Contributors
J. Michael Schmidt, PhD, Assistant Professor of Neuropsychology (in Neurology) Neurological Intensive Care Unit, Columbia University College of Physicians and Surgeons,
4 Surgical Management of Aneurysmal Subarachnoid Hemorrhage
Quoc-Anh Thai, MD, Assistant Chief of Service, Instructor Gustavo Pradilla, MD, Resident
Daniele Rigamonti , MD, FACS, Vice-Chairman and Professor Department of Neurosurgery , Johns Hopkins University School of Medicine, Johns Hopkins Medical Institutions , Baltimore , Maryland , USA
INTRODUCTION
Aneurysmal subarachnoid hemorrhage (aSAH) is caused by the rupture of intracranial aneurysms. Although it represents a small proportion of cerebrovascular accidents, aSAH leads to a disproportionately high morbidity and mortality. Twenty-fi ve percent of cerebrovascular mortality is due to aSAH ( 1 ), which represents only 3% of all strokes ( 2 ). The case-fatality rate is reported to be between 25% and 67% ( 1,3 ). Of those who survive, 50% have a disability requiring aid in performing activities of daily living ( 1,4 ). Refi nements of diagnostic tools, such as computed tomography angiography (CTA) and magnetic resonance angiography (MRA), as well as the advent of therapeutic options in the fi eld of endovascular interventional neuroradi-ology, have facilitated treatment for these patients, but they have also presented new challenges in management decisions for health care professionals. In this chapter, we will focus on the surgical management of aSAH and briefl y discuss the presentation, diagnosis, and grading of SAH, as well as the prognostic factors and treatment options.
CLINICAL PRESENTATION OF aSAH
Chapter 7contains a detailed review of the clinical presentation of aSAH. In brief, the classic clinical presentation is the sudden onset of a severe headache, often described as the “worst headache of my life.” Approximately 50% of patients with SAH report an instantaneous onset, and the other half describe its onset in seconds or minutes ( 5 ). Signs of meningismus, with com-plaints of nuchal discomfort or changes in mental status, often follow the headache in patients with a ruptured aneurysm. The blood can also cause irritation of the meninges and result in photophobia, neck soreness/stiffness, Brudzinski’s sign, Kernig’s sign, and even a low-grade fever that occurs within 6 to 24 hr after an aSAH ( 6 ). As a result of the thick blood clots in the basal cisterns, a communicating hydrocephalus can develop, and, in cases with intraventricular hemorrhages (IVHs), a noncommunicating hydrocephalus can occur from blockage of the foram-ina of Magendie and Luschka, resulting in the characteristic dilatation of all 4 ventricles ( 7 ).
DIAGNOSIS OF SUBARACHNOID HEMORRHAGE AND ANEURYSMS
The fi rst diagnostic test for a suspected aSAH is a noncontrast head CT ( Fig. 1 ). The sensitivity of detecting an aSAH within the fi rst 24 hr of hemorrhage is 92% and decreases by about 7%
each 24 hr thereafter ( 8 ). A false positive may occur in the rare case of generalized brain edema that causes venous congestion in the subarachnoid space, mimicking an aSAH ( 9 ). The Fisher Scale ( Table 1 ) assigns a numeric rating of the hemorrhage and facilitates prediction of the risk for vasospasm by grading the amount of blood on initial presentation.
In suspected aSAH cases, if the head CT is not diagnostic, a lumbar puncture is manda-tory. The lumbar puncture remains the most sensitive test for aSAH. Once a hemorrhage occurs in the subarachnoid space and blood becomes mixed in the cerebrospinal fl uid (CSF), suffi cient lysis of the red blood cells and formation of bilirubin and oxyhemoglobin form within 6 to 12 hr
( 9 ), giving the CSF a yellow tinge, or xanthochromia, after centrifugation. Therefore, in addition to routine CSF labs, CSF bilirubin should be checked.
The gold standard in the diagnosis of aneurysms is intra-arterial (IA) digital subtraction angiography. This enables visualization of the aneurysm in relation to its parent vessel, defi nition of the collateral circulation, and assessment for vasospasm. To assess all of these characteris-tics thoroughly, it is imperative that the angiogram includes contrast injection of both carotid arteries and both vertebral arteries a 4-vessel angiogram), with multiple views (anteroposterior, lateral, and oblique) of each injection. The risk of such a study in qualifi ed centers is very low.
