SAH From Cerebral Aneurysm Rupture

| 14.02.23 - 13:48 87 SAH from Cerebral Aneurysm Rupture 87.1 Epidemiology of cerebral aneurysms The incidence of cerebral aneurysms is di !cult to estimate. Range of autopsy prevalence of aneur- ysms: 0.2 –7.9% (variability depends on use of dissecting microscope, hospital referral and autopsy pat...

| 14.02.23 - 13:48 87 SAH from Cerebral Aneurysm Rupture 87.1 Epidemiology of cerebral aneurysms The incidence of cerebral aneurysms is di !cult to estimate. Range of autopsy prevalence of aneur- ysms: 0.2 –7.9% (variability depends on use of dissecting microscope, hospital referral and autopsy pattern, overall interest …). Estimated prevalence of incidental aneurysms range from 1–5% of the population, 1,2,3,4,5 and detection is increased with widespread use of CTand MRI. 6Ratio of ruptured: unruptured (incidental) aneurysm is 5:3 to 5:6 (rough estimate is 1:1, i.e., 50% of these aneurysmsrupture). 7Unruptured intracranial aneurysms are more common in women (!3:1 ratio) 8,9and in the elderly, 10and only 2% of aneurysms present during childhood. 11When present in children, they tend to occur more frequently in males (2:1) and to a greater degree in the posterior circulation(40–45%). 12,13 87.2 Etiology of cerebral aneurysms The exact pathophysiology of the development of aneurysms is still controversial. In contrast toextracranial blood vessels, there is less elastic in the tunica media and adventitia of cerebral bloodvessels, the media has less muscle, the adventitia is thinner, and the internal elastic lamina is moreprominent. 14,15 This, together with the fact that large cerebral blood vessels lie within the subarach- noid space with little supporting connective tissue, 16(p1644) may predispose these vessels to the development of saccular aneurysms. Aneurysms tend to arise in areas where there is a curve in theparent artery, in the angle between it and a significant branching artery, and point in the directionthat the parent artery would have continued had the curve not been present. 17 The etiology of aneurysms may be:1. congenital predisposition (e.g., defect in the muscular layer of the arterial wall, referred to as amedial gap)2.“atherosclerotic ”or hypertensive: presumed etiology of most saccular aneurysms, probably interacts with congenital predisposition described above3. embolic: as in atrial myxoma4. infectious —so called “mycotic aneurysms ”(p. 1492) 5. traumatic: see Traumatic aneurysms (p. 1491)6. associated with other conditions (see below) 87.3 Location of cerebral aneurysms Saccular aneurysms, AKA berry aneurysms are usually located on major named cerebral arteries atthe apex of branch points, which is the site of maximum hemodynamic stress in a vessel. 18More peripheral aneurysms do occur, but tend to be associated with infection (mycotic aneurysms) ortrauma. Fusiform aneurysms are more common in the vertebrobasilar system. Dissecting aneurysmsshould be categorized with arterial dissection (p. 1577).Saccular aneurysms location:1. 85 –95% in carotid system, with the following 3 most common locations: a) ACoA (single most common): 30% (ACoA & ACA more common in males)b) PComA: 25%c) middle cerebral artery (MCA): 20%2.5–15% in posterior circulation (vertebro-basilar)a)!10% on basilar artery: basilar bifurcation, AKA basilar tip, is the most common, followed byBA-SCA, BA-VA junction, AICAb)!5% on vertebral artery: VA-PICA junction is the most common 3. 20 –30% of aneurysm patients have multiple aneurysms (p. 1490) 19 87.4 Natural history of cerebral aneurysms This is an overview. Many of these items will be addressed in detail in following sections.1. major rupture (see below): typically into the subarachnoid space (subarachnoid hemorrhage(SAH)). Possible other sites include: ventricles, brain parenchyma, subdural space …(see below) a)forpreviously ruptured aneurysms, this is the risk of rebleeding (p. 1437) b) see forunruptured aneurysms (p. 1486) SAH from Cerebral Aneurysm Rupture 1453 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 2. spontaneous thrombosis of an aneurysm is a rare occurrence 20,21,22 (estimate in autopsy series is 9–13% 22). However, thrombosed aneurysms may re-open, 23,24 and delayed rupture may occur sometimes even years later3. aneurysms can also cause symptoms without a major rupture (e.g., cranial neuropathies, hemi-paresis, endocrine disturbances, proptosis, strokes …): see below 4. some incidental aneurysms may lie “dormant ”and be amenable to observation (see unruptured aneurysms (p. 1486)) 87.5 Presentation of cerebral aneurysms 87.5.1 Major rupture The most frequent presentation. This may produce:1. subarachnoid hemorrhage (SAH) (p. 1437): the most common sequela of aneurysmal rupture.The following may occur with or without SAH2. intracerebral hemorrhage: occurs in 20 –40% (more common with aneurysms distal to the Circle of Willis, e.g., MCA aneurysms)3. intraventricular hemorrhage: occurs in 13 –28% 25(see below) 4. hemorrhage into vascular space (producing an arteriovenous fistula), e.g., with cavernous carotidartery aneurysms (p. 1489)5. subdural blood occurs in 2–5% !Intraventricular hemorrhage. See also other etiologies of intraventricular hemorrhage (IVH) (p. 1671).IVH occurs in 13 –28% of ruptured aneurysms in clinical series (higher in autopsy series) 25and appears to carry a worse prognosis (64% mortality). 25The size of the ventricles on admission was the most important prognosticator (large vents being worse). Patterns that may occur:1. distal PICA aneurysms: may rupture directly into 4th ventricle through the foramen of Luschka 26 2. AComA aneurysm: it has been asserted that IVH occurs from rupture through the lamina termi- nalis into the anterior 3rd or lateral ventricles; however, this is not always borne out at the timeof surgery3. distal basilar artery or carotid terminus aneurysms: may rupture through the f loor of the 3rdventricle (rare) 87.5.2 Presentation other than major rupture General information May be thought of as possible “warning signs. ” 1. mass e"ect: usually associated with enlargement of the aneurysm. May be gradual as with giant aneurysms, or acute often associated with minor enlargementa) giant aneurysms: including brainstem compression producing hemiparesis and cranialneuropathiesb) cranial neuropathy (average latency from symptom to SAH was 110 days; note: the average latency quoted for some of these symptoms comes from a retrospective study of patients pre-senting with SAH who were identified as having a warning symptom 27) (see below) c) intra- or suprasellar aneurysm producing endocrine disturbance 28due to pituitary gland or stalk compression 2. minor hemorrhage: warning or sentinel hemorrhage; see Headache (p. 1418). This group had theshortest latency (10 days) between symptom and SAH (note: the average latency quoted for some of these symptoms comes from a retrospective study of patients presenting with SAH whowere identified as having a warning symptom 27) 3. small infarcts or transient ischemia due to distal embolization (including amaurosis fugax,homonymous hemianopsia …)29: average latency from symptom to SAH was 21 days 4. seizures: at surgery, an adjacent area of encephalomalacia may be found. 29The seizures may arise as a result of localized gliosis and do not necessarily represent aneurysmal expansion as there isno data to indicate an increased risk of hemorrhage in this group5. headache 29without hemorrhage: abates after treatment in most cases a) acute: may be severe and “thunderclap ”in nature, 30some describe as “worst headache of my life. ”Has been attributed to aneurysmal expansion, thrombosis, or intramural bleeding, 31all without rupture Subarachnoid Hemorrhage and Aneurysms 1454 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 b) present for "2 weeks: unilateral in about half (often retro-orbital or periorbital), possibly due to irritation of overlying dura. Di "use or bilateral in the other half, possibly due to mass e"ect !increased ICP 6. incidentally discovered (i.e., asymptomatic, e.g., those found on angiography, CT, or MRI obtained forother reasons) Cranial neuropathies from aneurysmal compression 1. oculomotor (3rd nerve) palsy (ONP): occurs in !9% of PComA aneurysms 32(ruptured and unrup- tured), less common with basilar apex aneurysm. Symptoms of ONP may include:a) extraocular muscle palsy (eye deviates “down and out ”!diplopia) b) ptosisc) dilated unreactive pupil (p. 591): !non-pupil-sparing third nerve palsy is the classic finding of 3rd nerve compression 2. visual loss due to 29 a) compressive optic neuropathy with ophthalmic artery aneurysms: characteristically producesnasal quadrantanopsiab) chiasmal syndromes due to ophthalmic, AComA, or basilar apex aneurysms3. facial pain syndromes in the ophthalmic or maxillary nerve distribution that may mimic trigemi-nal neuralgia can occur with intracavernous or supraclinoid aneurysms 29,33 !Note. The development of a third nerve palsy in a patient with an unruptured aneurysm is a med- ical emergency as it probably results from aneurysmal expansion and may portend impendingrupture. 