Journal of Intensive

Care Medicine
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ICU Management of Aneurysmal Subarachnoid Hemorrhage

Deborah M. Green, Joseph D. Burns and Christina M. DeFusco
J Intensive Care Med 2013 28: 341 originally published online 11 February 2012
DOI: 10.1177/0885066611434100
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http://jic.sagepub.com/content/28/6/341

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Analtyic Review

ICU Management of Aneurysmal

Subarachnoid Hemorrhage

Journal of Intensive Care Medicine

28(6) 341-354
The Author(s) 2013
Reprints and permission:
sagepub.com/journalsPermissions.nav
DOI: 10.1177/0885066611434100
jic.sagepub.com

Deborah M. Green, MD1, Joseph D. Burns, MD1, and

Christina M. DeFusco, RN, ANP2

Abstract
Introduction. Aneurysmal subarachnoid hemorrhage (SAH) has very high morbidity and mortality rates. Optimal intensive care
unit (ICU) management requires knowledge of the potential complications that occur in this patient population. Methods. Review
of the ICU management of SAH. Level of evidence for specific recommendations is provided. Results. Grading scales utilizing
clinical factors and brain imaging studies can help in determining prognosis and are reviewed. Misdiagnosis of SAH is fairly
common so the clinical symptoms and signs of SAH are summarized. The ICU management of SAH is discussed beginning
with a focus on avoiding aneurysm re-rupture and securing the aneurysm, followed by a review of the neurologic and medical
complications that may occur after the aneurysm is secured. Detailed treatment strategies and areas of current and future
research are reviewed. Conclusions. The ICU management of the patient with SAH can be particularly challenging and requires
an awareness of all potential neurologic and medical complications and their urgent treatments.
Keywords
subarachnoid hemorrhage, ICU management, cerebral aneurysm, cerebral vasospasm
Received January 14, 2011, and in revised form September 16, 2011. Accepted for publication September 19, 2011.

Introduction

Summary of Recommendations

Aneurysmal subarachnoid hemorrhage (SAH) makes up only

about 5% of all strokes but has significant morbidity and high
mortality ratesup to 45% in population-based studies, with
the majority of deaths occurring within the first few days.1,2
Risk factors for SAH include hypertension, tobacco smoking,
drug and alcohol use, and family history.3
Factors associated with poor outcome are older age, poor
neurologic examination on admission, and amount of blood
on initial head computed tomography (CT) imaging. Two
clinical scales used are the Hunt and Hess and the World
Federation of Neurological Surgeons (WFNS; Table 1). Hunt
and Hess grade ranges from 1 in a person who is normal
except for a mild headache to grade 5 in a person who is
comatose.4 The WFNS combines Glasgow Coma scale and
focal neurological signs for a score5 from 1 to 5. Prognosis
is worse the higher the score for both of these clinical scales.
The Fisher scale grades SAH based on its appearance on CT
and the modified Fisher scale factors in both the clot thickness
and presence of intraventricular hemorrhage (IVH) on the CT
scan (Table 1, Figure 1).6,7 According to a prediction model
from the International Subarachnoid Aneurysm Trial (ISAT)
data, Fisher scale and modified Fisher scale are predictive
of outcome, the latter being more predictive when compared
in the same population.8,9

The Hunt and Hess or WFNS clinical grading scale as well as

the Fisher or modified Fisher CT grading scale should be used
to classify the patients condition and severity of hemorrhage
on admission in order to guide prognosis (class I, level B; refer
to Table 2 for evidence rating scheme).

Recognition/Clinical Manifestations/
Diagnosis
Subarachnoid hemorrhage has a reported misdiagnosis rate of
around 12%.1,10 Misdiagnosis is associated with a higher likelihood of death or disability at 1 year.10 A sentinel bleed or
warning leak may occur within weeks of the major SAH and
be associated with a sudden headache, nausea, and vomiting
1
Neurology and Neurosurgery, Boston University School of Medicine, Boston
Medical Center, Boston, MA, USA
2
Department of Neurology, Boston University School of Medicine, Boston
Medical Center, Boston, MA, USA

Corresponding Author:
Deborah M. Green, Neurocritical Care, Boston University School of Medicine,
Boston Medical Center, 72 East Concord Street, C3, Boston, MA 02118, USA.
Email: deborah.green@bmc.org

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Table 1. Subarachnoid Hemorrhage Grading Scales.

Hunt and Hess Clinical Grading System4
1 Asymptomatic or mild headache and slight nuchal rigidity
2 Severe headache, neck stiffness, no neurologic deficit except
cranial nerve palsy
3 Drowsy or confused, mild focal neurologic deficit
4 Stuporous, moderate, or severe hemiparesis
5 Coma, decerebrate posturing
World Federation of Neurological Surgeons Clinical Grading scale5
1 GCS 15 and no motor deficit
2 GCS 13-14 and no motor deficit
3 GCS 13-14 and motor deficit
4 GCS 7-12 with or without motor deficit
5 GCS 3-6 with or without motor deficit
Modified Fisher Head CT scale7
0 No SAH or IVH
1 Minimal/thin SAH with no IVH in either lateral ventricle
2 Minimal/thin SAH with IVH in both lateral ventricles
3 Thick SAH with no IVH in either lateral ventricle
4 Thick SAH with IVH in both lateral ventricles
Abbreviations: GCS, Glasgow Coma scale; IVH, intraventricular hemorrhage;
SAH, subarachnoid hemorrhage.

which resolves after minutes to hours. Some of the typical

presenting symptoms of aneurysmal SAH are sudden onset
of severe headache, nausea, vomiting, neck pain, loss of consciousness, and seizures. On physical examination, there may
be focal neurologic signs, meningismus, and retinal subhyaloid hemorrhages. Noncontrast head CT is 98% to 100% sensitive for diagnosing SAH within 12 hours, but this rate drops
to 93% at 24 hours and may be as low as 57% at 6 days.11
Head CT is also useful in diagnosing hydrocephalus. If the
CT scan is negative and clinical suspicion exists, then a diagnostic lumbar puncture should be performed. Subarachnoid
hemorrhage is diagnosed by elevated red blood cells and
xanthochromic centrifugate in the cerebrospinal fluid.
Xanthochromia is due to the enzyme-dependent breakdown
of hemoglobin to bilirubin in the subarachnoid space and
therefore can take several hours after the initial development
of hemorrhage.12
Computed tomography angiography or magnetic resonance
angiography (MRA) can be used to diagnose the aneurysm or
aneurysms with a sensitivity of 95% to 100% for CTA and
85% to 100% for MRA with aneurysms 5 mm and closer to
64% to 83% for CTA and 56% for MRA with aneurysms
<5 mm.13,14 Conventional catheter angiography is still considered the standard for diagnosing cerebral aneurysms. All
vessels should be evaluated as many patients have multiple
aneurysms. If conventional angiogram does not detect the
aneurysm, a repeat imaging study is typically performed in
1 to 2 weeks to be sure the aneurysm was not missed due to
focal vasospasm or thrombus. An MRI of the brain and spinal
cord to look for a vascular malformation has been suggested by
some when the repeat imaging study still reveals no source for
the bleed.15 Sometimes nonaneurysmal perimesencephalic

