c a re o f t h e pat i e nt w i t h aneurysmal subarachnoid hemorrhage

8/21/2019 C a re o f t h e Pat i e nt w i t h Aneurysmal Subarachnoid Hemorrhage

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American Association of Neuroscience Nurses4700 W. Lake Avenue

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Care of t he Patient with

Aneurysmal Subarachnoid Hemorrhage

AANN Clinical Practice Guideline Series


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Clinical Practice Guideline Series EditorHilaire J. Thompson, PhD ACNP BC CNRN

Content AuthorsSheila Alexander, PhD RN, ChairMatthew Gallek, BSN RNMary Presciutti, RN CNRN CCRNPat Zrelak, PhD RN CNRN CNAA-BC

Content ReviewersPatricia Blissitt, PhD RN APRN-BC CCRN CNRN CCMAmanda Brill, MSN RN ACNPDonna Lindsay, MN RNRobin Saiki, MSN RN ACNP

Joanne Turner, MSN RN CCRN CNRN CCNS

Clinical Practice Guideline Series Editorial Board2007–2009Patricia Blissitt, PhD RN APRN-BC CCRN CNRN CCMMatthew Hendell, MSN CNRN CPNPTess Slazinski, MN RN APRN CCRN CNRNPat Zrelak, PhD RN CNRN CNAA-BC

AANN National OfficeStacy Sochacki, MSExecutive Director

Kari L. Lee Managing Editor

Sonya L. JonesSenior Graphic Designer

Publisher’s NoteThe author, editors, and publisher of this document neither represent nor guarantee that the practices described hereinwill, if followed, ensure safe and effective patient care. The authors, editors, and publisher further assume no liability orresponsibility in connection with any information or recommendations contained in this document. These recommenda-tions reflect the American Association of Neuroscience Nurses’ judgment regarding the state of general knowledge andpractice in their field as of the date of publication and are subject to change based on the availability of new scientificinformation.

Copyright © 2007, revised December 2009, by the American Association of Neuroscience Nurses. No part of this publica-tion may be reproduced, photocopied, or republished in any form, print or electronic, in whole or in part, without writ-ten permission of the American Association of Neuroscience Nurses.


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Preface .................................................................................................................................................................................. 4

Introduction ......................................................................................................................................................................... 5

Purpose ....................................................................................................................................................................... 5

Rationale for Guideline ............................................................................................................................................ 5

Goals of Clinical Practice Guidelines ..................................................................................................................... 5

Assessment of Scientific Evidence .......................................................................................................................... 5

Statement of the Problem .................................................................................................................................................. 5

Incidence of Aneurysm Formation and aSAH ...................................................................................................... 5

Mortality and Morbidity .......................................................................................................................................... 6

Secondary Injury After aSAH .................................................................................................................................. 7

Background .......................................................................................................................................................................... 8

Cerebral Vasculature Anatomy and Physiology ................................................................................................... 8

Pathophysiology and Etiology of aSAH ................................................................................................................ 9

Signs and Symptoms of aSAH .............................................................................................................................. 10

Diagnostic Studies ....................................................................................................................................................11

Treatment of Aneurysm .......................................................................................................................................... 13

Patient Care ........................................................................................................................................................................ 14

Preaneurysm Securement ...................................................................................................................................... 14

Postaneurysm Securement ..................................................................................................................................... 17

Patient and Family Education ............................................................................................................................... 24

Documentation ........................................................................................................................................................ 25

References ........................................................................................................................................................................... 26

Bibliography ...................................................................................................................................................................... 30

Contents


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Care of the Patient with Aneurysmal Subarachnoid Hemorrhage 4

To meet its members’ needs for educational tools, theAmerican Association of Neuroscience Nurses (AANN)has created a series of guides to patient care called theAANN Clinical Practice Guidelines. Each guide has beendeveloped based on current literature and is built uponevidence-based practice.

The purpose of this document is to assist registerednurses, patient care units, and institutions in providing safeand effective care to patients recovering from aneurysmalsubarachnoid hemorrhage (aSAH).

The personal and societal impact of aSAH is significantwith some 30,000 Americans suffering aSAH each year.Aneurysmal SAH occurs across the lifespan with risk in-creasing with increased age. The mean age of individualssuffering aSAH is 55 years old. Individuals of all races andethnic backgrounds suffer aSAH equally. Approximate-ly 50% of individuals suffering aSAH do not survive theinitial injury. Of those who do survive, an additional 30%–50% will suffer a secondary injury from one or more of the

following: rebleed, cerebral edema, increased intracranial

pressure, or cerebral vasospasm (the most common compli-cation of aSAH). The end result of primary and secondaryinjury from aSAH is a high rate of mortality and disability.

When a patient suffers aSAH, neuroscience nurses play apivotal role in patient monitoring and management of careto prevent secondary injury thereby improving outcomes.

Resources and recommendations for practice will provideneuroscience nurses with a tool to maximize outcome of in-dividuals suffering aSAH and secondary sequelae.

This reference is an essential resource for neurosciencenurses responsible for the care of this patient populationwith a multitude of biopsychosocial needs. This guideis not intended to replace formal learning, but rather toaugment the knowledge base of clinicians and provide areadily available reference tool.

Neuroscience nursing and AANN are indebted to thevolunteers who have devoted their time and expertise tothis valuable resource, created for those who are commit-ted to neuroscience patient care.

Preface


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I. IntroductionA. Purpose

The purpose of this document is to assist regis-tered nurses, patient care units, and institutions inproviding safe and effective care to adults recov-ering from aneurysmal subarachnoid hemorrhage(aSAH). The goal of the guideline is to provide

background on the biological processes occurring

during and after rupture of a cerebral aneurysmand provide evidence-based guidelines for provid-ing nursing care to this population.

B. Rationale for GuidelineThe impact of aSAH is significant, affecting peo-ple of all ages, races, and genders. Recovery fromaSAH is complicated by secondary injuries, somespecific to individuals recovering from this diseaseprocess. The mortality and disability rates for theaSAH population are high. Nurses providing quali-ty care based on empirical evidence with a focus onpreventing secondary injury will maximize recoveryfor this population.

C. Goals of Clinical Practice GuidelinesWhen presented with a patient with a possi-

ble aSAH, it is imperative that nurses and otherhealthcare professionals are able to recognize theunderlying clinical components, understand theseverity of the situation, initiate early treatment,and act judiciously in order to prevent secondarycomplications and further deterioration in this rel-atively infrequent and often misdiagnosed clinicalencounter. The goals for caring for a patient withaSAH are as follows:• early recognition and accurate diagnosis

• stabilization of the aneurysm• prevention of complications• early recognition of complications• treatment• rehabilitation.

D. Assessment of Scientific EvidenceA review of the published literature from Janu-ary 1982 to November 2006 was conducted usingMedline/PubMed, CINAHL, and Evidence-BasedMedicine Reviews using the following search terms:subarachnoid hemorrhage, cerebral vasospasm, manage-ment, and outcomes. Monographs, textbooks, andreview articles were also consulted. Studies not

directly pertaining to aSAH or not written in Eng-lish were excluded from further evaluation.

For the AANN Clinical Practice Guidelines, dataquality is classified as follows:• Class I: Randomized control trial without signifi-

cant limitations or metaanalysis• Class II: Randomized control trial with important

limitations (e.g., methodological flaws or incon-sistent results), observational studies (e.g., cohortor case-control)

• Class III: Qualitative studies, case study, or series• Class IV: Evidence from reports of expert com-

mittees and/or expert opinion of the guidelinepanel, standards of care, and clinical protocols

The Clinical Practice Guidelines and recommen-dations for practice are established based uponthe evaluation of the available evidence (AANN,2006, adapted from Guyatt & Rennie, 2002; Melnyk,

2004):• Level 1 recommendations are supported by class

I evidence.• Level 2 recommendations are supported by class

II evidence.• Level 3 recommendations are supported by class

III and IV evidence.

II. Statement of the ProblemAneurysmal subarachnoid hemorrhage (aSAH) ishemorrhagic stroke whereby blood from the vas-culature enters the subarachnoid space. Saccular or

berry aneurysms, the most common type of cerebral

aneurysms, are acquired lesions that develop at ves-sel bifurcations or branching points in the cerebralvasculature that resemble small, thin-walled blisters.Other types of aneurysms include fusiform aneu-rysms (also called atherosclerotic aneurysms) or dis-secting aneurysms (because of a tear in the vesselwall). Aneurysms typically form in the bifurcationsof the large vessels that make up the circle of Willis.When one of these vascular lesions ruptures, bloodleaks into the subarachnoid space and is known asan aSAH. Cerebral aneurysms are thought to arisefrom defective layers of arterial lamina and tunicamedia from which an outpouching or ballooning ofthe vessel develops into what is known as the domeof the aneurysm. It is this dome that usually ruptures,leading to blood extravasation into the subarachnoidspace. An aSAH is a catastrophic, emergent eventand is the leading cause of nontraumatic SAH andthe fourth most frequently occurring cerebrovasculardisorder. Immediate attention is warranted at the timeof rupture as a delay in treatment will adversely affectoutcome (Level 2; Kowalski et al., 2004; Lorenzi, Kerr,Yonas, Alexander, & Crago, 2003).A. Incidence of Aneurysm Formation and aSAH The prevalence of unruptured aneurysm is prob-

ably underestimated with up to 5% of the popu-lation having undiagnosed aneurysms found onautopsy. Saccular aneurysms can range in size from24 mm (2%). There arefew known risk factors for aneurysm formation,including familial history (more than two immedi-ate relatives with history of intracranial aneurysm)and select inherited connective tissue disorders(e.g., fibromuscular dysplasia, Marfan syndrome,sickle cell disease, polycystic kidney disease, and other



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connective tissue diseases), anomalous vessels (e.g.,coarctation of the aorta) and high-flow states (e.g.,vascular malformations, fistulae). Aneurysms thathave not ruptured but have manifested with othersymptoms, such as a new-onset third nerve palsy(an emergency that requires urgent treatment of theaneurysm), brain stem compression, or visual loss(caused by an ophthalmic artery aneurysm), should

be treated because the risk of rupture is believed to be significantly higher than that of incidentally dis-covered lesions.