One meta-analysis reported a transient or permanent neurologic complication risk of 1.8% in patients with aSAH and 0.3% in patients without aSAH ( 10 ). The risk of permanent neurologic damage is as low as 0.09% ( 11 ).
Procedural risks are eliminated in MRA or CTA, but their detection rate is lower. They are especially useful in planning for surgery when defi nition of the surrounding anatomy is necessary, as three-dimensional reconstruction with interactive manipulation of the views is possible. However, they remain inadequate replacements for IA angiography in the diagnosis of aneurysms at this time. Direct comparisons of CTA and MRA with IA angiograms showed that the accuracy of CTA/MRA is approximately 90% and is improving ( 12 ). CTA sensitivity and speci-fi city are 91% and 95%, respectively ( 13 ). In the period prior to 1995, CTA accuracy was 84%, and in the period subsequent to that, it was 93% ( 12 ). MRA sensitivity and specifi city have been reported at 83% and 97%, respectively ( 14 ). However, the detection rate decreases dramatically with smaller aneurysms and becomes negligible for sizes less than 3 mm. MRA accuracy is reported at 90% and has not changed signifi cantly. Although further improvements are expected for these noninvasive tests, IA angiograms remain the gold standard for detection of intracranial aneurysms. Therefore, it is crucial that patients with suspected aSAH have the following tests in this order: 1) noncontrast head CT, 2) lumbar puncture if head CT is nondiagnostic, and 3) IA angiography in cases with confi rmed aSAH.
Figure 1 Noncontrast head computed tomography showing aneu-rysmal subarachnoid hemorrhage. Acute blood in the subarachnoid space appears as diffuse hyperintensities in the chiasmatic, Sylvian, and interhemispheric cisterns. Also note in tra ventricular hemorrhage in the fourth ventricle associated with hydrocephalus (enlarged temporal horns).
Table 1 The Fisher Scale Grades the Amount of Hemorrhage on a Diagnostic Head Computed Tomography, Which Then Can Be Used to Assess for Risk of Vasospasm Blood on computed tomography (direct measurement, Fisher grade no calibration to actual thickness)
1 No subarachnoid blood detected
2 Diffuse or vertical layers <1 mm thick
3 Localized clot and/or vertical layer <1 mm thick
4 Intracerebral or intraventricular clot with diffuse or no aSAH Abbreviation : aSAH, aneurysmal subarachnoid hemorrhage.
GRADING AND PROGNOSIS OF aSAH
The single most important predictor of outcome after an aSAH is the presenting level of consciousness. The mental status and consciousness level seen during triage are routinely quanti-fi ed by health care personnel using the Glasgow Coma Scale (GCS) ( Table 2 ). The assessments of eye opening, verbal responses, and motor commands contribute to the initial assessment and refl ect the sum of the other prognostic factors associated with SAH, such as extent of hem-orrhage, injury to the brain, size of ruptured aneurysm, patient’s age, contributing medical illnesses, and others ( 15 ). Proper assessment of all these factors provides an accurate probabil-ity of outcome. The accuracy of assessment of all these factors greatly infl uences the accuracy of predicting outcome and, therefore, greatly infl uences patient management decisions.
The Hunt and Hess SAH scale ( 16 ) ( Table 3 ) was introduced to quantify the severity of SAH and includes the signs of SAH, such as nuchal rigidity, cranial nerve palsy, hemiparesis, and others. The scale also relied on the patients’ subjective report of their headache. Although these integrated assessments result in a strong predictive factor, the subjective components of the scale are vulnerable to variances in interpretation between different examiners and examinees. For example, “mild” versus “moderate” headaches reported by the patient could change the rating of SAH severity. The reported high interobserver disagreement ( 15 ) makes the scale less reliable.
The World Federation of Neurological Surgeons (WFNS) scale ( Table 4 ) eliminates the sub-jective aspects of the Hunt and Hess scale and incorporates the GCS score as the basis for grading SAH. It effectively uses the objective criteria of the GCS to yield a WFNS SAH scale. Although this scale is easier to memorize and use, its categories have not been validated clinically.