Figure 1. Axial head CT in a patient with aneurysmal SAH showing

thick clot and IVH in both lateral ventricles, consistent with a modified
Fisher scale of 4. CT indicates computed tomography; SAH, subarachnoid hemorrhage; IVH, intraventricular hemorrhage.

SAH occurs. These patients are usually alert and headache

onset is less suddenover minutes rather than a secondand
no aneurysm is found on repeat angiogram a week or 2 later.
The etiology is unclear but may involve venous bleeding. This
disorder has a benign course.

Summary of Recommendations
1. Noncontrast head CT should be obtained in any patient
with signs and symptoms suggestive of aneurysmal SAH
(class I, level B).
2. Lumbar puncture should be obtained in any patient with
signs and symptoms suggestive of aneurysmal SAH when
the CT is negative (class I, level B).
3. Conventional catheter angiography should be performed to
locate aneurysms in patients with clinical evidence of
aneurysmal SAH (class I, level B).
4. Both CTA and MRA can be used to locate aneurysms
in patients with aneurysmal SAH when an immediate
conventional angiogram cannot be obtained (class IIa,
level B).

Treatment Pre-Securing of Aneurysm

The main goal prior to securing the aneurysm is the avoidance
of rebleeding. The risk of ultra-early rebleeding within 24 hours
of initial SAH may be 15%, with recurrent hemorrhage fatality
around 70%.16,17 Higher-admission Hunt and Hess grade and

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343

Table 2. Modified AHA Stroke Council Evidence Rating Scheme.1

Class I

Conditions for which there is evidence for and/or general agreement that the procedure or
treatment is useful
Conditions for which there is conflicting evidence and/or a divergence of opinion about the
usefulness/efficacy of a procedure or treatment
Class IIa: the weight of evidence or opinion is in favor of the procedure or treatment
Class IIb: usefulness/efficacy is less well established by evidence or opinion
Conditions for which there is evidence and/or general agreement that the procedure or
treatment is not useful/effective and in some cases may be harmful

Class II

Class III
Therapeutic recommendations
Level A
Level B
Level C
Diagnostic/prognostic recommendations
Level A
Level B
Level C

Data derived from multiple randomized clinical trials

Data derived from a single randomized clinical trial or nonrandomized studies
Consensus opinion of experts
Data derived from multiple prospective cohort studies using a reference standard applied by a
masked evaluator
Data derived from a single grade A study or 1 casecontrol studies or studies using a
reference standard applied by an unmasked evaluator
Consensus opinion of experts

aneurysm size predict rebleeding.18 Blood pressure control is

initiated with either intermittent intravenous (IV) labetalol
(10-15 mg every 15 minutes as needed [prn]) or hydralazine
(10-20 mg every 20 minutes) if bradycardia is present. If these
are ineffective or frequent dosing is required, then continuous
infusions of short-acting IV medications such as nicardipine
(5-15 mg/h) or labetalol are typically used. Sodium nitroprusside is generally avoided because of its tendency to raise intracranial pressure and possible toxicity with prolonged use.1
Carefully titrated analgesia may also be needed, balancing
patient comfort and the intent to blunt the hyperadrenergic state
with the need to continuously assess the neurologic status of the
patient. There is no clear evidence on what target blood pressure should be maintained, but some retrospective series have
suggested that a target systolic blood pressure of less than
150 to 160 mm Hg was associated with lower risk of rebleeding.17-19
While prolonged use of antifibrinolytic agents such as epsilon aminocaproic acid and tranexamic acid administered before
delayed aneurysm securing can reduce the risk of rebleeding,
this has been associated with a higher risk of both cerebral
and systemic thrombotic events and is therefore generally
avoided.20 However, recent evidence indicates that the shortterm use of antifibrinolytic therapy in conjunction with early
securing of the aneurysm followed by discontinuation of the
antifibrinolytic agents may decrease the risk of early rebleeding
without elevating the risk of thrombotic complications.1,16
We have not typically used antifibrinolytic therapy due to our
practice of early securing of the ruptured aneurysm and our
concern for thrombotic events.

Summary of Recommendations
1.

The blood pressure should be closely monitored and

controlled to a maximum systolic blood pressure of 150
to 160 mm Hg in the pre-securing phase (class I, level B).

2. Sodium nitroprusside should be avoided in patients with

aneurysmal SAH (class III, level C).
3. A short course (24 hours) of antifibrinolytic therapy that
is discontinued after early aneurysm securing may be
considered to reduce the risk of rebleeding (class IIb, level B).

Treatment of Aneurysm
Coiling Versus Clipping
Early ruptured aneurysm treatment is recommended to reduce
the risk of rebleeding and to facilitate treatment of cerebral
vasospasm.1 Endovascular coiling was first described 20 years
ago and involves detachable platinum coils of different thickness and length which are introduced into the aneurysm via a
microcatheter. The aneurysm is packed with coils to induce
thrombosis which in effect eliminates its connection with the
parent blood vessel.21
The large, prospective, randomized International Subarachnoid Aneurysm Trial found that in patients for whom clipping
and coiling were equally appropriate, coiling was associated
with a better 1-year functional outcome.22,23 Of 9559 patients
with SAH, 2143 were selected for randomization into endovascular or surgical aneurysm treatment. Recurrent SAH occurred
after treatment at significantly higher annual rates in the coiling
(2.9%) versus the clipping group (0.9%). However, at 1 year
after treatment there were lower disability rates in coiled
patients (15.6% coiling vs 21.6% clipping), and there was no
significant difference in mortality rates (8.1% coiling vs
10.1% clipping). The 5-year mortality rate in the coiling group
(11%) was significantly lower than that of the clipping group
(14%).24
The decision on endovascular coiling of the aneurysm
versus surgical clipping is complex and generally based on the
individual patient and the characteristics of the aneurysm. Vertebrobasilar artery aneurysms and paraophthalmic aneurysms
tend to be more easily accessed by endovascular coiling. Wide