Multiple intracranial aneurysms occur in 10%–30% of all cases with a stronger predilection infemales. About 75% of patients with multiple intrac-ranial aneurysms have two aneurysms, 15% havethree, and 10% have more than three intracranialaneurysms.

Intracranial aneurysms are uncommon in chil-dren, accounting for less than 2% of all cases.Aneurysms in children are more commonly post-traumatic or mycotic, have a slight male predilec-

tion, and tend to be larger than those found inadults (average diameter is 17 mm).

Aneurysm rupture can occur with any sizeaneurysm, but is more typical in those >3–5 mm.Aneurysmal SAH accounts for 6%–8% of all strokes,yet unlike other types of stroke, the incidenceof aSAH has not declined in the last 30 years.Incidence of aSAH in the general U.S. populationis approximately 8–10 cases per 100,000 annually,resulting in approximately 24,000–27,000 new caseseach year.

Risk of aneurysm rupture and aSAH is positivelycorrelated with aneurysm size, hypertension, andsmoking (Level 2; Juvela, Hillbom, Numminen,& Koskinen, 1993; Wiebers et al., 2003). The riskof aSAH increases linearly with age from 25 to 64years when data is corrected for the age distributionwithin the population and peaks between 50 and60 years old depending on the population or studyreferenced (Level 2; Wermer, van der Schaaf, Algra,& Rinkel, 2007). Aneurysmal SAH occurs morecommonly in women than men (Level 2; Wermeret al.). Reports regarding racial differences alsovary from no difference in the rate or prevalence ofSAH to a two-fold increase in black versus white

Americans (Level 2; Broderick, Brott, Tomsick,Huster, & Miller, 1992). Certain hypertensivestates such as those induced by use of stimulants(e.g., cocaine, amphetamines) have been shown topromote aneurysm growth and rupture (Level 2; Brisman, Song, & Newell, 2006; Levine et al., 1990;Mayberg et al., 1994). Reports of oral contraceptiveuse, heavy alcohol consumption, illicit drug use,hormone replacement therapy, hypercholesterolemia,

and vigorous physical activity do not appear to berobust independent risk factors (Level 2; Brisman etal.; Mayberg et al.). Although there are many pos-tulated risk factors for aSAH, there is little conclu-sive evidence to support most of them, other thanfemale gender, increasing age, hypertension, andcigarette smoking.

B. Mortality and Morbidity Most saccular aneurysms are asymptomatic until

they rupture, at which time they are associatedwith extreme morbidity and mortality despiteimprovements in care during the last 3 decades.Approximately 10%–15% (and in some referencesup to 30%) of patients with aSAH die before obtain-ing medical attention (Level 2; Broderick, Brott,Duldner, Tomsick, & Leach, 1994; Olafsson, Hauser,& Gudmundsson, 1997). For those who survive untilhospital arrival, another 30%–60% will die because ofthe initial hemorrhage or secondary sequelae (Ingall,Asplund, Mähönen, & Bonita, 2000). Thirty-day mor-tality is approximately 50% with the highest numberof deaths occurring within the first 14 days (Level

2; Broderick et al., 1994; Ingall et al.; Olafsson et al.).Survival is inversely proportional to aSAH gradeupon presentation (Table 1 and Table 2) as well asage and overall health. Even in patients who pres-ent in good clinical condition, only 55% have goodoutcomes at 90 days. Outcomes are better for patientsadmitted to major medical centers, especially thosewith interventional neuroradiology, within 7 hours ofhemorrhage (Level 2; Lorenzi et al., 2003).

Table 1. Hunt and Hess Classification Scale

Grade I Asymptomatic, mild headache, slight nuchal rigidity

Grade II Moderate to severe headache, nuchal rigidity, noneurological deficit other than cranial nerve palsy

Grade III Drowsiness, confusion, mild focal neurological deficit

Grade IV Stupor, moderate to severe hemiparesis

Grade V Coma, decerebrate posturing

Note. From “Surgical Risks as Related to Time of Intervention in the Repair of IntracranialAneurysms,” by W. E. Hunt and R. M. Hess, 1968, Journal of Neurosurgery, 28, pp. 14–20.

Table 2. Fisher Grading Scale

0 Unruptured

I No subarachnoid blood detected

II Diffuse or vertical layer 1 mm thick

IV Intracerebral or intraventricular clot with diffuse or no

subarachnoid blood

Note. From “Relation of Cerebral Vasospasm to Subarachnoid Hemorrhage Visualized by CTScanning,” by C. M. Fisher, J. P. Kistler, and J. M. Davis, 1980, Neurosurgery, 6, pp. 1–9.


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Patients that survive aSAH are most often leftwith cranial nerve palsies, paralysis, aphasia, cog-nitive impairments, behavioral disorders, andpsychiatric disturbances (Level 2; Bellebaum et al.,2004; Hutter, Kreitschmann-Andermahr, & Gils-

bach, 1998, 2001; Mavaddat, Sahakian, Hutchinson,& Kirkpatrick, 1999).

C. Secondary Injury After aSAH

Functional sequelae after initial aSAH are sig-nificant. Secondary injury from aSAH is a majorconcern and typically results from three sources:(1) increased volume within the cranial vault fromhemorrhage into the subarachnoid space leadingto compressive force, injury to local tissues, masseffect, and increase in intracranial pressure (ICP);(2) meningeal irritation from contact with blood;and (3) compromise of cerebral blood flow becauseof cerebral vasospasm.1. Aneursymal rebleeding

One of the most feared and earliest complica-tions in patients who survive the initial aSAH

is rebleeding of the aneurysm. A second hem-orrhage is a significant contributor of morbidityand mortality following aSAH and is of immedi-ate concern. There is a 2%–4% risk of aneurysmalrebleed within the first 24 hours of ictus andthat risk increases to 15%–20% during the next2 weeks (Brisman et al., 2006). Untreated rup-tured aneurysms have a very high rebleedingrisk (20%–50%) after the initial hemorrhage,especially in the first 24 hours (Mayer, Bernardi-ni, Solomon, & Brust, 2005). The mortality rateafter a rehemorrhage is extremely high (50%–80%; Suarez, Tarr, & Selman, 2006). In addition toincreased mortality related to aneurysm rebleed-ing, 30% of these patients suffer other seriouscomplications (Suarez et al., 2006). Symptomsof aneurysm rebleed are typically related toincreased ICP and include increase in headache,decrease in level of consciousness, and new onsetof focal symptoms.

In one study a reduction in the rebleeding ratefrom 10.8% to 2% was achieved when antifibrin-olytic therapy was administered for fewer than72 hours (Level 1; Hillman, Fridriksson, Nilsson, &

Jakobsson, 2002). Prolonged antifibrinolytic admin-

istration (e.g., aminocaproic acid tablets [Amicar])is complicated by ischemia and thromboembolicevents and no overall improvement in outcome(Level 2; Suarez et al., 2006; van Gijn & Rinkel,2001). For these reasons, antifibrinolytic therapyhas been abandoned (or is typically avoided) as astandard therapy.

2. Acute hydrocephalusAcute hydrocephalus, indicated by an enlargement

of the ventricles, occurs in up to 65% of SAHpatients depending on diagnostic criteria usedand can be life threatening (Level 2; Hasan, Ver-meulen, Wijdicks, Hijdra, & van Gijn, 1989;Mehta, Holness, Connolly, Walling, & Hall,1996; Milhorat, 1987). It usually presents with-in the first 24 hours and is characterized byabrupt mental status change with or without

sixth nerve palsy or gaze deviation and progress-es to an obtunded state if left untreated. Late orchronic hydrocephalus, occurring in 10%–15% ofpatients, is typically because of a blood clot with-in the ventricular system (Level 2; Demirgil et al.,2003). Late or chronic hydrocephalus generallyoccurs 10 or more days after SAH and is char-acterized by incontinence, gait instability, andcognitive deterioration (Level 2; Demirgil et al.).

