Diagnosis and Management of Subarachnoid Hemorrhage

Review Article
Diagnosis and
Management of
Subarachnoid
Hemorrhage
Address correspondence to
Dr Jose I. Suarez, Baylor
College of Medicine, One
Baylor Plaza, NB:302, Houston,
TX 77030, jisuarez@bcm.edu.
Relationship Disclosure:
Dr Suarez reports no disclosure.
Unlabeled Use of
Products/Investigational
Use Disclosure:
Dr Suarez reports no disclosure.
* 2015, American Academy
of Neurology.
Jose I. Suarez, MD, FNCS, FANA

ABSTRACT
Purpose of Review: The purpose of this article is to present the epidemiology, clinical
presentation, and management of patients with subarachnoid hemorrhage (SAH). SAH
is a neurologic emergency that carries high morbidity and mortality. Patients with SAH
are at risk for several significant neurologic complications, including hydrocephalus, cerebral edema, delayed cerebral ischemia, rebleeding, seizures, and neuroendocrine abnormalities that lead to impaired body regulation of sodium, water, and glucose.
Recent Findings: The incidence of SAH has remained stable, but mortality of hospitalized patients has significantly declined over the past 3 decades. Many common
therapies for SAH have created controversy, and various recent neuroprotective clinical
trials have produced negative results. However, the publication of two consensus guidelines by the American Heart Association/American Stroke Association and the Neurocritical
Care Society have provided a clarification for what should constitute best practice for
patients with SAH. The most important of those recommendations include the following: admission of patients to high-volume centers (defined as more than 35 patients
with SAH per year) under the management of a specialized and multidisciplinary team;
early identification and management of the bleeding source; evaluation and treatment
decision for unsecured aneurysms by a multidisciplinary team made up of cerebrovascular neurosurgeons, endovascular practitioners, and neurointensivists; management
of patients in the neurocritical care unit with oral nimodipine, blood pressure control,
euvolemia, and frequent monitoring for neurologic and systemic complications; and
delayed cerebral ischemia secondary to cerebral vasospasm should be treated with
induced hypertension and endovascular therapies once confirmed.
Summary: SAH is a devastating neurologic disease. Management of patients with SAH
should adhere to currently available treatment guidelines. Several aspects of SAH management remain controversial and need further studies to clarify their role in improving
patient outcome.
Continuum (Minneap Minn) 2015;21(5):12631287.
INTRODUCTION
Nontraumatic subarachnoid hemorrhage (SAH) represents about 3% of
all strokes in the United States.1 The
worldwide incidence of SAH ranges
from 2 to 16 per 100,000 people and
has not changed in the past 3 decades.2
Most epidemiologic studies have shown
Continuum (Minneap Minn) 2015;21(5):12631287
that women are more likely to have SAH

compared to men (1.24:1.0) and that
minority groups (particularly African
American and Hispanic populations)
are more frequently affected compared
to white Americans.1,2 The incidence
of SAH increases with age, with a typical mean age of onset of 50 years or
www.ContinuumJournal.com
Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.
1263
Subarachnoid Hemorrhage
KEY POINTS
h Subarachnoid hemorrhage
is more frequent in
women than men and
more frequent in
minority populations
compared to
white Americans.
h Case-fatality rates of
hospitalized patients
with subarachnoid
hemorrhage have
decreased with the
advent of neurocritical care,
endovascular therapy,
and more refined
microsurgical techniques.
h The most important

points in the management
of patients with
subarachnoid hemorrhage
are prompt evaluation
and diagnosis, immediate
transfer to appropriate
centers, expeditious
diagnosis and treatment of
the bleeding source, and
overall good neurocritical
care adhering to available
treatment guidelines.
1264
older.2 In about 80% of SAH cases, a

ruptured cerebral aneurysm is found.
However, neuroimaging techniques
may show no source of bleeding in 15%
of SAH cases or show other abnormalities (eg, arteriovenous malformation,
vasculitis) in the remaining 5% of cases.
SAH causes significant morbidity and
mortality. Mortality rates vary widely
among studies, ranging from 8% to 67%
(median of 30% in the United States),
with the caveat that most of these studies
did not account fully for prehospital
deaths, which have been estimated to
be between 10% and 15%.3 However,
there has been a significant decrease in
case-fatality rates of SAH across the
globe,3 which has been attributed to improved survival of hospitalized patients
and is most likely owing to changes in
management of patients with SAH, including neurocritical care, endovascular
therapy, and more refined microsurgical
techniques. Nevertheless, it is important
to emphasize that despite the decrease
in case-fatality rates, about half of survivors experience significant chronic reductions in health-related quality of life.4,5
For example, a large proportion of survivors do not return to their previous level
of employment, social independence and
interactions, or personal or family relationships even 5 years after the event.
This reduction in health-related quality of life may be due to a combination
of factors, including impaired physical
functioning, cognitive deficits (particularly executive function and memory),
mood and emotional symptoms (eg, anxiety, depression, and posttraumatic
stress disorder), and personality changes.
Several risk factors for SAH have been
identified (Table 1-1).2,6Y10 Whether
any of these factors plays a predominant
role in an individual patient remains unclear. Genetic and environmental factors also can increase the risk of SAH,
and some of these factors can interact.
For instance, the size at which cerebral
aneurysms rupture may be smaller for

those patients with concomitant hypertension and cigarette smoking than for
those with either factor alone.
SAH remains one of the top neurologic
emergencies, and neurologists must familiarize themselves with this devastating
disease. This review discusses the main
features of diagnosis and management of
SAH. The main areas of emphasis when
caring for patients with SAH should include the following: prompt evaluation
and diagnosis,11 immediate transfer to
appropriate centers,2,12 expeditious diagnosis and treatment of the bleeding
source,13,14 and overall good neurocritical care adhering to available treatment guidelines.2,12
CLINICAL PRESENTATION
SAH typically presents with sudden and
severe headache (usually described as
the worst headache ever) accompanied by nausea, vomiting, photophobia,
neck pain, and loss of consciousness
(Case 1-1A).15 Physical examination
should include determination of level
of consciousness, funduscopic evaluation, determination of meningeal signs,
and presence of focal neurologic deficits (Table 1-2). The latter are present
in about 10% of patients with SAH and
are associated with worse prognosis when
due to the presence of thick subarachnoid clot or parenchymal hemorrhage.
Transient elevation in the intracranial pressure (ICP) causes nausea, vomiting, and
syncope. However, more sustained and
severe increases in ICP can lead to coma
and brain death. Terson syndrome (vitreous hemorrhage associated with SAH)
can present in up to 40% of patients
with SAH.16,17 The sudden spike in ICP
is thought to lead to preretinal hemorrhages, which are associated with more
severe SAH and increased mortality.
Some patients with SAH can have a
more atypical presentation.11,15 Occasionally, patients may present with seizures,
October 2015
TABLE 1-1 Risk Factors for Subarachnoid Hemorrhage

b Nonmodifiable Risk Factors
Age
Female sex
Prior history of aneurysmal subarachnoid hemorrhage
Family history of subarachnoid hemorrhage
History of aneurysm in first-degree relatives (especially in two or more relatives)
b Modifiable Risk Factors
Hypertension
Cigarette smoking
Heavy alcohol use
Sympathomimetic drug use (eg, cocaine)
b Other
Certain genetic disorders (eg, autosomal dominant polycystic kidney disease,
type IV Ehlers-Danlos syndrome)
Anterior circulation aneurysms are more likely to rupture in patients who are
younger than 55 years of age
Posterior circulation aneurysms are more likely to rupture in men
Significant financial or legal problems within the past 30 days
Cerebral aneurysms of more than 7 mm in diameter
Case 1-1A
A 45-year-old right-handed woman presented to a primary stroke center with sudden onset of severe
headache accompanied by nausea, vomiting, and syncope, which developed 1 hour prior to
presentation while she was moving furniture at her house. She had a past history of heavy smoking
and cocaine use. Upon arrival to the emergency department, her blood pressure was 180/100 mm Hg,
heart rate was 105 beats per minute, arterial oxygen saturation (SaO2) was 97% on room air, and
her temperature was 36.5-C (97.7-F). Her examination revealed a Glasgow Coma Scale score of 15,
normal cranial nerves, and no motor or sensory deficits. Her World Federation of Neurological Surgeons
Scale (WFNSS) score was 1 and her modified Fisher Scale score was 3. She reported neck pain
throughout the interview. She was treated with 4 mg of IV morphine sulfate and 10 mg of IV labetalol
without much response. She was then started on a nicardipine drip to maintain a systolic blood pressure
less than 160 mm Hg. A noncontrast head CT showed a subarachnoid hemorrhage (SAH) with
predominance in the anterior interhemispheric fissure (Figure 1-1A). The patient was immediately
transferred by helicopter to a comprehensive stroke center for further care. Digital subtraction
angiography (DSA) revealed an irregular, multilobed, and wide-neck anterior communicating artery
aneurysm (Figure 1-1B and 1-1C). After discussion among the neuroradiologist, the cerebrovascular
neurosurgeon, and neurointensivists, the patient underwent surgical clipping of the unsecured aneurysm.
Following surgery, the patient was transferred to the neurocritical care unit, where she received oral
nimodipine, pain control, IV levetiracetam (seizure prophylaxis for 3 days), and fluids to maintain euvolemia.
Nicardipine was discontinued, and she maintained her systolic blood pressure between 140 and 160 mm Hg
spontaneously. Her neurologic examination remained unchanged and she was mobilized out of bed.
Continued on page 1266

