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Mayo Clin Proc. April 2005;80(4):550-559 www.mayoclinicproceedings.com550

SUBARACHNOID HEMORRHAGE

From the Department of Neurology (E.F.M.W., E.M.M., J.R.F.), Department ofRadiology (D.F.K.), and Department of Neurologic Surgery (D.G.P.), MayoClinic College of Medicine, Rochester, Minn.

Individual reprints of this article are not available. The entire Symposium onCerebrovascular Diseases will be available for purchase as a bound bookletfrom the Proceedings Editorial Office at a l ater date.

2005 Mayo Foundation for Medical Education and Research

SYMPOSIUM ON CEREBROVASCULAR DISEASES

Subarachnoid Hemorrhage:Neurointensive Care and Aneurysm Repair

EELCO F. M. W IJDICKS , MD; D AVID F. K ALLMES , MD; E DWARD M. M ANNO , MD; J IMMY R. F ULGHAM , MD;AND DAVID G. P IEPGRAS , MD

Aneurysmal subarachnoid hemorrhage (SAH) is oft en a neurologiccatastrophe. Diagnosing SAH can be challenging, and treatmentis complex, sophisticated, multidisciplinary, and rarely routine.This review emphasizes treatment in the intensive care unit,surgical and endovascular therapeutic options, and the currentstat e of t reatment of major complicat ions such as cerebral vaso-spasm, acute hydrocephalus, and rebleeding. Outcome assess-ment in survivors of SAH and controversies in screening of familymembers are discussed.

Mayo Clin Proc . 2005;80(4) :550-559

CSF = cerebrospinal fluid; CT = computed tomography; MCA = middlecerebral art ery; SAH = subarachnoid hemorrhage

R upture of an intracranial aneurysm into the subarach-noid compartment immediately leaves patients incritical condition. Some patients do not receive care intime. Sudden death from a massive increase in intracranialpressure occurs in approximately 1 of 10 patients (with40% in a posterior circulation aneurysm), and another 10%to 20% of patients who arrive at the emergency departmentare comatose and need immediate respiratory support. 1,2 Atthe other end of the clinical spectrumand certainly morecommonlypatients present with acute excruciating head-

ache, confusion, or abnormal behavior. Because of thecomparatively infrequent presentation of subarachnoidhemorrhage (SAH) (approximately 1 in 10,000 Americansannually), physicians who encounter patients with SAH arenot attuned to its severity and may find recognizing its keycomponents difficult. 3

The care of a patient with aneurysmal SAH involves earlyrepair of the recently ruptured aneurysm. In most largerinstitutions, patients are admitted to a neurologic-neurosur-gical intensive care unit and receive aggressive care to pre-vent further deterioration, which can substantially affect out-come. We describe aspects of initial evaluation, neurologicintensive care, and methods of definitive repair. This care

involves a multidisciplinary team with immediate availabil-ity that can be provided only in tertiary care medical centers.

CHALLENGES IN DIAGNOSIS

A ruptured cerebral aneurysm causes an unexpected, sud-den headache and may lead to loss of consciousness. Pa-tients describe a thunderclap headache (an unfortunateterm because no sound is heard). The patient reports theworst headache of his or her life, more precisely, a split-second, extremely intense, and overwhelming headachethat fails to subside. Many patients report feeling as if thetop of my head is blown off or as though someone hit mein the head with a hammer, but these key elements in themedical history may be difficult to elicit in confused pa-tients. Rarely, there are other nonaneurysmal causes of thunderclap headache present. These disorders include pi-tuitary apoplexy, arterial dissection, cerebral venous throm-bosis, and hypertensive encephalopathy. Also, thunderclapheadache may be idiopathic. 4 In these conditions (otherthan SAH), computed tomography (CT) or results of ce-rebrospinal fluid (CSF) examination may be normal, inwhich case magnetic resonance imaging is indicated.