87.6 Conditions associated with aneurysms 87.6.1 Overview 1. autosomal dominant polycystic kidney disease (see below)2. fibromuscular dysplasia (FMD) : prevalence of aneurysms in renal FMD is 7%, in aortocranial FMD 21% 3. arteriovenous malformations (AVM) including moyamoya disease; see AVMs and aneurysms (p. 1507) 4. connective tissue disorders 34: a) Ehlers-Danlos, especially type IV (deficient collagen type III) which also has a high rate ofarterial dissection, including with angiography or coilingb) Marfan syndrome (p. 1576)c) pseudoxanthoma elasticum 5. multiple other family members with intracranial aneurysms. Familial intracranial aneurysm syndrome (FIA): 2 or more relatives, third-degree or closer, harbor radiographically provenintracranial aneurysms. Also, see Familial aneurysms (p. 1490) 6. coarctation of the aorta 35 7. hereditary hemorrhagic telangiectasia 36(Osler-Weber-Rendu syndrome) 8. atherosclerosis 37 9. bacterial endocarditis10. multiple endocrine neoplasia type I38 11. neurofibromatosis type I39 87.6.2 Autosomal dominant polycystic kidney disease General information Adult polycystic kidney disease is seen in 1 of every 500 autopsies, and approximately 500,000 peo - ple in the U.S. carry the mutant gene for autosomal dominant polycystic kidney disease (ADPKD ; there is also an autosomal recessive polycystic kidney disease ). Renal function is usually normal dur- ing the first few decades of life, with progressive chronic renal failure ensuing. HTN is a common sequelae. Transmission is autosomal dominant, with 100% penetrance by 80 yrs of age. 40Cystic dis- ease of other organs may occur (viz.: liver in !33%, and occasionally lung, pancreas). 41 The first association between ADPKD and cerebral aneurysms is attributed to Dunger in 1904.Reported prevalence of intracranial aneurysms with ADPKD: 10 –30%, 42with 15% being a reasonable estimate. 43Most were located on the MCA, with multiple aneurysms present in 31%. 44In addition to SAH from Cerebral Aneurysm Rupture 1455 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 the increased incidence of aneurysms, there appears to be an increased risk of rupture, 45with 64% occurring before age 50. Asa result, patients with ADPKD carry a 10 –20-fold increased risk of SAH compared to the general population. 46Aneurysms are rarely detectable before age 20 years. The average rate of rupture of incidental aneurysms is !2%/yr (p. 1437). Recommendations Using the above statistics, together with the life expectancy of patients with ADPKD and other esti-mations (of operative morbidity and mortality, etc.), the result of decision analysis is that arteriogra-phy not be routinely employed in patients older than 25 years. 42However, patients with symptoms possibly due to unruptured aneurysms, and those with SAH, should undergo angiography and sub - sequent treatment of any aneurysms discovered (especially those > 1 cm diameter). A decision analy - sis study 43determined that screening with MRA was beneficial compared to treating patients once they became symptomatic. Repeat MRA screening may be e"ectively repeated as follows: 1. every !2–3 years for a young patient with ADPKD with either a) a history of aneurysms, orb) a kindred of ADPKD with aneurysms2. every 5–20 years for a patient with ADPKD in a kindred of ADPKD with no history of aneurysms 43 87.7 Treatment options for aneurysms 87.7.1 General information The optimal treatment for an aneurysm depends on the age and condition of the patient, the anat-omy of the aneurysm and associated vasculature, the ability of the surgeon and the availability ofendovascular treatment options, and must be weighed against the natural history (p. 1453) of thecondition. Also, treatment of the aneurysm facilitates treatment of cerebrovascular vasospasm(p. 1439), should it occur.In general, the appropriateness of endovascular treatment should be assessed initially in treatingruptured and unruptured aneurysms (not all will be amenable). 