3. Cerebral vasospasmSecondary injury because of cerebral vasospasmmay occur in as many as 70% of patients with upto 40% demonstrating clinical symptoms (Level

2; Adams, Kassell, Torner, & Haley, 1987; Al-Yamany & Wallace, 1999; Dehdashti, Mermillod,Rufenacht, Reverdin, & de Tribolet, 2004; Dorsch,2002). The cause of cerebral vasospasm appearsto be due to the direct effect of blood and metab-olites on the adventitia of the artery. Prolongedsmooth muscle contraction is mediated by oxy-hemoglobin and release of vasoactive substancesfrom the vessel wall causing inflammatorychanges (Level 2; Arai, Takeyama, & Tanaka,1999; Fujii & Fujitsu, 1988; Macdonald et al., 2001;Takenaka et al., 1991). Cellular response fromprolonged smooth muscle contraction causes inti-mal hyperplasia and subendothelial fibrosis ofthe vessel. Subsequent leukocyte infiltration andplatelet aggregation leads to further reduction inthe caliber of the vessel (Level 2; Janjua & Mayer,2003; Treggiari-Venzi, Suter, & Romand, 2001). Ultimately, cerebral vasospasm results in thefocal narrowing of large arteries and can leadto impaired cerebral autoregulation, cerebralischemia, and infarction. The most common-ly involved arteries are the internal carotid andproximal portions of the anterior and middlecerebral arteries. Vessels undergoing vasospasm

are typically unrelated to the initial aneurysmlocation. Cerebral vasospasm typically occurswithin 4–14 days following hemorrhage in thecase of virgin bleeds and earlier with recurrenthemorrhage. Risk of vasospasm is positive-ly correlated with subarachnoid blood volume,clinical severity of the initial bleed, female gen-der, younger age, and smoking. Symptomaticvasospasm can be manifested by one or more of


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the following: severe headache, change in men-tal status from acute confusion and lethargy toobtunded state, or appearance or exacerbationof a focal deficit (Mayer et al., 2005; Treggiari-Venzi et al., 2001). Symptoms vary, but patientstypically present with a new onset of a gener-al decrease in level of consciousness or with newfocal neurological deficit. Angiographic cerebral

vasospasm occurs in up to 70% of individualsrecovering from aSAH, and up to 40% will sufferdevastating neurological sequelae from ischemiaor infarcts (Level 2; Kassell, Sasaki, Colohan, &Nazar, 1985; Treggiari-Venzi et al.).

4. SeizuresSeizures occur in as many as 25% of patients andare most common after middle cerebral artery(MCA) ruptures. Seizures can lead to increasedcerebral blood flow, hypertension, and elevatedICP, thus escalating the risk of aneurysm rebleedand neurologic deterioration. Seizures at onsethave been shown to be an independent risk fac-

tor for late seizures and a predictor of pooroutcome (Butzkueven & Hart, 2000).

5. Cardiac abnormalitiesElectrocardiogram (EKG) abnormalities frequent-ly occur (Jain, Deveikis, & Thompson, 2004;Zaroff, Rordorf, Newell, Ogilvy, & Levinson,1999). Most are benign and reversible; however,differentiating myocardial ischemia and left ven-tricular dysfunction from the benign changes isimportant (Khush et al., 2005; Zaroff et al., 1999;Zaroff, Rordorf, Ogilvy, & Picard, 2000). Chang-es resembling acute myocardial ischemia arenoted in 25%–80% of patients. In approximate-ly 20% of cases the arrhythmias can be severe orlife threatening. The current theory is that EKGchanges after aSAH are due to release of excesscatecholamines and increased sympathetic tone.There is some thought that they may also berelated to vascular vasospasm in the coronarysystem. Other researchers have postulated thatcontraction band necrosis or myofibrillar degen-eration may be the underlying pathology drivingthis phenomenon. Typical EKG changes seenafter aSAH include prolonged QT and T wavechanges (Jain et al., 2004; Zaroff et al., 1999). Cardi-

ac isoenzymes such as troponin and creatine kinaseMB fraction are often increased (Zaroff et al., 1999).Myocardial injury after aSAH may increase the riskof cerebral ischemia because of inadequate cardiacoutput leading to inadequate cerebral perfusion.

6. Cerebral hyponatremiaCerebral hyponatremia occurs in up to 50% of cas-es and is correlated with poor outcomes (Level 2;

Doczi, Bende, Huszka, & Kiss, 1981; Qureshi etal., 2002; Revilla-Pacheco, Herrarda-Pineda, Loyo-Varela, & Modiano-Esquenazi, 2005; Wijdicks,Vermeulen, Hijdra, & van Gijn, 1985). This isthought to be due to excessive renal secretion ofsodium leading to a syndrome known as cerebralsalt wasting (CSW) rather than a dilutional effectfrom inappropriate antidiuretic hormone secre-

tion (Doczi et al.; Revilla-Pacheco et al.; Wijdickset al.). Besides the direct neural effects on renalfunction, CSW is associated with disturbanc-es in levels of atrial natriuretic, brain natriuretic,and C-type natriuretic peptides (Level 2; McGirtet al., 2004). Lower serum sodium concentrationresults in hypoosmolality; this tonicity gradientacross the blood-brain barrier can lead to cerebraledema. In addition, these patients are at partic-ular risk of developing cerebral ischemic deficitsas a result of increased blood viscosity.

7. FeverPatients with aSAH are at risk for developing

both infectious and noninfectious fever (Commi-chau, Scarmeas, & Mayer, 2003) and are often notresponsive to treatment. Fever occurs in as manyas 54% of patients recovering from aSAH and isa predictor of poor prognosis (Wartenberg et al.,2006). Fever increases cerebral metabolic rate andis thought to cause release of excitatory neuro-transmitters, increased production of oxygen freeradicals, and cellular cytoskeletal degradation, aswell as break down the blood brain barrier (Bad-

jatia et al., 2004), all resulting in an increased riskfor ischemia.

III. BackgroundA. Cerebral Vasculature Anatomy and Physiology Arterial blood flow to the brain occurs through four

major arteries: two large internal carotids providing blood to the anterior portion of the brain and twosmaller vertebral arteries providing blood to theposterior portion of the brain, brainstem, and spinalcord. The two internal carotid arteries branch off theaortic arch and extend to the level of midbrain wherethey enter the circle of Willis. The MCA and ante-rior cerebral arteries (ACA) branch off the internalcarotid arteries at this junction. The MCA provides

blood to lateral portions of the brain in the frontal (including the primary motor strip), parietal (includ-ing the primary sensory strip), and occipital lobes.The ACAs provide blood to the medial portion of the

brain, optic tract, and subcortical structures of the brain. The anterior communicating artery (ACOMM)connects the two ACAs, allowing for bilateral bloodflow in the presence of lesions to one ACA before theACA–ACOMM junction. The two vertebral arteries


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unite at the level of the brainstem toform the basilar artery. The basilarartery continues up the brain stem

before branching into two posteriorcommunicating arteries (PCOMM),which form the posterior portion ofthe circle of Willis. The PCOMM arter-ies connect to the internal carotid arter-

ies on either side, closing the circle ofWillis. PCOMM arteries provide bloodto the anterior vessels of the circleof Willis in the face of lesions to theinternal carotid arteries. The posteriorcerebral arteries (PCA) branch off the

basilar artery at the same junction asthe PCOMMs and supply blood flowto the occipital lobe and portions ofthe temporal lobe. See Figure 1 for thevessels of the circle of Willis.

Unlike other areas in the body, thevenous system does not mimic arte-

rial system design. Deep veins andthe dural sinuses are responsible for the majority ofvenous drainage; both empty into the internal jugu-lar veins. The exception is a small amount of venous

blood that drains through the ophthalmic andpterygoid venous plexuses into the emissary veinsto the scalp and down the system of paravertebralveins in the spinal canal.

A normal arterial wall consists of three layers: theintima, which is the innermost endothelial layer; themedia, which consists of smooth muscle; and theadventitia, the outermost layer, which consists ofconnective tissue (Figure 2).

Normal cerebral circulation requires a constant,total cerebral blood flow under varying conditions.Factors affecting cerebral blood flow include arte-rial pressure, venous pressure, intracranial pressure,

blood viscosity, and the degree of active constrictionor dilation of the cerebral arterioles. Because theskull is not pliable and brain tissue and spinal fluidare essentially incompressible, the volume of blood,spinal fluid, and brain in the cranium at any onetime must be relatively constant (Monro-Kellie doc-trine). Normal cranial capacity for blood and spinalfluid is 125–150 ml.

B. Pathophysiology and Etiology of aSAH The occurrence, growth, thrombosis, and rupture ofintracranial saccular aneurysms can best be explained

by abnormal hemodynamic shear stress on the wallsof large cerebral arteries, particularly at bifurcationpoints, although other factors such as congenitalweakness in the arterial or degenerative changesfrom conditions such as atherosclerosis may act astriggers or cofactors in the disease process. Most

saccular intracranial aneurysms (86.5%) occur inthe anterior (carotid) circulation within or near thecircle of Willis (Brisman et al., 2006). Approximately60% of these aneurysms occur at the MCA bifurca-tion and along the ACA. Other common vessels inthe anterior circulation include the bifurcation ofthe PCA and ophthalmic artery.

Approximately 10% of cerebral aneurysms arisefrom the vertebral and basilar arteries in the posteri-or circulation with the tip of the basilar artery beingthe most common location followed by the origin ofthe posterior inferior cerebellar arteries. The remain-

ing 3.5% of aneurysms occur in sites such as wherethe superior cerebellar and the anterior inferior cer-ebellar arteries branch from the basilar artery. SeeFigure 3 for common aneurysm locations.

The aneurysmal sac itself is usually composed of

Figure 1. Circle of Willis

Note. Copyright © 2007 by Zygote Media Group, Inc. Reprinted with permission.

Figure 2. Layers of a Normal Arterial Wall


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only the intima and adventitia vessel layers. Theintima is typically normal, although subintimal cel-lular proliferation may be present. The internal elasticmembrane is reduced or absent, and the mediaends at the junction of the aneurysm neck with the

parent vessel. Lymphocytes and phagocytes mayinfiltrate the adventitia and fill the lumen of theaneurysmal sac with thrombotic debris. Crucial tothis model is the impact vascular and internal flowhemodynamics has on the origin, growth, and con-figuration of the aneurysms. One of the most impor-tant relationships on flow pattern is the geometricrelationship between the aneurysm and its parentartery. Understanding the flow patterns not onlyhelps understand the pathogenesis of the aneurysm

but is important in selecting the type and placementof a treatment device. In lateral aneurysms, such asones arising from the internal carotid artery (ICA),

blood typically moves into the aneurysm at thedistal aspect of its ostium and exits at the proximalaspect. This causes a slow-flow vortex in the aneu-rysm center. Opacification of the lumen occurs in acranial-to-caudal fashion leading to flow stagnation.In contrast, intraaneurysmal circulation associatedwith vessels, arising at the origin or branching ves-sels or a terminal bifurcation, is rapid. Vortex for-mation with blood stasis is rare.

