Continuum-Diagnosis and Management of Subarachnoid Hemorrhage

Review Article
Diagnosis and
Address correspondence to
Dr Jose I. Suarez, Baylor
College of Medicine, One
Management of
Baylor Plaza, NB:302, Houston,
TX 77030, jisuarez@bcm.edu.
Relationship Disclosure:
Subarachnoid
Dr Suarez reports no disclosure.
Unlabeled Use of
Products/Investigational
Hemorrhage
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, ce-
rebral edema, delayed cerebral ischemia, rebleeding, seizures, and neuroendocrine ab-
normalities that lead to impaired body regulation of sodium, water, and glucose.
Recent Findings: The incidence of SAH has remained stable, but mortality of hos-
pitalized 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 guide-
lines 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 fol-
lowing: 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 cerebrovas-
cular 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 man-
agement remain controversial and need further studies to clarify their role in improving
patient outcome.
Continuum (Minneap Minn) 2015;21(5):1263–1287.
INTRODUCTION that women are more likely to have SAH

Nontraumatic subarachnoid hemor- compared to men (1.24:1.0) and that
rhage (SAH) represents about 3% of minority groups (particularly African
all strokes in the United States.1 The American and Hispanic populations)
worldwide incidence of SAH ranges are more frequently affected compared
from 2 to 16 per 100,000 people and to white Americans.1,2 The incidence
has not changed in the past 3 decades.2 of SAH increases with age, with a typi-
Most epidemiologic studies have shown cal mean age of onset of 50 years or
Continuum (Minneap Minn) 2015;21(5):1263–1287 www.ContinuumJournal.com 1263
Copyright © American Academy of Neurology. Unauthorized reproduction of this article is prohibited.

Subarachnoid Hemorrhage
KEY POINTS
h Subarachnoid hemorrhage older.2 In about 80% of SAH cases, a aneurysms rupture may be smaller for
is more frequent in ruptured cerebral aneurysm is found. those patients with concomitant hyper-
women than men and However, neuroimaging techniques tension and cigarette smoking than for
more frequent in may show no source of bleeding in 15% those with either factor alone.
minority populations of SAH cases or show other abnormali- SAH remains one of the top neurologic
compared to ties (eg, arteriovenous malformation, emergencies, and neurologists must fa-
white Americans. vasculitis) in the remaining 5% of cases. miliarize themselves with this devastating
h Case-fatality rates of SAH causes significant morbidity and disease. This review discusses the main
hospitalized patients mortality. Mortality rates vary widely features of diagnosis and management of
with subarachnoid among studies, ranging from 8% to 67% SAH. The main areas of emphasis when
hemorrhage have (median of 30% in the United States), caring for patients with SAH should in-
decreased with the with the caveat that most of these studies clude the following: prompt evaluation
advent of neurocritical care, did not account fully for prehospital and diagnosis,11 immediate transfer to
endovascular therapy, deaths, which have been estimated to appropriate centers,2,12 expeditious di-
and more refined be between 10% and 15%.3 However, agnosis and treatment of the bleeding
microsurgical techniques.
there has been a significant decrease in source,13,14 and overall good neurocrit-
h The most important case-fatality rates of SAH across the ical care adhering to available treat-
points in the management globe,3 which has been attributed to im- ment guidelines.2,12
of patients with proved survival of hospitalized patients
subarachnoid hemorrhage CLINICAL PRESENTATION
and is most likely owing to changes in
are prompt evaluation
management of patients with SAH, in- SAH typically presents with sudden and
and diagnosis, immediate
transfer to appropriate
cluding neurocritical care, endovascular severe headache (usually described as
centers, expeditious therapy, and more refined microsurgical ‘‘the worst headache ever’’) accompa-
diagnosis and treatment of techniques. Nevertheless, it is important nied by nausea, vomiting, photophobia,
the bleeding source, and to emphasize that despite the decrease neck pain, and loss of consciousness
overall good neurocritical in case-fatality rates, about half of survi- (Case 1-1A).15 Physical examination
care adhering to available vors experience significant chronic reduc- should include determination of level
treatment guidelines. tions in health-related quality of life.4,5 of consciousness, funduscopic evalua-
For example, a large proportion of survi- tion, determination of meningeal signs,
vors do not return to their previous level and presence of focal neurologic defi-
of employment, social independence and cits (Table 1-2). The latter are present
interactions, or personal or family rela- in about 10% of patients with SAH and
tionships even 5 years after the event. are associated with worse prognosis when
This reduction in health-related qual- due to the presence of thick subarach-
ity of life may be due to a combination noid clot or parenchymal hemorrhage.
of factors, including impaired physical Transient elevation in the intracranial pres-
functioning, cognitive deficits (partic- sure (ICP) causes nausea, vomiting, and
ularly executive function and memory), syncope. However, more sustained and
mood and emotional symptoms (eg, an- severe increases in ICP can lead to coma
xiety, depression, and posttraumatic and brain death. Terson syndrome (vit-
stress disorder), and personality changes. reous hemorrhage associated with SAH)
Several risk factors for SAH have been can present in up to 40% of patients
identified (Table 1-1).2,6Y10 Whether with SAH.16,17 The sudden spike in ICP
any of these factors plays a predominant is thought to lead to preretinal hemor-
role in an individual patient remains un- rhages, which are associated with more
clear. Genetic and environmental fac- severe SAH and increased mortality.
tors also can increase the risk of SAH, Some patients with SAH can have a
and some of these factors can interact. more atypical presentation.11,15 Occasion-
For instance, the size at which cerebral ally, patients may present with seizures,
1264 www.ContinuumJournal.com 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

Continued from page 1265
FIGURE 1-1 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).
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.