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Journal of Intensive Care Medicine 28(6)

neck aneurysms, middle cerebral artery (MCA) aneurysms, and

those associated with intraparenchymal hematomas tend to be
more appropriate for surgical clipping. Advances in coil and
stent technology may allow broader indications for an endovascular approach.1 When an aneurysm cannot be treated by either
direct surgical clipping or coil embolization, the parent vessel
can be occluded by either surgical clipping or coil embolization
at the risk of ischemic sequelae.
A team approach to the decision making involving the neurosurgeon, interventional neurologist or neuroradiologist, and
neurointensivist is the best approach for reviewing all the
patients individual characteristics and determining the best
course for securing the aneurysm. If endovascular coiling is
deemed appropriate, it should be performed at the time of the
diagnostic angiogram, reducing the time to treatment and risk
of rebleeding.1

Summary of Recommendations
1.

2.
3.

Ruptured aneurysms should be secured by surgical

clipping or endovascular coiling to reduce the risk of
rebleeding (class I, level B).
Ruptured aneurysms should be secured early (class IIa,
level B).
The decision to treat with surgical clipping or endovascular coiling should be made by teams with expertise in both
techniques and should be based on characteristics of the
individual patient and aneurysm (class I, level B).
For patients with ruptured aneurysms for which treatment
by surgical clipping and endovascular coiling are determined to be equally appropriate by a team of neurosurgeons and neurointerventionalists, endovascular coiling
is the preferred technique (class I, level B)

Intracranial hypertension. Raised intracranial pressure may

occur for a number of reasons, including hydrocephalus, rerupture of aneurysm, and cerebral edema. Some signs of raised
intracranial pressure include somnolence, headache, nausea,
vomiting, pupil changes such as dilation, and/or sluggish to
no constriction to light stimulus. Monitoring may be performed
by the placement of either an external ventricular drain or an
intraparenchymal monitor. Intracranial pressures sustained
above 20 mm Hg are considered abnormal and warrant treatment. Treatment may include cerebrospinal fluid diversion
with an external ventricular drain (see above section on
Hydrocephalus), sedation and pain management (balancing
the need to monitor the neurologic examination), induced
normothermia, maintenance of normocapnea (PaCO2 goal of
35-42 mm Hg), elevated head of bed, and osmotic agents.
Either mannitol or hypertonic saline may be used for osmotic
agents, but in our practice hypertonic saline in the form of
3% normal saline (NS) 250 mL bolus over 20 to 30 minutes has
been preferred when cerebral vasospasm is a concern as mannitol may lead to greater intravascular volume depletion and
higher risk of vasospasm. If medical measures are ineffective
for intracranial hypertension, a hemicraniectomy may be considered by the neurosurgeon.

Other unsecured aneurysms. A careful evaluation during CTA

or conventional angiogram of all cerebral vessels should be
obtained as about 15% to 20% of patients will have multiple
aneurysms. If other unsecured aneurysms are present, this may
impact the use of hypertensive treatment for cerebral
vasospasm.

Seizures. Seizures have been reported in up to 20% of patients

and are more common after SAH from MCA aneurysms or when
there is a history of hypertension, intraparenchymal hematoma, or
infarcts. It is unclear what impact seizures have on outcome as
there are conflicting reports in the literature.25,26 Prophylactic
anticonvulsant administration may be considered in the immediate
post SAH period. Given the theoretical increased risk of rebleeding with a seizure in the setting of an unsecured, recently
ruptured aneurysm, our approach has been to administer on admission either phenytoin (15-20 mg/kg IV loading dose followed by
100 mg IV every 8 hours) or levetiracetam (500-1000 mg IV load
followed by 500-1000 mg IV every 12 hours). We stop the
anticonvulsant once the aneurysm is secured unless the patient
has had seizures. Routine ongoing use of anticonvulsant medication is not recommended after the aneurysm is secured.1 Continuous EEG monitoring may be considered in any patient who is in
coma. One series of patients with SAH who had continuous
EEG monitoring found that 19% of patients had nonconvulsive
seizures and all of these patients died.27

Hydrocephalus. Acute ventricular enlargement with or without intraventricular blood occurs within 72 hours of SAH in
20% to 30% of patients. If hydrocephalus is present and the
patient is symptomatic (eg, has a decreased level of consciousness), an external ventricular drain should be placed. Typically,
it is kept open at 10 to 20 cm above the external auditory canal.
Reports of up to 40% to 80% of patients had some improvement after ventriculostomy placement. Up to 26% of patients
who survive may need permanent cerebrospinal fluid shunting.
Predictive factors for the need for shunting include female
gender, older age, poor clinical grade on admission, and IVH.1

Pain management. Headaches are best initially treated with

acetaminophen (650 mg orally [po]/per rectum [pr] every 4 hours
prn) and, if needed, codeine (30-60 mg po every 4 hours prn).
Alternatively, tramadol 25 to 50 mg po every 4 hours prn may
be used. If these are ineffective, then fentanyl 12.5 to 25 mcg
IV every 1 hour prn, dilaudid 0.2 to 0.4 mg IV every 3 to 4 hours
prn, or morphine sulfate 2 to 4 mg IV every 1 hour prn may be
used, trying to avoid oversedation and inability to distinguish
signs of neurologic worsening from cerebral vasospasm or other
causes.

4.

Treatment Post-Securing of Aneurysm

Neurologic Complications

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345

Table 3. Modified Fisher Score and Risk of Vasospasm.