1265
Continued from page 1265
Initial imaging studies of the patient in Case 1-1. A, Nonenhanced head CT

shows diffuse subarachnoid hemorrhage with predominance in anterior interhemispheric
fissure without cerebral edema or significant hydrocephalus. B, A two-dimensional
digital subtraction angiogram shows an anterior communicating artery aneurysm on a lateral
view (arrow). C, A three-dimensional rotational digital subtraction angiogram reveals that the
anterior communicating artery aneurysm is irregular and trilobed and has a wide neck (arrow).
FIGURE 1-1
Comment. This case delineates the initial management of a patient with SAH. The key issues to
consider include early identification, transfer to a high-volume center, admission to a specialized
neurocritical care unit, identification and treatment of the bleeding source, and multidisciplinary
discussion to undertake best treatment for an unsecured aneurysm. In addition, this patient
underwent blood pressure control prior to aneurysm treatment to prevent rebleeding, and received
oral nimodipine, which has been shown to improve long-term outcomes in patients with SAH.
1266
October 2015
TABLE 1-2 Focal Physical Findings in Patients With Subarachnoid Hemorrhage

Findings
Likely Cause
Third nerve palsy
Usually posterior communicating aneurysm; also posterior cerebral

artery and superior cerebellar artery aneurysms
Sixth nerve palsy
Elevated intracranial pressure (false localizing sign)
Combination of hemiparesis and

aphasia or visuospatial neglect
Middle cerebral artery aneurysm, thick subarachnoid clots, or

parenchymal hematomas
Bilateral leg weakness and abulia
Anterior communicating artery aneurysm
Ophthalmoplegia
Internal carotid artery aneurysm impinging upon the cavernous sinus
Unilateral visual loss or bitemporal

hemianopia
Internal carotid artery aneurysm compressing optic nerve or optic chiasm
Impaired level of consciousness and

impaired upward gaze
Pressure on the dorsal midbrain due to hydrocephalus
Brainstem signs
Brainstem compression by basilar artery aneurysm
Neck stiffness
Meningeal irritation by the presence of subarachnoid blood
Retinal and subhyaloid hemorrhages
Sudden increase of intracranial pressure
Preretinal hemorrhages (Terson syndrome)
Vitreous hemorrhage due to severe elevations of intracranial pressure
acute encephalopathy, and concomitant

subdural hematoma and head trauma,
making the underlying diagnosis of SAH
more elusive. A minority of patients may
have a warning sentinel headache days
to weeks before an aneurysmal SAH,
which is thought to represent a small aneurysmal leak.18,19 Regrettably, this piece
of information is only obtained retrospectively as most of the time the headache is transient and head CT scanning
is unrevealing in about 50% of cases.
DIAGNOSIS
Head CT Scan
The most appropriate initial diagnostic test for patients suspected of having
SAH is a noncontrast head CT scan
(Figure 1-2) (Case 1-1A).15 The sensitivity of a CT scan has been reported
to be 98% to 100% for the detection
of subarachnoid blood within 12 hours
of symptom onset when compared to
lumbar puncture. However, the sensitivity of a CT scan decreases to 93% at
24 hours and 50% at 7 days.20,21 The

characteristic appearance of extravasated
blood in the basal subarachnoid cisterns
is hyperdense (Figure 1-1A). Other locations include the sylvian fissures; interhemispheric fissure; interpeduncular
fossa; and suprasellar, ambient, and
quadrigeminal cisterns. CT also can detect
intracerebral hemorrhage, intraventricular hemorrhage, and hydrocephalus.
Although MRI may be as sensitive as CT
scan in the first 2 days of SAH presentation, it is rarely performed in this scenario because of logistical issues.22,23 MRI
with hemosiderin-sensitive sequences
(gradient echo and susceptibility-weighted
imaging) or with fluid-attenuated inversion recovery (FLAIR) sequences is more
sensitive than CT scan when performed
several days after the onset of SAH.
KEY POINTS
h In some instances,
diagnosis of
can be elusive owing to
atypical findings on
presentation such as
seizures at onset, acute
encephalopathy, and
concomitant subdural
hematoma and
head trauma.
h The sensitivity of CT for

detection of subarachnoid
blood may be 98% to
100% when obtained
within 12 hours of onset
of symptoms, compared
to lumbar puncture.
Lumbar Puncture
A lumbar puncture is recommended in
any patient with suspected SAH and negative or equivocal results on head CT
1267
FIGURE 1-2
Diagnostic algorithm for subarachnoid hemorrhage.

CT = computed tomography.
15
Reprinted with permission from Suarez JI, et al, N Eng J Med.

NEJMra052732.
KEY POINT
h The diagnosis of
is supported by the finding
of xanthochromia in CSF.
1268
B 2006 Massachusetts Medical Society. www.nejm.org/doi/full/10.1056/
scan (Figure 1-2). CSF should be collected four consecutive tubes, and red
blood cell count should be determined
in tubes one and four.11,15 The diagnosis of SAH is supported by the following:
elevated opening pressure, elevated red
blood cell count that does not significantly decrease from tube one to tube
four, and especially xanthochromia. The
latter, which indicates red blood cell
breakdown, can be determined by visual
inspection or by spectrophotometry.
Xanthochromia takes about 12 hours to
develop after SAH, and spectropho-
tometry seems to be more sensitive

than visual inspection. However, most
hospitals in the United States use visual
inspection, and no well-conducted clinical studies exist that allow clinicians to
know with certainty what the falsenegative rate for xanthochromia is at various time intervals from SAH onset.24
Identification of Bleeding Source
All patients with a diagnostic CT scan or
with either equivocal or diagnostic lumbar
puncture must undergo further imaging
with CT angiography (CTA) or cerebral
October 2015
digital subtraction angiography (DSA)

(Figure 1-1).11,15 The latter has traditionally been considered the gold standard to elucidate the source of bleeding
in SAH (particularly aneurysmal), but
CTA has become widely available and
is being commonly performed as firstline vascular imaging or even in lieu of
DSA in some centers. CTA has a sensitivity and specificity ranging from 90%
to 97% and 93% to 100%, respectively,
depending on technique (16-detector
rows versus 64-detector rows, slice thickness, and data processing algorithms)
and the readers experience.25,26 CTA
may not be reliable for the detection of
smaller (ie, less than 4 mm) or distal aneurysms. The decision to perform CTA
or DSA will vary depending on resource
availability and institutional practices.
However, loss of consciousness at the
onset of SAH may be a strong predictor
for the detection of ruptured cerebral
aneurysm on subsequent DSA.27 Thus,
in those patients with a negative CTA,
this presentation should still prompt a
DSA. In the authors institution, a combination of two-dimensional and threedimensional DSA are performed as the
standard diagnostic testing for aneurysm
detection in all SAH cases. Patients with
a negative DSA should have a repeat
study 7 to 14 days after initial presentation, and if negative, MRI should be performed to uncover a possible vascular
malformation of the brain, brainstem,
or spinal cord.15,23
Misdiagnosis
Misdiagnosis of SAH is still common
because the classic findings may occur
inconsistently or patients may present
with atypical findings. Misdiagnosis is
associated with significantly increased
mortality and disability (up to fourfold)
in those patients presenting without
neurologic deficits at their initial hospital
visit. Fortunately, the frequency of SAH
misdiagnosis has decreased from more
than 60% in the early 1980s to less than
15% more recently.28,29 Nevertheless, it