The GCS for grading SAH ( 17 ) remains the simplest scale to use, with the highest predictive value for discharge GCS and lowest interobserver variability. The GCS SAH scale incorporates the clinically validated GCS as the objective criteria for grading aSAH ( Table 5 ), utilizing a known scoring system and eliminating any subjective aspects. The GCS SAH Grade I is equiva-lent to a GCS of 15. Thereafter, the GCS SAH grade increases by 1 for decremental changes of 3 points on the GCS. For example, GCS SAH Grade II equals GCS of 14, 13, or 12, and GCS SAH Grade III equals GCS of 11, 10, or 9, etc. This facilitates memorization, but even if the initial care providers do not know the GCS SAH scale, their record of the GCS, itself, is documentation of the SAH scale. The validity of the GCS SAH scale is clear in direct comparison with the Hunt and Hess and WFNS scales ( 17 ). In our opinion, the high predictive value, low interobserver variability, and ease of use make the GCS SAH scale a preferred scale.
COMPLICATIONS AFTER aSAH
The major initial complications after an aSAH associated with high morbidity and mortality are hydrocephalus and rebleeding. Hydrocephalus is present radiographically in 15% to 20%
Table 3 Hunt and Hess Subarachnoid Hemorrhage Scale
Grade Clinical assessment
I Asymptomatic or mild headache
II Moderate to severe headache, nuchal rigidity, cranial nerve palsy III Lethargy, confusion, mild focal defi cit
IV Stupor, moderate to severe hemiparesis, early decerebrate rigidity V Deep coma, decerebrate rigidity, moribund
Table 2 The Glasgow Coma Scale Assesses Patient’s Mental State on Arrival
Points Best eye Best verbal Best motor
6 N/A N/A Obeys
5 N/A Oriented Localizes pain
4 Spontaneous Confused Withdraws to pain
3 To speech Inappropriate Flexor (decorticate)
2 To pain Incomprehensible Extensor (decerebrate)
1 None None None
of patients with aSAH on admission ( 18 ), and an additional 3% develop hydrocephalus within 1 week after aSAH ( 19 ), resulting in shunt-dependent hydrocephalus in more than 20% of all aSAH patients ( 20–23 ). When associated with IVH, CSF outfl ow is blocked at the foramina of Magendie and Luschka, resulting in a noncommunicating 4-ventricle dilation hydrocephalus ( 7 ). However, approximately 50% of patients with hydrocephalus do not have radiographically evident IVH ( 18 ). When decreasing mental status is in the setting of hydrocephalus, the stan-dard of care is insertion of an intraventricular catheter for external CSF drainage, which can be done under standard sterility at the bedside and improves the level of consciousness in 78%
of patients ( 19 ). However, rebleeding rate is reported to increase to 43% with intraventricular drainage, versus 15% in patients without drainage ( 19 ). To prevent this dreadful complication, it is recommended to set the initial pop-off pressure at ≥20 mmHg to prevent the creation of a pressure gradient that could cause re-rupture of the aneurysm.
Rebleeding increases morbidity and mortality signifi cantly. One study reported a mortality rate for rebleeding of 80%, compared to 41% in patients without rebleeding ( 24 ). Rebleeding is a major risk in all patients with aSAH within the fi rst 24 hr and remains high during the fi rst 2 weeks. The actual rate is unknown but has been reported to be as high as 15% ( 25 ) in the initial hours. Afterward, the rate of rebleeding drops to 1.5% per day and continues to decline over the next 2 weeks. The total risk of rebleeding for the fi rst 2 weeks has been reported at 19% ( 25 ). Considering the high mortality associated with rebleeding and the incidence of early rebleeding, prompt medical and surgical management is critical in the setting of an aSAH.