When the patient is seen hours after onset of symptoms,neurologic examination may reveal nuchal rigidity, cranialneuropathy (third or sixth cranial nerve most commonly),

or other localized neurologic deficit (aphasia, hemipare-sis); however, major neurologic signs generally are absent.Seizures may occur in a small percentage of surviving pa-tients, and epilepsy may develop in less than 10%, particu-larly in those who had a subdural hematoma or cerebralinfarction during their hospital course. 5 Subarachnoid hem-orrhage usually is graded by using the World Federation of Neurosurgical Societies grading scale, which is based onthe Glasgow Coma Scale (Table 1). Poor-grade SAH is de-fined arbitrarily as grade IV and V; when caused by rupturealone, immediate definitive treatment may be deferred, withmany neurosurgeons awaiting patient improvement. 6

Computed tomography is the first-line diagnostic proce-

dure in patients with suspected SAH (Figure 1). Histori-cally, CT has 90% to 95% sensitivity for recent SAH; withmodern CT equipment, sensitivity is closer to 98%. 7,8

On CT, an aneurysm is rarely seen but when presentindicates large size (>10 cm) (Figure 1). Examination of CSF is necessary when CT is normal and has been reviewedfor subtle areas of subarachnoid blood (posterior horns,sylvian fissure, and sulci). Prompt ascertainment of a diag-nosis of SAH is warranted because a ruptured aneurysm has

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Mayo Clin Proc. April 2005;80(4):550-559 www.mayoclinicproceedings.com 551


TABLE 1. Grading System Proposed by the World Federation ofNeurosurgical Societies (WFNS) for the Classification of

Subarachnoid Hemorrhage

WFNS Glasgow Coma Scalegrade score Motor deficit

I 15 AbsentII 14-13 AbsentIII 14-13 PresentIV 12-7 Present or absentV 6-3 Present or absent

FIGURE 1. Computed tomograms show blood in basal cisterns, sulci, and visible giantaneurysm of the anterior communicating artery (left) and basilar artery (right).

the highest rate of rerupture within the initial 48 hours.However, no evidence suggests that lumbar puncture in-creases the risk of aneurysmal rehemorrhage. Testing CSFfor the presence of xanthochromia, the yellow tinge in CSFcaused by the breakdown products of hemoglobin, is thegold standard for diagnosis of SAH, with a sensitivity greaterthan 99%. Xanthochromia is present as early as 6 hours afterSAH and along with bilirubin remains detectable until about2 to 3 weeks after SAH. 9,10 When gross blood is present in theinitial CSF specimen tube, a decrease in the quantity of redblood cells in successive specimen tubes is a frequently used(albeit unreliable) marker for the absence of SAH. (Themedicolegal implications can be substantial if cerebral an-giography is deferred on the basis of this loose criterion.)

Determining the presence of xanthochromia is the bestmethod to document disintegrated erythrocytes, but vialsshould be held against a bright light and white back-ground to appreciate the discoloration (Figure 2 11). Visualinspection is far from perfect, and, although used rarely inthe United States, spectrophotometry of CSF may docu-ment oxyhemoglobin or bilirubin if visual assessments of the vial with centrifuged CSF are conflicting. Bilirubinabsorbance at 473 is diagnostic (note that iodine usedduring the procedure may lead to a false-positive effect). 9

Once a diagnosis of SAH is confirmed, 4-vessel cerebralangiography is needed to identify and characterize thesource of hemorrhage. Noninvasive imaging techniquessuch as magnetic resonance angiography and CT angiogra-phy continue to improve and are being used for makingfundamental treatment decisions for intracranial aneurysm.

Three-dimensional rotational angiography allows volumet-

ric data acquisition during conventional catheter angiogra-phy (Figure 3). The technique is used routinely in manymedical centers. Its primary advantage over 2-dimensionalangiography is that it allows a better understanding of thecomplex relationships between aneurysm necks and adja-cent arteries. In some circumstances, angiography shouldbe repeated several weeks later to detect abnormalities notvisualized on earlier studies. One important entity thatneeds to be recognized is nonaneurysmal pretruncal (orperimesencephalic) SAH. 12-17 This type of hemorrhage hascertain CT characteristics (Figure 4), mainly with a focalclot in the front of the brainstem. The major concern is thepresence of a posterior circulation aneurysm that may pro-duceat least in 1 studysimilar CT patterns in up to 17%of cases. 18

