed by an increase in peripheral vascular resistance
and, finally, enhancement of cardiac contractility. Blood
pressure augmentation may substantially improve ischemic
neurologic deficit. If medical therapy for symptomatic va-
sospasm has been maximized and neurologic symptoms
prove refractory, endovascular therapies can be considered
(Table 3). Intra-arterial papaverine infusion acts immedi-
ately and increases arterial caliber and cerebral blood
flow, but its effects are short-lived. A recent study using
intra-arterial verapamil suggested safety, but results were
far from impressive.36 Balloon angioplasty is particular-
ly effective as a durable means of alleviating arterial
narrowing and preventing stroke in patients with symp-
tomatic vasospasm after aneurysmal SAH. However, the
procedure has risk, particularly in inexperienced hands.
The timing of endovascular intubation and use of ino-
tropes in patients with cardiac dysfunction are unresolved
issues.
ANEURYSM TREATMENT
As stated previously, the treatment strategy for aneurysmal
SAH is focused on (1) treatment of the primary brain injury
of the hemorrhage itself; (2) the necessary associated gen-
eral supportive therapy, prophylactic therapy, and, if neces-
sary, interventive therapies for the secondary effects of the
hemorrhage such as cerebral vasospasms/delayed ischemic
deficit and hydrocephalus; and (3) last but not least in
importance or priority, treatment of the aneurysm that gave
rise to the hemorrhage.
Definitive treatment of the aneurysm is recommended
as soon as feasible, particularly for patients with good-
grade SAH, to minimize risk of recurrent aneurysmal hem-
orrhage. Early aneurysm treatment necessarily must take
into account the general medical priorities of the patient,
particular complexities of the aneurysm itself, and avail-
ability of the appropriate surgical team. Currently, the 2
primary options for aneurysm treatment are craniotomy
and aneurysm neck clipping or transvascular endosaccular
coiling. Only in rare situations is occlusion of the arterial
trunk proximal to the aneurysm the best therapeutic option.
ENDOVASCULAR TREATMENT
In 1995, the Food and Drug Administration approved use
of the Guglielmi Detachable Coil (Target Therapeutics,
Fremont, Calif) for endovascular therapy for aneurysms
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 SUBARACHNOID HEMORRHAGE

FIGURE 5. Anteroposterior angiograms show a bilobed basilar apex aneurysm (left) and oblitera-
tion of the aneurysm after coil embolization (right).

not considered amenable to surgical treatment. In the 8
years since initial Food and Drug Administration approval,
more than 100,000 patients worldwide with cerebral aneu-
rysms have been treated with endovascular coil occlusion.
In some medical centers, indications for use of endovascu-
lar therapy have evolved to include a broader array of
patients beyond those with “nonsurgical aneurysms” ini-
tially treated with the device.
Even though documentation of numerous case series
of coiling procedures exist,37-41 few controlled trials have
compared surgery to endovascular treatment of aneurysms.
A small series comparing the 2 treatments in patients with
basilar apex aneurysms showed slight decreases in mortal-
ity, costs, and length of hospital stay in patients treated
with coil embolization compared with those who under-
went surgery.42 A recent series comparing surgery to coil
embolization in unruptured aneurysms showed improved
outcomes and fewer complications in the surgical group
compared with the coil group.40 A large prospective trial
comparing surgery with coiling in ruptured aneurysms, the
International Subarachnoid Aneurysm Trial (ISAT), showed
a modest decrease in morbidity associated with coiling com-
pared with clipping.43 Because of the relative lack of pro-
spective controlled trials, most patients are treated individu-
ally on the basis of numerous considerations.
Choice of the ideal treatment option, either surgical
clipping or endovascular treatment, depends on multiple
factors, including those related to the patient’s overall
clinical status, the anticipated surgical difficulty, and the
technical details of the proposed coiling procedure. These
technical features include the anatomy of the access ves-
sels, including the aortic arch and the brachiocephalic ves-
sels, as well as the morphology of the aneurysm and the
adjacent parent artery. With the advent of multiple coil
shapes, even aneurysms with highly complex anatomy can
be embolized safely (Figure 5).
In many ways, clipping and coiling can be seen as
complementary. For example, surgical treatment of basi-
lar apex aneurysms has relatively high morbidity rates,
whereas coil embolization of basilar apex aneurysms is
often straightforward, depending on the breadth of the
aneurysm neck. Conversely, aneurysms in the region of
the MCA trifurcation are usually difficult to treat with
coils, given the proximity of branch vessels to the aneu-
rysm neck, but are often readily treated with surgical
clipping.
Vascular access should be carefully considered in all
patients. The difficulty and risk of the procedure are highly
dependent on the anatomy of all vessels that will be tra-
versed. However, primary consideration should be focused
on the caliber, tortuosity, and extent of atherosclerotic
change in the cervical and intracranial portions of the ac-
cess vessel. For example, tortuosity or loop formation in
the cervical carotid artery can markedly increase the diffi-
culty of a coiling procedure. Furthermore, tortuosity of the
carotid siphon may affect the safety of performing the
coiling procedure, especially in broad-necked aneurysms
in which adjunctive treatments such as balloon remodeling
or stent placement are anticipated.
Perhaps the primary factor in deciding whether to at-
tempt a coiling procedure is the breadth of the aneurysm
neck compared with that of the dome and adjacent parent
artery. Various definitions of “wide neck” have been used
in relation to coiling procedures, but difficulty in coiling
can be anticipated if the dome-neck ratio is less than 1.5:1.
In some locations, especially along the supraclinoid inter-