Modified Fisher Score
0
1
2
3
4

Risk of Vasospasm9
0%
6%
15%
35%
34%

Cerebral Vasospasm. Cerebral vasospasm is the most common neurologic complication after aneurysmal SAH. It typically occurs between days 4 and 14 after SAH and can be
focal or diffuse, involving multiple cerebral vessels, and may
occur suddenly or gradually. Angiographic vasospasm has been
reported in up to 30% to 70% of the patients with SAH and
leads to stroke or death in 15% to 20%.28,29 Some predictors
of cerebral vasospasm include amount of blood on initial head
CT, pulmonary complications, and cardiomyopathy. Kramer
and colleagues, using the modified Fisher scale, found that the
risk of vasospasm increased with increasing grade (Table 3).9
When not effectively treated, vasospasm can lead to delayed
cerebral ischemia (DCI) and worsen clinical outcome.
Vasospasm can manifest in different ways, such as elevated
blood flow velocity measured by transcranial Doppler (TCD)
ultrasound, conventional angiographic evidence of narrowed
vessels, decline in neurologic function on physical examination
in the absence of other causes, or CT or MRI evidence of
infarction with no other explanation. Symptomatic vasospasm
is defined by either TCD ultrasound or angiographic evidence
of vasospasm combined with new or worsening headache or
alteration in the level of consciousness (confusion, delirium,
or somnolence). Focal neurologic deficits, such as hemiparesis,
aphasia, or other signs, may occur, indicating the involved
vascular territory or territories. Delayed cerebral ischemia is
defined as symptomatic vasospasm or CT or MRI evidence
of infarction attributed to vasospasm. Some patients who have
imaging evidence of vasospasm (TCD or angiography) do not
exhibit clinical signs or imaging evidence of ischemia or infarction, while some patients who clearly have clinical signs of focal
brain ischemia do not have imaging evidence of vasospasm.30
This lack of overlap between the various manifestations of
vasospasm makes interpreting clinical data and guiding treatment at the level of the individual patient challenging.
We screen for vasospasm with daily TCD ultrasound of the
cerebral vessels. Mean velocities of TCD in the 120s to 130s
cm/s for anterior (ACA) and MCA vessels suggest mild vasospasm, 140s to 170s moderate vasospasm, and 180 and higher
severe vasospasm when in conjunction with a Lindegaard ratio
(MCA to extracranial internal carotid artery mean velocities)
>3. Transcranial Doppler has limitations due to being operator
dependent and technical factors such as inability to obtain temporal windows. Cerebral angiography can be used to confirm
vasospasm and to potentially treat intra-arterially.
In patients whose baseline neurologic function is sufficient
to examine cortical function on neurologic examination, we

use the presence of changes in the examination to trigger hemodynamic and endovascular treatment for vasospasm (discussed
below). If such patients have elevated TCD velocities but no
clinical changes, we increase the frequency of neurologic
assessments, carefully maintain normal intravascular volume,
and aim to keep the systolic blood pressure from dipping below
120 mm Hg. High-grade patients with poor baseline neurologic
examinations represent a challenge, as the clinical examination
cannot be relied on to assess the adequacy of brain perfusion. In
this group, the addition of surveillance imaging using conventional angiography, CT or MR angiography and perfusion imaging and/or invasive physiologic monitoring of intracranial
pressure, brain tissue oxygen tension (Licox; Integra Licox1
Brain Oxygen Monitoring System; Integra LifeSciences
Corporation, cerebral blood flow, or microdialysis during the
highest risk period (post-bleed days 4-14) may be reasonable.31
Nimodipine (60 mg orally every 4 hours for 21 days) is indicated to reduce poor outcome after aneurysmal SAH,1 although
its effect may be modest and it has not clearly been demonstrated to prevent cerebral vasospasm and DCI. It may act more
as a neuroprotectant. The trials of nimodipine were conducted
before neurocritical care management with the introduction of
aggressive hemodynamic augmentation so it is unclear whether
these treatments are additive in effect.32 This recommendation
for the use of nimodipine thus far has not been extended to
other calcium channel antagonists. When blood pressure has
been adversely affected by the nimodipine, we have divided
up the dosing to 30 mg orally every 2 hours or even stopped
it completely with significant hypotension or when induced
hypertensive treatment is introduced.
Hemodynamic augmentation, including hypervolemia,
hypertension, and hemodilution (Triple-H therapy), to overcome the increased resistance to flow of spastic vessels has
been the mainstay of the medical treatment of cerebral vasospasm for decades. The theory behind it rests on the HagenPoiseuille law governing flow in blood vessels:
Q DPpr4 =8LZ

Where Q blood flow rate; DP the pressure gradient across the

vessel; r vessel radius; L vessel length; Z blood viscosity.
If brain tissue ischemia in vasospasm occurs because of
blood flow reduction due to reduction in the diameter of the
vessel, then this can be counteracted by raising the driving
pressure across the vessel (hypervolemia and hypertension) and
reducing blood viscosity (hemodilution). The effectiveness of
this strategy, while never definitively established in a randomized, controlled trial, is fairly well documented.33 Most studies suggest a success rate in terms of clinical improvement of
about 50% to 75%.34 However, hemodynamic augmentation
has many important shortcomings and, while necessary in the
face of brain ischemia, must be used with great care. First,
existing evidence does not indicate that prophylactic Triple-H
therapy, initiated before vasospasm is apparent, effectively
prevents DCI or poor clinical outcome.35-37 Second, existing
physiologic evidence suggests that hypertension, but not

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Journal of Intensive Care Medicine 28(6)

hypervolemia or hemodilution, causes desirable improvements

in key physiologic parameters such as cerebral blood flow,
brain tissue oxygenation, and cerebral delivery rate of oxygen.38,40 Third, it is associated with a number of serious complications including exacerbation of cerebral edema,
hemorrhagic transformation of cerebral infarctions, epidural
hematoma formation, pulmonary edema, myocardial infarction, hyponatremia, coagulopathy related to the use of nonalbumin colloid solutions, and complications related to pulmonary
artery catheters.38,41,42
Given these considerations, it is our practice to strictly
maintain euvolemia rather than inducing hypervolemia in all
patients with SAH. This is accomplished by aggressively
repleting any volume deficit that is present on admission with
NS, followed by the infusion of maintenance fluids in the
form of NS at 1 to 1.5 mL/kg per h. We use 24-hour fluid balance (goal: even to 1 L positive to account for insensible
losses), urine output (goal: >0.5 cc/kg per h), and central
venous pressure (goal: 6-8 mm Hg) as objective indicators
of volume status. Once the aneurysm is secured, we stop all
antihypertensive medications and allow the blood pressure
to rise to a systolic of 200 mm Hg before considering treatment. This removes the possibility of inadvertently exacerbating previously well-compensated vasospasm by lowering the
blood pressure.
The balance of oxygen carrying capacity and viscosity is
most optimal at a hematocrit of 30% to 35%.32 This is usually
accomplished with IV fluids and the routine ICU phlebotomy
done for diagnostic testing.
Once it is clear from clinical and/or imaging evidence that
brain tissue perfusion is reduced due to vasospasm, it is necessary to act quickly to restore perfusion and avoid infarction. We
immediately induce hypertension with a 1 to 2 L bolus of NS
and vasopressors (typically phenylephrine or norepinephrine)
titrated to resolution of the relevant clinical or imaging
abnormality, with an upper limit of mean arterial pressure
(MAP) 40% above the estimated premorbid MAP or a systolic blood pressure of 180 to 200 mm Hg. During hemodynamic
augmentation, we carefully monitor for the previously mentioned complications and continue to strictly maintain euvolemia, as defined above. This often requires a high-rate NS
infusion (up to 200 mL/h) as well as intermittent NS boluses
of 500 to 1000 mL. Infrequent 250 mL boluses of 5% albumin
can be useful in this situation both to restore intravascular
volume and to limit ongoing renal sodium and water loss.43
Sometimes the cerebral perfusion pressure can be indirectly
raised if the intracranial pressure is reduced a few points by
lowering the external ventricular drain, thereby limiting vasopressor use.
For the 25% to 50% of patients who do not respond to
hemodynamic augmentation, urgent endovascular treatment
is crucial. The ideal timing for this intervention is not clear, but
a number of studies suggest that the response is best when it
occurs within 2 hours of the onset of symptomatic vasospasm.44 Therefore, we alert the neurointerventional team as
soon as a patient develops symptomatic vasospasm. Patients