INITIAL TREATMENT

Although surgical and endovascular therapeutic options

have substantially changed the approach to SAH, medical



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treatment also has shifted considerably. On the basis of evidence from randomized trials, several therapies havebeen discarded because of a serious concern of doing more

harm than good, including antifibrinolytic agents, sublin-gual nifedipine, fluid restriction for hyponatremia, delayed

FIGURE 2. Xanthochromia from a patient with recent subarachnoidhemorrhage. Vial with cerebrospinal fluid is compared with water.Note that xanthochromia is hardly recognizable when vial is heldagainst blue sky (left ) vs a light box (right). Adapted from Catastrophic Neurologic Disorders in the Emergency Department , 2nd ed, by EelcoF. M. Wijdicks. 11 Copyright 2004 by Oxford University Press, Inc. Usedby permission of Oxford University Press, Inc.

clipping of ruptured aneurysm, and nitroprusside and othervasodilators. 19-22

Close neurologic monitoring in the neurologic-neuro-surgical intensive care unit should lead to prompt identifi-cation and treatment of new neurologic deterioration due toaneurysmal rebleeding, acute hydrocephalus, early cere-bral vasospasm, or other medical complications. Before ananeurysm has been treated definitively, blood pressure gen-erally is controlled, with a target systolic pressure of lessthan 180 mm Hg and a target mean arterial pressure be-tween 100 and 120 mm Hg. Use of antifibrinolytic agentstypically is avoided. Although long-term (21 day) anti-fibrinolytic agents decrease the risk of rehemorrhage, theyincrease the incidence of ischemic neurologic deficit due tocerebral vasospasm and do not improve overall out-come. 19,20 A large pilot study of short-term antifibrinolyticuse did not suggest reduced rebleeding. 20

Our approach to initial treatment is shown in Table 2. 23

The guiding principles by organ systems are aimed atpreservation of homeostasis, use of prophylactic drugs,and preparation for definitive aneurysm treatment. Nor-mal CSF circulation may become obstructed secondary tointraventricular blood due to a thick clot in the basal cis-terns or a clot at the level of the arachnoid villi. Certainclinical and radiographic features may predict the occur-rence of acute hydrocephalus: intracerebral extension of hemorrhage, posterior circulation aneurysm, and reducedGlasgow Coma Scale score on admission. 24 Acute hydro-cephalus after SAH is a necessary consideration in pa-tients presenting with altered consciousness; by CT crite-

ria, it is present in 20% of patients. Acute neurologicdeterioration in the setting of progressive ventricular en-

FIGURE 3. Left, Lateral view of a conventional digital subtraction angiogram from which a diagnosis of anteriorchoroidal artery infundibulum was made because a vessel appeared to emanate from the dome. LT ICA = leftinternal carotid artery. Right, Three-dimensional rotational angiography shows that an aneurysm is presentrather than an infundibulum because the anterior choroidal artery originated separately from the dome.



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TABLE 2. Initial Treatment of Subarachnoid Hemorrhage*

Type Treatment

Airway Intubation and mechanical ventilation if patient hasaspiration, neurogenic pulmonary edema, GlasgowComa Scale motor score of withdrawal, or worse

Fluid 2-3 L of 0.9% NaCl per 24 hoursFludrocortisone acetate, 0.3 mg/d if patient has

hyponatremia

Blood Accept MAP of 130 mm Hg. If MAP is >130 mm Hg,pressure esmolol bolus, 500 g/kg in 1 min; or labetalol, 20 mg

IV in 2 min; or enalaprilat, 0.625 mg IV in 5 min

Nutrition Enteric nutrition with continuous infusion on day 2

Additional Nimodipine, 60 mg 6 times a day for 21 daysmeasures Stool softener

Pneumatic compression devicesAcetaminophen with codeine or morphine, 1-2 mg, or

tramadol (if no seizures), 50-100 mg, orally every4 hours for pain management

Phenytoin, 20 mg/kg if seizures have occurred

*b.i.d. = twice daily; IV = intravenously; MAP = mean arterial pressure.Adapted from Wijdicks. 23

largement on CT is a clear indication for external ven-tricular drainage. 25,26 However, the treatment of patientswho arrive at the hospital in a comatose state with ven-tricular enlargement on CT is more controversial becausethe neurologic impairment may be a result of the effect of the initial hemorrhage rather than due to hydrocephalus.Such patients can be observed initially for 24 hours, andsome will improve clinically without intervention. If se-rial CT scans reveal progressive ventricular enlargementor if the neurologic condition deteriorates, external ven-tricular drainage is indicated. Other clinicians may advo-cate early placement of external ventricular drains andthen observation for possible improvement. The mostrecent data suggest that external ventricular drainage doesnot increase the likelihood of aneurysmal rehemorrhagewhen drainage is performed at moderate pressures (