C. Signs and Symptoms of aSAH Patients with aSAH typically present with a char-

acteristic intense, unrelenting, and overwhelming

headache of sudden onset (occurring within sec-onds). It is often referred to as a “thunderclap head-ache,” although no sound is heard. A patient oftendescribes the headache as “the worst headache ofhis life” or “as if the top of his head is being blownoff.” In patients with a history of headaches, includ-ing migraines, aSAH headache is typically different,

being more severe and associated with a feeling ofdoom. Patients with less severe hemorrhage may

present only with headache or with a headache ofmoderate intensity that may or may not be associ-ated with nonspecific symptoms, or with neck painAn aSAH headache can be difficult to assess inpatients with decreased levels ofconsciousness.

Symptoms of meningeal irritation, such as neckstiffness, photophobia, and low back pain, are

fairly common, as is nausea, vomiting and doublevision from an increase in ICP or meningeal irrita-tion. Depending on the vessel involved, aneurysmsize, aneurysm location, and resultant changes in

blood flow to brain parenchyma, focal neurologicaldeficits including hemiparesis may also be present.Approximately 10%–25% of patients may presentwith seizure because of a sudden increase in ICPor cortical irritation from blood, or both. An alteredlevel of consciousness, ranging from mild confusionto coma, is frequently present.

Approximately 10%–15% of patients with rup-tured aSAH report having prodromal symptoms in

the days or weeks prior to rupture. Prodromal signspresent 10–20 days prior to rupture and are presentin up to 50% of cases. The most common of thesesigns are headache (48%), dizziness (10%), orbitalpain (7%), diplopia (4%), and vision loss (4%). Otherless common prodromal signs include sensory ormotor disturbance (6%), seizures (4%), ptosis (3%),

bruits (3%), and dysphasia (2%). Jallo and Becske(2007) suggest that these premonitory signs andsymptoms either represent small sentinel leaks oraneurysm expansion.

Neurologic examination may demonstrate nuchalrigidity, meningismus, retinal hemorrhage, and toa lesser extent cranial neuropathy (most commonlythird [oculomotor] or sixth cranial [abducens] nerveinvolvement), or other localized neurologic deficitsuch as aphasia or hemiparesis. Ocular hemorrhage,papilledema, and hypertension may also be present.Many of these findings are clues to the underlyingarea of brain involved.

There are three prognostic scales widely usedas adjuncts for treatment decision making in theSAH population: (1) the Hunt and Hess classifica-tion scale, (2) the World Federation of NeurologicalSurgeons subarachnoid hemorrhage grading scale,

and (3) the Fisher grading scale. The patient’slevel of consciousness is a cardinal determinantin outcome in the first two scales. The Hunt andHess classification scale classifies patients basedon initial presentation (see Table 1). The WorldFederation of Neurological Surgeons subarachnoidhemorrhage grading scale has better outcome pre-dictive power, especially in high-grade patients(Table 3). The Fisher grading scale is based on

Note. Copyright © 2007 by eMedicine.com. Reprinted with permission.

Figure 3. Common Aneurysm Locations Within theCircle of Willis


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initial computed tomography (CT) scan findingsand specifically predicts risk of cerebral vasospasm(Table 2). These grading systems—in addition toinformation such as age and medical conditionof the patient, aneurysm size and location, acces-sibility of the aneurysm, presence of a clot, patientwishes, and institutional experience—are usedin making clinical decisions regarding treatment

(Class I, Level 2; Bederson, et. al, 2009).D. Diagnostic Studies There are three categories for common diagnostic

studies for aSAH: (1) tests to identify subarachnoid blood; (2) tests to identify aneurysm presence, size,and location; and (3) tests that monitor for cerebraledema and cerebral vasospasm and for further bleed-ing and tissue damage (i.e., stroke). The followingsection describes tests used to identify subarachnoid

blood and identify aneurysm presence, size, andlocation; however, the same tests may be used laterin the patient’s stay to monitor for further bleeding,cerebral edema, cerebral vasospasm, and stroke.

1. CT scanNonenhanced brain CT scan is consideredthe first study of choice in the initial evalua-tion of patients presenting with suspected SAH(aneurysmal, traumatic, or other cause) withsensitivity approaching 98% with modern CTscanners when performed within 24 hours ofsymptom onset. Films should be read by a neu-ro expert (e.g., neuroradiologist, neurosurgeon,or neurologist experienced in diagnosing SAH;Class I, Level 2; Bederson, et al., 2009) for subtlefindings such as subarachnoid blood in the pos-

terior horns, Sylvian fissure, and sulci. Failure toundergo an initial head CT in suspect patients isone of the risk factors in misdiagnosis of aSAH(Kowalski et al., 2004). CT scans use X-ray technology to characterizedensity within the cranial vault. Substances withincreased density appear lighter on the CT scan,and less dense substances appear darker. There-fore, bone and blood appear white and cerebro-spinal fluid (CSF) appears black on the CT scan.SAH blood on the CT scan appears as a high-attenuating and formless matter in the subarach-noid space around the brain, thus making what

would normally be dark appear white. This effecttypically appears as a white star shape in the cen-ter of the brain (Figure 4).

The location of blood within the subarachnoidspace correlates with the location of the aneurysmin 70% of cases. Generally, blood that is localizedto the basal cisterns, the Sylvian fissure, or theinterhemispheric fissure indicates rupture of a sac-cular aneurysm. Blood found over the convexities

or within the superficial parenchyma of the brainoften is indicative of arteriovenous malformation

(AVM) or mycotic (from an infectious process) an-eurysm rupture.

Intraparenchymal hemorrhage may occur withmiddle-communicating artery and posterior-communicating artery aneurysms, whereas inter-hemispheric and intraventricular hemorrhages areoften seen with anterior communicating artery an-eurysms. The outcome is worse for patients withextensive clots in basal cisterns than for those witha thin, diffuse hemorrhage. Over the cerebral hemispheres, SAH blood ismost conspicuous the first 24 hours after hemor-

rhage. Decreased visualization of the normallyhypoattenuating fluid within the sulci and bas-al cisterns and enlargement of the ventricles may

be signs of a communicating hydrocephalus. Theamount of SAH is evaluated by the Fisher gradingscale, which was initially formulated to predictthe risk of cerebral vasospasm but also has prog-nostic value in predicting overall patient outcome(Table 2). A Fisher grade ≥3 is robustly associatedwith the likelihood of developing vasospasm.

A false-negative CT scan can result from se-vere anemia or small-volume SAH. If theCT scan is positive for possible SAH, fur-

ther imaging such as cerebral angiography,CT angiography (CTA), or magnetic resonanceangiography (MRA) will be required to charac-terize the hemorrhage source (see pages 12 &13). Extremely large aneurysms may be visibleon CT scans, but further testing to obtain moredetailed information about size and angle of theaneurysm as well as vessel involvement is usual-ly required for treatment.

Table 3. World Federation of Neurological SurgeonsSubarachnoid Hemorrhage Grading Scale

World Federationof NeurologicalSurgeonsSubarachnoidHemorrhageGrading Scale

Glasgow ComaScale Score Motor Deficit

I 15 Absent

II 14–13 Absent

III 14–13 Present

IV 12–7 Present or absent

V 6–3 Present or absent

Note. From “Report of the World Federation of Neurological Surgeons Committee on aUniversal Subarachnoid Hemorrhage Grading Scale,” by C. G. Drake, 1988, Journal ofNeurosurgery, 68, pp. 985–986.


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2. Lumbar puncture

If imaging studies such as noncontrast CT arenegative in the presence of strong clinical suspi-cion of an aSAH, a lumbar puncture (LP) should

be performed to confirm the diagnosis (Class I,Level 2; Bederson, et al., 2009). A CT scan shouldalways be performed prior to the LP to rule outany significant intracranial mass effect or obvi-ous intracranial bleed. LP is contraindicated inthe presence of mass effect, obvious intracranial

bleed, and in cases where there is an increase inICP because of the risk of potential herniation.

A lumbar puncture involves the insertion ofa large bore needle into the subarachnoid space between the lumbar vertebrae. CSF is drainedfrom the spinal column and analyzed for bloodcells. Presence of xanthochromia (yellow-tingedCSF caused by the breakdown of hemoglobin)is very suggestive of a diagnosis of SAH (sensi-tivity greater than 99%). Xanthochromia may bepresent as early as 6 hours following SAH andremains detectable until about 2–3 weeks afterhemorrhage. LP is most sensitive 6–12 hours af-ter symptom onset. When gross blood is present,as from a traumatic spinal tap and not an SAH,

there should be a successive decrease in blood insuccessive specimen tubes. It is important if re-lying on visual inspection for xanthochromia,instead of spectrography, that the correct lightand a white background be used to fully appre-ciate any discoloration. The increase in CSF red

blood cells (RBCs) related to a traumatic LP andpain to the patient during the procedure makeLP a less commonly used method for diagnosing

SAH. If the CSF reveals evidence of SAH, eitherovert hemorrhage or xanthochromia, a cerebralangiography, CTA, or MRA should be performed.