who fail to respond to hemodynamic augmentation undergo

angiography and are treated with endovascular intervention if
a suitable target is found. Neurointerventionalists can treat
vasospasm in 2 ways: injection of vasodilators directly into the
spastic vessel or vascular territory and balloon angioplasty.
Intra-arterial vasodilators, including nicardipine, verapamil,
and milrinone, are generally safer than angioplasty and are
especially useful for improving vasospasm in smaller, distal
vessels.45 Their duration of effect, however, can last for as little
as 1 to 2 days, often necessitating multiple treatments.46 Angioplasty can safely be performed in only the largest cerebral
vessels: internal carotid artery, M1 and M2 segments of the
MCA, A1 and A2 segments of the ACA, P1 and P2 segments
of the posterior cerebral artery, vertebral arteries, and the basilar artery. The major advantage of angioplasty over vasodilators is the improved durability of vessel widening, which is
particularly important in patients who develop vasospasm
early. This advantage comes with a price: angioplasty is associated with a 5% risk of major complications, including a 1%
risk of vessel rupture.45 Figure 2 demonstrates symptomatic
and angiographic vasospasm, its intra-arterial treatment, and its
consequences.

Summary of Recommendations
1.

2.

3.

4.

5.
6.

7.

8.

An external ventricular drain should be urgently placed in

patients with SAH with imaging evidence of hydrocephalus and altered consciousness (class IIa, level B).
Intracranial pressure monitoring should be considered in
those patients with SAH having somnolence, headache,
nausea, vomiting, and pupil changes such as dilation
and/or sluggish to no constriction to light stimulus (class
IIa, level C).
The choice of osmotic agent for the treatment of intracranial hypertension in patients with SAH should be based
on the hemodynamic status of the individual patient.
However, hypertonic saline may be more beneficial than
mannitol as it does not lead to volume depletion (class
IIb, level C).
The prophylactic use of antiepileptic drugs such as phenytoin or levetiracetam should be considered in the presecuring phase (class IIb, level B).
Antiepileptic drugs should not be routinely used after the
aneurysm is secured (class IIb, level B).
The treatment of head and neck pain after SAH should be
carefully treated, balancing patient comfort with avoidance of oversedation and inability to distinguish signs
of neurologic worsening from cerebral vasospasm or
other causes. Use of a tiered system of analgesics may
help achieve this goal (class IIb, level C).
The modified Fisher scale should be applied to the admission CT to determine the patients risk of vasospasm
(class IIa, level B).
Frequent serial neurologic examinations and TCD studies
should be used to detect the earliest evidence of vasospasm (class IIa, level B).

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Figure 2. Vasospasm, its treatment, and its consequences. Angiographic and CT images are from the same 35 year-old woman with SAH from a
ruptured right MCA aneurysm. A, Pretreatment conventional angiogram on postbleed day 5 demonstrating severe vasospasm in the M1 segment
of the right MCA (arrow). B, Posttreatment images from the same treatment session showing significant improvement in the caliber of the M1
segment and flow distal to it after intra-arterial injection of nicardipine followed by balloon angioplasty. C, Noncontrast head CT from postbleed day 12, showing large right MCA infarction and R hemicraniectomy. Unfortunately, right MCA vasospasm recurred in this patient and
resulted in a large stroke. CT indicates computed tomography; SAH, subarachnoid hemorrhage; MCA, middle cerebral artery.

9.

10.

11.

Enteral nimodipine at a dose of 60 mg every 4 hours

should be used to prevent poor outcome in all patients
with aneurysmal SAH (class I, level A).
Euvolemia, as determined by fluid balance, urine output, and/or central venous pressure, should be strictly
maintained with the use of isotonic fluids (class IIa,
level B).
Hemodynamic augmentation in the form of euvolemic
hypertension should be used as the first-line treatment
of symptomatic vasospasm (class IIa, level B).

12. Urgent endovascular therapy is indicated for patients with

symptomatic vasospasm who do not respond within 2 to 4
hours of adequate hemodynamic augmentation (class IIb,
level B).

Medical Complications
Between 79% to 100% of patients with SAH have at least 1
medical complication which can have an impact on prognosis.47,48 While older age, aneurysm size >10 mm, aneurysm

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Journal of Intensive Care Medicine 28(6)

rebleeding, stroke from cerebral vasospasm, and neurologic

grade on presentation are well-known predictors of poor outcome from SAH, medical complications have been found to
be similarly associated with poor outcome and mortality.48
Some of the more important medical factors that have been
described as prognostic indicators are fever, hyperglycemia,
and anemia.48