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 Middle cerebral artery aneurysm, thick subarachnoid clots, or
aphasia or visuospatial neglect 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 Internal carotid artery aneurysm compressing optic nerve or optic chiasm
hemianopia
Impaired level of consciousness and Pressure on the dorsal midbrain due to hydrocephalus
impaired upward gaze
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 24 hours and 50% at 7 days.20,21 The KEY POINTS
subdural hematoma and head trauma, characteristic appearance of extravasated h In some instances,
making the underlying diagnosis of SAH blood in the basal subarachnoid cisterns diagnosis of
subarachnoid hemorrhage
more elusive. A minority of patients may is hyperdense (Figure 1-1A). Other loca-
can be elusive owing to
have a warning ‘‘sentinel’’ headache days tions include the sylvian fissures; inter-
atypical findings on
to weeks before an aneurysmal SAH, hemispheric fissure; interpeduncular presentation such as
which is thought to represent a small an- fossa; and suprasellar, ambient, and seizures at onset, acute
eurysmal leak.18,19 Regrettably, this piece quadrigeminal cisterns. CT also can detect encephalopathy, and
of information is only obtained retro- intracerebral hemorrhage, intraventricu- concomitant subdural
spectively as most of the time the head- lar hemorrhage, and hydrocephalus. hematoma and
ache is transient and head CT scanning Although MRI may be as sensitive as CT head trauma.
is unrevealing in about 50% of cases. scan in the first 2 days of SAH presen- h The sensitivity of CT for
tation, it is rarely performed in this sce- detection of subarachnoid
DIAGNOSIS nario because of logistical issues.22,23 MRI blood may be 98% to
Head CT Scan with hemosiderin-sensitive sequences 100% when obtained
The most appropriate initial diagnos- (gradient echo and susceptibility-weighted within 12 hours of onset
tic test for patients suspected of having imaging) or with fluid-attenuated inver- of symptoms, compared
SAH is a noncontrast head CT scan sion recovery (FLAIR) sequences is more to lumbar puncture.
(Figure 1-2) (Case 1-1A).15 The sen- sensitive than CT scan when performed
sitivity of a CT scan has been reported several days after the onset of SAH.
to be 98% to 100% for the detection
of subarachnoid blood within 12 hours Lumbar Puncture
of symptom onset when compared to A lumbar puncture is recommended in
lumbar puncture. However, the sensi- any patient with suspected SAH and neg-
tivity of a CT scan decreases to 93% at ative or equivocal results on head CT

FIGURE 1-2 Diagnostic algorithm for subarachnoid hemorrhage.

CT = computed tomography.
15
Reprinted with permission from Suarez JI, et al, N Eng J Med. B 2006 Massachusetts Medical Society. www.nejm.org/doi/full/10.1056/
NEJMra052732.
KEY POINT scan (Figure 1-2). CSF should be col- tometry seems to be more sensitive
h The diagnosis of lected four consecutive tubes, and red than visual inspection. However, most
subarachnoid hemorrhage blood cell count should be determined hospitals in the United States use visual
is supported by the finding
in tubes one and four.11,15 The diagno- inspection, and no well-conducted clin-
of xanthochromia in CSF.
sis of SAH is supported by the following: ical studies exist that allow clinicians to
elevated opening pressure, elevated red know with certainty what the false-
blood cell count that does not signifi- negative rate for xanthochromia is at var-
cantly decrease from tube one to tube ious time intervals from SAH onset.24
four, and especially xanthochromia. The
latter, which indicates red blood cell Identification of Bleeding Source
breakdown, can be determined by visual All patients with a diagnostic CT scan or
inspection or by spectrophotometry. with either equivocal or diagnostic lumbar
Xanthochromia takes about 12 hours to puncture must undergo further imaging
develop after SAH, and spectropho- with CT angiography (CTA) or cerebral

KEY POINTS
digital subtraction angiography (DSA) 15% more recently.28,29 Nevertheless, it h All patients with a
(Figure 1-1).11,15 The latter has tradition- is important to emphasize that practi- diagnostic CT scan or
ally been considered the ‘‘gold stan- tioners should have a high level of sus- with either equivocal or
dard’’ to elucidate the source of bleeding picion for any patient presenting with diagnostic lumbar
in SAH (particularly aneurysmal), but new-onset headache and understand puncture must undergo
CTA has become widely available and the possible pitfalls in the diagnosis of further imaging with CT
is being commonly performed as first- SAH (Table 1-3). A recent study reported angiography or digital
line vascular imaging or even in lieu of 100% sensitivity to detect SAH in pa- subtraction angiography.
DSA in some centers. CTA has a sensi- tients older than 40 years of age using h Any of the following
tivity and specificity ranging from 90% clinical decision-making rules that in- clinical factors should
to 97% and 93% to 100%, respectively, clude any of the following factors: neck prompt a workup for
depending on technique (16-detector pain or stiffness, witnessed loss of con- subarachnoid hemorrhage
rows versus 64-detector rows, slice thick- sciousness, and symptom onset during in patients older than 40:
ness, and data processing algorithms) exertion plus thunderclap headache neck pain or stiffness,
and the reader’s experience.25,26 CTA and pain on neck flexion.30 witnessed loss of
may not be reliable for the detection of consciousness, and
smaller (ie, less than 4 mm) or distal an- Perimesencephalic Subarachnoid symptom onset during
eurysms. The decision to perform CTA Hemorrhage exertion plus thunderclap
or DSA will vary depending on resource headache and pain on
As previously mentioned, in about 15%
neck flexion.
availability and institutional practices. of patients with SAH, imaging studies
However, loss of consciousness at the fail to demonstrate the source of bleed-
onset of SAH may be a strong predictor ing. Approximately 38% of these patients
for the detection of ruptured cerebral have nonaneurysmal perimesencephalic
aneurysm on subsequent DSA.27 Thus, SAH.31 Most patients with nonaneurys-
in those patients with a negative CTA, mal perimesencephalic SAH (about 54%)
this presentation should still prompt a are male and have a low risk of com-
DSA. In the author’s institution, a complications and better outcomes than pa-
bination of two-dimensional and three- tients with aneurysmal SAH. A correct
dimensional DSA are performed as the diagnosis is important because of the
standard diagnostic testing for aneurysm catastrophic consequences of missing
detection in all SAH cases. Patients with a ruptured cerebral aneurysm. Nona-
a negative DSA should have a repeat neurysmal perimesencephalic SAH is
study 7 to 14 days after initial presenta- confirmed in the presence of a nega-
tion, and if negative, MRI should be per- tive CTA or DSA in patients with the
formed to uncover a possible vascular
following head CT scan pattern32: cen-
malformation of the brain, brainstem,
ter of hemorrhage located immediately
or spinal cord.15,23
anterior to the midbrain, with or without
Misdiagnosis extension of blood to the anterior part
of the ambient cistern or to the basal
Misdiagnosis of SAH is still common
part of the sylvian fissures; no complete
because the classic findings may occur
filling of the anterior interhemispheric
inconsistently or patients may present
with atypical findings. Misdiagnosis is fissure and no extension to the lateral
associated with significantly increased sylvian fissures, except for minute
mortality and disability (up to fourfold) amounts of blood; and absence of frank
in those patients presenting without intraventricular blood (Figure 1-3).
neurologic deficits at their initial hospital
visit. Fortunately, the frequency of SAH INITIAL EVALUATION
misdiagnosis has decreased from more Initial evaluation and management
than 60% in the early 1980s to less than of patients with SAH should focus on