3. Cerebral angiogramAfter the diagnosis of SAH is confirmed, a cere-

bral angiography is performed to visualizethe cerebrovascular anatomy; identify the loca-tion, size, and shape of the aneurysm; establish

the orientation of the aneurysm dome and neck;determine the relationship of the aneurysm tothe parent artery and perforating arteries; andto establish the presence of multiple aneurysms(Class I, Level 2; Bederson, et al., 2009). Newerthree-dimensional rotational angiography, whichallows for 360° imaging that can be rotated inthree-dimensional space, is particularly helpful inproviding a more accurate depiction of the aneu-rysm than two-dimensional films.

Despite development of diagnostic testing,cerebral angiography—with its high degreeof accuracy—remains the gold standard in

determining the presence and location of an in-tracranial aneurysm. Cerebral angiography is aninvasive procedure with a small but significantrisk of complications, including perforation of thevasculature and hemorrhage from the catheter in-sertion site. A cerebral angiogram is a procedurewhere a catheter is inserted into the femoral ar-tery in the groin and guided up into the cerebralvasculature. After the catheter is in the cerebralvasculature, a radiographic, iodine-based dye isinjected into the catheter. The dye is held in thevasculature, and X rays are taken that permit

visualization of the vasculature. An unsecured an-eurysm fills with dye-infused blood and appearsas an opaque, dark bulb on the X ray (Figure 5).Cerebral angiography has a small, false-negativerate, so another cerebral angiogram must be re-peated within 10–14 days if the initial angiogramis negative.

4. CTAMany hospitals now have the capabilities to per-form computed tomography angiogram (CTA).Because of the risk associated with cerebralangiography, CTA was developed as a nonin-vasive test to visualize the cerebral vasculature

and identify size and location of a cerebral aneu-rysm. A baseline CT scan is obtained, and a dyeis injected. An additional CT scan is obtained asthe dye is filling the cerebral blood vessels. Thestrength of the signal is stronger in the blood ves-sels where the dye-filled blood exists. Computerprocessing by either a neurosurgeon or neuro-radiologist removes static from bone and otherstructures leaving a clear, three-dimensional

Note. Copyright © 2007 by Michael Horowitz, MD. Reprinted with permission.

Figure 4. CT Scan Showing Subarachnoid Blood


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figure of the blood vessels. The dye-filled aneu-rysm is easily identified in the three-dimensionalfigure. CTA can be easily performed immediate-ly after a noncontrast CT scan and is becominga routine test in the work-up of patients with sus-pected SAH or aneurysm. CTA has the advantagesof being noninvasive with the sensitivity andspecificity approaching that of cerebral angiog-raphy (Jayaraman et al., 2004), especially inlesions greater than 3 mm; however, the comput-

er processing required when obtaining imagesintroduces potential error. CTA can be useful inplanning interventional procedures such as coil-ing or surgery.

5. MRI and MRAUse of magnetic resonance imaging (MRI) isgaining popularity in identification of aneurysmsafter aSAH. However, because blood can be moredifficult to distinguish on MRI and because of thelack of sensitivity, availability, and increased costof MRI compared to CT, it is rarely performedas a first-line test, but exceptions to this rule aregrowing. MRI is similar to CT; both use radiant

energy that is directed at the patient. MRI dif-fers in that it uses radio frequency pulsing ratherthan an X ray. The radio frequency pulse excitesthe hydrogen ions and then can be measured aschanges in the corresponding emanating radiofrequency pulses. A patient is placed in a magnetto align the protons of the hydrogen atoms, anda radio frequency (RF) is administered. Signalintensity is measured at a time interval, known

as time to echo (TE), following RF administra-tion. The RF pulse is administered many times ingenerating an image. The time to repetition (TR)is the time between these RF pulses. Signals char-acteristic of intracerebral hemorrhage dependon hemoglobin degradation. Deoxyhemoglobinis the MRI substrate for demonstration of blood

because of its paramagnetic properties causing

signal loss on susceptibility-weighted sequences.The two basic MRI sequences in common us-

age are T1- (short TE and TR) and T2- (long TE andlong TR) weighted images. Other MRI sequences incommon usage include fluid-attenuated inversionrecovery (FLAIR) and susceptibility- and diffusion-weighted imaging. Diffusion-weighted imaging isvalued for its ease of interpretation because isch-emia appears as a bright, white light against a darkgray or black background. MRI can be helpful when angiography find-ings are negative, in patients with multipleaneurysms, in bleeds that are several days old,

and for identifying small infarcts. In some cas-es, MRI may provide greater sensitivity thanCT in detecting small areas of subarachnoid clotand in helping to determine the particular lesionresponsible. FLAIR imaging is particularly use-ful for demonstrating early or subtle T2 signalchanges such as changes associated with edema.Diffusion-weighted MRI is extremely helpful indetecting early ischemia and stroke.

MRA provides a noninvasive means of exam-ining blood flow in the intra- and extracranialvasculature and may be performed in cases where

the angiogram failed to show the etiology of theaneurysm (e.g., in dissection, AVM, delayed im-aging, or when a patient cannot undergo CT orconventional angiography; Level 2; Bederson, etal., 2009). In general, MRA is still considered lesssensitive than catheter angiography, especiallyin its ability to detect posterior inferior com-municating artery and anterior communicatingartery aneurysms, but this technology is rapidlyevolving.

Gadolinium is the contrast agent used in MRA.Gadolinium-enhanced images are usually ac-quired with a T1-weighted sequence. There is no

cross-reactivity between contrast used for CT andgadolinium. Gadolinium does not have the neph-rotoxicity of iodinated contrast used in CTA andconventional angiography. MRI or MRA may on-ly be safely used in the absence of metal objects(foreign bodies, plates, and screws) and pacemak-er and defibrillator devices. Some people withclaustrophobia cannot tolerate MRI.


Figure 5. Angiographic Film Showing Cerebral Aneurysm BeforeTreatment


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E. Treatment of Aneurysm Initially, treatment of the aSAH patient is focused

on preventing rebleeding of the aneurysm.Although there are many nursing interventionsdesigned to prevent rebleed of the aneurysm (seepages 14–17), securement of the aneurysm is para-mount. Newer surgical and endovascular thera-peutics options have significantly changed the

approach to aSAH management. Definitive treat-ment is recommended as soon as possible, espe-cially for good-grade patients (i.e., patients withlow Hunt and Hess scores or low Fisher grade onadmission). Use of an accepted grading system,such as the Hunt and Hess or Fisher Scale, to deter-mine the degree of neurological impairment can

be useful for prognosis and triage (Class IIa, Level2; Bederson, et al., 2009). The two primary optionsfor aneurysm treatment include (1) craniotomy andaneurysm neck clipping and, less commonly, wrap-ping or ligation and (2) endovascular coiling.

Surgery requires an incision and removal of bone.

After the bone has been removed, the temporal lobecan be separated from the parietal and frontal lobealong the Sylvian fissure. Separation of the lobesprovides a window through which the aneurysm isvisualized. When the aneurysm can be clearly seen,a surgical clip is attached at the base of the aneu-rysm (where it bulges away from the blood vessel).Application of the surgical clip prevents bloodfrom entering the aneurysm and rebleeding. Whenthe surgical clip is in place, the dome of the aneu-rysm is punctured or excised, and the aneurysm ismonitored shortly to assure no more blood is enter-ing the aneurysm. Many aneurysms are either in aposition that is difficult to reach via craniotomy, asin aneurysms in the posterior circulation, or havea very broad base (or neck) that is not amenableto clip placement. Surgical clipping of an aneu-rysm is still a surgical procedure and, as such, hasinherent risks. Risks from surgical aneurysm clip-ping are similar to risks associated with any other

brain surgery and include infection, cerebral edema,pneumocephalus, and risks associated with admin-istration of general anesthesia.

Coil embolization, developed in 1991 as a min-imally invasive, nonsurgical method of securing

aneurysms, was approved in 1995 by the U.S. Foodand Drug Administration and represents a signifi-cant and rapidly evolving advancement in the care ofthe aSAH patient. Coil embolization involves cere-

bral angiographic techniques to guide a catheterto the location of the aneurysm. Platinum coils areattached to the end of a guide wire and advancedthrough a microcatheter into the dome of the aneu-rysm, where they are detached. Coils are packed

into the aneurysm until it is filled. After the aneu-rysm is filled with coils, blood can no longer enterthe aneurysm, and it is considered secure. The

blood in the aneurysm where the coils are placedwill clot and solidify, but there is no additional

blood entering the aneurysm, and there is no fur-ther risk of rebleed. Newer techniques includeadjuvant use of stents as well as balloons for assist-

ing with broad-neck aneurysms. Although this is aminimally invasive procedure and does not have therisks related to craniotomy, coil embolization has thesame risks as cerebral angiography—primarily perfo-ration of vasculature and bleeding from the catheterinsertion site. Currently, both methods are safe andeffective when performed by experienced, qualifiedpersonnel; however, endovascular coiling is associ-ated with improved outcome and is the preferredmethod for post-circulation, cavernous segment,and internal carotid artery aneurysm (Bederson,et al., 2009). In cases where both surgical clippingand endovascular coiling are potential therapeutic

options, endovascular coiling is the preferred meth-od of aneurysm securement (Level 2; Molyneux etal., 2002); however, there is still controversy regard-ing this subject. Early treatment reduces the risk ofrebleeding and is probably indicated in the majorityof cases (Level 2; Bederson, et al., 2009). See Figure6 for an angiogram showing an aneurysm pre- andpostcoiling.

Beginning 24–48 hours after hemorrhage, cerebral edema often develops increasing risk of pooroutcome if a surgical intervention is attempted. Inaddition, risk of cerebral vasospasm dramatical-ly increases 48–96 hours after hemorrhage. Surgicalintervention on a patient experiencing even mildcerebral vasospasm greatly increases risk of tissuedamage and stroke after surgery. For these reasons,a patient whose aneurysm is not secured in the firstfew days after aSAH may not be eligible for surgi-cal securement for several days. Nursing care of thepatient with an unsecured aneurysm is commonin the first 1–2 days after hemorrhage; however,specific portions of this care may be required forlonger periods of time in patients who have delayedsecurement of the aneurysm.