Fever
Fever (temperature >38.3 C) was the most frequent complication of SAH and a significant predictor of poor outcome in
1 study of 580 patients with SAH.48 Fever with SAH has been
associated with higher risk of symptomatic cerebral vasospasm
and consequent worse outcome.49 Fever may be due to infectious causes such as pneumonia, urinary tract infection, bacteremia, or, in patients with a ventriculostomy, ventriculitis
should be considered. Other noninfectious causes include deep
venous thrombosis and central fever. The diagnosis of central fever should be reached only after infectious etiologies are
meticulously excluded. It is thought to be due to the inflammatory response to the subarachnoid blood or hypothalamic
damage.
We generally treat patients initially with acetaminophen
every 6 hours when febrile and then add on a surface cooling
device (Arctic Sun) if this is ineffective. In a casecontrol study
of 120 febrile patients with SAH, conventional fever control
was compared with advanced fever control.50 The group with
advanced fever control had a better outcome at 1 year; however, this required increased sedation and longer ICU length
of stay. The use of aggressive fever control measures to maintain normothermia deserves further study in a larger, prospective multicenter trial.

atrial fibrillation, and ventricular arrhythmias.52 Elevation of troponin I occurs in up to 30% of patients with SAH especially those
with more severe Hunt and Hess grade SAH.53 Typically the
increase in troponin is less than that seen with acute myocardial
infarction. Regional wall motion abnormalities extend beyond a
single coronary vessel territory and there may be large regions
of akinesis on echocardiogram despite the mild increase in
troponin.51
Neurogenic stunned myocardium is characterized by
improvement in ejection fraction within days to weeks often
with complete recovery of function. Unfortunately, this complication can occur during the peak period of cerebral vasospasm, exacerbating cerebral ischemia due to associated
hypotension and hypoxia and making hemodynamic augmentation more difficult and dangerous. Similar to tako-tsubo cardiomyopathy, this condition occurs more frequently in
postmenopausal women. More severe grade SAH patients are
also at higher risk of neurogenic cardiomyopathy. There is
likely significant overlap of neurogenic cardiomyopathy and
neurogenic pulmonary edema which will be discussed further
in the following section on pulmonary complications.
Prevention of cardiac complications may involve early identification of those patients at higher risk and implementation of
early treatment for the presumed catecholamine toxicity with
alpha or beta blockade. This strategy, however, is based only
on small studies and larger prospective trials are needed.51
Treatment for neurogenic stunned myocardium is supportive
as the condition is generally temporary. Where the difficulty
arises is with hemodynamic augmentation therapy for cerebral
vasospasm in a patient with reduced left ventricular function.
Rather than using sympathetic vasopressor medications such
as phenylephrine or norepinephrine, these patients should be
treated with inotropic medications such as milrinone or dobutamine during cerebral vasospasm.

Cardiac Complications
Cardiac complications of SAH may occur within minutes to
hours of the aneurysm rupture and range from electrocardiograph (EKG) changes to myocardial infarction to congestive
heart failure termed neurogenic stunned myocardium. Delays
in diagnosis of aneurysmal rupture occur when SAH-induced
congestive heart failure is mistakenly thought to be due to myocardial infarction. The pathogenesis of SAH-induced cardiac
dysfunction is thought to be due to a catecholamine surge following aneurysm rupture with the resultant explosive increase
in intracranial pressure and presumed hypothalamic injury.
Myocardial contraction band necrosis, also known as myocytolysis or myofibrillary degeneration characterized by hypercontracted sarcomeres, eosinophilic bands, and mononuclear
inflammation, is the typical pathologic injury associated with
SAH but can also be seen with other conditions that involve
a rapid sympathetic surge such as traumatic brain injury and
tako-tsubo cardiomyopathy.51
The EKG changes in SAH occur in up to 80% of patients and
can include ST-T wave changes, sinus tachycardia, and sinus bradycardia more commonly but also associated are atrial flutter,

Pulmonary Complications
Pulmonary complications were the cause of half of all fatal
medical complications in one study and have been associated
with higher frequency of symptomatic vasospasm which may
be related to less aggressive hypertension, hypervolemia, and
hemodilution (HHH) treatment.47,54 The most common pulmonary abnormality is impaired oxygenation, present in
approximately 80% of patients when defined as an alveolar
arterial gradient of >100 mm Hg or a PaO2:FIO2 (fraction of
inspired oxygen) ratio of <300.55 In accordance with these findings, one large retrospective cohort study of 620 patients with
SAH found a 27% incidence of acute lung injury (ALI) and an
18% incidence of acute respiratory distress syndrome
(ARDS).56 Neurogenic pulmonary edema, thought to be a consequence of the catecholamine surge that occurs in the early
stages of severe acute brain injury, affects both the pulmonary
vascular endothelium and myocardium (see Cardiac Complications above) and may account for an important proportion
of patients with ALI in SAH.57 In a retrospective study of
patients with 477 SAH, neurogenic pulmonary edema occurred

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in 8% and was associated with poor clinical and radiologic

grades at presentation and with posterior circulation aneurysms.58 Other common pulmonary complications include
pneumonia (15%-20%), congestive heart failure (8%), pneumothorax (3%), and pulmonary embolism (0.2%-0.6%).47,48,54
As prevention of these complications is more effective than
treatment once they occur, meticulous application of prophylactic measures against hospital-acquired and ventilator-associated
pneumonia, deep venous thrombosis/pulmonary embolism, and
ventilator-associated lung injury are essential to the respiratory
management of patients with SAH. This includes the routine use
of a lung-protective, low tidal volume strategy in all mechanically ventilated patients. We typically use volume-control ventilation with a tidal volume of 0.7 to 0.8 mL/kg ideal body weight
and aim for a PaO2 >80 mm Hg and a low-normal PaCO2 of 35
to 42 mm Hg by adjusting the positive end-expiratory pressure
(PEEP), FIO2, and respiratory rate. Judicious fluid management
with the avoidance of volume overload (see Cerebral Vasospasm above) is important in avoiding iatrogenic pulmonary
edema and in limiting neurogenic pulmonary edema. In cases
of severe neurogenic pulmonary edema, we use diuretics sparingly, if at all, because of its generally self-limited course, the
lack of a role of volume overload in its pathophysiology, and the
potential negative consequences of diuretics on cerebral perfusion. Instead, we focus on maintaining adequate oxygenation
by increasing PEEP and, when neurogenic stunned myocardium
coexists, normalizing cardiac output with inotropic agents.