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 stabilization of airway, breathing, and or a systolic blood pressure of less than
h Mean arterial blood circulation.2,12,15,22,23 Once patients 160 mm Hg until the ruptured aneu-
pressure should be
are deemed stable, a head CT scan must rysm is secured, while using premorbid
maintained at less than
be performed. Patients who are unable to baseline blood pressures to refine tar-
110 mm Hg or systolic
blood pressure at less
protect their airway should be intubated gets and avoid hypotension. Commonly,
than 160 mm Hg until immediately. The most common indica- pain control may be sufficient to achieve
the ruptured aneurysm tions for endotracheal intubation include blood pressure control; otherwise, admin-
is secured, while coma, hydrocephalus, seizure, and need istration of IV labetalol (5 mg to 20 mg),
avoiding hypotension. for sedation for significant agitation. In hydralazine (5 mg to 20 mg), or continu-
addition, extreme blood pressure values ous infusion of nicardipine (5 mg/h to
should be avoided. Hypertension control 15 mg/h) is preferred. Pain control is
is predicated on the premise that it may best achieved with the administration
precipitate rebleeding.33 No data from of short-acting opiates (Case 1-1A).
randomized controlled clinical trials exist,
but usual practice and current recommen- Disease Severity Scoring
dations are to maintain a mean arterial The severity of neurologic impair-
blood pressure of less than 110 mm Hg ment and the amount of subarachnoid

FIGURE 1-3 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).
KEY POINT
bleeding on admission are the strongest to perform (Table 1-415,34,35).23 Higher
h The severity of neurologic
predictors of neurologic complications WFNSS and modified Fisher Scale
impairment and the
and outcome.15,23 Therefore, it is scores are associated with worse clin- amount of subarachnoid
essential that patients with SAH be ical outcome and a higher proportion bleeding on admission are
scored promptly after arrival and sta- of neurologic complications. the strongest predictors
bilization. There are several scoring of neurologic complications
systems available. However, the World Admission to High-Volume and outcome.
Federation of Neurological Surgeons Centers
Scale (WFNSS) and the modified Fisher The next immediate steps are to transfer
Scale are the most reliable and simple the patient to a high-volume center (if not
a
TABLE 1-4 Clinical and Radiologic Grading Scales for Subarachnoid Hemorrhage
World Federation of Neurological

Surgeons Scale34 Modified Fisher Scale35
Glasgow Neurologic Subarachnoid Intraventricular
Grade Coma Scale Examination Grade Hemorrhage Hemorrhage
1 15 No motor deficit 0 Absent Absent
2 13Y14 No motor deficit 1 Minimal Absent in both lateral ventricles
3 13Y14 Motor deficit 2 Minimal Present in both lateral ventricles
4 7Y12 With or without 3 Thickb Absent in both lateral ventricles
motor deficit
5 3Y6 With or without 4 Thickb Present in both lateral ventricles
motor deficit
a
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.
b
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.

already in one), admit the patient to a It has been shown that admission of pa-
dedicated neurocritical care unit, and have tients with SAH to low-volume centers
the patient undergo a multidisciplinary is associated with higher 30-day mor-
evaluation for the management of an un- tality compared to admission to high-
secured cerebral aneurysm (Table 1-5).2,12 volume centers. In addition, admission
TABLE 1-5 Summary of Key Recommendations for the Management of Patients With
Treatment American Heart Association/American

Decision Stroke Association2,a Neurocritical Care Society12,b
Hospital/system Low-volume hospitals (eg, less than Patients with SAH should be treated at
characteristics 10 subarachnoid hemorrhage [SAH] cases high-volume centers (moderate quality
per year) should consider early transfer of of evidence, strong recommendation).
patients with SAH to high-volume centers
High-volume centers should have
(eg, more than 35 SAH cases per year) with
appropriate specialty neurointensive
experienced cerebrovascular surgeons,
care units, neurointensivists, vascular
endovascular specialists, and
neurosurgeons, and interventional
multidisciplinary neurointensive care
neuroradiologists to provide the
services (Class I, Level B).
essential elements of care
After discharge, it is reasonable to refer (moderate quality of evidence,
patients with SAH for a comprehensive strong recommendation).
evaluation, including cognitive, behavioral,
and psychosocial assessments
(Class IIa, Level B).
Aneurysm treatment Surgical clipping or endovascular coiling of Early aneurysm repair should be
the ruptured aneurysm should be undertaken, when possible and reasonable
performed as early as feasible in the to prevent rebleeding (high quality of
majority of patients to reduce the rate of evidence, strong recommendation).
rebleeding after SAH (Class I, Level B).
An early, short course of antifibrinolytic
For patients with ruptured aneurysms therapy prior to early aneurysm repair
judged to be technically amenable to either (begun at diagnosis and continued up to
endovascular coiling and neurosurgical the point at which the aneurysm is secured
clipping, endovascular coiling should be or at 72 hours post ictus, whichever is
considered (Class I, Level B). shorter) should be considered (low quality
of evidence, weak recommendation).
Complete obliteration of the aneurysm is
recommended whenever possible Delayed (more than 48 hours after the
(Class I, Level B). ictus) or prolonged (more than 3 days)
Stenting of a ruptured aneurysm is associated antifibrinolytic therapy exposes patients
with increased morbidity and mortality to side effects of therapy when the risk
(Class III, Level C). of rebleeding is sharply reduced and
should be avoided (high quality of
For patients with an unavoidable delay in evidence, strong recommendation).
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
(Class IIa, Level B).