is important to emphasize that practitioners should have a high level of suspicion for any patient presenting with
new-onset headache and understand
the possible pitfalls in the diagnosis of
SAH (Table 1-3). A recent study reported
100% sensitivity to detect SAH in patients older than 40 years of age using
clinical decision-making rules that include any of the following factors: neck
pain or stiffness, witnessed loss of consciousness, and symptom onset during
exertion plus thunderclap headache
and pain on neck flexion.30
Perimesencephalic Subarachnoid
Hemorrhage
As previously mentioned, in about 15%
of patients with SAH, imaging studies
fail to demonstrate the source of bleeding. Approximately 38% of these patients
have nonaneurysmal perimesencephalic
SAH.31 Most patients with nonaneurysmal perimesencephalic SAH (about 54%)
are male and have a low risk of complications and better outcomes than patients with aneurysmal SAH. A correct
diagnosis is important because of the
catastrophic consequences of missing
a ruptured cerebral aneurysm. Nonaneurysmal perimesencephalic SAH is
confirmed in the presence of a negative CTA or DSA in patients with the
following head CT scan pattern32: center of hemorrhage located immediately
anterior to the midbrain, with or without
extension of blood to the anterior part
of the ambient cistern or to the basal
part of the sylvian fissures; no complete
filling of the anterior interhemispheric
fissure and no extension to the lateral
sylvian fissures, except for minute
amounts of blood; and absence of frank
intraventricular blood (Figure 1-3).
KEY POINTS
h All patients with a

diagnostic CT scan or
with either equivocal or
diagnostic lumbar
puncture must undergo
further imaging with CT
angiography or digital
subtraction angiography.
h Any of the following

clinical factors should
prompt a workup for
in patients older than 40:
neck pain or stiffness,
witnessed loss of
consciousness, and
symptom onset during
exertion plus thunderclap
headache and pain on
neck flexion.
INITIAL EVALUATION
Initial evaluation and management
of patients with SAH should focus on
1269
a
TABLE 1-3 Reasons for Misdiagnosis of Subarachnoid Hemorrhage
b Failure to Recognize Spectrum of Presentation of Subarachnoid Hemorrhage

Not obtaining complete history from patients with unusual (for the patient) headaches
(Was the onset abrupt? Is the quality different and severity greater than prior headaches?)
Failure to appreciate that the headache can improve spontaneously or with non-narcotic analgesics
Focusing on the secondary head injury resulting from syncope and fall or motor vehicle collision
Focusing on ECG findings
Focusing on elevated blood pressure
Overreliance on the classic presentation
Assuming symptoms may be related to other disorders (eg, viral syndrome, viral meningitis, migraine,
tension-type headache, sinus-related headache, psychiatric disorder)
b Failure to Understand the Limitations of Head CT Scanning
Sensitivity decreases with increasing time from onset of headache
False-negative results with small-volume bleeds
Lack of experience of physician reader
Motion artifacts or lack of thin cuts of posterior fossa
False-negative results due to hematocrit of less than 30%
b Failure to Perform Lumbar Puncture or Interpret the CSF Findings Correctly
Failure to perform lumbar puncture in patients with negative or inconclusive CT scans
Failure to distinguish a traumatic tap from true subarachnoid hemorrhage
Failure to recognize that xanthochromia may be absent very early (less than 12 hours) and very late
(more than 2 weeks)
CSF = cerebrospinal fluid; CT = computed tomography; ECG = electrocardiogram.
a
Data from Edlow JA, et al, J Emerg Med.11 www.jem-journal.com/article/S0736-4679(07)00729-9/abstract.
KEY POINT
h Mean arterial blood

pressure should be
maintained at less than
110 mm Hg or systolic
blood pressure at less
than 160 mm Hg until
the ruptured aneurysm
is secured, while
avoiding hypotension.
1270
stabilization of airway, breathing, and

circulation.2,12,15,22,23 Once patients
are deemed stable, a head CT scan must
be performed. Patients who are unable to
protect their airway should be intubated
immediately. The most common indications for endotracheal intubation include
coma, hydrocephalus, seizure, and need
for sedation for significant agitation. In
addition, extreme blood pressure values
should be avoided. Hypertension control
is predicated on the premise that it may
precipitate rebleeding.33 No data from
randomized controlled clinical trials exist,
but usual practice and current recommendations are to maintain a mean arterial
blood pressure of less than 110 mm Hg
or a systolic blood pressure of less than

160 mm Hg until the ruptured aneurysm is secured, while using premorbid
baseline blood pressures to refine targets and avoid hypotension. Commonly,
pain control may be sufficient to achieve
blood pressure control; otherwise, administration of IV labetalol (5 mg to 20 mg),
hydralazine (5 mg to 20 mg), or continuous infusion of nicardipine (5 mg/h to
15 mg/h) is preferred. Pain control is
best achieved with the administration
of short-acting opiates (Case 1-1A).
Disease Severity Scoring
The severity of neurologic impairment and the amount of subarachnoid
October 2015
Noncontrast head CT scan of a patient with nonaneurysmal perimesencephalic subarachnoid hemorrhage.

The center of the hemorrhage is located immediately anterior to the midbrain (A and C, arrows) and extends
to the anterior part of the ambient cistern (B, arrow).
FIGURE 1-3
bleeding on admission are the strongest

predictors of neurologic complications
and outcome.15,23 Therefore, it is
essential that patients with SAH be
scored promptly after arrival and stabilization. There are several scoring
systems available. However, the World
Federation of Neurological Surgeons
Scale (WFNSS) and the modified Fisher
Scale are the most reliable and simple
to perform (Table 1-415,34,35).23 Higher

WFNSS and modified Fisher Scale
scores are associated with worse clinical outcome and a higher proportion
of neurologic complications.
KEY POINT
h The severity of neurologic
Admission to High-Volume
Centers
The next immediate steps are to transfer
the patient to a high-volume center (if not
impairment and the

amount of subarachnoid
bleeding on admission are
the strongest predictors
of neurologic complications
and outcome.
a
TABLE 1-4 Clinical and Radiologic Grading Scales for Subarachnoid Hemorrhage
World Federation of Neurological

Surgeons Scale34
Modified Fisher Scale35
Grade
Glasgow
Coma Scale
Neurologic
Examination
Grade
Subarachnoid
Hemorrhage
Intraventricular
Hemorrhage
15
No motor deficit
Absent
Absent
13Y14
No motor deficit
Minimal
Absent in both lateral ventricles
13Y14
Motor deficit
Minimal
Present in both lateral ventricles
7Y12
With or without
motor deficit
Thickb
Absent in both lateral ventricles
3Y6
With or without
motor deficit
Thickb
Present in both lateral ventricles
a
b
Modified with permission from Suarez JI, et al, N Engl J Med.15 B 2006 Massachusetts Medical Society. www.nejm.org/doi/full/10.1056/NEJMra052732.
Thick is defined as a hemorrhage filling one or more cisterns or fissures out of a total of 10: interhemispheric fissure, the quadrigeminal
cistern, both suprasellar cisterns, both ambient cisterns, both basal sylvian fissures, and both lateral sylvian fissures.
1271
already in one), admit the patient to a

dedicated neurocritical care unit, and have
the patient undergo a multidisciplinary
evaluation for the management of an unsecured cerebral aneurysm (Table 1-5).2,12
It has been shown that admission of patients with SAH to low-volume centers
is associated with higher 30-day mortality compared to admission to highvolume centers. In addition, admission
TABLE 1-5 Summary of Key Recommendations for the Management of Patients With
Treatment
Decision
American Heart Association/American

Stroke Association2,a
Hospital/system
characteristics
Low-volume hospitals (eg, less than

10 subarachnoid hemorrhage [SAH] cases
per year) should consider early transfer of
patients with SAH to high-volume centers
(eg, more than 35 SAH cases per year) with
experienced cerebrovascular surgeons,
endovascular specialists, and
multidisciplinary neurointensive care
services (Class I, Level B).
After discharge, it is reasonable to refer
patients with SAH for a comprehensive
evaluation, including cognitive, behavioral,
and psychosocial assessments
(Class IIa, Level B).
Aneurysm treatment
Surgical clipping or endovascular coiling of

the ruptured aneurysm should be
performed as early as feasible in the
majority of patients to reduce the rate of
rebleeding after SAH (Class I, Level B).
For patients with ruptured aneurysms
judged to be technically amenable to either
endovascular coiling and neurosurgical
clipping, endovascular coiling should be
considered (Class I, Level B).
Complete obliteration of the aneurysm is
recommended whenever possible
(Class I, Level B).
Stenting of a ruptured aneurysm is associated
with increased morbidity and mortality
(Class III, Level C).
For patients with an unavoidable delay in
obliteration of aneurysm, a significant risk
of rebleeding, and no compelling medical
contraindications, short-term (less than
72 hours) therapy with tranexamic acid or
aminocaproic acid is reasonable to reduce
the risk of early aneurysm rebleeding
Neurocritical Care Society12,b