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TABLE 3. Mayo Clinic Protocol for Hemodynamic Augmentationin the Treatment of Cerebral Vasospasm

in Aneurysmal SAH*

SAH, clinically asymptomatic but TCD or CT evidence of diffuse cerebralvasospasm

Place central venous catheterObtain hourly readings of fluid balance and body weightAccomplish volume repletion with crystalloidsNote end points of volume resuscitation: CVP 8 mm Hg, urine

output >250 mL/hAvoid antihypertensive and diuretic agents

SAH, secured aneurysm, clinical evidence of cerebral vasospasmNotify interventional neuroradiologist for possible cerebral

angiographyPlace pulmonary artery catheterGive crystalloid bolus or albumin 5% until increase in stroke volume

index is 250 mL/h, start administration of

fludrocortisone acetate, 0.2 mg b.i.d.Wait 1 hour for clinical improvement

If no improvement, start administration of phenylephrine,10-30 g/min with increase in MAP 25% above baseline or>120 mm Hg

Start administration of dobutamine, 5-15 g/kg/min to increase cardiacindex >3.5 L/min/m 2

Consider replacing phenylephrine with norepinephrine if desiredeffect is not attained

If no effect, perform cerebral angiography for angioplasty orpapaverine infusion

*b.i.d. = twice daily; CT = computed tomography; CVP = central venouspressure; MAP = mean arterial pressure; SAH = subarachnoid hemor-rhage; TCD = transcranial Doppler ultrasonography.

See Treatment of Symptomatic Cerebral Vasospasm in text. Typically,fluctuation in level of consciousness or a localizing sign such as aphasia,hemiparesis, paraparesis, or apraxia.

From Wijdicks. 23

noted that multiple systemic and operator-dependent factorscould influence these flow velocities, limiting their useful-ness as a prognostic tool. 31,32 More recently, 1 study claimedthat MCA flow velocities slower than 120 cm/s and fasterthan 200 cm/s, respectively, have strong negative and posi-tive predictive powers for determining which patients willdevelop ischemic deficits. 33

TREATMENT OF SYMPTOMATICCEREBRAL VASOSPASM

For patients who become symptomatic with delayed is-

chemic deficit due to vasospasm, more aggressive intravas-cular volume expansion and induced hypertension areused. To ensure appropriate intravascular volume and car-diac output in symptomatic patients, invasive monitoring inthe form of right atrial or pulmonary artery catheterizationis recommended. Nimodipine, a calcium channel blockeradministered orally, improves overall patient outcome afterSAH. Of note, the drug does not increase the caliber of narrowed cerebral arteries on cerebral angiography. Rather,

the calcium channel blockade seems to have a neuro-protective effect mediated through an uncharacterizedmechanism. 34,35

Our approach to cerebral vasospasm is stepwise, hemo-dynamic augmentation with improvement of volume statusfollowed by an increase in peripheral vascular resistanceand, finally, enhancement of cardiac contractility. Bloodpressure augmentation may substantially improve ischemicneurologic deficit. If medical therapy for symptomatic va-sospasm has been maximized and neurologic symptomsprove refractory, endovascular therapies can be considered(Table 3). Intra-arterial papaverine infusion acts immedi-ately and increases arterial caliber and cerebral bloodflow, but its effects are short-lived. A recent study usingintra-arterial verapamil suggested safety, but results werefar from impressive. 36 Balloon angioplasty is particular-ly effective as a durable means of alleviating arterialnarrowing and preventing stroke in patients with symp-tomatic vasospasm after aneurysmal SAH. However, theprocedure has risk, particularly in inexperienced hands.The timing of endovascular intubation and use of ino-tropes in patients with cardiac dysfunction are unresolvedissues.