IV. Patient CareA. Preaneurysm Securement1. Assessment

Upon admission of the patient to the intensivecare unit (ICU), hourly neurologic exam checks(including a complete neurologic exam, NationalInstitutes of Health Stroke Scale, Glasgow ComaScale, and hemodynamic monitoring) are per-formed and compared to baseline to detect earlydeterioration because of aneurysmal rebleed,


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acute hydrocephalus, ischemia related to inad-equate cerebral perfusion (from early cerebralvasospasm or other causes), or other medicalcomplications.

2. Airway and oxygenationIntubation and mechanical ventilation may beindicated for patients with decreased mentalstatus, compromised airways, or acute lung inju-ries from subarachnoid hemorrhage (SAH; e.g.,neurogenic pulmonary edema), aspiration, or aGlasgow Coma Scale motor score of withdrawal.

Modes of ventilation vary, especially in patientswho have pulmonary complications following SAH.The goal is to maintain adequate oxygenation andventilation without compromising both intrac-ranial and cerebral perfusion pressures. Positiveend-expiratory pressure of 5 cm H20 may be usedcautiously in the aSAH patient; however, it doesdecrease blood pressure (BP) and may lead tocerebral ischemia (Level 2; Meunch et al., 2005).Pressure-controlled ventilation should be consid-ered if the patient has significant aspiration orearly acute respiratory distress syndrome.

Patients recovering from aSAH are critically

ill patients at risk for many common secondaryinjuries such as atelectasis and pneumonia. Hour-ly monitoring of breath sounds and frequent deep

breathing should be encouraged. Coughing is dis-couraged in the SAH patient before aneurysmsecurement because of the increased risk of aneu-rysm rupture with the increased ICP and BP thatoccurs during coughing.

3. BP managementThe exact relationship between aneurysmal rebleedand BP remains to be identified; however, most cli-nicians agree that to prevent rebleed, BP control isachieved before aneurysm securement. Systolic BPis kept between 90 and 140 mm Hg before aneu-rysm securement (Level 3; Suarez et al., 2006).There are a variety of vasoactive agents used tomaintain BP within an acceptable range. Choiceof vasoactive agent and BP target range variesdepending upon institutional policy (i.e., policy and

procedures) and managing clinician preference.Some institutions require clinicians to followsystolic BP, and other institutions follow meanarterial pressure. Typically, BP is maintainedwithin the target range using an initial bolus fol-lowed by commencement of an intravenous (IV)drip that is titrated to maintain BP within thetarget range (Level 2; Kraus, Metzler, & Coplin,2002). Use of sublingual agents that may cause arapid drop in BP is not recommended. BP should

be lowered in a controlled manner as a suddendrop in BP increases the risk of cerebral ischemia.

Hypotension occurring before aneurysm

securement places the patient recovering fromaSAH at risk for ischemia. Hypotension should

be treated with rapid IV fluid replacement begin-ning with isotonic saline (0.9%) and colloids asnecessary. For persistent hypotension, IV vaso-pressors should be instituted.

4. Intracranial pressure monitoringWhen a patient shows symptoms of increas-ing ICP, or is at increased risk of increased ICP

Figure 6. Cerebral Angiogram Showing an Aneurysm (A) and the Same Aneurysm Postcoiling (B)

Note.

Copyright © 2007 by Michael Horowitz, MD. Reprinted with permission.

A B


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because of large blood load, an external ventric-ular catheter or subarachnoid bolt is inserted.This can be done in the operating room (duringsurgical clipping or as a separate surgical proce-dure) or emergently at the bedside to decreaseICP. Poor clinical grade on admission, acute neu-rologic deterioration, or progressive enlargementof ventricles on CT scan are clear indications for

the use of an external ventricular device (Level 2; Mayberg et al., 1994; Rordorf, Ogilvy, Gress, Crow-ell, & Choi, 1997; Suzuki, Otawara, Doi, Ogasawara,& Ogawa, 2000). Newer data suggest that externalventricular drainage does not include likelihoodof aneurysm rehemorrhage when drainage isperformed at moderate pressures (38.3 °C or as

per institutional policy), fever reduction should be achieved with administration of acetamino-phen every 4–6 hours to achieve normothermia(Level 3; Suarez et al., 2006). Surface or intra-vascular cooling is instituted to maintaintemperature


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to a speech pathologist to evaluate swallowingcapability and aid in diet-type selection is recom-mended for any patient whose ability to swallow isin question.

Although there is significant ongoingresearch to identify ideal glycemic control inICU populations, no specific guidelines areroutinely applied to the aSAH population.

Hyperglycemia has been found to be associatedwith increased risk of morbidity and mortality fol-lowing aSAH, therefore, serum glucose should bekept within the range of 80–120 mg/dl with insulininfusion if necessary (Level 3; Suarez et al., 2006).

9. ActivityTypically, activity is limited in patients with anunsecured aneurysm. All activities that increaseBP (and, therefore, ICP) are limited to preventrebleed. The patient should be maintained ina quiet environment with limited visitors untilafter aneurysm securement (Level 3; Suarez et al.,2006).

10. Deep vein thrombosis prophylaxisBecause of limited mobility, patients with anunsecured aneurysm are at risk for deep veinthrombosis (DVT). In these patients, thigh-highstockings and pneumatic (sequential) compres-sion devices should be implemented as soon aspossible (Level 3; Suarez et al., 2006). Anticoag-ulants (e.g., heparin) should be avoided untilafter aneurysm securement (Level 3; Suarez et al.,2006).

11. Medicationsa. Seizure prophylaxis

The administration of prophylactic anticon-vulsants may be considered in the immediatepost-hemorrhagic period (Level 2). The routinelong-term use of anticonvulsants is not recom-mended (Level 2) but may be considered forpatients with risk factors such as prior seizure,parenchymal hematoma, infarct, or middlecerebral artery aneurysms (Level 2; Bederson,et al., 2009).

Controversy exists on the need for andlength of anticonvulsant therapy in patientswithout a history of seizures because someanticonvulsants have been associated with

poor outcomes, and the percentage of aSAHpatients developing seizures is small (Level2; Naidech et al., 2005). If using anticonvul-sants, use those that do not change the level ofconsciousness.

b. Stool softenersStool softeners are initiated. The patient withan unsecured aneurysm should not strain tohave a bowel movement, and stool softeners

maintain soft stool so straining is not required(Level 3). For patients able to take oral nutri-tion, a high-fiber diet is instituted. For patientson parenteral nutrition, a high-fiber feeding isinstituted.

c. Pain managementHeadache pain is usually intense after aSAH.Analgesics are administered as needed for

pain. Pain causes increased BP, heart rate, andanxiety. All of these can increase risk for aneu-rysmal rebleed and, therefore, must be treated(Level 3). Use short-acting and reversible med-ications when possible.

d. SedativesAgitation can lead to increases in activity, dis-lodging of catheters, and aneurysmal rebleed.Sedation is administered as needed to patientswho are agitated. A short-acting sedativeshould be used to facilitate frequent neuro-logic exams free of sedatives. It is not alwayspossible to obtain a neurologic exam free of

sedatives, but use of short-acting sedativesincreases this likelihood.

e. AntiemeticsPrevention and treatment of nausea and vom-iting are also important for the aSAH patient,

both before and after aneurysm securement,especially during the first 24 hours. Vomit-ing increases ICP and can cause aneurysmalrebleed. Patients with nausea should receivean antiemetic routinely.

f. Gastrointestinal hemorrhage prophylaxisHistamine-receptor antagonists or pro-ton pump inhibitors are instituted toprevent ulcer formation and gastrointestinalhemorrhage.

12. PsychosocialAlleviate anxiety by explaining procedures andICU routine to patients and families. Incorporatea multidisciplinary approach, including pasto-ral care and social work, to address the patients’needs.

B. Postaneurysm Securement1. aSAH patient in the ICU

After the aneurysm has been secured, many ofthe previous care guidelines are maintained;

however, some adjustments should be made.a. AssessmentTypically, monitoring of neurologic examand vital signs are performed every hourafter surgery or embolization. If the patientremains stable, exam and vital-sign assess-ment are decreased to every 2 hours and asnecessary. Serial complete neurological assess-ment, including level of consciousness, cranial


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nerve assessment, and motor exam performedat the bedside, detects subtle changes fromthe patient’s baseline status. Any changes inneurologic exam are reported to the attend-ing physician, resident, or nurse practitionerimmediately. Initial assessment will iden-tify changes related to surgery or possiblerebleeding of the aneurysm, cerebral edema,

or increasing ICP. Continued assessment isvital to optimize outcomes in this population

because cerebral vasospasm is a common sec-ondary sequelae to aSAH and develops verysuddenly. Prompt identification of changesin neurologic exam initiates further testing todetermine cause of the change and interven-tion, thereby preventing long-term damage tothe brain.

b. Airway and oxygenationFor patients who do not require intubation andmechanical ventilation, frequent assessmentof airway patency and oxygenation contin-

ue. Along with hourly vital-sign assessment, breath sounds are auscultated. Any chang-es in breath sounds should be reported to theattending physician, resident, or nurse prac-titioner immediately. Proper oxygenation isnecessary to prevent hypoxia and cerebral isch-emia. Suctioning may be performed as neededfor short intervals with appropriate hyperoxy-genation provided prior to suctioning in apatient recovering from aSAH after the aneu-rysm has been secured.

c. BP managementWhen the aneurysm is secure, an increase in BPis permitted. Maintaining the systolic pressureat less than 200 mm Hg has been recommend-ed (Level 3; Suarez et al., 2006). The targetrange for ideal BP after aneurysm securementhas not been thoroughly defined; however, thegoal of BP management is to maintain perfu-sion of brain tissue and prevent ischemia.

d. ICP monitoringIn many patients recovering from aSAH, ICPmonitoring will continue after securement ofthe aneurysm. Any patient at risk for increasedICP should have continued ICP monitoring.