SURGICAL INTERVENTION
The high risks of rebleeding, poor medical management options for treating vasospasm in the set-ting of an unsecured aneurysm, and time course of vasospasm are all factors that make prompt, defi nitive surgical intervention the best therapy. Neurosurgical treatment of aneurysms began in 1937, when Walter Dandy surgically treated the fi rst aneurysm patient at Johns Hopkins Hospital. Modern microsurgical treatment of aneurysm evolved in the 1960s and 1970s under the innovative leadership of Charles Drake and Gazi Yasargil, who incorporated the use of the operating microscope for clipping of aneurysms. Since then, the techniques of microneurosur-gery and skull-base surmicroneurosur-gery have reached maturity, and aneurysm clips are routinely used to occlude the neck of the aneurysm and exclude the weak saccular portion from the cerebral circulation.
Table 4 World Federation of Neurological Surgeons Subarachnoid Hemorrhage Scale
Grade GCS and clinical assessment I 15
II 13 –14, without focal defi cit III 13 –14, with focal defi cit IV 7–12
V 3 – 6
Abbreviation : GCS, Glasgow Coma Scale.
Table 5 Glasgow Coma Scale for Aneurysmal Subarachnoid Hemorrhage
Grade GCS score
I 15
II 14 –12
III 11– 9
IV 8 – 6
V 5 – 3
Abbreviation : GCS, Glasgow Coma Scale .
Timing of surgery is essential in achieving optimal outcome, and the time course of vasospasm is the major consideration. “Early surgery” has been advocated for several obvious practical reasons. Prompt clipping of an aneurysm eliminates the risk of rebleeding, which is theoretically associated with increased morbidity and mortality. Also, once an aneurysm is secured, treatment of vasospasm is facilitated with the use of triple-H therapy (hypertension, hypervolemia, and hemodilution), an option that is dangerous in an unsecured aneurysm. Vaso-spasm and edema may complicate surgery that is delayed from 7 to 10 days after aSAH, when vasospasm is at its peak. Another surgical option is that of “late surgery,” in which clipping is accomplished after 12 to 14 days, when vasospasm has resolved and edema has subsided.
The Cooperative Study on the Timing of Aneurysm Surgery showed that the results of early surgery were equivalent to those of late surgery ( 26,27 ). This was a prospective observational study involving 3521 patients from 60 centers collected over a period of 2.5 years. Comparably good outcomes were reported for surgery that was performed on days 0 to 3 (63%) and days 4 to 6 (60%) post-aSAH. Delayed surgery on days 11 to 14 post-aSAH also yielded similar results (62%), as did late surgery on days 15 to 32 (63%). Surgery during days 7 to 10 after aSAH had the worst outcome, and this period coincides with the peak of vasospasm.
The intraoperative dissection technique is crucial for aneurysm clipping. Using an oper-ating microscope, dissection should focus on sharply separoper-ating arachnoid tissues to facilitate separation of vascular structures from the parenchyma. The fi rst goal of the dissection is to gain proximal control. Prior to attempting dissection near the aneurysm, the surgeon must be able to emergently occlude the vessel that supplies the aneurysm in the case of an intraopera-tive rupture. In cases in which intracranial proximal control is not an option (e.g., ophthalmic artery aneurysms), an extracranial neck dissection for proximal control is required prior to the craniotomy. Blunt dissection should be avoided, especially near the aneurysm due to the high risk of tearing the frail dome. Also, a blunt tear is much more diffi cult to repair than a punc-tate tear made using sharp dissection techniques. Once the aneurysm is reached, meticulous dissection of the aneurysm neck is required, to ensure optimal clip placement and to reduce iatrogenic rupture of the aneurysm.
Temporary arterial occlusion is a useful option to aid in the surgical dissection and, ulti-mately, in the clipping of aneurysms. This technique, when used properly, can reduce the risk of intraoperative rupture when dissecting near the aneurysm, can facilitate optimal placement of the permanent clip, and is indicated in cases where more involved neck dissection is required and those in which extensive adhesions are located near the aneurysm. Prior to applying tem-porary clips, hemodynamic status must be stable and the patient’s intravascular volume and systemic blood pressure should be normalized (higher blood pressure should be maintained for hypertensive patients). The patient should be anesthetized to electroencephalographic burst suppression. The temporary arterial occlusion should be applied with a “temporary clip” that has a closing pressure approximately half that of a permanent clip. This will decrease the risk of intimal damage to the vessel. Although the exact placement of the temporary clip is case specifi c, the general guideline is that it should allow maximal aneurysm exposure while minimizing the risk of infarction.