Subarachnoid Hemorrhage Continued from page 1272

Blood pressure control Between the time of SAH symptom onset Treat extreme hypertension in patients
and aneurysm obliteration, blood pressure with an unsecured, recently ruptured
should be controlled with a titratable aneurysm. Modest elevations in blood
agent to balance the risk of stroke, pressure (mean blood pressure of less than
hypertension-related rebleeding, and 110 mm Hg) do not require therapy.
maintenance of cerebral perfusion Premorbid baseline blood pressures should
pressure (Class I, Level B). be used to refine targets and hypotension
The magnitude of blood pressure control should be avoided (low quality of evidence,
to reduce the risk of rebleeding has not strong recommendation).
been established, but a decrease in systolic
blood pressure to less than 160 mm Hg
is reasonable (Class IIa, Level C).
Intravascular Maintenance of euvolemia and normal Intravascular volume management should
volume status circulating blood volume is recommended target euvolemia and avoid prophylactic
to prevent delayed cerebral ischemia hypervolemic therapy. In contrast, there is
(Class I, Level B). evidence for harm from aggressive
administration of fluid aimed at achieving
hypervolemia (moderate quality
of evidence, strong recommendation).
Cardiopulmonary No recommendations given. Baseline cardiac assessment with serial
complications 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 Routine use of anticonvulsant prophylaxis
may be considered in the immediate with phenytoin is not recommended
posthemorrhagic period (Class IIb, Level B). after SAH (low quality of evidence,
strong recommendation).
The routine long-term use of anticonvulsants
is not recommended (Class III, Level B). 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,


Fever treatment Aggressive control of fever to a target of During the period of risk for delayed cerebral
normothermia by use of standard or ischemia, control of fever is desirable;
advanced temperature-modulating systems intensity should reflect the individual
is reasonable in the acute phase of SAH patient’s relative risk of ischemia (low
(Class IIa, Level B). 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
evidence, strong recommendation).
Glucose control Careful glucose management with strict Hypoglycemia (serum glucose of less than
avoidance of hypoglycemia may be 80 mg/dL) should be avoided (high quality
considered as part of the general critical of evidence, strong recommendation).
care management of patients with SAH
(Class IIb, Level B). Serum glucose should be maintained
below 200 mg/dL (moderate quality of
evidence, strong recommendation).
Deep venous Heparin-induced thrombocytopenia and Measures to prevent deep venous
thrombosis deep venous thrombosis are relatively thrombosis should be employed in all
prophylaxis frequent complications after SAH. Early patients with SAH (high quality of evidence,
identification and targeted treatment are strong recommendation).
recommended, but further research is needed The use of unfractionated heparin for
to identify the ideal screening paradigms prophylaxis could be started 24 hours
(Class I, Level B). after undergoing aneurysm obliteration
(moderate quality of evidence,
Delayed cerebral Oral nimodipine should be administered to Oral nimodipine (60 mg every 4 hours)
ischemia all patients with SAH (Class I, Level A). should be administered after SAH for
Maintenance of euvolemia and normal a period of 21 days (high quality of
circulating blood volume is recommended evidence, strong recommendation).
to prevent delayed cerebral ischemia The goal should be maintaining
(Class I, Level B). euvolemia, rather than attempting
Prophylactic hypervolemia or balloon hypervolemia (moderate quality
angioplasty before the development of of evidence, strong recommendation).
angiographic spasm is not recommended Transcranial Doppler may be used for
(Class III, Level B). monitoring and detection of large artery
Transcranial Doppler is reasonable to vasospasm with variable sensitivity
monitor for the development of arterial (moderate quality of evidence,
vasospasm (Class IIa, Level B). strong recommendation).
Digital subtraction angiography is the
Perfusion imaging with CT or MRI can be
gold standard for detection of large
useful to identify regions of potential
artery vasospasm (high quality of evidence,
brain ischemia (Class IIa, Level B).


Induction of hypertension is recommended Patients clinically suspected of delayed
for patients with delayed cerebral ischemia cerebral ischemia should undergo a
unless blood pressure is elevated at trial of induced hypertension
baseline or cardiac status precludes it (moderate quality of evidence,
(Class I, Level B). strong recommendation).
Cerebral angioplasty and/or selective Endovascular treatment using
intra-arterial vasodilator therapy is intra-arterial vasodilators and/or
reasonable in patients with symptomatic angioplasty may be considered for
vasospasm, particularly those who are vasospasm-related delayed cerebral
not responding to hypertensive therapy ischemia (moderate quality of evidence,
(Class IIa, Level B). strong recommendation).
Anemia and The use of packed red blood cell Patients should receive packed red blood
transfusion transfusion to treat anemia might be cell transfusions to maintain hemoglobin
reasonable in patients with SAH who concentration above 8Y10 g/dL (moderate
are at risk of cerebral ischemia. The quality of evidence, strong
optimal hemoglobin goal is still to be recommendation).
determined (Class IIb, Level B).
Hyponatremia The use of fludrocortisone acetate and Fluid restriction should not be used to
hypertonic saline solution is reasonable treat hyponatremia (weak quality of
for preventing and correcting evidence, strong recommendation).
hyponatremia (Class IIa, Level B).
Early treatment with hydrocortisone
or fludrocortisone may be used to
limit natriuresis and hyponatremia
(moderate quality of evidence,
weak recommendation).
Mild hypertonic saline solutions can be used
to correct hyponatremia (very low quality
of evidence, strong recommendation).
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
Council’s methods of classifying the level of certainty of the treatment effect and the class of evidence.
b
For the Neurocritical Care Society’s 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 st- ing. The choice of treatment depends KEY POINT
affed by dedicated neurointensivists is on several factors, including the pa- h Admission of patients
associated with decreased in-hospital with subarachnoid
tient’s age and aneurysm location,
hemorrhage to
mortality.36 morphology, and relationship to ad-
low-volume centers is
jacent vessels. Because of the complex- associated with higher
Treatment of Unsecured ity of determining the most appropriate 30-day mortality
Aneurysms treatment for individual patients, it compared to admission
Treatment of unsecured aneurysms has is recommended that a multidisciplin- to high-volume centers.
evolved, and two accepted efficacious ary team made up of cerebrovascular
management modalities currently exist: neurosurgeons, endovascular practi-
surgical clipping and endovascular coil- tioners, and neurointensivists confer