87.7.2 Therapies that do not directly address the aneurysm The hope here is that the aneurysm will not bleed and that it will thrombose (see above).1. continue medical management initiated on admission: i.e., control of HTN, continue calcium-channel blockers, stool softeners, activity restrictions … 2. treatment options generally not used a) antifibrinolytic therapy (e.g., !-aminocaproic acid (EACA)): !NB: NOT USED . Reduces rebleed- ing, but increases the incidence of arterial vasospasm and hydrocephalus 47 b) serial LPs: an historical treatment, 48may increase the risk of aneurysmal re-rupture 87.7.3 Endovascular techniques to treat the aneurysm 1. thrombosing the aneurysm:a)“coiling ”with Guglielmi electrolytically detachable coils (see below) b) Onyx HD 500 has been used forwide-necked or giant ICA aneurysms. 49Out of 22 patients, there was 1 parent ICA stenosis and 2 ICA occlusions caused by Onyx migration c)“flow diversion ”with “covered stents ”(p. 1924) (tightly woven stents) which promotes thrombosis of the aneurysm 2. trapping: e"ective treatment requires distal AND proximal arterial interruption, usually by endo- vascular techniques, 50occasionally by direct surgical means (ligation or clip occlusion), or some combination. May also incorporate vascular bypass (e.g., EC-IC bypass) to maintain f low distal to trapped segment 51 3. proximal ligation (so-called hunterian ligation after Hunter ligated the popliteal artery proximalto a peripheral aneurysm in 1784 52): useful forgiant aneurysms. 53,54 For non-giant aneurysms provides little benefit and adds the risk of thromboembolism (which may be reduced by occlud- ing the CCA rather than the ICA 54). May also elevate the risk of developing aneurysms in the con- tralateral circulation 55 Subarachnoid Hemorrhage and Aneurysms 1456 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 87.7.4 Surgical treatment options for aneurysms 1. clipping: the surgical gold standard. Surgical placement of a clip across the neck of the aneurysm to exclude the aneurysm from the circulation (see below) without occluding normal vessels2. wrapping or coating the aneurysm: although this should never be the goal of surgery, situationsmay arise in which there is little else that can be done (e.g., fusiform basilar trunk aneurysms,aneurysms with significant branches arising from the dome, or part of the neck within the caver-nous sinus)a) with muscle: the first method used to surgically treat an aneurysm 56(the patient described died from rebleeding)b) with cotton or muslin: popularized by Gillingham. 57An analysis of 60 patients showed that 8.5% rebled in #6 mos, and the annual rebleeding rate was 1.5% thereafter 58(similar to the natural history)c) with plastic resin or other polymer: may be slightly better than muscle or gauze. 59One study with long follow-up found no protection from rebleeding during the first month, but there-after the risk was slightly lower than the natural history. 59Other studies show no di "erence from natural course 60 d)tef lon and fibrin glue 61 87.7.5 Treatment decisions: coiling vs. clipping General information The use of endovascular treatment for aneurysms has increased, with coil embolization being the most common endovascular modality (see above for other options). From 2002 –2008, the rate of aneurysm coiling in the U.S. and U.K. increased from 17 and 35% to 58 and 68%, respectively. 62,63 There is considerable controversy and debate as to the best therapeutic approach for aneurysms(ruptured and unruptured). Impediments to resolving the debate include methodological shortcom-ings of published studies, the fact that endovascular methods are still rapidly evolving, which ren-ders many studies obsolete before completion, and the critical need for long-term follow-up of endovascular results.This section reviews some of the available information comparing surgical treatment to coilembolization. Ruptured intracranial aneurysms Todate, four randomized controlled trials have been published comparing functional outcome aftercoil embolization versus surgical clip ligation for ruptured intracranial aneurysms: the “Finnish Study, ”64ISAT 2002, 65the “Chinese Study, ”66and BRAT 2012. 