signs of hypovolemia such as tachycardia. In practice, however, the distinction between the 2 can be quite difficult.62
Hyponatremia should not be corrected faster than 12 to 24
mmol/L in 24 hours to avoid central pontine myelinolysis. For
patients with SIADH, treatment begins with restriction of free
water by administering all IV fluids as NS. If the patient is taking fluids orally, we find it helpful to restrict all oral fluid
intake to salty solutions such as V8 or Gatorade mixed from
powder with half the recommended amount of water. It is crucial to maintain euvolemia despite free water restriction.
Unlike in other patients with SIADH, total fluid restriction
should not be instituted in the setting of SAH as this has clearly
been shown to increase the risk of DCI.63 Therefore, if free
water restriction alone is not sufficient, sodium supplementation in the form of enteric sodium chloride tablets (2-8 g daily
divided between twice daily and four times a day [bid-qid]) or
IV hypertonic saline is necessary. Demeclocycline hydrochloride up to 1200 mg/d divided between bid and qid may also be
used. Due to the difficulty in distinguishing SIADH from CSW
and the consequences of volume dysregulation in SAH
patients, our use of vasopressin antagonists such as conivaptan
in this population is limited. In patients with CSW, treatment is
aimed at simultaneous replacement of sodium and water. This
can be accomplished by first replacing any volume deficit and
compensating for ongoing fluid losses with IV NS, then
correcting the hyponatremia with the use of fludrocortisone
acetate (0.1-0.2 mg po bid), hypertonic saline, or some combination of the 2 depending upon its severity. Sodium chloride
tablets can also be administered.

Hyponatremia
Hyponatremia is very common in patients with SAH, occurring
in up to 57%.59 It tends to occur more often in the setting of
anterior communicating artery aneurysm, hydrocephalus, and
poor clinical grade patients.1,60 Its consequences are significant, and range from subtle abnormalities such as inattention
and gait disturbance with relatively mild hyponatremia to seizures, increased cerebral edema, and even death in acute,
severe hyponatremia.61 The importance of these consequences
is substantially magnified in the setting of the acute brain injury
and cerebral edema present in patients with SAH.
The syndrome of inappropriate antidiuretic hormome
(SIADH) and cerebral salt wasting (CSW) are by far the predominant causes of hyponatremia in SAH. The SIADH is caused
by unregulated release of ADH with resultant unregulated reabsorption of free water in the distal tubule and collecting ducts of
the kidney. This results in euvolemic to slightly hypervolemic
hyponatremia. CSW, on the other hand, is the result of natriuresis (probably due to dysregulated release of circulating
natriuretic peptide), thus leading to a hypovolemic hyponatremic state. Both disorders are associated with an inappropriately
elevated urine osmolality and sodium concentration. Accordingly, distinguishing between SIADH and CSW is primarily
based on an assessment of the patients volume status and urine
output. The CSW is suggested by a negative fluid balance, a
decrease in weight, elevated blood urea nitrogen, and clinical

Hypernatremia
Hypernatremia is probably less common in SAH than hyponatremia.64 In most cases, it is the result of either hypovolemia or
the administration of hypertonic saline or mannitol for treatment of cerebral edema, but it is occasionally caused by neurogenic diabetes insipidus. Diabetes insipidus is suggested by
hypernatremia in the setting of hypovolemia and hypotonic
urine.
As in other patients with hypernatremia, the severity of the
disorder and rapidity of its development should guide treatment
in patients with SAH. However, since there is a risk of fatal
worsening of cerebral edema due to overzealous correction of
hypernatremia, we generally tolerate high serum sodium concentrations in patients with SAH (up to 155 mEq/L). When
we do treat, we typically aim only to keep the sodium concentration 155 mEq/L and do so slowly using a goal reduction of
no more than 2 to 4 mEq/L over 24 hours. Treatment starts with
correction of hypovolemia followed, if necessary, by either
water administration enterically or 0.45% NS IV. Serum
sodium should be checked serially to avoid overcorrection. If
the patient has neurogenic diabetes insipidus, the urine output
is replaced with IV 0.9% or 0.45% NS to maintain an even fluid
balance and 2 mcg of desmopressin IV is typically
administered.

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Hypomagnesemia
Hypomagnesemia is a common occurrence in patients with
SAH, with one large study reporting a frequency of 38% at the
time of admission and 55% at some point during the first 3
weeks after hemorrhage. In the same study, a magnesium level
<0.7 mmol/L occurred more commonly in patients with
poor clinical or radiologic grades and was an independent
predictor of DCI.65 These findings are in agreement with the
well-established role of magnesium supplementation as a neuroprotective agent in animal models of ischemic stroke and
vasospasm after SAH and may be related to magnesiums role
as an antagonist of calcium at the N-methyl-D-aspartate glutamate receptor and voltage-dependent calcium channels in vascular smooth muscle.66 Numerous randomized, controlled
human clinical trials have investigated the utility of moderateand high-dose magnesium supplementation in preventing DCI
and improving clinical outcomes.66-68 Their results have unfortunately been conflicting, although this may be related to differences in outcome definitions and achieved magnesium
concentrations in the treatment groups. The topic remains an
active area of clinical investigation. Until the safety and efficacy of magnesium supplementation has been clearly established, its use cannot be recommended. However, given that
magnesium is generally safe and has only been associated with
poor outcomes in SAH at ultra-high serum concentrations, it is
reasonable to meticulously maintain normal serum magnesium
concentrations by monitoring levels daily and repleting with IV
magnesium sulfate.69

Hyperglycemia
Hyperglycemia (>200 mg/dL) has been described as a predictor
of poor outcome after SAH.48 Whether treating it leads to better
outcome is not clear. The large prospective randomized trials of
intensive insulin therapy did not report numbers of patients
with SAH included, but the Normoglycemia in Intensive Care
EvaluationSurvival Using Glucose Algorithm Regulation
(NICE-SUGAR) trial of critically ill medical and surgical
patients did include patients with traumatic brain injury and
found higher mortality with a blood glucose goal of 80 to
110 mg/dL.70 One small prospective study found no difference
in outcome with intensive insulin therapy (target blood glucose
of 80-110 mg/dL) versus conventional insulin therapy (target
blood glucose less than 151 mg/dL) in a neuro ICU population
which included patients with SAH.71 We have now adopted a
blood glucose goal of 120 to 180 mg/dL.