KEY POINTS
h Overall, when to reach a consensus.2,12,15,22,23,29 The glucose. Furthermore, SAH unleashes
considering treatment of International Subarachnoid Aneurysm hypothalamic-mediated changes, includ-
unruptured aneurysms, Trial (ISAT) was a prospective random- ing increased sympathetic and parasym-
endovascular coiling ized controlled clinical trial that evalu- pathetic drive, that result in cardiac and
should be preferred over ated patients with unsecured aneurysms pulmonary complications. For example,
surgical clipping who were considered suitable for either increased circulating catecholamines are
whenever possible. endovascular coiling or surgical clip- thought to be the cause for several cardiac
h Patients with ping.13,14 Patients assigned to the endo- manifestations, including ECG changes,
subarachnoid vascular coiling group had a significantly arrhythmias, impaired cardiac contrac-
hemorrhage are at risk higher favorable outcome (defined as tility (eg, Takotsubo cardiomyopathy),
for several significant troponinemia, and myocardial necrosis.
survival free of disability at 1 year)
neurologic complications,
and lower risk of epilepsy compared Pulmonary complications, such as neu-
including hydrocephalus,
cerebral edema,
to those assigned to the surgical clip- rogenic pulmonary edema, most likely
delayed cerebral ischemia, ping group. However, the risk of have a similar underlying pathophysi-
rebleeding, seizures, rebleeding and partial occlusion of ologic mechanism. It is important to
and neuroendocrine aneurysms was lower with surgical recognize and treat all these systemic
abnormalities. clipping. Overall, endovascular coil- complications as they are associated
h The best measure to ing should be preferred over surgical with increased risk for delayed cerebral
reduce the risk of clipping whenever possible; however, ischemia and poor neurologic outcome
rebleeding is the many aneurysms are not equally suit- after SAH.
early treatment of able for either surgical clipping or endo-
unsecured aneurysms. vascular coiling (Table 1-6) (Case 1-1A). Neurologic Complications
Regardless of the treatment modality Rebleeding. Rebleeding is a major dis-
chosen, unsecured aneurysms must be abling complication of SAH, which car-
treated as soon as possible to prevent ries high mortality and morbidity. In
rebleeding (Table 1-5). In the author’s the first 24 hours, 4% to 15% of pa-
institution, the median time for aneu- tients will rebleed, with the highest risk
rysm treatment is 7 hours from initial occurring less than 6 hours from symp-
hospital arrival. tom onset.33 Rebleeding risk decreases
over the following 2 weeks. The main
INTENSIVE CARE UNIT risk factors associated with rebleeding
MANAGEMENT include high systolic blood pressure
SAH is often accompanied by more se- (ie, greater than 160 mm Hg), poor neu-
vere initial systemic and intracranial re- rologic grade, intracerebral or intraven-
sponses than other cerebral insults.37Y40 tricular hematomas, ruptured posterior
More than 75% of patients with SAH circulation aneurysms, and aneurysms
experience systemic inflammatory re- of greater than 10 mm in size.33
sponse syndrome (SIRS), which is likely The best measure to reduce the risk
related to elevated levels of inflammatory of rebleeding is the early treatment of
cytokines. SIRS has been associated with unsecured aneurysms (Table 1-5).2,12
permanent neurocognitive dysfunction. However, in some instances there may
In addition, patients with SAH are at risk be a delay in surgical clipping or endo-
for several significant neurologic com- vascular coiling of the aneurysm, and
plications, including hydrocephalus, cere- short-term (ie, less than 72 hours) treat-
bral edema, delayed cerebral ischemia, ment with tranexamic acid or amino-
rebleeding, seizures, and neuroendo- caproic acid has been recommended if
crine abnormalities that lead to impaired no contraindications exist. The use of
body regulation of sodium, water, and these antifibrinolytic agents is based

KEY POINT
TABLE 1-6 Preferences for Treatment of Unsecured Aneurysms h About 60% of patients
with subarachnoid
Preferred Treatment hemorrhage who undergo
Characteristics Modality external ventricular drain
insertion will have
Advanced age Endovascular coiling
successful weaning and
Poor clinical grade Endovascular coiling the others may require
Multiple underlying systemic conditions Endovascular coiling chronic ventriculoperitoneal
shunt insertion.
Aneurysms with wide neck-to-body ratio Surgical clipping
Normal arterial branches arising from dome or body Surgical clipping
of aneurysm
Middle cerebral artery aneurysm Surgical clipping
Top-of-the-basilar aneurysm Endovascular coiling
Aneurysm associated with large parenchymal hematoma Surgical clipping
High surgical risk Endovascular coiling
Patient preference Endovascular coiling
a
Clinical equipoise Endovascular coiling
a
Unsecured aneurysm is considered equally suitable for either endovascular coiling or surgical clipping.
on the premise that early risk for re- head CT scan is warranted in any patient
bleeding is a consequence of activated with suspected symptomatic hydroceph-
fibrinolysis and reduced clot stability alus and must be followed by insertion
during the first 6 hours. In addition, of an external ventricular drain (EVD).
blood pressure control is also very im- Some centers perform lumbar drain in-
portant to prevent rebleeding prior to sertion instead of EVD in patients with
aneurysm obliteration, as previously SAH who have communicating hydro-
mentioned. Patients suspected of re- cephalus. Weaning the patient of an EVD
bleeding should be evaluated promptly, should begin shortly after aneurysm ob-
have a follow-up head CT scan and DSA literation or within 48 hours of insertion
(if not already done), and immediately if the patient is neurologically stable. A
undergo aneurysm obliteration. Endo- rapid weaning protocol is preferred.
vascular treatment of ruptured cere- About 60% of patients with SAH who
bral aneurysms should include coiling undergo EVD insertion will have suc-
only. Stenting of cerebral aneurysms in cessful weaning, and the others may
the setting of SAH should be avoided require chronic ventriculoperitoneal
as it is associated with higher bleeding shunt insertion (Case 1-1B).
complications and poor outcome.2 Seizures. Delineating the true fre-
Hydrocephalus. Acute symptomatic quency of seizures in patients with SAH
hydrocephalus occurs in about 20% of has been difficult and controversial as
patients with SAH, usually within the many patients (20% to 26%) present with
first few days after symptom onset.2,15,22 seizurelike episodes that are not easy to
Patients manifest decreased levels of con- characterize as many of them occur at
sciousness and other signs of increased the time of symptom onset.2,12Y15 In
ICP, such as impaired upward gaze and general, patients with middle cerebral
hypertension. An immediate follow-up artery (MCA) aneurysms, concomitant