ANEURYSM TREATMENT

As stated previously, the treatment strategy for aneurysmalSAH is focused on (1) treatment of the primary brain injuryof the hemorrhage itself; (2) the necessary associated gen-eral supportive therapy, prophylactic therapy, and, if neces-

sary, interventive therapies for the secondary effects of thehemorrhage such as cerebral vasospasms/delayed ischemicdeficit and hydrocephalus; and (3) last but not least inimportance or priority, treatment of the aneurysm that gaverise to the hemorrhage.

Definitive treatment of the aneurysm is recommendedas soon as feasible, particularly for patients with good-grade SAH, to minimize risk of recurrent aneurysmal hem-orrhage. Early aneurysm treatment necessarily must takeinto account the general medical priorities of the patient,particular complexities of the aneurysm itself, and avail-ability of the appropriate surgical team. Currently, the 2primary options for aneurysm treatment are craniotomy

and aneurysm neck clipping or transvascular endosaccularcoiling. Only in rare situations is occlusion of the arterialtrunk proximal to the aneurysm the best therapeutic option.

ENDOVASCULAR TREATMENT

In 1995, the Food and Drug Administration approved useof the Guglielmi Detachable Coil (Target Therapeutics,Fremont, Calif) for endovascular therapy for aneurysms



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not considered amenable to surgical treatment. In the 8years since initial Food and Drug Administration approval,more than 100,000 patients worldwide with cerebral aneu-rysms have been treated with endovascular coil occlusion.In some medical centers, indications for use of endovascu-lar therapy have evolved to include a broader array of patients beyond those with nonsurgical aneurysms ini-tially treated with the device.

Even though documentation of numerous case seriesof coiling procedures exist, 37-41 few controlled trials havecompared surgery to endovascular treatment of aneurysms.

A small series comparing the 2 treatments in patients withbasilar apex aneurysms showed slight decreases in mortal-ity, costs, and length of hospital stay in patients treatedwith coil embolization compared with those who under-went surgery. 42 A recent series comparing surgery to coilembolization in unruptured aneurysms showed improvedoutcomes and fewer complications in the surgical groupcompared with the coil group. 40 A large prospective trialcomparing surgery with coiling in ruptured aneurysms, theInternational Subarachnoid Aneurysm Trial (ISAT), showeda modest decrease in morbidity associated with coiling com-pared with clipping. 43 Because of the relative lack of pro-spective controlled trials, most patients are treated individu-

ally on the basis of numerous considerations.Choice of the ideal treatment option, either surgical

clipping or endovascular treatment, depends on multiplefactors, including those related to the patients overallclinical status, the anticipated surgical difficulty, and thetechnical details of the proposed coiling procedure. Thesetechnical features include the anatomy of the access ves-sels, including the aortic arch and the brachiocephalic ves-sels, as well as the morphology of the aneurysm and the

adjacent parent artery. With the advent of multiple coilshapes, even aneurysms with highly complex anatomy canbe embolized safely (Figure 5).

In many ways, clipping and coiling can be seen ascomplementary. For example, surgical treatment of basi-lar apex aneurysms has relatively high morbidity rates,whereas coil embolization of basilar apex aneurysms isoften straightforward, depending on the breadth of theaneurysm neck. Conversely, aneurysms in the region of the MCA trifurcation are usually difficult to treat withcoils, given the proximity of branch vessels to the aneu-

rysm neck, but are often readily treated with surgicalclipping.Vascular access should be carefully considered in all

patients. The difficulty and risk of the procedure are highlydependent on the anatomy of all vessels that will be tra-versed. However, primary consideration should be focusedon the caliber, tortuosity, and extent of atheroscleroticchange in the cervical and intracranial portions of the ac-cess vessel. For example, tortuosity or loop formation inthe cervical carotid artery can markedly increase the diffi-culty of a coiling procedure. Furthermore, tortuosity of thecarotid siphon may affect the safety of performing thecoiling procedure, especially in broad-necked aneurysms

in which adjunctive treatments such as balloon remodelingor stent placement are anticipated.

