Diagnosis and management of subarachnoid hemorrhage

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

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 cece-rebral 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, endovascerebrovas-cular 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

Nontraumatic subarachnoid

hemor-rhage (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

that women are more likely to have SAHcompared to men (1.24:1.0) and thatminority groups (particularly AfricanAmerican and Hispanic populations)are more frequently affected compared

to white Americans.1,2 The incidence

of SAH increases with age, with a cal mean age of onset of 50 years or

typi-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.

1263 Review Article

older.2 In about 80% of SAH cases, aruptured cerebral aneurysm is found.

However, neuroimaging techniquesmay show no source of bleeding in 15%

of SAH cases or show other ties (eg, arteriovenous malformation,vasculitis) in the remaining 5% of cases

abnormali-SAH causes significant morbidity andmortality Mortality rates vary widelyamong studies, ranging from 8% to 67%

(median of 30% in the United States),with the caveat that most of these studiesdid not account fully for prehospitaldeaths, which have been estimated to

be between 10% and 15%.3 However,there has been a significant decrease incase-fatality rates of SAH across theglobe,3which has been attributed to im-proved survival of hospitalized patientsand is most likely owing to changes inmanagement of patients with SAH, in-cluding neurocritical care, endovasculartherapy, and more refined microsurgicaltechniques Nevertheless, it is important

to emphasize that despite the decrease

in case-fatality rates, about half of vors experience significant chronic reduc-tions in health-related quality of life.4,5For example, a large proportion of survi-vors do not return to their previous level

survi-of employment, social independence andinteractions, or personal or family rela-tionships even 5 years after the event

This reduction in health-related ity of life may be due to a combination

qual-of factors, including impaired physicalfunctioning, cognitive deficits (partic-ularly executive function and memory),mood and emotional symptoms (eg, an-xiety, depression, and posttraumaticstress disorder), and personality changes

Several risk factors for SAH have beenidentified (Table 1-1).2,6Y10 Whetherany of these factors plays a predominantrole in an individual patient remains un-clear Genetic and environmental fac-tors 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 forthose patients with concomitant hyper-tension and cigarette smoking than forthose with either factor alone

SAH remains one of the top neurologicemergencies, and neurologists must fa-miliarize themselves with this devastatingdisease This review discusses the mainfeatures of diagnosis and management ofSAH The main areas of emphasis whencaring for patients with SAH should in-clude the following: prompt evaluationand diagnosis,11immediate transfer toappropriate centers,2,12 expeditious di-agnosis and treatment of the bleedingsource,13,14 and overall good neurocrit-ical care adhering to available treat-ment guidelines.2,12

CLINICAL PRESENTATIONSAH typically presents with sudden andsevere headache (usually described as

‘‘the worst headache ever’’) nied by nausea, vomiting, photophobia,neck pain, and loss of consciousness(Case 1-1A).15 Physical examinationshould include determination of level

accompa-of consciousness, funduscopic tion, determination of meningeal signs,and presence of focal neurologic defi-cits (Table 1-2) The latter are present

evalua-in about 10% of patients with SAH andare associated with worse prognosis whendue to the presence of thick subarach-noid clot or parenchymal hemorrhage.Transient elevation in the intracranial pres-sure (ICP) causes nausea, vomiting, andsyncope However, more sustained andsevere increases in ICP can lead to comaand brain death Terson syndrome (vit-reous hemorrhage associated with SAH)can present in up to 40% of patientswith SAH.16,17The sudden spike in ICP

is thought to lead to preretinal rhages, which are associated with moresevere SAH and increased mortality.Some patients with SAH can have amore atypical presentation.11,15Occasion-ally, patients may present with seizures,

decreased with the

advent of neurocritical care,

endovascular therapy,

and more refined

microsurgical techniques.

hThe 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.

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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 (SaO 2 ) 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

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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.

FIGURE 1-1 Initial imaging studies of the patient in Case 1-1 A, Nonenhanced head CTshows 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).

Continued from page 1265

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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

an-eurysmal leak.18,19Regrettably, this piece

of information is only obtained

retro-spectively as most of the time the

head-ache is transient and head CT scanning

is unrevealing in about 50% of cases

DIAGNOSIS

Head CT Scan

The most appropriate initial

diagnos-tic test for patients suspected of having

SAH is a noncontrast head CT scan

(Figure 1-2) (Case 1-1A).15 The

sen-sitivity 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

sensi-tivity of a CT scan decreases to 93% at

24 hours and 50% at 7 days.20,21 Thecharacteristic appearance of extravasatedblood in the basal subarachnoid cisterns

is hyperdense (Figure 1-1A) Other tions include the sylvian fissures; inter-hemispheric fissure; interpeduncularfossa; and suprasellar, ambient, andquadrigeminal cisterns CT also can detectintracerebral hemorrhage, intraventricu-lar hemorrhage, and hydrocephalus

loca-Although MRI may be as sensitive as CTscan in the first 2 days of SAH presen-tation, it is rarely performed in this sce-nario because of logistical issues.22,23 MRIwith hemosiderin-sensitive sequences(gradient echo and susceptibility-weightedimaging) or with fluid-attenuated inver-sion recovery (FLAIR) sequences is moresensitive than CT scan when performedseveral days after the onset of SAH