KEY POINTS
h Anticonvulsant intraparenchymal hematomas, and poor Delayed cerebral ischemia. Delayed
administration clinical grade are at higher risk for sei- cerebral ischemia is one of the most
(particularly phenytoin) zures, whereas patients treated with dreaded complications after SAH and is
has been associated endovascular coiling have lower rates the most important factor impacting func-
with worse of seizures. Long-term risk for epilepsy tional outcome.39Y41 Delayed cerebral
clinical outcome. is low. ischemia occurs in about 30% of pa-
h Delayed cerebral ischemia The administration of prophylactic tients with SAH, usually between 4 and
is defined as any anticonvulsants in patients with SAH was 14 days after the onset of symptoms.
neurologic deterioration common practice; however, anticonvul- Delayed cerebral ischemia is defined as
(focal or global) presumed sant administration (particularly phenyt-
any neurologic deterioration (focal or
secondary to cerebral oin) has been associated with worse
global) presumed secondary to cerebral
ischemia that persists for clinical outcome and a high frequency
more than 1 hour and of medication-related complications.2,12 ischemia that persists for more than 1
cannot be explained by Current recommendations are to avoid hour and cannot be explained by any
any other neurologic or phenytoin, and, if desirable, short-term other neurologic or systemic condition.
systemic condition. anticonvulsant administration for 3 to The latter implies an absence of signif-
7 days could be administered. In addi- icant hydrocephalus, sedation, hypox-
tion, concern exists that the frequency emia, seizures, and electrolyte or renal or
of subclinical seizures may be high in hepatic impairment. Thus, delayed cere-
patients with poor-grade SAH, and con- bral ischemia is a diagnosis of exclusion.
tinuous EEG has been recommended in Several factors have been impli-
this setting.12 cated 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 patient’s 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 patient’s 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.

Continued from page 1278
FIGURE 1-4 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.
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.

KEY POINTS
h Possible underlying cerebral ischemia, including cerebral va- hypotension. The latter could be prob-
conditions implicated sospasm, microcirculatory constriction, lematic as it could lead to hypoperfusion
in the pathogenesis microthrombosis, cortical spreading due to decreased cerebral perfusion pres-
of delayed cerebral depression, and delayed cellular apo- sure (CPP). Therefore, it is important that
ischemia include ptosis.39 Most likely, the main driver of systolic blood pressure not be compro-
cerebral vasospasm, all these processes is the release of oxy- mised when administering nimodipine.
microcirculatory hemoglobin and erythrocyte contents One solution employed by the author is
constriction, to half the nimodipine dose to 30 mg
through hemolysis, which unleashes a
microthrombosis, cortical every 2 hours while maintaining ade-
host of inflammatory and proapoptotic
spreading depression, and quate intravascular volume.
delayed cellular apoptosis. factors. The risk for cerebral vasospasm
increases with the thickness, density, Patients with SAH frequently experi-
h Nimodipine should be ence decreased intravascular volume and
location, and persistence of the sub-
administered to all negative fluid balance, which have been
patients with arachnoid blood. In addition, poor
clinical grade, loss of consciousness at associated with higher incidence of cere-
subarachnoid
ictus, cigarette smoking, cocaine use, bral infarction and poor neurologic out-
hemorrhage to decrease
come. These findings led to the institution
the risk of delayed SIRS, hyperglycemia, and hydrocepha-
of prophylactic hypervolemic therapy.
cerebral ischemia lus also increase the risk of delayed
and poor However, this strategy has not been shown
cerebral ischemia and poor neurologic
functional outcome. to improve cerebral blood flow (CBF) or
outcome.39,40 However, predicting who
decrease the frequency of cerebral vaso-
h Euvolemia should be will develop delayed cerebral ischemia
maintained at all times,
spasm or delayed cerebral ischemia, and
has proven very difficult. The latter has
while prophylactic it increases the frequency of cardiopul-
important implications for the reduc- monary complications. Therefore, pro-
hypervolemia should
tion of level of monitoring in patients phylactic hypervolemia should not be
be avoided.
with SAH who are at low risk for delayed pursued. Current recommendations are
cerebral ischemia, thus avoiding poten- to maintain euvolemia at all times after
tial adverse effects of aggressive man- SAH.2,12 It is important to emphasize
agement and potentially decreasing that controversy still exists about the
resource utilization. The best predic- methodology to follow to determine
tors for patients requiring less frequent euvolemia. Many neurointensivists use a
monitoring include older age (more than combination of methods, including strict
65 years), a WFNSS score of 1 to 3, and monitoring of fluid balance, central
a modified Fisher Scale score less than venous pressure, echocardiogram, and
3 (Table 1-5).39 stroke volume variation, among others.
Prophylaxis. The best studied of the In practice, maintenance of euvolemia
available interventions aimed at prevent- can generally be ensured by replacing
ing delayed cerebral ischemia are calcium urine output and even administering
channel blockers and intravascular vol- fludrocortisone or hydrocortisone in pa-
ume status. The use of nimodipine to tients with significant diuresis (Table 1-5).
decrease the risk of delayed cerebral Diagnosis and monitoring. Diagnos-
ischemia and poor functional outcome ing delayed cerebral ischemia is not easy.
is well supported and recommended However, the combination of neurologic
(Table 1-5).2,12,23,39 Nimodipine is ad- examination and imaging studies can
ministered by enteral route at 60 mg enhance the chances of early detection
every 4 hours for 21 days. Nimodipine and management. Patients with SAH must
affords neuroprotection without decreas- be in the neurocritical care unit where
ing the frequency of angiographic vaso- they can be examined very frequently,
spasm. The most common adverse effects preferably at least every 2 hours. Delayed
of nimodipine include constipation and cerebral ischemia must be suspected