Perhaps the primary factor in deciding whether to at-tempt a coiling procedure is the breadth of the aneurysmneck compared with that of the dome and adjacent parentartery. Various definitions of wide neck have been usedin relation to coiling procedures, but difficulty in coilingcan be anticipated if the dome-neck ratio is less than 1.5:1.In some locations, especially along the supraclinoid inter-

FIGURE 5. Anteroposterior angiograms show a bilobed basilar apex aneurysm (left) and oblitera-tion of the aneurysm aft er coil embolization (right).



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nal carotid artery, balloon remodeling or stent placementcan be used to facilitate coil placement 44-47 (Figure 6). Inother locations, including branch points such as the basilarapex, adjunctive techniques are difficult to use. Coil embo-lization in extremely wide neck aneurysms with dome-neck ratios of less than 1:1 would be unlikely to be effec-tive, even with use of adjunctive measures.

Multiple clinical studies have shown that the efficacy of

coil embolization, defined as the rate of complete, persis-tent aneurysmal occlusion, is intimately related to both theaneurysm size and the width of the aneurysm neck. 38,48-50

There is a sharp reduction in the rate of complete aneurys-mal occlusion for aneurysms greater than 8 to 10 mm indiameter and in aneurysms with necks broader than 4mm. 38,49,50 Recent advances such as use of the balloon re-modeling technique, in which a soft balloon is temporarilyinflated in the parent artery to hold coils within the aneu-rysm cavity, and use of endovascular stents have improvedthe ability to treat difficult aneurysms. 51-54 Even so, the rateof complete occlusion remains frustratingly low, about50% to 70% in most series. Perhaps more importantly, the

rate of late aneurysmal regrowth after coil embolization isextremely high, 33% or more, for aneurysms 10 mm andgreater in diameter. Other factors associated with increasedrisk of aneurysmal recurrence include treatment of rup-tured rather than unruptured aneurysms and incompletecoiling in the initial procedure. 48-50

Several modifications of simple coils aimed at improv-ing aneurysmal occlusion rates have been reported wide-ly. Two such modifications are commercially avail-

able, 55,56 but no clinical data are yet available to assesstheir efficacy.

Coiling represents an important adjunct to aneurysmsurgery in selected patients. Apparent improvements inoutcome with coils compared with surgery in patients withruptured aneurysm may speed adoption of coils in somemedical centers. Currently, the lack of persistent occlusionand the need for long-term surveillance limit the applica-

tion of coils, but these limitations may be overcome withthe advent of modified coil devices.

SURGICAL TREATMENT

Definitive treatment of saccular intracranial aneurysms,whether ruptured or unruptured, evolved over the lasthalf of the 20th century with major refinements of directaneurysm obliteration by clamping or clipping of theaneurysm neck (Figure 7). Microsurgical techniques en-hanced by adjuncts such as temporary proximal trunk occlusion, bipolar coagulation for shrinkage of the aneu-rysm sac, and improved aneurysm clips have ensured

a high degree of treatment efficacy, with permanentaneurysm obliteration in more than 90% of patients whensurgery is performed by experienced aneurysm sur-geons. 57,58 Furthermore, such treatments can be accom-plished with low morbidity and mortality, ranging from5% to 15% for most intracranial aneurysms in the carotidand vertebrobasilar circulation, exclusive of giant aneu-rysms. 59,60 As such, craniotomy and microsurgical clip-ping has been established as the gold standard for treat-

FIGURE 6. Left, Anteroposterior angiogram reveals a broad-necked ophthalmic-segment aneurysm. The dome-neck ratiois approximately 1.2:1. Previously, an attempt was made to coil the aneurysm, but coils persistently herniated through

the broad neck, and the procedure was aborted. Middle, After placement of a single coil with a balloon inflated acrossthe aneurysm neck, the coil shows excellent conformation and stability and was therefore detached in the aneurysm.Right, After balloon-assisted embolization, the aneurysm was obliterated completely, with preservation of the parentartery.