Patients with SAH should be treated at
high-volume centers (moderate quality
of evidence, strong recommendation).
High-volume centers should have
appropriate specialty neurointensive
care units, neurointensivists, vascular
neurosurgeons, and interventional
neuroradiologists to provide the
essential elements of care
(moderate quality of evidence,
strong recommendation).
Early aneurysm repair should be

undertaken, when possible and reasonable
to prevent rebleeding (high quality of
evidence, strong recommendation).
An early, short course of antifibrinolytic
therapy prior to early aneurysm repair
(begun at diagnosis and continued up to
the point at which the aneurysm is secured
or at 72 hours post ictus, whichever is
shorter) should be considered (low quality
of evidence, weak recommendation).
Delayed (more than 48 hours after the
ictus) or prolonged (more than 3 days)
antifibrinolytic therapy exposes patients
to side effects of therapy when the risk
of rebleeding is sharply reduced and
should be avoided (high quality of
1272
October 2015
Subarachnoid Hemorrhage Continued from page 1272
Treatment
Decision

Blood pressure control
Between the time of SAH symptom onset

and aneurysm obliteration, blood pressure
should be controlled with a titratable
agent to balance the risk of stroke,
hypertension-related rebleeding, and
maintenance of cerebral perfusion
pressure (Class I, Level B).
The magnitude of blood pressure control
to reduce the risk of rebleeding has not
been established, but a decrease in systolic
blood pressure to less than 160 mm Hg
is reasonable (Class IIa, Level C).

Treat extreme hypertension in patients
with an unsecured, recently ruptured
aneurysm. Modest elevations in blood
pressure (mean blood pressure of less than
110 mm Hg) do not require therapy.
Premorbid baseline blood pressures should
be used to refine targets and hypotension
should be avoided (low quality of evidence,
Intravascular
volume status
Maintenance of euvolemia and normal

circulating blood volume is recommended
to prevent delayed cerebral ischemia
(Class I, Level B).
Intravascular volume management should

target euvolemia and avoid prophylactic
hypervolemic therapy. In contrast, there is
evidence for harm from aggressive
administration of fluid aimed at achieving
hypervolemia (moderate quality
Cardiopulmonary
complications
No recommendations given.
Baseline cardiac assessment with serial

enzymes, ECG, and echocardiography is
recommended, especially in patients
with evidence of myocardial dysfunction
(low quality of evidence, strong
recommendation).
Monitoring of cardiac output may be useful
in patients with evidence of hemodynamic
instability or myocardial dysfunction
(low quality of evidence, strong
recommendation).
Seizures
The use of prophylactic anticonvulsants

may be considered in the immediate
posthemorrhagic period (Class IIb, Level B).
The routine long-term use of anticonvulsants
is not recommended (Class III, Level B).
Routine use of anticonvulsant prophylaxis

with phenytoin is not recommended
after SAH (low quality of evidence,
If anticonvulsant prophylaxis is used, a short
course (3Y7 days) is recommended (low
quality of evidence, weak recommendation).
Continuous EEG monitoring should be
considered in patients with poor-grade
SAH who fail to improve or who have
neurologic deterioration of undetermined
etiology (low quality of evidence,
1273
Treatment
Decision

Fever treatment
Aggressive control of fever to a target of

normothermia by use of standard or
advanced temperature-modulating systems
is reasonable in the acute phase of SAH
During the period of risk for delayed cerebral

ischemia, control of fever is desirable;
intensity should reflect the individual
patients relative risk of ischemia (low
quality of evidence, strong recommendation).
Surface cooling or intravascular devices
are more effective and should be employed
when antipyretics fail in cases where fever
control is highly desirable (high quality of
Glucose control
Deep venous
thrombosis
prophylaxis
Delayed cerebral
ischemia
Careful glucose management with strict

avoidance of hypoglycemia may be
considered as part of the general critical
care management of patients with SAH
(Class IIb, Level B).
Hypoglycemia (serum glucose of less than

80 mg/dL) should be avoided (high quality
Heparin-induced thrombocytopenia and

deep venous thrombosis are relatively
frequent complications after SAH. Early
identification and targeted treatment are
recommended, but further research is needed
to identify the ideal screening paradigms
(Class I, Level B).
Measures to prevent deep venous

thrombosis should be employed in all
patients with SAH (high quality of evidence,
Oral nimodipine should be administered to

all patients with SAH (Class I, Level A).
Oral nimodipine (60 mg every 4 hours)

should be administered after SAH for
a period of 21 days (high quality of
Maintenance of euvolemia and normal

circulating blood volume is recommended
to prevent delayed cerebral ischemia
(Class I, Level B).
Prophylactic hypervolemia or balloon
angioplasty before the development of
angiographic spasm is not recommended
(Class III, Level B).
Transcranial Doppler is reasonable to
monitor for the development of arterial
vasospasm (Class IIa, Level B).
Perfusion imaging with CT or MRI can be
useful to identify regions of potential
brain ischemia (Class IIa, Level B).
Serum glucose should be maintained

below 200 mg/dL (moderate quality of
The use of unfractionated heparin for

prophylaxis could be started 24 hours
after undergoing aneurysm obliteration
The goal should be maintaining

euvolemia, rather than attempting
hypervolemia (moderate quality
Transcranial Doppler may be used for
monitoring and detection of large artery
vasospasm with variable sensitivity
Digital subtraction angiography is the
gold standard for detection of large
artery vasospasm (high quality of evidence,
1274
October 2015
Treatment
Decision

Induction of hypertension is recommended

for patients with delayed cerebral ischemia
unless blood pressure is elevated at
baseline or cardiac status precludes it
(Class I, Level B).
Patients clinically suspected of delayed

cerebral ischemia should undergo a
trial of induced hypertension
Cerebral angioplasty and/or selective

intra-arterial vasodilator therapy is
reasonable in patients with symptomatic
vasospasm, particularly those who are
not responding to hypertensive therapy
Endovascular treatment using

intra-arterial vasodilators and/or
angioplasty may be considered for
vasospasm-related delayed cerebral
ischemia (moderate quality of evidence,
Anemia and
transfusion
The use of packed red blood cell

transfusion to treat anemia might be
reasonable in patients with SAH who
are at risk of cerebral ischemia. The
optimal hemoglobin goal is still to be
determined (Class IIb, Level B).
Patients should receive packed red blood

cell transfusions to maintain hemoglobin
concentration above 8Y10 g/dL (moderate
quality of evidence, strong
recommendation).
Hyponatremia
The use of fludrocortisone acetate and

hypertonic saline solution is reasonable
for preventing and correcting
hyponatremia (Class IIa, Level B).
Fluid restriction should not be used to

treat hyponatremia (weak quality of
Early treatment with hydrocortisone
or fludrocortisone may be used to
limit natriuresis and hyponatremia
weak recommendation).
Mild hypertonic saline solutions can be used
to correct hyponatremia (very low quality
CT = computed tomography; ECG = electrocardiogram; EEG = electroencephalogram; MRI = magnetic resonance imaging.
a
American Heart Association/American Stroke Association recommendations follow the American Heart Association Stroke
Councils methods of classifying the level of certainty of the treatment effect and the class of evidence.
b
For the Neurocritical Care Societys guidelines, the quality of the data was assessed and recommendations developed using the
Grading of Recommendations, Assessment, Development, and Evaluation (GRADE) system.
to dedicated neurocritical care units staffed by dedicated neurointensivists is

associated with decreased in-hospital
mortality.36
Treatment of Unsecured
Aneurysms
Treatment of unsecured aneurysms has
evolved, and two accepted efficacious
management modalities currently exist:
surgical clipping and endovascular coilContinuum (Minneap Minn) 2015;21(5):12631287
ing. The choice of treatment depends

on several factors, including the patients age and aneurysm location,
morphology, and relationship to adjacent vessels. Because of the complexity of determining the most appropriate
treatment for individual patients, it
is recommended that a multidisciplinary team made up of cerebrovascular
neurosurgeons, endovascular practitioners, and neurointensivists confer
KEY POINT
h Admission of patients
with subarachnoid
hemorrhage to
low-volume centers is
associated with higher
30-day mortality
compared to admission
to high-volume centers.
1275
KEY POINTS
h Overall, when
considering treatment of
unruptured aneurysms,
endovascular coiling
should be preferred over
surgical clipping
whenever possible.
h Patients with
subarachnoid
hemorrhage are at risk
for several significant
neurologic complications,
including hydrocephalus,
cerebral edema,
delayed cerebral ischemia,
rebleeding, seizures,
and neuroendocrine
abnormalities.
h The best measure to

reduce the risk of
rebleeding is the
early treatment of
unsecured aneurysms.
to reach a consensus.2,12,15,22,23,29 The