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SUBARACHNOID HEMORRHAGE

FIGURE 6. Left, Anteroposterior angiogram reveals a broad-necked ophthalmic-segment aneurysm. The dome-neck ratio
is approximately 1.2:1. Previously, an attempt was made to coil the aneurysm, but coils persistently herniated through
the broad neck, and the procedure was aborted. Middle, After placement of a single coil with a balloon inflated across
the aneurysm neck, the coil shows excellent conformation and stability and was therefore detached in the aneurysm.
Right, After balloon-assisted embolization, the aneurysm was obliterated completely, with preservation of the parent
artery.

nal carotid artery, balloon remodeling or stent placement
can be used to facilitate coil placement44-47 (Figure 6). In
other locations, including branch points such as the basilar
apex, adjunctive techniques are difficult to use. Coil embo-
lization in extremely wide neck aneurysms with dome-
neck ratios of less than 1:1 would be unlikely to be effec-
tive, even with use of adjunctive measures.
Multiple clinical studies have shown that the efficacy of
coil embolization, defined as the rate of complete, persis-
tent aneurysmal occlusion, is intimately related to both the
aneurysm size and the width of the aneurysm neck.38,48-50
There is a sharp reduction in the rate of complete aneurys-
mal occlusion for aneurysms greater than 8 to 10 mm in
diameter and in aneurysms with necks broader than 4
mm.38,49,50 Recent advances such as use of the balloon re-
modeling technique, in which a soft balloon is temporarily
inflated in the parent artery to hold coils within the aneu-
rysm cavity, and use of endovascular stents have improved
the ability to treat difficult aneurysms.51-54 Even so, the rate
of complete occlusion remains frustratingly low, about
50% to 70% in most series. Perhaps more importantly, the
rate of late aneurysmal regrowth after coil embolization is
extremely high, 33% or more, for aneurysms 10 mm and
greater in diameter. Other factors associated with increased
risk of aneurysmal recurrence include treatment of rup-
tured rather than unruptured aneurysms and incomplete
coiling in the initial procedure.48-50
Several modifications of simple coils aimed at improv-
ing aneurysmal occlusion rates have been reported wide-
ly. Two such modifications are commercially avail-
able,55,56 but no clinical data are yet available to assess
their efficacy.
Coiling represents an important adjunct to aneurysm
surgery in selected patients. Apparent improvements in
outcome with coils compared with surgery in patients with
ruptured aneurysm may speed adoption of coils in some
medical centers. Currently, the lack of persistent occlusion
and the need for long-term surveillance limit the applica-
tion of coils, but these limitations may be overcome with
the advent of modified coil devices.
SURGICAL TREATMENT
Definitive treatment of saccular intracranial aneurysms,
whether ruptured or unruptured, evolved over the last
half of the 20th century with major refinements of direct
aneurysm obliteration by clamping or “clipping” of the
aneurysm neck (Figure 7). Microsurgical techniques en-
hanced by adjuncts such as temporary proximal trunk
occlusion, bipolar coagulation for shrinkage of the aneu-
rysm sac, and improved aneurysm clips have ensured
a high degree of treatment efficacy, with permanent
aneurysm obliteration in more than 90% of patients when
surgery is performed by experienced aneurysm sur-
geons.57,58 Furthermore, such treatments can be accom-
plished with low morbidity and mortality, ranging from
5% to 15% for most intracranial aneurysms in the carotid
and vertebrobasilar circulation, exclusive of giant aneu-
rysms.59,60 As such, craniotomy and microsurgical clip-
ping has been established as the gold standard for treat-

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 SUBARACHNOID HEMORRHAGE

FIGURE 7. A, Typical microsurgical exposure during craniotomy and clipping of a middle

cerebral artery (MCA) aneurysm after opening of the sylvian fissure between the frontal and
temporal lobes; the aneurysm arises at the bifurcation of the MCA with a broad base. B,
The aneurysm is occluded completely with an aneurysm clip while blood flow is preserved
in the MCA branches.