KEY POINTS
when patients with SAH develop focal with a high degree of specificity. CTP h Delayed cerebral
neurologic impairment or a decrease findings of an elevated mean transit time ischemia must be
of at least 2 points on the Glasgow Coma (MTT) of greater than 6.4 seconds may suspected when patients
Scale that lasts for more than 1 hour be additive to CTA in predicting delayed with subarachnoid
and cannot be explained by any other cerebral ischemia and has been recom- hemorrhage develop
cause. In addition, all patients with SAH mended as a threshold for decreased focal neurologic
should undergo head CT or MRI 24 to cerebral perfusion. Qualitative visual in- impairment or a decrease
48 hours after aneurysm occlusion. terpretation of CTP can also be useful. of at least 2 points on
Therefore, any new hypodensities on Brain tissue oxygenation and CBF moni- the Glasgow Coma Scale
CT imaging after this period not attri- toring can provide additional information that lasts for more than
1 hour and cannot
butable to EVD insertion or intra- when used in the context of a multimo-
be explained
parenchymal hematoma should be dality approach, bearing in mind their
by any other cause.
regarded as cerebral infarctions from limitations, such as limited tissue sam-
delayed cerebral ischemia regardless of pling and location in relation to pathology. h Any new hypodensities
on CT imaging 24 to
clinical signs.41 Continuous EEG offers the advantage of
48 hours after aneurysm
The general consensus among prac- being able to monitor broad regions of
treatment should be
titioners indicates that patients with SAH the brain to detect epileptiform dis- regarded as cerebral
should undergo additional imaging and/or charges noninvasively. Continuous EEG infarctions from delayed
physiologic monitoring routinely during is particularly useful in patients with poor- cerebral ischemia.
the risk period for delayed cerebral isch- grade SAH where neurologic examina-
h Transcranial Doppler
emia (Table 1-5).2,12 Such monitoring is tion is limited. thresholds for vasospasm
usually multimodal and includes ICP, Some variability exists regarding the include mean cerebral
CPP, CBF, EEG, transcranial Doppler timing and frequency of use of the var- blood flow velocities of
(TCD), DSA, CTA, CT perfusion (CTP), ious neuromonitoring techniques men- less than 120 cm/s for
and brain tissue oxygenation. TCD has tioned above. The author’s institution absence and more than
been the longest and best studied of all follows an algorithm for identifying and 200 cm/s or a Lindegaard
the monitoring modalities. TCD has treating subarachnoid hemorrhage sim- ratio of greater than
adequate sensitivity and specificity to ilar to the one proposed by Macdonald 6 for presence.
detect delayed cerebral ischemia sec- as shown in Figure 1-5.39 Patients with h Digital subtraction
ondary to cerebral vasospasm in large SAH are stratified into low risk (ie, older angiography is the gold
arteries compared to DSA, but is limited age, a WFNSS score of 1 to 2, and a mod- standard for detection of
by the operator’s experience and the ified Fisher Scale score of less than 3), large artery vasospasm.
patient’s cranial windows.42 TCD thresh- high risk (ie, a WFNSS score of 1 to 3 h CT perfusion findings of
olds for vasospasm are the following: and a modified Fisher Scale score of 3), elevated mean transit
mean cerebral blood flow velocities of and high risk with poor neurologic time of greater than
less than 120 cm/s for absence and more status (ie, clouded examination due to 6.4 seconds may be
than 200 cm/s or a Lindegaard ratio (MCA additive to CT angiography
sedation, a WFNSS score of 3 to 5, and
mean cerebral blood flow velocity/extra- in predicting delayed
a modified Fisher Scale score of 4). All
cerebral ischemia and
cranial internal carotid artery mean patients with aneurysmal SAH undergo has been recommended
cerebral blood flow velocity) of greater TCD (daily or every other day) and head as a threshold for decreased
than 6 for presence. In addition, mean CT/CTA/CTP on admission and on days cerebral perfusion.
cerebral blood flow velocity increases by 3 to 5 and days 7 to 10 for screening of
more than 50 cm/s within 24 to 48 hours decreased cerebral perfusion or vaso-
also have been associated with delayed spasm. DSA also can be performed in
cerebral ischemia. lieu of CTA/CTP. High-risk patients
DSA is the gold standard for detection with poor neurologic status undergo
of large artery vasospasm.2,12 CTA has additional neuromonitoring, includ-
become more widely available and may ing EEG, brain tissue oxygenation, and
replace DSA for screening of vasospasm CBF determination.

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.
39
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.
Management. All of the patients with of care as early as 5 days post ictus.
SAH in the author’s institution are treated High-risk patients who have good
with nimodipine and euvolemia as men- neurologic status and whose neurologic
tioned above (Table 1-5) (Figure 1-5). examination remains unchanged along
Low-risk patients whose neurologic ex- with normal TCD and CTA/CTP are
amination remains unchanged along transferred out of the neurocritical care
with absence of vasospasm and hypo- unit as early as 7 days after symptom
perfusion on TCD and CTA/CTP are onset. High-risk patients with poor
considered for transfer to a lower level neurologic status, whose examination

KEY POINTS
remains unchanged, and all neuro- ment of delayed cerebral ischemia may h Once patients experience
monitoring values remain within normal be somewhat subjective and mostly neurologic deterioration
limits, are considered for transfer to a based on neuromonitoring findings. suggestive of delayed
lower level of care 14 days after SAH. If The protocol at the author’s institu- cerebral ischemia, rescue
at any given time low-risk or high-risk tion dictates induced hypertension therapies are initiated with
patients develop elevated TCD mean ce- and CT/CTA/CTP or DSA when these induced hypertension as
rebral blood flow velocities or abnormal patients experience elevated TCD mean first-line modality.
CTA/CTP, the intensity and frequency of cerebral blood flow velocities indica- h In high-risk patients
neurologic monitoring is escalated. tive of vasospasm, abnormal brain tis- with poor neurologic
Once patients experience neuro- sue oxygenation, or CBF (Figure 1-5). status, diagnosis and
logic deterioration suggestive of delayed treatment of delayed
cerebral ischemia, rescue therapies are Medical Complications cerebral ischemia may
initiated. Current guidelines indicate Cardiopulmonary. Cardiopulmonary al- be somewhat subjective
that induced hypertension is indicated terations are among the most common and mostly based on
neuromonitoring findings.
(Table 1-5) (Figure 1-5).2,12 At the au- systemic complications of SAH and can
thor’s institution, typically, an IV fluid range from minor ECG changes to se- h Cardiopulmonary
bolus (1 to 2 liters of 0.9% saline) is ad- alterations are
vere dilated cardiomyopathy and acute
among the most
ministered and hypertension is induced respiratory distress syndrome (ARDS).38
common systemic
with norepinephrine as our drug of ECG alterations and cardiac enzyme complications of
choice. Blood pressure augmentation (troponin T) elevations are quite frequent subarachnoid hemorrhage.
progresses in stepwise fashion with fre- after SAH and, depending on their se-
quent assessment of neurologic function verity, are also significant surrogates for
at each 10 mm Hg change in systolic clinical outcome. ECG changes include
(up to 200 mm Hg) or mean arterial sinus tachycardia, peaked T waves, T-wave
blood pressures to determine whether
inversions, ST segment depression or
a higher blood pressure target is needed.
elevation, and QT prolongation. Tro-
The author’s institution reserves the use
ponin elevation can be seen in up to
of inotropes (dobutamine or milrinone)
30% of patients. The exact pathogenesis
for those patients with known poor car-
behind cardiac abnormalities is not com-
diac function. If neurologic deficits per-
sist, then the patient undergoes CT/CTA/ pletely understood but may reflect a
CTP or DSA with subsequent endovas- catecholamine-related myocardial injury.
cular therapy once cerebral vasospasm Echocardiogram can help differentiate
is confirmed. Endovascular treatment patients with diffuse cardiac dysfunction
using intra-arterial vasodilators and/or related to SAH from those with underly-
angioplasty is supported by prospective ing cardiac ischemia showing regional
and retrospective observational data and wall motion abnormalities restricted to
is currently recommended (Table 1-5).2,12 the territory of a coronary vessel. Clin-
Induced hypertension is maintained ically, patients with SAH can develop sig-
for at least 72 hours or until stability is nificant cardiac dysfunction manifesting
achieved and is slowly weaned off after as left ventricular failure, with impaired
that. We do not perform prophylactic cardiac output, hypotension, and pul-
angioplasty when cerebral vasospasm monary edema. These cardiovascular
is discovered during the screening dysfunctions can lead to severe hypo-
CT/CTA/CTP or DSA without neurologic perfusion, reduced CPP or brain tissue
deterioration because this practice is oxygenation, with added catastrophic
associated with higher complication consequences for an already-injured
rates.2,12 In high-risk patients with poor brain prone to delayed cerebral ische-
neurologic status, diagnosis and treat- mia and poor neurologic outcome.