Prolonged elevations in ICP are associatedwith decreased cerebral perfusion pressure andincrease the risk of cerebral ischemia and pooroutcome (Level 2; Mayberg et al., 1994; Rordorfet al., 1997; Suzuki et al., 2000).

e. Fever managementIn febrile patients (temperature ≥38.3 °C or as perinstitutional policy), fever reduction is achievedwith administration of acetaminophen every

4–6 hours to achieve normothermia (Level 3;Suarez et al., 2006). Surface or intravascularcooling is instituted to maintain temperature


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al., 1982; Muizelaar & Becker). Vigilant moni-toring of patients is warranted because triple Htherapy includes complications such as myocar-dial injury, pulmonary edema, hyponatremia,cerebral edema, and bleeding of unsecuredaneurysm (Awad et al.; Janjua & Mayer; Kassellet al., 1982; Mocco, Zacharia, Komotar, & Con-nolly, 2006; Muizelaar & Becker; Solomon, Fink,

& Lennihan, 1988; Treggiari-Venzi et al., 2001).Although not yet used as a standard of care inall facilities, invasive monitoring, such as a pul-monary artery catheter, is warranted in patientswith cardiac dysfunction to adequately monitorand treat the patient recovering from an aSAH(Level 3; Mayer et al., 2005; Suarez et al., 2006).See Figure 7 for an angiogram showing cerebralvasospasm before and after treatment (see pag-es 18 & 21–23 for treatment of the patient withcerebral vasospasm).

h. NutritionPatients recovering from aSAH must be

screened for ability to swallow prior toreceiving any food, fluid, or medication

by mouth. A validated bedside screen thatincludes a water test should be used. A for-mal swallow evaluation from a speechtherapist should be obtained if there are anyquestions about the patient’s ability to safeyswallow. After it has been determined thatswallowing is normal, the patients’ usu-al diet with increased fiber may be followed.Patients with impaired swallowing shouldhave a diet prescribed by the speech therapistto prevent aspiration.

i. ActivityAfter the aneurysm has been secured, patientsgradually increase activity. Physical andoccupational therapists are consulted post-operatively when patients are stable.

j. DVT prophylaxisThigh-high stockings and pneumatic (sequen-tial) compression devices are maintainedpostaneurysm securement (Level 3; Suarez etal., 2006). When the aneurysm has been secured,heparin therapy for prevention of DVT may beconsidered. Additional factors, such as future

need for surgery or angiography, are weighedinto the decision to institute heparin therapy.k. Medications

(1) Anticonvulsants—If seizures have occurredor the patient is at higher risk for seizuredevelopment, prophylaxis is maintained. Ifusing anticonvulsants, use those that do notchange the level of consciousness.

(2) Stool softeners—Stool softeners should becontinued because narcotics, other medica-tions, and decreased physical mobility and

bowel motility may cause constipation.(3) Sedation—Sedation may be warranted par-

ticularly in patients who are intubated, haveICP monitors and central lines, or both.

(4) Antiemetics—Use of antiemetics may be

continued as needed.(5) Cerebral edema treatment—In patients

with cerebral edema, 2% or 3% hyperton-ic saline may be administered at a rate of


Figure 7. Angiogram Showing Cerebral Vasospasm (A) andAngiogram Showing Cerebral Vessels After Being Treated forCerebral Vasospasm (B)

A

B


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75–150 cc/hr unless contraindicated (Level2; Suarez et al., 1999). Frequent electro-lyte monitoring is indicated at least every6 hours. Monitor and replace potassium tomaintain normal levels. Monitor serum sodi-um to a goal of 145–155 meq/L and serumosmolarity 300–320 mOsm/L levels. Noti-fy the provider on call if the serum sodium

is >155 meq/L. Hypertonic saline therapy can be tapered slowly if no longer indicated (i.e.,improving mental status or cerebral edema orthe serum sodium rises to dangerous levels>155 meq/L; Level 2; Suarez et al., 1999).

(6) BP treatment—A variety of pharmacologi-cal agents may be used to maintain BPwithin the target range. See page 18 fortreatment of BP.

(7) Calcium channel blockers—Nimodipine(Nimotop), a calcium channel blocker, is theonly drug currently approved by the FDAfor the prevention and treatment of vasos-

pasm following aSAH. Nimodipine crossesthe blood–brain barrier and inhibits calciumentry into cells, subsequently reducing thecontractile state of the vascular smooth mus-cle. It is indicated to reduce the incidenceand severity of delayed ischemic deficitsfrom vasospasm following aSAH and has

been shown to improve outcomes followingaSAH despite a lack of evidence of arterio-graphic efficacy (Level 1; Allen et al., 1983;Neil-Dwyer, Mee, Dorrance, & Lowe, 1987;Petruk et al., 1988; Philippon et al., 1986; Pic-kard et al., 1989). Solomon and colleagues(1988) proposed that the improved outcomewith nimodipine was related to it inhibitingcalcium entry into ischemic neurons, there-

by increasing viability of these cells. Oralor enteral administration of 60 mg of nimo-dipine every 4 hours is instituted within 96hours after hemorrhage and continued forup to 21 days.

l. Other tests and treatmentsSeveral tests are used to monitor for presenceof cerebral vasospasm. Transcranial Doppler(TCD) ultrasonography uses ultrasound waves

projected through a thin spot in the skull tothe cerebral blood vessels. The ultrasoundwaves bounce off of the RBCs as they flowthrough the cerebral blood vessel. A decreasein the internal lumen of the blood vesselrequires the blood (and hence, the RBCs) tomove at a higher velocity. Although TCDultrasonography is not sensitive or specificenough to use to diagnose cerebral vasospasm,

it is a noninvasive diagnostic tool that can beused in conjunction with neurologic exam andother diagnostic tests to manage the aSAHpatient. TCD ultrasonography has severallimitations. It is only as good as thetechnologist performing the exam, so a neu-rophysiologist should be consulted wheneveravailable. There are multiple physiologic

states that will increase blood flow, thereby increasing blood velocity. Independent ofneurologic exam, TCD can consistently mea-sure MCA mean velocities and can detectincreasing mean MCA velocities. MCA flowvelocities 200 cm/secrespectively have a strong negative and posi-tive predictive power for determining whichpatients will develop ischemic deficits (Lev-el 3; Aaslid, Huber, & Nornes, 1984). Someclinicians and institutions prefer to moni-tor patients using the Lindegaard index. TheLindegaard index was developed to predict

cerebral vasospasm using TCD. It is calcu-lated as mean MCA velocity/mean ICA velocity.A Lindegaard index ≥3 is indicative of MCAvasospasm and ≥6 as severe vasospasm (Level2; Aaslid et al.; Lee et al., 1997; Lindegaard,Nornes, Bakke, Sorteberg, & Nakstad, 1988).TCD velocity associated with a decrease inneurological function, or independently incomatose patients, can be used as a prelim-inary screening method to identify patientsrequiring further intervention (i.e., CT scan orcerebral angiogram).

Cerebral angiography is the gold standardfor diagnosing cerebral vasospasm. The pro-cedure is the same as described on pages 12 &13 for aneurysm identification. The angiogramprovides a clear visualization of the cerebral

blood vessels, and a decrease in lumen sizeis indicative of cerebral vasospasm. Variationin the decrease in lumen size also quantifiesseverity of cerebral vasospasm. A blood ves-sel with a significant decrease in lumen sizerequires intervention.

In patients with symptomatic vasospasm, itis often managed with triple H therapy. More

severe symptomatic vasospasm requires moreaggressive treatment. Endovascular therapiesfor refractory vasospasm include both intra-arterial vasodilators and mechanical dilatationof vessels with balloon angioplasty. The deter-mination of which of these therapies to useis an individual decision and depends uponthe patient’s general health and severity ofvasospasm. Papaverine is a widely used agent


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(Fandino, Kaku, Schuknecht, Valavanis, &Yonekawa, 1998; Kaku, Yonekawa, Tsukahara,& Kazekawa, 1992; Polin, Hansen, German,Chadduck, & Kassell, 1998; Sawada et al.,1997), although, there is preliminary evidencethat verapamil (Feng et al., 2002), nicardipine(Kasuya, Onda, Sasahara, Takeshita, & Hori,2005; Kasuya, Onda, Takeshita, Okada, & Hori,

2002), nimodipine (Biondi et al., 2004; Hui& Lau, 2005; Tanaka et al., 1982), and fasudilhydrochloride (Tachibana et al., 1999; Tanaka,Minami, Kota, Kuwamura, & Kohmura, 2005)may be of benefit (Level 2). A review of intra-arterial treatment of cerebral vasospasm andmechanisms of action of these drugs was pro-vided by Sayama, Liu, and Couldwell (2006).