International Subarachnoid Aneurysm
Trial (ISAT) was a prospective randomized controlled clinical trial that evaluated patients with unsecured aneurysms
who were considered suitable for either
endovascular coiling or surgical clipping.13,14 Patients assigned to the endovascular coiling group had a significantly
higher favorable outcome (defined as
survival free of disability at 1 year)
and lower risk of epilepsy compared
to those assigned to the surgical clipping group. However, the risk of
rebleeding and partial occlusion of
aneurysms was lower with surgical
clipping. Overall, endovascular coiling should be preferred over surgical
clipping whenever possible; however,
many aneurysms are not equally suitable for either surgical clipping or endovascular coiling (Table 1-6) (Case 1-1A).
Regardless of the treatment modality
chosen, unsecured aneurysms must be
treated as soon as possible to prevent
rebleeding (Table 1-5). In the authors
institution, the median time for aneurysm treatment is 7 hours from initial
hospital arrival.
INTENSIVE CARE UNIT
MANAGEMENT
SAH is often accompanied by more severe initial systemic and intracranial responses than other cerebral insults.37Y40
More than 75% of patients with SAH
experience systemic inflammatory response syndrome (SIRS), which is likely
related to elevated levels of inflammatory
cytokines. SIRS has been associated with
permanent neurocognitive dysfunction.
In addition, patients with SAH are at risk
for several significant neurologic complications, including hydrocephalus, cerebral edema, delayed cerebral ischemia,
rebleeding, seizures, and neuroendocrine abnormalities that lead to impaired
body regulation of sodium, water, and
1276
glucose. Furthermore, SAH unleashes

hypothalamic-mediated changes, including increased sympathetic and parasympathetic drive, that result in cardiac and
pulmonary complications. For example,
increased circulating catecholamines are
thought to be the cause for several cardiac
manifestations, including ECG changes,
arrhythmias, impaired cardiac contractility (eg, Takotsubo cardiomyopathy),
troponinemia, and myocardial necrosis.
Pulmonary complications, such as neurogenic pulmonary edema, most likely
have a similar underlying pathophysiologic mechanism. It is important to
recognize and treat all these systemic
complications as they are associated
with increased risk for delayed cerebral
ischemia and poor neurologic outcome
after SAH.
Neurologic Complications
Rebleeding. Rebleeding is a major disabling complication of SAH, which carries high mortality and morbidity. In
the first 24 hours, 4% to 15% of patients will rebleed, with the highest risk
occurring less than 6 hours from symptom onset.33 Rebleeding risk decreases
over the following 2 weeks. The main
risk factors associated with rebleeding
include high systolic blood pressure
(ie, greater than 160 mm Hg), poor neurologic grade, intracerebral or intraventricular hematomas, ruptured posterior
circulation aneurysms, and aneurysms
of greater than 10 mm in size.33
The best measure to reduce the risk
of rebleeding is the early treatment of
unsecured aneurysms (Table 1-5).2,12
However, in some instances there may
be a delay in surgical clipping or endovascular coiling of the aneurysm, and
short-term (ie, less than 72 hours) treatment with tranexamic acid or aminocaproic acid has been recommended if
no contraindications exist. The use of
these antifibrinolytic agents is based
October 2015
KEY POINT
h About 60% of patients
TABLE 1-6 Preferences for Treatment of Unsecured Aneurysms

Characteristics
Preferred Treatment
Modality
Advanced age
Endovascular coiling
Poor clinical grade
Multiple underlying systemic conditions
Aneurysms with wide neck-to-body ratio
Surgical clipping
Normal arterial branches arising from dome or body

of aneurysm
Surgical clipping
Middle cerebral artery aneurysm
Surgical clipping
Top-of-the-basilar aneurysm
Aneurysm associated with large parenchymal hematoma
Surgical clipping
High surgical risk
Patient preference
Clinical equipoise
a
with subarachnoid
hemorrhage who undergo
external ventricular drain
insertion will have
successful weaning and
the others may require
chronic ventriculoperitoneal
shunt insertion.
Unsecured aneurysm is considered equally suitable for either endovascular coiling or surgical clipping.
on the premise that early risk for rebleeding is a consequence of activated

fibrinolysis and reduced clot stability
during the first 6 hours. In addition,
blood pressure control is also very important to prevent rebleeding prior to
aneurysm obliteration, as previously
mentioned. Patients suspected of rebleeding should be evaluated promptly,
have a follow-up head CT scan and DSA
(if not already done), and immediately
undergo aneurysm obliteration. Endovascular treatment of ruptured cerebral aneurysms should include coiling
only. Stenting of cerebral aneurysms in
the setting of SAH should be avoided
as it is associated with higher bleeding
complications and poor outcome.2
Hydrocephalus. Acute symptomatic
hydrocephalus occurs in about 20% of
patients with SAH, usually within the
first few days after symptom onset.2,15,22
Patients manifest decreased levels of consciousness and other signs of increased
ICP, such as impaired upward gaze and
hypertension. An immediate follow-up
head CT scan is warranted in any patient

with suspected symptomatic hydrocephalus and must be followed by insertion
of an external ventricular drain (EVD).
Some centers perform lumbar drain insertion instead of EVD in patients with
SAH who have communicating hydrocephalus. Weaning the patient of an EVD
should begin shortly after aneurysm obliteration or within 48 hours of insertion
if the patient is neurologically stable. A
rapid weaning protocol is preferred.
About 60% of patients with SAH who
undergo EVD insertion will have successful weaning, and the others may
require chronic ventriculoperitoneal
shunt insertion (Case 1-1B).
Seizures. Delineating the true frequency of seizures in patients with SAH
has been difficult and controversial as
many patients (20% to 26%) present with
seizurelike episodes that are not easy to
characterize as many of them occur at
the time of symptom onset.2,12Y15 In
general, patients with middle cerebral
artery (MCA) aneurysms, concomitant
1277
KEY POINTS
h Anticonvulsant
administration
(particularly phenytoin)
has been associated
with worse
clinical outcome.
h Delayed cerebral ischemia

is defined as any
neurologic deterioration
(focal or global) presumed
secondary to cerebral
ischemia that persists for
more than 1 hour and
cannot be explained by
any other neurologic or
systemic condition.
intraparenchymal hematomas, and poor

clinical grade are at higher risk for seizures, whereas patients treated with
endovascular coiling have lower rates
of seizures. Long-term risk for epilepsy
is low.
The administration of prophylactic
anticonvulsants in patients with SAH was
common practice; however, anticonvulsant administration (particularly phenytoin) has been associated with worse
clinical outcome and a high frequency
of medication-related complications.2,12
Current recommendations are to avoid
phenytoin, and, if desirable, short-term
anticonvulsant administration for 3 to
7 days could be administered. In addition, concern exists that the frequency
of subclinical seizures may be high in
patients with poor-grade SAH, and continuous EEG has been recommended in
this setting.12
Delayed cerebral ischemia. Delayed