ment of unruptured and ruptured aneurysms, with early
surgery recommended for patients who present with SAH
and are in good condition to reduce risk of recurrent
bleeding.61
Although several studies indicate that endovascular
coiling can be accomplished with lower procedural risks
than clipping,43,62 particularly for aneurysms located along
the basilar trunk and at the basilar caput,42 efficacy for
complete obliteration of the aneurysm is clearly less than
clipping, ranging from 75% in optimal circumstances to
40% in patients with suboptimal aneurysm anatomy.38 Fur-
thermore, features such as broad aneurysm base, intra-
aneurysmal thrombus, and arterial branches exiting from
the aneurysm dome or neck constitute relative specific
indications for aneurysm clipping over coiling. Of all loca-
tions, the MCA bifurcation region has been the least opti-
mal for coiling, particularly related to the tendency for
broader aneurysm neck and branches arising at this site.63
In cases of ruptured aneurysm, the presence of major in-
tracerebral hemorrhage with mass effect causing neuro-
logic consequences constitutes a specific indication for
craniotomy to permit expeditious evacuation of the clot and
definitive aneurysm treatment with clipping. Furthermore,
extremely large or giant aneurysms, although posing in-
creased risk for treatment due to their size and complexity,
are in most cases still best treated by direct clipping of the
aneurysm neck or other reconstructive techniques.
As technology advances, particularly in endovascular
therapies, more intracranial aneurysms undoubtedly will be
treated by such means. However, it seems highly likely that
many aneurysms, particularly those of large size and com-
plicated anatomy, will continue to be best treated by open
craniotomy and microsurgical clipping because of the
proven durability of this procedure.
OUTCOME IN SURVIVORS AND
FURTHER CONSEQUENCES
An SAH is a major life experience that leads to additional
morbidity in up to 25% of surviving patients. Many pa-
tients do not return to work, retire early, and are unable to
function at the same intellectual level as before the rup-
ture.64-67 Numerous clinical factors may influence outcome
after SAH, including the presenting clinical condition of
the patient, age older than 65 years, presence of posterior
distribution aneurysms, rupture, intracerebral extension,
and development of cerebral vasospasm or cerebral in-
farctions. Preexisting medical conditions and aneurysm
size do not appear to affect outcome.65 Recovery in young
patients may be protracted and better than expected.68
The most important clinical factor in predicting poor
patient outcome after SAH is the presenting level of con-
sciousness (World Federation of Neurosurgical Societies
grade IV or V). The natural history of such patients is
dismal with higher than 90% mortality. Population-based
studies that eliminate the selection bias of referral centers
have estimated that approximately 30% of patients have
poor outcome after SAH.
Despite numerous clinical factors associated with poor
outcome after SAH, individual prediction of outcome may

Mayo Clin Proc. • April 2005;80(4):550-559 • www.mayoclinicproceedings.com 557

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SUBARACHNOID HEMORRHAGE
be imprecise. Traditionally, patients with poor-grade (IV
and V) SAH have been treated conservatively with sup-
portive care and, if needed, placement of external ventricu-
lar drains. Patients who improve clinically are selected for
subsequent repair of the ruptured aneurysm. This treatment
strategy has improved patient outcome but nevertheless
results in approximately 50% mortality. Only about 20% to
30% of patients treated conservatively have favorable out-
comes.69 Outcome in patients with poor-grade SAH has been
consistent throughout several decades, which has led to an
attitude of therapeutic nihilism for such patients. Neverthe-
less, with aggressive treatment, a subset of patients with
poor-grade SAH can survive with favorable outcome in up to
50% (grade IV) and 20% (grade V) of cases.38,66,69
The experience of an aneurysmal SAH often prompts
other family members to seek advice on screening for
aneurysm. If screened on a large scale, aneurysms would be
found in approximately 7% of first-degree relatives (par-
ents, siblings, and children), with a higher chance of an
unruptured aneurysm in a sibling. Certain families have
more than 1 member with a documented aneurysm, and
there is some suggestion that aneurysms in such family
members have a higher risk of rupture than those found
incidentally and that rupture may occur at a younger age.70-73
Screening for aneurysm is a complicated and unresolved
issue. The rupture risk of incidentally detected aneurysm is
low (<0.5% annually), but the morbidity of surgical or
endovascular repair (5%) is potentially substantial. More-
over, noninvasive imaging tests are suboptimal for detect-
ing unruptured aneurysm.
Some family members may decide not to know whether
they have an unruptured aneurysm. One should understand
the anxiety of the patient screened for an aneurysm (be-
cause of 2 ruptured aneurysms in the family) who is found
to have a 3-mm aneurysm and then is told to leave it alone
and return for follow-up annually. (The anxiety may be even
greater when an inconsiderate physician has told the patient
that his or her head contains a “ticking time bomb.”) Some
experts argue against screening; we are also hesitant but are
more inclined in high-risk populations such as patients with
autosomal dominant polycystic kidney disease.74
Follow-up with magnetic resonance angiography is
warranted and growth of the aneurysm is more likely in
medium or large (>9 mm) aneurysms or when multiple
lobes are present.75
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