Anemia
Anemia is one of the most common medical complications of
SAH, occurring in as many as 47% of patients.72 It is associated
with surgical aneurysm treatment, poor clinical grade on
admission, higher admission systemic inflammatory response
syndrome (SIRS) score, female sex, baseline hematocrit
<36%, and a history of hypertension.72 Like hyperglycemia,

however, it is not clear whether anemia is an epiphenomenon

that serves only as a marker of disease severity or if its treatment can lead to better outcomes. The issue is further complicated by the fact that the most common treatment for anemia,
transfusion of packed red blood cells (pRBCs), is itself associated with the potential to exacerbate vasospasm and its consequent ischemia through depletion of endogenous nitric
oxide, stimulation of neutrophil activity, and decreased
deformability of RBCs, leading to decreased flow in the
microcirculation. Furthermore, pRBC transfusions are associated with an increased rate of nosocomial infections and
ARDS.73 Clinical evidence illustrates this complicated relationship between anemia, transfusions, and outcome in SAH.
For example, even after adjustment for other factors such as
age and HuntHess grade, anemia requiring transfusion was
associated with mortality and poor outcome after SAH in one
study.48 In a retrospective cohort of 245 SAH patients, when
entered into the same multivariable logistic regression model,
transfusion but not anemia itself emerged as an independent
predictor of the combined outcome of death, severe disability,
or delayed infarction.74 However, when these patients were
dichotomized into those who developed symptomatic vasospasm and those who did not, anemia was a stronger predictor
of adverse outcomes in the vasospasm group, whereas transfusion assumed this role in the group without vasospasm.
Finally, Dhar and colleagues studied positron-emission tomography (PET) scans in a small group of patients with SAH and
found that transfusion of a single unit of pRBC led to
increased cerebral oxygen delivery in all brain regions except
those in the territory of vasospasm.75 In the absence of a clear
answer to these questions, we have adopted a middle-of-theroad approach to anemia in SAH, using pRBC transfusions
as needed to maintain a goal hemoglobin concentration of 8
g/dL. We typically do not adjust this goal for the occurrence
of vasospasm. The treatment of anemia in SAH remains a very
active area of investigation.

Other Medical Issues

Other general considerations in medical management include
deep venous thrombosis prophylaxis, stress ulcer prophylaxis,
and nutrition. All patients should have pneumatic compression devices placed. Heparin at a dose of 5000 units subcutaneously 2 to 3 times a day should be considered after the
aneurysm is secured. This usually can be started immediately
following endovascular coiling but may be delayed for 1 to 3
days after surgical clipping. Ondansetron 4 mg IV may be
given for nausea every 6 hours prn. Stress ulcer prophylaxis
with either a histamine H2 blocker or proton pump inhibitor
should be considered in every mechanically ventilated
patient. Stool softeners are initiated especially if the aneurysm
is unsecured or if the patient is on narcotics. Enteral nutrition
is usually started early after the aneurysm is secured. Hypotonic IV fluids should be avoided due to the risk of worsening
cerebral edema.

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Summary of Recommendations

Future Research

1.

Many potential preventative or treatment measures for cerebral

vasospasm are being studied. Statin medications may decrease
inflammation, increase cerebral arterial diameter, and decrease
thrombosis. Based on positive results in small trials, we have
used statins in some patients, but a meta-analysis of 4 small
studies did not show benefit.78-80 There is an ongoing trial to
further investigate the utility of statins in vasospasm.81 Erythropoietin, thought to potentially be neuroprotective, cannot
be recommended at this time based on limited data but one
small single-center randomized trial found the incidence of
DCI reduced in the group that received 3 doses every other day
initiated within 72 hours of SAH.82 Clazosentan, an endothelin
antagonist, showed promise in early research, but a phase II
trial was recently reported to show no difference in the primary
end point of vasospasm-related morbidity and all-cause mortality. It remains to be seen whether further studies will be performed with this drug class. Other promising treatments that
are under investigation are dantrolene, magnesium (see Hypomagnesemia section), and advanced fever control (see
Fever section).83

2.

3.
4.

Advanced fever control can be considered for patients with

SAH (class IIB, level B).
Patients with SAH should be investigated and monitored
for cardiac complications with electrocardiography and
continuous cardiac telemetry (class IIa, level B). Measurement of cardiac enzymes on admission, and transthoracic
echocardiography should also be considered (class IIb,
level B).
Volume overload should be avoided after SAH (class I,
level B).
Serum sodium levels should be carefully monitored after
SAH (class I, level B).

The major causes of hyponatremia after SAH are SIADH and

CSW. Treatment of hyponatremia in patients with SAH having
SIADH consists of some combination of restriction of free
water (but not total fluid), enteric sodium chloride tablets, IV
hypertonic saline, and demeclocycline. Treatment of CSW
consists of volume and sodium replacement with some combination of isotonic saline, hypertonic saline, enteric sodium
chloride tablets, and fludrocortisone (class IIa, level B).
1.
2.

3.

A high-normal serum magnesium level should be maintained in patients after SAH (class IIb, level C).
Serum glucose should be strictly maintained between 120
and 180 mg/dL in the acute period after SAH (class IIa,
level B).
The hemoglobin concentration should be maintained 8g/
dL in the acute period after SAH (class IIb, level C).

Neurointensivist/Neurologic Intensive
Care Unit
Length of intensive care unit (ICU) stay for patients with SAH
was significantly reduced after the initiation of neurointensivist
comanagement of all aspects of care in a recent retrospective
study.76 The percentage of patients requiring a ventriculoperitoneal shunt was cut in half when a neurointensivist managed
external ventricular drain weaning. This successful strategy
may be an example of an effective multidisciplinary approach
to the care of these patients and certainly warrants further prospective study. It is preferable for patients with SAH to be
admitted to a dedicated neurologic ICU.77 Frequent neurologic
examinations by nurses and physicians experienced in neurocritical care are essential to recognize the earliest signs of cerebral ischemia, raised intracranial pressure, and hydrocephalus
as deterioration can occur rapidly thereafter without early
detection and intervention.

Summary of Recommendations
1.

It is preferable for patients with SAH to be admitted to a

dedicated neurologic ICU (class IIa, level B).

Conclusions
The ICU management of the patients with SAH can be particularly challenging and requires awareness and vigilance for all
potential neurologic and medical complications that may occur
and require urgent intervention. The initial management is
focused on avoiding rebleeding and securing the aneurysm,
while the more prolonged subsequent ICU management
requires a broader view balancing the benefits of therapies
needed to treat vasospasm with potential cardiac, pulmonary,
and other medical complications. Wider use of endovascular
coiling, refinement of hemodynamic augmentation and intraarterial strategies for cerebral vasospasm treatment, and
increasing numbers of neurocritical care physician and nurse
specialists demonstrate how far the care of patients with SAH
has advanced in recent years. Ongoing and future research
trials offer potential strategies for even further improvement
in outcomes in patients with SAH.
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