KEY POINTS
h Pulmonary edema or The term stunned myocardium has Thromboembolism. The incidence
acute respiratory distress
been applied to patients with SAH who of deep venous thrombosis (DVT) after
syndrome in patients present with hypoxemia and cardiogenic SAH ranges from 2% to 20% depending
with subarachnoid shock with pulmonary edema within on the screening methodology used.12
hemorrhage should be hours of disease onset. Takotsubo cardio- The risk of DVT is higher in patients with
treated with judicious myopathy (typically characterized by apical poor neurologic status. Because of the
use of diuretics and other ballooning on echocardiogram) can be high incidence of DVT and its potential
standard heart failure seen in those patients with poor neuro- life-threatening consequences, prophy-
therapies targeting logic status and increases the risk of laxis should be administered to all
euvolemia and normal delayed cerebral ischemia.12 Current rec- patients with SAH. Sequential compres-
cerebral perfusion pressure. ommendations for the treatment of pul- sion devices are recommended for all
h Fever is the most monary edema or ARDS in patients with patients with SAH (Table 1-5). The use
common non-neurologic SAH are to avoid excessive fluid intake of unfractionated heparin for prophy-
complication in and to use diuretics judiciously to target laxis is indicated after aneurysm obliter-
patients with euvolemia. In addition, standard man- ation and can be started 24 hours after
subarachnoid hemorrhage.
agement of heart failure is indicated, the procedure.
h Fever in patients with keeping in mind that CPP should be main- Glucose abnormalities. Hyperglyce-
subarachnoid hemorrhage tained within normal limits.12 Although mia is a common phenomenon follow-
has been associated with
lung-protective mechanical ventilation ing SAH. Its real impact is still unclear,
poor clinical outcome.
should be tried whenever possible, hy- but hyperglycemia has been associated
h Deep venous thrombosis percarbia should be closely monitored with the development of delayed cere-
prophylaxis should be and managed to avoid ICP elevations. bral ischemia and poor clinical outcome.
administered to all
Cardiopulmonary function should be Hypoglycemia also is associated with
patients with
supported, even with the insertion of an worse clinical outcome. The methods,
subarachnoid hemorrhage.
intra-aortic balloon pump if necessary, timing, and aggressiveness of glucose
as these abnormalities usually improve control are not well studied in patients
a few days after onset. with SAH. Current recommendations
Fever. Fever is the most common non- are to maintain a blood glucose between
neurologic complication of SAH, occur- 80 mg/dL and 200 mg/dL pending further
ring in up to 70% of patients during their investigations (Table 1-5).12
hospitalization.2,12 Fever is more likely Hyponatremia. Hyponatremia is the
to occur in patients with poor neuro- most common electrolyte disorder in
logic status and higher modified Fisher SAH and can occur in about 30% of pa-
Scale scores. Fever in SAH has been as- tients.2,12,15 Hyponatremia has been as-
sociated with poor clinical outcome and sociated with development of delayed
is more likely related to SIRS rather than cerebral ischemia and poor clinical out-
infectious in origin. There is currently come. Hyponatremia can be secondary
no clear evidence indicating that fever to cerebral salt wasting or inappropriate
control is beneficial for patients with secretion of antidiuretic hormone. Tra-
SAH. However, current recommenda- ditionally, in patients without SAH, the
tions are to monitor body temperature former is treated with volume infusion
frequently and to seek and treat infec- and the latter with fluid restriction. How-
tious processes. In addition, during the ever, because determination of fluid status
period of risk for delayed cerebral ische- can be difficult in the neurocritical care
mia, fever control should be achieved in unit and because hypovolemia is asso-
a stepwise fashion starting with standard ciated with poor clinical outcome, fluid
antipyretic medications and escalating to restriction should be avoided in patients
surface cooling or intravascular devices with SAH. Treatment goals for hypona-
while avoiding shivering. tremia in SAH should be oral free water

KEY POINTS
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Continuum-Diagnosis and Management of Subarachnoid Hemorrhage

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Review Article

Continuum (Minneap Minn) 2015;21(5):1263–1287.

INTRODUCTION that women are more likely to have SAH

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b Nonmodifiable Risk Factors

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Continued from page 1265

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Findings Likely Cause

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FIGURE 1-2 Diagnostic algorithm for subarachnoid hemorrhage.

1268 www.ContinuumJournal.com October 2015

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b Failure to Recognize Spectrum of Presentation of Subarachnoid Hemorrhage

1270 www.ContinuumJournal.com October 2015

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World Federation of Neurological

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Treatment American Heart Association/American

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Treatment American Heart Association/American

Continued on page 1274

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Treatment American Heart Association/American

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Treatment American Heart Association/American

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1278 www.ContinuumJournal.com October 2015

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FIGURE 1-5 Management approach to delayed cerebral ischemia.

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