cerebral ischemia is one of the most
dreaded complications after SAH and is
the most important factor impacting functional outcome.39Y41 Delayed cerebral
ischemia occurs in about 30% of patients with SAH, usually between 4 and
14 days after the onset of symptoms.
Delayed cerebral ischemia is defined as
any neurologic deterioration (focal or
global) presumed secondary to cerebral
ischemia that persists for more than 1
hour and cannot be explained by any
other neurologic or systemic condition.
The latter implies an absence of significant hydrocephalus, sedation, hypoxemia, seizures, and electrolyte or renal or
hepatic impairment. Thus, delayed cerebral ischemia is a diagnosis of exclusion.
Several factors have been implicated in the pathogenesis of delayed
Case 1-1B
The patient discussed in Case 1-1A continued to evolve satisfactorily with normal mean cerebral blood
flow velocities by transcranial Doppler (TCD). On postbleed day 6, TCD revealed an increase in mean
cerebral blood flow velocity in the right middle cerebral artery (MCA) to 160 cm/s from 80 cm/s on
day 5. The next morning, the patient developed a sudden onset of left hemiparesis and confusion.
A head CT scan revealed no rebleeding, cerebral edema, or hydrocephalus. She was given an
IV bolus of 500 mL of 0.9% saline and was started on a norepinephrine drip with some improvement
of her left hemiparesis but without complete resolution. The patients electrolytes, blood urea nitrogen,
creatinine, and liver function tests were normal, and her white blood cell count was 14,000 cells/mm3.
A follow-up TCD after neurologic deterioration showed a further increase in mean cerebral blood flow
velocity of her right MCA to 220 cm/s and a Lindegaard ratio (MCA/extracranial internal carotid
artery mean blood flow velocities) of 6. Digital subtraction angiography (DSA) was performed 90 minutes
after symptom onset, showing severe vasospasm of her right MCA and anterior cerebral artery (ACA)
(Figure 1-4A). She underwent balloon angioplasty of the right MCA and subsequent intra-arterial
infusion of nicardipine in both the right MCA and ACA with radiologic and clinical improvement
(Figure 1-4B). The patients neurologic examination normalized, and her systolic blood pressure was
maintained at greater than 180 mm Hg for 3 more days. Her TCD showed improvement in mean
cerebral blood flow velocities to less than 100 cm/s by day 9, and the patient was slowly weaned off
norepinephrine by day 10. On day 11 she developed a decreased level of consciousness without focal
neurologic findings except for limited upward gaze. A follow-up head CT scan showed communicating
hydrocephalus, and an external ventricular drain (EVD) was inserted (Figure 1-4C). Several attempts at
weaning the patient off the EVD failed and, therefore, she underwent programmable ventriculoperitoneal
shunt placement (Figure 1-4D) on day 15, after which she was transferred to the regular floor. The
patient was discharged to home on day 17, after clearance by physical and occupational therapies, with
instructions to continue nimodipine for 4 more days and schedule follow-up in vascular neurology and
neurosurgery outpatient clinics.
1278
October 2015
Continued from page 1278
Subsequent imaging studies for the patient in Case 1-1. A, A two-dimensional

digital subtraction angiogram reveals severe vasospasm of the right middle
cerebral artery and anterior cerebral artery (arrows). B, A two-dimensional digital
subtraction angiogram after balloon angioplasty of the right middle cerebral artery and
intra-arterial infusion of nicardipine of the right middle cerebral artery and anterior cerebral
artery reveals improved vessel diameter of both arteries (arrows). C, Nonenhanced head CT scan
shows communicating hydrocephalus and placement of an external ventricular drain (arrow)
after patient developed decreased level of consciousness. D, Noncontrasted head CT scan shows
placement of a ventriculoperitoneal shunt.
FIGURE 1-4
Comment. This case exemplifies the clinical presentation and management of two of the most
common neurologic complications of SAH: delayed cerebral ischemia and hydrocephalus. This patient
was treated with recommended therapies, including maintenance of euvolemia, oral nimodipine,
and liberal blood pressure parameters. In addition, she was monitored in the neurocritical care unit
and had frequent TCDs. This patient had important risk factors for the development of delayed cerebral
ischemia secondary to vasospasm, including cigarette smoking, cocaine use, and a high burden of
subarachnoid blood. Her TCD recordings revealed an increase in mean cerebral blood flow velocities of
greater than 50 cm/s within 24 hours followed by focal neurologic signs. Once the diagnosis of cerebral
vasospasm was confirmed (after ruling out other neurologic and systemic disorders), she was treated
with induced hypertension and endovascular therapy with complete resolution of her symptoms.
As this case demonstrates, the management of delayed cerebral ischemia is carried out in a stepwise fashion,
and final confirmation and treatment of vasospasm must be done within 2 hours of symptom onset.
Furthermore, this case highlights that, frequently, more than one neurologic complication is present in the
same patient. Treatment of hydrocephalus entails the immediate insertion of an EVD.
1279
KEY POINTS
h Possible underlying
conditions implicated
in the pathogenesis
of delayed cerebral
ischemia include
cerebral vasospasm,
microcirculatory
constriction,
microthrombosis, cortical
spreading depression, and
delayed cellular apoptosis.
h Nimodipine should be
administered to all
patients with
subarachnoid
hemorrhage to decrease
the risk of delayed
cerebral ischemia
and poor
functional outcome.
h Euvolemia should be
maintained at all times,
while prophylactic
hypervolemia should
be avoided.
1280
cerebral ischemia, including cerebral vasospasm, microcirculatory constriction,

microthrombosis, cortical spreading
depression, and delayed cellular apoptosis.39 Most likely, the main driver of
all these processes is the release of oxyhemoglobin and erythrocyte contents
through hemolysis, which unleashes a
host of inflammatory and proapoptotic
factors. The risk for cerebral vasospasm
increases with the thickness, density,
location, and persistence of the subarachnoid blood. In addition, poor
clinical grade, loss of consciousness at
ictus, cigarette smoking, cocaine use,
SIRS, hyperglycemia, and hydrocephalus also increase the risk of delayed
cerebral ischemia and poor neurologic
outcome.39,40 However, predicting who
will develop delayed cerebral ischemia
has proven very difficult. The latter has
important implications for the reduction of level of monitoring in patients
with SAH who are at low risk for delayed
cerebral ischemia, thus avoiding potential adverse effects of aggressive management and potentially decreasing
resource utilization. The best predictors for patients requiring less frequent
monitoring include older age (more than
65 years), a WFNSS score of 1 to 3, and
a modified Fisher Scale score less than
3 (Table 1-5).39
Prophylaxis. The best studied of the
available interventions aimed at preventing delayed cerebral ischemia are calcium
channel blockers and intravascular volume status. The use of nimodipine to
decrease the risk of delayed cerebral
ischemia and poor functional outcome
is well supported and recommended
(Table 1-5).2,12,23,39 Nimodipine is administered by enteral route at 60 mg
every 4 hours for 21 days. Nimodipine
affords neuroprotection without decreasing the frequency of angiographic vasospasm. The most common adverse effects
of nimodipine include constipation and
hypotension. The latter could be problematic as it could lead to hypoperfusion

due to decreased cerebral perfusion pressure (CPP). Therefore, it is important that
systolic blood pressure not be compromised when administering nimodipine.
One solution employed by the author is
to half the nimodipine dose to 30 mg
every 2 hours while maintaining adequate intravascular volume.
Patients with SAH frequently experience decreased intravascular volume and
negative fluid balance, which have been
associated with higher incidence of cerebral infarction and poor neurologic outcome. These findings led to the institution
of prophylactic hypervolemic therapy.
However, this strategy has not been shown
to improve cerebral blood flow (CBF) or
decrease the frequency of cerebral vasospasm or delayed cerebral ischemia, and
it increases the frequency of cardiopulmonary complications. Therefore, prophylactic hypervolemia should not be
pursued. Current recommendations are
to maintain euvolemia at all times after
SAH.2,12 It is important to emphasize
that controversy still exists about the
methodology to follow to determine
euvolemia. Many neurointensivists use a
combination of methods, including strict
monitoring of fluid balance, central
venous pressure, echocardiogram, and
stroke volume variation, among others.
In practice, maintenance of euvolemia
can generally be ensured by replacing
urine output and even administering
fludrocortisone or hydrocortisone in patients with significant diuresis (Table 1-5).
Diagnosis and monitoring. Diagnosing delayed cerebral ischemia is not easy.
However, the combination of neurologic
examination and imaging studies can
enhance the chances of early detection
and management. Patients with SAH must
be in the neurocritical care unit where
they can be examined very frequently,
preferably at least every 2 hours. Delayed
cerebral ischemia must be suspected
October 2015
when patients with SAH develop focal