The technique used in treating the aneurysm is as important as the dissection and application of the clip. Clip selection is crucial in excluding the aneurysm from the systemic circula-tion. Careful measurement of the aneurysm on the angiogram should be correlated with the intraoperative fi ndings. The clip size should be at least 1.53 × the diameter of the aneurysm, as application of the clip will lead to collapse and elongation of the neck of the aneurysm.
In certain circumstances, application of a clip is not possible due to the anatomy or shape of the aneurysm. An alternative maneuver is wrapping the aneurysm, although the outcome of this technique is debatable. In another technique, called “trapping,” clips are placed proximal and distal to the aneurysm to interrupt fl ow. Depending upon the anatomic location, this procedure can be associated with ischemic sequelae.
Post-clipping protocol is as important as pre-clipping protocol. Once the clip is in place, careful visual inspection must be made to ensure that optimal placement has occurred and no other vessels are compromised, especially in cases where the clip is placed too close to the parent vessel, decreasing its diameter. Papaverine is applied to all exposed and manipulated arteries to facilitate redilatation to premanipulation diameters. Then, intraoperative angiography is per-formed to ensure proper clip placement. Improper clip placement that requires reexploration and clip adjustment was seen on intraoperative angiography in 11% of the cases in one study ( 28 ).
Endovascular intervention for aneurysms is a more recent technique and is a promising minimally invasive option for the treatment of aneurysms. Endovascular interventional neu-roradiology began in the 1970s, when Fedor Serbinenko used detachable latex balloons to occlude the supplying artery of the aneurysm or to occlude the aneurysm sac itself ( 29 ). Mod-ern endovascular treatment of aneurysms started in 1991, when Guido Guglielmi introduced an electrolytic detachable platinum coil (Guglielmi detachable coils) ( 30,31 ). These coils are inserted through a femoral artery cannula via a microcatheter that can be threaded to the loca-tion of the aneurysm. The coils are then packed into the saccular porloca-tion and separated from the microcatheter by electrolysis, thus excluding the aneurysmal sac from cerebral circulation.
The use of endovascular coiling for the treatment of aneurysms is rapidly increasing worldwide, which is a refl ection of improved coil design and refi nements of techniques, as more centers subspecialize in this area. A few centers are reserving surgery as a back-up option when coiling is deemed unsuitable. It is estimated that approximately 1500 patients worldwide per month are being treated by endovascular coiling, and more than 100,000 patients with aneurysms have been treated with endovas cular coiling ( 32 ).
The level of expertise at the neurosurgical center is a crucial determinant of outcome in patients who undergo surgical treatment of aneurysms, especially clipping. Microsurgical techniques of aneurysmal clipping are technically demanding and usually are not employed for most neurosurgical cases. The neurosurgical centers that treat the average patient popula-tion without a referral bias would typically not encounter a high volume of aneurysm patients, thus limiting the experience of the surgeons. A study on the effects of patient volume on the outcome of craniotomy and aneurysmal clipping showed that institutions that performed more than 30 craniotomies per year had a 43% reduction in mortality rates. Also, centers that per-formed more than 30 aneurysm clippings per year had a 43% reduction in mortality rates ( 33 ).
Similar results have been noted in other studies, suggesting that patients with aSAH will have improved outcome if their surgery is performed at a high-volume institution.
CONCLUSION
aSAH remains a devastating problem, with high morbidity and mortality. Improvements in CTA and MRA have aided in the detection of aneurysms and have facilitated planning for intervention.
Although their sensitivity and accuracy of detecting aneurysms (which have improved during the past decade) exceed 90%, the IA digital subtraction angiogram remains the gold standard for diagnosing aneurysms. Currently, aneurysm treatment should ideally be referred to specialized centers of excellence that have subspecialists in both cerebrovascular neurosurgery and endovas-cular interventional neuroradiology who perform a high volume of cases. The deciding factor for a good outcome is not necessarily the type of intervention, but the volume of procedures that have been performed at a particular center; center expertise can reduce mortality by 43% ( 33 ).
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