Lumbar Puncture

A lumbar puncture is recommended inany patient with suspected SAH and neg-ative or equivocal results on head CT

KEY POINTS

hIn some instances, diagnosis of subarachnoid hemorrhage can be elusive owing to atypical findings on presentation such as seizures at onset, acute encephalopathy, and concomitant subdural hematoma and head trauma.

hThe 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.

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

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

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scan (Figure 1-2) CSF should be lected four consecutive tubes, and redblood cell count should be determined

col-in tubes one and four.11,15The sis of SAH is supported by the following:

diagno-elevated opening pressure, diagno-elevated redblood cell count that does not signifi-cantly decrease from tube one to tubefour, and especially xanthochromia Thelatter, which indicates red blood cellbreakdown, can be determined by visualinspection or by spectrophotometry

Xanthochromia takes about 12 hours todevelop after SAH, and spectropho-

tometry seems to be more sensitivethan visual inspection However, mosthospitals in the United States use visualinspection, and no well-conducted clin-ical studies exist that allow clinicians toknow with certainty what the false-negative rate for xanthochromia is at var-ious time intervals from SAH onset.24Identification of Bleeding SourceAll patients with a diagnostic CT scan orwith either equivocal or diagnostic lumbarpuncture must undergo further imagingwith CT angiography (CTA) or cerebral

digital subtraction angiography (DSA)

(Figure 1-1).11,15The latter has

tradition-ally been considered the ‘‘gold

stan-dard’’ to elucidate the source of bleeding

in SAH (particularly aneurysmal), but

CTA has become widely available and

is being commonly performed as

first-line vascular imaging or even in lieu of

DSA in some centers CTA has a

sensi-tivity and specificity ranging from 90%

to 97% and 93% to 100%, respectively,

depending on technique (16-detector

rows versus 64-detector rows, slice

thick-ness, and data processing algorithms)

and the reader’s experience.25,26 CTA

may not be reliable for the detection of

smaller (ie, less than 4 mm) or distal

an-eurysms 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 author’s institution, a

com-bination of two-dimensional and

three-dimensional 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

presenta-tion, and if negative, MRI should be

per-formed 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.28,29Nevertheless, it

is important to emphasize that tioners should have a high level of sus-picion for any patient presenting withnew-onset headache and understandthe possible pitfalls in the diagnosis ofSAH (Table 1-3) A recent study reported100% sensitivity to detect SAH in pa-tients older than 40 years of age usingclinical decision-making rules that in-clude any of the following factors: neckpain or stiffness, witnessed loss of con-sciousness, and symptom onset duringexertion plus thunderclap headacheand pain on neck flexion.30

practi-Perimesencephalic SubarachnoidHemorrhage

As previously mentioned, in about 15%

of patients with SAH, imaging studiesfail to demonstrate the source of bleed-ing Approximately 38% of these patientshave nonaneurysmal perimesencephalicSAH.31Most patients with nonaneurys-mal perimesencephalic SAH (about 54%)are male and have a low risk of com-plications and better outcomes than pa-tients with aneurysmal SAH A correctdiagnosis is important because of thecatastrophic consequences of missing

a ruptured cerebral aneurysm neurysmal perimesencephalic SAH isconfirmed in the presence of a nega-tive CTA or DSA in patients with thefollowing head CT scan pattern32: cen-ter of hemorrhage located immediatelyanterior to the midbrain, with or withoutextension of blood to the anterior part

Nona-of the ambient cistern or to the basalpart of the sylvian fissures; no completefilling of the anterior interhemisphericfissure and no extension to the lateralsylvian fissures, except for minuteamounts of blood; and absence of frankintraventricular blood (Figure 1-3)

INITIAL EVALUATIONInitial evaluation and management

of patients with SAH should focus on

KEY POINTS

hAll 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.

hAny of the following clinical factors should prompt a workup for subarachnoid hemorrhage

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.