neurologic impairment or a decrease
of at least 2 points on the Glasgow Coma
Scale that lasts for more than 1 hour
and cannot be explained by any other
cause. In addition, all patients with SAH
should undergo head CT or MRI 24 to
48 hours after aneurysm occlusion.
Therefore, any new hypodensities on
CT imaging after this period not attributable to EVD insertion or intraparenchymal hematoma should be
regarded as cerebral infarctions from
delayed cerebral ischemia regardless of
clinical signs.41
The general consensus among practitioners indicates that patients with SAH
should undergo additional imaging and/or
physiologic monitoring routinely during
the risk period for delayed cerebral ischemia (Table 1-5).2,12 Such monitoring is
usually multimodal and includes ICP,
CPP, CBF, EEG, transcranial Doppler
(TCD), DSA, CTA, CT perfusion (CTP),
and brain tissue oxygenation. TCD has
been the longest and best studied of all
the monitoring modalities. TCD has
adequate sensitivity and specificity to
detect delayed cerebral ischemia secondary to cerebral vasospasm in large
arteries compared to DSA, but is limited
by the operators experience and the
patients cranial windows.42 TCD thresholds for vasospasm are the following:
mean cerebral blood flow velocities of
less than 120 cm/s for absence and more
than 200 cm/s or a Lindegaard ratio (MCA
mean cerebral blood flow velocity/extracranial internal carotid artery mean
cerebral blood flow velocity) of greater
than 6 for presence. In addition, mean
cerebral blood flow velocity increases by
more than 50 cm/s within 24 to 48 hours
also have been associated with delayed
cerebral ischemia.
DSA is the gold standard for detection
of large artery vasospasm.2,12 CTA has
become more widely available and may
replace DSA for screening of vasospasm
with a high degree of specificity. CTP

findings of an elevated mean transit time
(MTT) of greater than 6.4 seconds may
be additive to CTA in predicting delayed
cerebral ischemia and has been recommended as a threshold for decreased
cerebral perfusion. Qualitative visual interpretation of CTP can also be useful.
Brain tissue oxygenation and CBF monitoring can provide additional information
when used in the context of a multimodality approach, bearing in mind their
limitations, such as limited tissue sampling and location in relation to pathology.
Continuous EEG offers the advantage of
being able to monitor broad regions of
the brain to detect epileptiform discharges noninvasively. Continuous EEG
is particularly useful in patients with poorgrade SAH where neurologic examination is limited.
Some variability exists regarding the
timing and frequency of use of the various neuromonitoring techniques mentioned above. The authors institution
follows an algorithm for identifying and
treating subarachnoid hemorrhage similar to the one proposed by Macdonald
as shown in Figure 1-5.39 Patients with
SAH are stratified into low risk (ie, older
age, a WFNSS score of 1 to 2, and a modified Fisher Scale score of less than 3),
high risk (ie, a WFNSS score of 1 to 3
and a modified Fisher Scale score of 3),
and high risk with poor neurologic
status (ie, clouded examination due to
sedation, a WFNSS score of 3 to 5, and
a modified Fisher Scale score of 4). All
patients with aneurysmal SAH undergo
TCD (daily or every other day) and head
CT/CTA/CTP on admission and on days
3 to 5 and days 7 to 10 for screening of
decreased cerebral perfusion or vasospasm. DSA also can be performed in
lieu of CTA/CTP. High-risk patients
with poor neurologic status undergo
additional neuromonitoring, including EEG, brain tissue oxygenation, and
CBF determination.
KEY POINTS
h Delayed cerebral
ischemia must be
suspected when patients
with subarachnoid
hemorrhage develop
focal neurologic
impairment or a decrease
of at least 2 points on
the Glasgow Coma Scale
that lasts for more than
1 hour and cannot
be explained
by any other cause.
h Any new hypodensities

on CT imaging 24 to
48 hours after aneurysm
treatment should be
regarded as cerebral
infarctions from delayed
cerebral ischemia.
h Transcranial Doppler
thresholds for vasospasm
include mean cerebral
blood flow velocities of
less than 120 cm/s for
absence and more than
200 cm/s or a Lindegaard
ratio of greater than
6 for presence.
h Digital subtraction
angiography is the gold
standard for detection of
large artery vasospasm.
h CT perfusion findings of
elevated mean transit
time of greater than
6.4 seconds may be
additive to CT angiography
in predicting delayed
cerebral ischemia and
has been recommended
as a threshold for decreased
cerebral perfusion.
1281
FIGURE 1-5
Management approach to delayed cerebral ischemia.
BP = blood pressure; CPP = cerebral perfusion pressure; CT = computed tomography; CTA = computed
tomography angiography; CTP = computed tomography perfusion; DCI = delayed cerebral ischemia;
ICP = intracranial pressure; IVH = intraventricular hemorrhage; MTT = mean transit time; SAH = subarachnoid hemorrhage;
TCD = transcranial Doppler; WFNSS = World Federation of Neurological Surgeons Scale.
Reprinted with permission from Macdonald RL, Nat Rev Neurol. B 2014 Macmillan Publishers Limited. www.nature.com/nrneurol/journal/v10/n1/full/
nrneurol.2013.246.html.
39
Management. All of the patients with

SAH in the authors institution are treated
with nimodipine and euvolemia as mentioned above (Table 1-5) (Figure 1-5).
Low-risk patients whose neurologic examination remains unchanged along
with absence of vasospasm and hypoperfusion on TCD and CTA/CTP are
considered for transfer to a lower level
1282
of care as early as 5 days post ictus.

High-risk patients who have good
neurologic status and whose neurologic
examination remains unchanged along
with normal TCD and CTA/CTP are
transferred out of the neurocritical care
unit as early as 7 days after symptom
onset. High-risk patients with poor
neurologic status, whose examination
October 2015
remains unchanged, and all neuromonitoring values remain within normal

limits, are considered for transfer to a
lower level of care 14 days after SAH. If
at any given time low-risk or high-risk
patients develop elevated TCD mean cerebral blood flow velocities or abnormal
CTA/CTP, the intensity and frequency of
neurologic monitoring is escalated.
Once patients experience neurologic deterioration suggestive of delayed
cerebral ischemia, rescue therapies are
initiated. Current guidelines indicate
that induced hypertension is indicated
(Table 1-5) (Figure 1-5).2,12 At the authors institution, typically, an IV fluid
bolus (1 to 2 liters of 0.9% saline) is administered and hypertension is induced
with norepinephrine as our drug of
choice. Blood pressure augmentation
progresses in stepwise fashion with frequent assessment of neurologic function
at each 10 mm Hg change in systolic
(up to 200 mm Hg) or mean arterial
blood pressures to determine whether
a higher blood pressure target is needed.
The authors institution reserves the use
of inotropes (dobutamine or milrinone)
for those patients with known poor cardiac function. If neurologic deficits persist, then the patient undergoes CT/CTA/
CTP or DSA with subsequent endovascular therapy once cerebral vasospasm
is confirmed. Endovascular treatment
using intra-arterial vasodilators and/or
angioplasty is supported by prospective
and retrospective observational data and
is currently recommended (Table 1-5).2,12
Induced hypertension is maintained
for at least 72 hours or until stability is
achieved and is slowly weaned off after
that. We do not perform prophylactic
angioplasty when cerebral vasospasm
is discovered during the screening
CT/CTA/CTP or DSA without neurologic
deterioration because this practice is
associated with higher complication
rates.2,12 In high-risk patients with poor
neurologic status, diagnosis and treatContinuum (Minneap Minn) 2015;21(5):12631287
ment of delayed cerebral ischemia may

be somewhat subjective and mostly
based on neuromonitoring findings.
The protocol at the authors institution dictates induced hypertension
and CT/CTA/CTP or DSA when these
patients experience elevated TCD mean
cerebral blood flow velocities indicative of vasospasm, abnormal brain tissue oxygenation, or CBF (Figure 1-5).
Medical Complications
Cardiopulmonary. Cardiopulmonary alterations are among the most common
systemic complications of SAH and can
range from minor ECG changes to severe dilated cardiomyopathy and acute
respiratory distress syndrome (ARDS).38
ECG alterations and cardiac enzyme
(troponin T) elevations are quite frequent
after SAH and, depending on their severity, are also significant surrogates for
clinical outcome. ECG changes include
sinus tachycardia, peaked T waves, T-wave
inversions, ST segment depression or
elevation, and QT prolongation. Troponin elevation can be seen in up to
30% of patients. The exact pathogenesis
behind cardiac abnormalities is not completely understood but may reflect a
catecholamine-related myocardial injury.
Echocardiogram can help differentiate
patients with diffuse cardiac dysfunction
related to SAH from those with underlying cardiac ischemia showing regional
wall motion abnormalities restricted to
the territory of a coronary vessel. Clinically, patients with SAH can develop significant cardiac dysfunction manifesting
as left ventricular failure, with impaired
cardiac output, hypotension, and pulmonary edema. These cardiovascular
dysfunctions can lead to severe hypoperfusion, reduced CPP or brain tissue
oxygenation, with added catastrophic
consequences for an already-injured
brain prone to delayed cerebral ischemia and poor neurologic outcome.
KEY POINTS
h Once patients experience