For patients at risk for or with known cerebral vasospasm, more aggressive treatmentshould be used. Patients without symptoms

but with elevated TCD velocities or CT evi-dence of diffuse cerebral vasospasm require

at least a central venous catheter, repletionwith crystalloids, and the above end pointsfor volume resuscitation (CVP ≥8 and urineoutput ≥250 ml/hr). CVP monitoring is indicat-ed at least every 2 hours. Treatment with fluidor albumin bolus to keep CVP >5 for normov-olemia or CVP >8 mm Hg for hypervolemia isindicated (Level 3; Mayer et al., 2005; Suarez etal., 2006). Hypervolemia is desirable in patientswithout underlying cardiac disease to main-tain adequate cerebral perfusion pressure (Level3; Mayer et al.). Antihypertensive and diureticagents should be avoided (Level 3; Mayer et al.).

For patients with a secured aneurysm andclinical evidence of cerebral vasospasm, moreaggressive therapy is instituted. If not yetperformed, cerebral angiography may beperformed to accurately diagnose and treatcerebral vasospasm (see page 20 for angio-graphic treatment of cerebral vasospasm).Pulmonary pressure monitoring may be indi-cated in patients with cardiac dysfunctionwith the goal of maintaining pulmonary arterywedge pressure >12 mm Hg and cardiac index>4.0 L/min (Mayer et al., 2005). If desired

effect is not attained, cerebral angiography forangioplasty or drug infusion may be under-taken if qualified personnel are available (seepages 12 & 20 for angiographic treatment).

2. Patient monitoring in the ICUa. Neurological

(1) Frequent neurological assessment is indi-cated with a minimum of at least everyhour or more frequently when patients are

actively ischemic.(2) For patients with external ventricular

drain or subarachnoid bolt, see Guide to theCare of the Patient with Intracranial Pressure

Monitoring: AANN Reference Series for Clini-cal Practice.

(3) Monitor TCD values including systolicvelocities, mean velocities, and Lindegaard

ratio and compare them to baseline andprevious values. Discuss elevations (meanMCA velocity >120 mm Hg or Lindegaardratio ≥3) with attending physician, resi-dent, or nurse practitioner promptly.

(4) Electroencephalography (EEG) is common-ly used to monitor for seizure activity inmany patients with neurological condi-tions. Continuous EEG is used to monitorpatients with unexplained neurologi-cal deterioration to detect nonconvulsiveseizures by providing information aboutglobal cerebral activity and cortical func-

tion (Wartenberg et al., 2002). Electrodesare placed at distinct positions around theskull, and brain activity is monitored. Typ-ical brain activity shows much variation inthe brain waves, while seizure activity isevidenced by rhythmic waves indicatingneurons firing in unison. In patients withcontinuous EEG, collaborate with the EEGtechnician to ensure that leads are in place.Monitor for clinical seizures.

(5) Repeat CT scans and cerebral angiogra-phy are common tests used to monitor thepatient recovering from aSAH. CT scans areroutinely performed postoperatively andpostcoiling and are warranted when thepatient’s clinical exam changes. Cerebralangiography should be obtained postop-eratively, postcoiling (to ensure aneurysmobliteration), and when clinical exam orTCDs suggest cerebral vasospasm.

b. Cardiovascular(1) Hemodynamic monitoring is obtained at

least every hour or more frequently whentitrating vasoactive agents. Monitor periph-eral pulses and troponin levels during

vasopressor infusion.(2) CVP monitoring is indicated at least every2 hours to keep CVP >5 for normovolemia orCVP >8 mm Hg for hypervolemia (Mayer etal., 2005).

(3) Pulmonary artery pressure monitoringis indicated in patients with cardiac dys-function, with pulmonary artery diastolicpressure kept >14 mm Hg or a cardiac


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index >4.0 L/min (Mayer et al., 2005). Someinstitutions have incorporated pulmonaryartery pressure monitoring as a standardof care for all aSAH patients, although theliterature is not clear on the efficacy of thispractice.

c. Respiratory(1) In patients requiring mechanical ventilation,

frequent arterial blood gases, pulse oxim-etry (SaO2) and end tidal CO2 (ETCO2) areindicated. Arterial blood gases should beobtained daily and with each change in ven-tilator settings. Continuous SaO2 or ETCO2 monitoring should be incorporated to main-tain SaO2 ≥90% or ETCO2 ≥35–37 mm Hg.

(2) Suctioning should be performed only as nec-essary to maintain clear lungs and limitedto 15 seconds, hyperoxygenating the patientprior to the procedure. Saline lavage prior tosuctioning should be avoided.

d. Gastrointestinal

(1) Abdominal assessment is indicated at leastevery shift.

(2) Nutritional support is obtained via tubefeeding if the patient is unable to takeorally.

e. Renal(1) Urine output is monitored precisely. A uri-

nary catheter is often warranted to assureaccurate monitoring.

(2) Urine electrolytes and specific gravityshould be monitored as these patients areat risk for CSW and the syndrome of inap-propriate antidiuretic hormone secretion(SIADH).

(3) It is important to be aware that patientsreceiving triple H therapy often have highurine output.

f. Integumentary(1) In patients on complete bed rest, skin

assessment is performed every shift.(2) Frequent turning (at least every 2 hours)

is performed for patients unable to movethemselves.

(3) Skin-care techniques are performed everyshift with the assessment.

g. Endocrine Tight glycemic control is to be maintained,using an insulin drip if necessary. Glu-cose should be monitored at least daily in allpatients recovering from aSAH. In patientsrequiring an insulin drip, glucose should beevaluated hourly until reaching the target

blood glucose (100–120 mg/dl) and thenevery 2–4 hours.

h. Psychosocial Social workers and pastoral personnel areconsulted to assist in alleviating concerns ofpatients and families. Social workers should alsocollaborate with the critical care team to identifyand facilitate appropriate after-discharge care.

i. Current research and future therapies(1) Pharmacologic therapeutics

(a) MagnesiumIntravenous magnesium sulfate(MgSO4) is currently being researchedfor its potential clinical use in the pre-vention and reversal of cerebralvasospasm. It is especially attractive

because it is readily available, inexpen-sive, and has been shown to be safe inhumans (Veyna et al., 2002). Magnesiumhas many neuroprotective mechanismsof action. It has cerebral vasodilatoryeffects (Pyne, Cadoux-Hudson, & Clark,2001), inhibits excitatory amino acid

release, and provides N-methyl D-aspar-tate receptor blockade (Lin, Chung, Lin,& Cheng, 2002; Nowak, Bregestovski,Ascher, Herbet, & Prochiantz, 1984). Pre-liminary studies in humans have showna significant reduction in cerebral vasos-pasm development (55%; Chia, Hughes,& Morgan, 2002) and delayed cerebralischemia (35%; van den Bergh et al.,2005) in patients randomized to receiveIV MgSO4. Current research is ongo-ing to determine therapeutic dosagesfor preventing cerebral vasospasm anddelayed cerebral ischemia while avoid-ing initiating side effects.

(b) StatinsSeveral small randomized clinical trials,consistent with animal research, havedemonstrated that the initiation of sta-tin therapy after aSAH to significantlyreduce the incidence of vasospasm anddelayed ischemic deficits, and slightlyreduce mortality. These studies sup-port the routine use of statins in the careof patients with aSAH (Sillberg, 2008).

However, Kramer and Fletcher (2009),in a recent review article, do not rec-ommend statin therapy in aSAH andreport no associated with improve-ment in neurological outcomes. Moreresearch is needed in this area.

(2) Advance neuromonitoring(a) Brain tissue oxygen monitoring

PtiO2 monitoring is a method to directly


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monitor brain tissue oxygenation.Currently, there is only one systemcommercially available—the Licox sys-tem (GMS-Integra; Kiel-Mielkendorf,Germany). It contains a polarograph-ic cell embedded in the catheter thatis placed in the brain tissue of inter-est. When oxygen passes through the

electrolyte chamber of the catheter,an electrical current is generated. Theelectrical current is then translatedinto tissue oxygenation. The samplingarea of the catheter is approximately14 mm2.

The catheter measures the tissue envi-ronment of a small portion of the brain.It is difficult to predict which area of

brain tissue is at highest risk of cerebralvasospasm; hence, there is not standard-ization as to where the catheter should

be placed in a patient recovering from

aSAH. Recent research suggests thatPtiO2 monitoring is a safe neuromonitor-ing device that accurately reflects tissueoxygenation (Lang, Mulvey, Mudaliar,& Dorsch, 2007). With future research,PtiO2 monitoring may be an excellentmethod to monitor for pending isch-emia in the aSAH population. Langand colleagues recently presented areview of literature surrounding thesafety and efficacy of these cathetersand their utility in neurocritical care.

(b) NeurochemistryFor cerebral application, the microdi-alysis technique allows clinicians toprecisely monitor brain chemistry bycontinuously monitoring biochem-ical markers of energy metabolismsuch as glucose, lactate, pyruvate,and lactate-pyruvate ratio; cell mem-

brane degradation such as glycerol; orexcitotoxic and other metabolic path-ways. A 10-mm catheter is insertedinto the region at risk for vasospasmin patients with subarachnoid hemor-

rhage (Ungerstedt & Rostami, 2004).The microdialysis catheter has asemipermeable membrane at the distalend which functions as a blood cap-illary. Standard catheters can measuremolecules of 20 kDa such as glucose,lactate, and pyruvate. When perfusionfluid is pumped at a rate of 0.3 µl/mininto the catheter, it flows through the

distal end of the membrane and equili- brates with the extracellular fluid. Aftersome time, the molecules will dif-fuse into the perfusion fluid. Recoveryof these molecules is about 70%. Themolecules are extracted hourly andanalyzed with the microdialysis ana-lyzer (CMA Microdialysis, Stockholm,

Sweden) at the bedside. Immediate bedside analysi

c a re o f t h e pat i e nt w i t h aneurysmal subarachnoid hemorrhage

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