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ment of unruptured and ruptured aneurysms, with earlysurgery recommended for patients who present with SAHand are in good condition to reduce risk of recurrentbleeding. 61

Although several studies indicate that endovascularcoiling can be accomplished with lower procedural risksthan clipping, 43,62 particularly for aneurysms located alongthe basilar trunk and at the basilar caput, 42 efficacy for

complete obliteration of the aneurysm is clearly less thanclipping, ranging from 75% in optimal circumstances to40% in patients with suboptimal aneurysm anatomy. 38 Fur-thermore, features such as broad aneurysm base, intra-aneurysmal thrombus, and arterial branches exiting fromthe aneurysm dome or neck constitute relative specificindications for aneurysm clipping over coiling. Of all loca-tions, the MCA bifurcation region has been the least opti-mal for coiling, particularly related to the tendency forbroader aneurysm neck and branches arising at this site. 63

In cases of ruptured aneurysm, the presence of major in-tracerebral hemorrhage with mass effect causing neuro-logic consequences constitutes a specific indication for

craniotomy to permit expeditious evacuation of the clot anddefinitive aneurysm treatment with clipping. Furthermore,extremely large or giant aneurysms, although posing in-creased risk for treatment due to their size and complexity,are in most cases still best treated by direct clipping of theaneurysm neck or other reconstructive techniques.

As technology advances, particularly in endovasculartherapies, more intracranial aneurysms undoubtedly will betreated by such means. However, it seems highly likely that

many aneurysms, particularly those of large size and com-plicated anatomy, will continue to be best treated by opencraniotomy and microsurgical clipping because of theproven durability of this procedure.

OUTCOME IN SURVIVORS ANDFURTHER CONSEQUENCES

An SAH is a major life experience that leads to additionalmorbidity in up to 25% of surviving patients. Many pa-tients do not return to work, retire early, and are unable tofunction at the same intellectual level as before the rup-ture. 64-67 Numerous clinical factors may influence outcomeafter SAH, including the presenting clinical condition of the patient, age older than 65 years, presence of posteriordistribution aneurysms, rupture, intracerebral extension,and development of cerebral vasospasm or cerebral in-farctions. Preexisting medical conditions and aneurysmsize do not appear to affect outcome. 65 Recovery in youngpatients may be protracted and better than expected. 68

The most important clinical factor in predicting poor

patient outcome after SAH is the presenting level of con-sciousness (World Federation of Neurosurgical Societiesgrade IV or V). The natural history of such patients isdismal with higher than 90% mortality. Population-basedstudies that eliminate the selection bias of referral centershave estimated that approximately 30% of patients havepoor outcome after SAH.

Despite numerous clinical factors associated with pooroutcome after SAH, individual prediction of outcome may

FIGURE 7. A, Typical microsurgical exposure during craniotomy and clipping of a middle

cerebral artery (MCA) aneurysm after opening of the sylvian fissure between the frontal andtemporal lobes; the aneurysm arises at the bifurcation of the MCA with a broad base. B,The aneurysm is occluded completely with an aneurysm clip while blood flow is preservedin the MCA branches.



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be imprecise. Traditionally, patients with poor-grade (IVand V) SAH have been treated conservatively with sup-portive care and, if needed, placement of external ventricu-lar drains. Patients who improve clinically are selected forsubsequent repair of the ruptured aneurysm. This treatmentstrategy has improved patient outcome but neverthelessresults in approximately 50% mortality. Only about 20% to30% of patients treated conservatively have favorable out-comes. 69 Outcome in patients with poor-grade SAH has beenconsistent throughout several decades, which has led to anattitude of therapeutic nihilism for such patients. Neverthe-less, with aggressive treatment, a subset of patients withpoor-grade SAH can survive with favorable outcome in up to50% (grade IV) and 20% (grade V) of cases. 38,66,69

The experience of an aneurysmal SAH often promptsother family members to seek advice on screening foraneurysm. If screened on a large scale, aneurysms would befound in approximately 7% of first-degree relatives (par-ents, siblings, and children), with a higher chance of anunruptured aneurysm in a sibling. Certain families havemore than 1 member with a documented aneurysm, andthere is some suggestion that aneurysms in such familymembers have a higher risk of rupture than those foundincidentally and that rupture may occur at a younger age. 70-73

Screening for aneurysm is a complicated and unresolvedissue. The rupture risk of incidentally detected aneurysm islow (9 mm) aneurysms or when multiplelobes are present. 75

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End of the Symposium on Cerebrovascular Diseases.


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