neurologic deterioration
suggestive of delayed
cerebral ischemia, rescue
therapies are initiated with
induced hypertension as
first-line modality.
h In high-risk patients
with poor neurologic
status, diagnosis and
treatment of delayed
cerebral ischemia may
be somewhat subjective
and mostly based on
neuromonitoring findings.
h Cardiopulmonary
alterations are
among the most
common systemic
complications of
subarachnoid hemorrhage.
1283
KEY POINTS
h Pulmonary edema or
acute respiratory distress
syndrome in patients
with subarachnoid
hemorrhage should be
treated with judicious
use of diuretics and other
standard heart failure
therapies targeting
euvolemia and normal
cerebral perfusion pressure.
h Fever is the most

common non-neurologic
complication in
patients with
h Fever in patients with

has been associated with
poor clinical outcome.
h Deep venous thrombosis

prophylaxis should be
administered to all
patients with
1284
The term stunned myocardium has

been applied to patients with SAH who
present with hypoxemia and cardiogenic
shock with pulmonary edema within
hours of disease onset. Takotsubo cardiomyopathy (typically characterized by apical
ballooning on echocardiogram) can be
seen in those patients with poor neurologic status and increases the risk of
delayed cerebral ischemia.12 Current recommendations for the treatment of pulmonary edema or ARDS in patients with
SAH are to avoid excessive fluid intake
and to use diuretics judiciously to target
euvolemia. In addition, standard management of heart failure is indicated,
keeping in mind that CPP should be maintained within normal limits.12 Although
lung-protective mechanical ventilation
should be tried whenever possible, hypercarbia should be closely monitored
and managed to avoid ICP elevations.
Cardiopulmonary function should be
supported, even with the insertion of an
intra-aortic balloon pump if necessary,
as these abnormalities usually improve
a few days after onset.
Fever. Fever is the most common nonneurologic complication of SAH, occurring in up to 70% of patients during their
hospitalization.2,12 Fever is more likely
to occur in patients with poor neurologic status and higher modified Fisher
Scale scores. Fever in SAH has been associated with poor clinical outcome and
is more likely related to SIRS rather than
infectious in origin. There is currently
no clear evidence indicating that fever
control is beneficial for patients with
SAH. However, current recommendations are to monitor body temperature
frequently and to seek and treat infectious processes. In addition, during the
period of risk for delayed cerebral ischemia, fever control should be achieved in
a stepwise fashion starting with standard
antipyretic medications and escalating to
surface cooling or intravascular devices
while avoiding shivering.
Thromboembolism. The incidence

of deep venous thrombosis (DVT) after
SAH ranges from 2% to 20% depending
on the screening methodology used.12
The risk of DVT is higher in patients with
poor neurologic status. Because of the
high incidence of DVT and its potential
life-threatening consequences, prophylaxis should be administered to all
patients with SAH. Sequential compression devices are recommended for all
patients with SAH (Table 1-5). The use
of unfractionated heparin for prophylaxis is indicated after aneurysm obliteration and can be started 24 hours after
the procedure.
Glucose abnormalities. Hyperglycemia is a common phenomenon following SAH. Its real impact is still unclear,
but hyperglycemia has been associated
with the development of delayed cerebral ischemia and poor clinical outcome.
Hypoglycemia also is associated with
worse clinical outcome. The methods,
timing, and aggressiveness of glucose
control are not well studied in patients
with SAH. Current recommendations
are to maintain a blood glucose between
80 mg/dL and 200 mg/dL pending further
investigations (Table 1-5).12
Hyponatremia. Hyponatremia is the
most common electrolyte disorder in
SAH and can occur in about 30% of patients.2,12,15 Hyponatremia has been associated with development of delayed
cerebral ischemia and poor clinical outcome. Hyponatremia can be secondary
to cerebral salt wasting or inappropriate
secretion of antidiuretic hormone. Traditionally, in patients without SAH, the
former is treated with volume infusion
and the latter with fluid restriction. However, because determination of fluid status
can be difficult in the neurocritical care
unit and because hypovolemia is associated with poor clinical outcome, fluid
restriction should be avoided in patients
with SAH. Treatment goals for hyponatremia in SAH should be oral free water
October 2015
restriction while maintaining euvolemia.

Patients can be treated with continuous
infusion of hypertonic saline (1.5% to 3%)
and fludrocortisone if diuresis is active
and impedes maintenance of adequate
fluid balance. It is important to test for
thyroid and adrenal dysfunction, particularly in those patients with SAH who
require vasopressors to maintain blood
pressure goals.
Hemoglobin. The majority of patients
with SAH experience a drop in hemoglobin during hospitalization, which could
be due to several factors, including excessive blood draws, blood loss for other
reasons, or systemic inflammation.12 Anemia has been associated with delayed
cerebral ischemia and poor clinical outcome in patients with SAH. However,
the optimal hemoglobin concentration
in patients with SAH has not been determined, and whether blood transfusion
improves clinical outcome remains to
be proven. Current recommendations
are to minimize blood loss from blood
drawing and to maintain a hemoglobin
concentration of above 8 g/dL to 10 g/dL
(Table 1-5).
CONCLUSION
SAH is a neurologic emergency associated
with high morbidity and mortality. SAH
is more frequent in women than men
and more frequent in minority populations compared to white Americans. The
main areas of emphasis when caring for
patients with SAH should be the following: prompt evaluation and diagnosis,
immediate transfer to appropriate centers,
expeditious diagnosis and treatment of the
bleeding source, and overall good neurocritical care adhering to available treatment
guidelines. The main neurologic complications of SAH include hydrocephalus,
seizures, cerebral edema, delayed cerebral
ischemia, and neuroendocrine disorders.
Patients with SAH frequently experience
cardiopulmonary complications, which
can be life threatening.
KEY POINTS
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1287

Diagnosis and Management of Subarachnoid Hemorrhage

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Review Article

Jose I. Suarez, MD, FNCS, FANA

that women are more likely to have SAH

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

h The most important

older.2 In about 80% of SAH cases, a

aneurysms rupture may be smaller for

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

TABLE 1-1 Risk Factors for Subarachnoid Hemorrhage

Continued on page 1266

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Continued from page 1265

Initial imaging studies of the patient in Case 1-1. A, Nonenhanced head CT

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

TABLE 1-2 Focal Physical Findings in Patients With Subarachnoid Hemorrhage

Third nerve palsy

Usually posterior communicating aneurysm; also posterior cerebral

Sixth nerve palsy

Elevated intracranial pressure (false localizing sign)

Combination of hemiparesis and

Middle cerebral artery aneurysm, thick subarachnoid clots, or

Bilateral leg weakness and abulia

Anterior communicating artery aneurysm

Internal carotid artery aneurysm impinging upon the cavernous sinus

Unilateral visual loss or bitemporal

Internal carotid artery aneurysm compressing optic nerve or optic chiasm

Impaired level of consciousness and

Pressure on the dorsal midbrain due to hydrocephalus

Brainstem compression by basilar artery aneurysm

Meningeal irritation by the presence of subarachnoid blood

Retinal and subhyaloid hemorrhages

Sudden increase of intracranial pressure

Preretinal hemorrhages (Terson syndrome)

Vitreous hemorrhage due to severe elevations of intracranial pressure

acute encephalopathy, and concomitant

24 hours and 50% at 7 days.20,21 The

h The sensitivity of CT for

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Diagnostic algorithm for subarachnoid hemorrhage.

Reprinted with permission from Suarez JI, et al, N Eng J Med.

B 2006 Massachusetts Medical Society. www.nejm.org/doi/full/10.1056/

tometry seems to be more sensitive

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

digital subtraction angiography (DSA)

15% more recently.28,29 Nevertheless, it

h All patients with a

h Any of the following

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

b Failure to Recognize Spectrum of Presentation of Subarachnoid Hemorrhage

h Mean arterial blood

stabilization of airway, breathing, and

or a systolic blood pressure of less than

Copyright American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Noncontrast head CT scan of a patient with nonaneurysmal perimesencephalic subarachnoid hemorrhage.

bleeding on admission are the strongest

to perform (Table 1-415,34,35).23 Higher

h The severity of neurologic

impairment and the

World Federation of Neurological

Modified Fisher Scale35

Absent in both lateral ventricles

Present in both lateral ventricles

Absent in both lateral ventricles

Present in both lateral ventricles