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stabilization of airway, breathing, andcirculation.2,12,15,22,23 Once patientsare deemed stable, a head CT scan must

be performed Patients who are unable toprotect their airway should be intubatedimmediately The most common indica-tions for endotracheal intubation includecoma, hydrocephalus, seizure, and needfor sedation for significant agitation Inaddition, extreme blood pressure valuesshould be avoided Hypertension control

is predicated on the premise that it mayprecipitate rebleeding.33 No data fromrandomized controlled clinical trials exist,but usual practice and current recommen-dations are to maintain a mean arterialblood pressure of less than 110 mm Hg

or a systolic blood pressure of less than

160 mm Hg until the ruptured rysm is secured, while using premorbidbaseline blood pressures to refine tar-gets and avoid hypotension Commonly,pain control may be sufficient to achieveblood pressure control; otherwise, admin-istration of IV labetalol (5 mg to 20 mg),hydralazine (5 mg to 20 mg), or continu-ous infusion of nicardipine (5 mg/h to

aneu-15 mg/h) is preferred Pain control isbest achieved with the administration

of short-acting opiates (Case 1-1A).Disease Severity ScoringThe severity of neurologic impair-ment and the amount of subarachnoid

TABLE 1-3 Reasons for Misdiagnosis of Subarachnoid Hemorrhagea

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.

1270

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

sta-bilization 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 HigherWFNSS and modified Fisher Scalescores are associated with worse clin-ical outcome and a higher proportion

of neurologic complications

Admission to High-VolumeCenters

The next immediate steps are to transferthe patient to a high-volume center (if not

KEY POINT

hThe severity of neurologic impairment and the amount of subarachnoid bleeding on admission are the strongest predictors

of neurologic complications and outcome.

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).

TABLE 1-4 Clinical and Radiologic Grading Scales for Subarachnoid Hemorrhagea

World Federation of Neurological

Intraventricular 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

motor deficit

3 Thickb Absent in both lateral ventricles

5 3Y6 With or without

motor deficit

4 Thick b Present in both lateral ventricles

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.

1271

already in one), admit the patient to adedicated neurocritical care unit, and havethe patient undergo a multidisciplinaryevaluation for the management of an un-secured cerebral aneurysm (Table 1-5).2,12

It has been shown that admission of tients with SAH to low-volume centers

pa-is associated with higher 30-day tality compared to admission to high-volume centers In addition, admission

mor-TABLE 1-5 Summary of Key Recommendations for the Management of Patients With

Subarachnoid Hemorrhage

Treatment

Decision

American Heart Association/American

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).

Patients with SAH should be treated at high-volume centers (moderate quality

of evidence, strong recommendation).

After discharge, it is reasonable to refer patients with SAH for a comprehensive evaluation, including cognitive, behavioral, and psychosocial assessments

(Class IIa, Level B).

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).

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).

Early aneurysm repair should be undertaken, when possible and reasonable

to prevent rebleeding (high quality of evidence, strong recommendation).

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).

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).

Complete obliteration of the aneurysm is recommended whenever possible

(Class I, Level B).

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 evidence, strong recommendation).

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 (Class IIa, Level B).

Continued on page 1273

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TABLE 1-5 Summary of Key Recommendations for the Management of Patients With

Subarachnoid Hemorrhage Continued from page 1272

Treatment

Decision

American Heart Association/American

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).

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, strong recommendation).

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).

of evidence, strong recommendation).

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).

Routine use of anticonvulsant prophylaxis with phenytoin is not recommended 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,

strong recommendation).

Continued on page 1274

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TABLE 1-5 Summary of Key Recommendations for the Management of Patients With

Subarachnoid Hemorrhage Continued from page 1273

Treatment

Decision

American Heart Association/American

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 (Class IIa, Level B).

During the period of risk for delayed cerebral ischemia, control of fever is desirable;

intensity should reflect the individual patient’s 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 evidence, strong recommendation).

Glucose control 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

of evidence, strong recommendation) Serum glucose should be maintained below 200 mg/dL (moderate quality of evidence, strong recommendation).

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, strong recommendation).

The use of unfractionated heparin for prophylaxis could be started 24 hours after undergoing aneurysm obliteration (moderate quality of evidence,

hypervolemia (moderate quality

of evidence, strong recommendation).

Prophylactic hypervolemia or balloon angioplasty before the development of angiographic spasm is not recommended (Class III, Level B). Transcranial Doppler may be used formonitoring and detection of large artery

vasospasm with variable sensitivity (moderate quality of evidence, strong recommendation).

Transcranial Doppler is reasonable to monitor for the development of arterial vasospasm (Class IIa, Level B).

Digital subtraction angiography is the gold standard for detection of large artery vasospasm (high quality of evidence, strong recommendation).

Perfusion imaging with CT or MRI can be useful to identify regions of potential brain ischemia (Class IIa, Level B).

Continued on page 1275

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