67!Table 87.1 summarizes the treat- ment data from the 4 RCTs. Table 87.1 Summary of rebleeding, complete occlusion, and retreatment rates as a function of treatment modal- ity (clip vs. coil) for the 4 randomized controlled trials Rebleed a: Clip Rebleed a: Coil Completeocclusion: Clip Completeocclusion: Coil Retreatment:Clip Retreatment:Coil Finnish 0% 0% 73.7% b 50% b 7% 23.1% ISAT 1.0% 2.6% 82% 66% 4.2% 15.1% ISAT 5c 0.3%* 0.9%* n/a n/a ———— ———— ISAT 10c 0.4% 1.6% n/a n/a ———— ———— Chinese 3.3% 3.2% 83.7%* 64.9%* ———— ———— BRAT d 0.8% e 0% 85% 58% 4.5%* 10.6%* BRAT 3d 0% 0% 87% 52% 5%* 13%* *statistically significant difference (p < 0.05)aRebleeding from target aneurysm after first procedurebResult achieved after treatment during first hospitalizationcISAT 5& ISAT 10refer to the 5- and 10-year follow-up studies. Rebleeding results for these studies refer to recurrent SAH after the 1styear of follow-up dBRAT 3refers to the 3-year follow-up study. BRAT & BRAT 3are “as-treated ”results eBoth rebleeding events occurred during the initial hospitalization SAH from Cerebral Aneurysm Rupture 1457 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 !ISAT. The largest trial, the International Subarachnoid Hemorrhage Aneurysm Trial (ISAT), enrolled 2143 patients and ran from 1997 to 2002, and was stopped prematurely because of a signif- icant outcome di "erence between the 2 groups favoring endovascular coil embolization. Despite the limitations of ISAT (see below), the findings have often been generalized to all patients with aneur-ysms, resulting in a dramatic change in management.Results: At 1 year, there was an absolute reduction of risk of having a poor outcome (i.e., !Table 98.5, modified Rankin Scale score > 2) by 7% with coiling (24%) compared to open surgery(31%; p=0.0019). Although not statistically significant, rebleeding in the first year after treatmentwas higher for coiling (2.6%) than clipping (1.0%). Assuch, the durability of coil embolization and its ability to prevent subsequent rebleeding of the treated aneurysm were questioned. Additionally,ISAT had many important shortcomings, as detailed in !Table 87.2. Following the initial report, medium-term follow-up results have been published. 68In the endo- vascular cohort, there were 10 episodes of rebleeding from the treated aneurysm after 1 year, in8,447 person-years of follow-up. In the surgical cohort, 3 patients rebled from the treated aneurysmafter 1 year, in 8,177 person-years of follow-up (one of these patients had declined surgery after ran-domization and underwent coiling instead). There was a non-significant increased risk of rebleeding from the treated aneurysm in the endovascular cohort (p=0.06), by an intention-to-treat analysis,but a significant di "erence when analysis was by actual treatment (p=0.02). The probability of death at 5 years was significantly lower in the coiled group (11%) than in the clipping group (14%; p=0.03). However, when patients who died before treatment are excluded from this analysis, the statisticaldi"erence is no longer present (p=0.1). 69The probability of independent survival for those patients alive at 5 years was no di "erent between groups (83% coil; 82% clip). The 10-year results have been reported for the U.K. cohort from the initial trial. 70Similar to the 5- year results, the proportion of patients with a good outcome did not di "er between the two groups, but the probability of being alive with a good outcome compared with death or dependence was sig- nificantly better for the endovascular group. Thirteen patients in the endovascular group rebledfrom the target aneurysm (1 per 641 patient-years) compared to 4 in the surgical group (1 per 2,041patient-years). Although the risk of rebleeding was higher in the endovascular group, the overall risk was small and the risk of death or dependency from a rebleed did not di "er between the groups. A follow-up study, ISAT II (multicenter RCT), is currently being conducted to help elucidate di "er- ences in outcomes between treatment modalities. 71 !Chinese study 66.192 patients with aSAH randomized to coiling or clipping. Surgical clipping increased the risk of symptomatic vasospasm (OR 1.24), and there were significantly more new cere-bral infarctions in the clipping group (21.7 vs. 12.8%). Incidence of complete aneurysm occlusion was significantly lower in the coiling group (64.9 vs. 83.7%). Rebleeding rates were similar in both groups(!3%). At 1 year, there was no significant di "erence in probability of mortality (coiling: 10.6%, clip - ping: 15.2%). Furthermore, there was no significant di "erence in probability of a good outcome (coil- ing: 75%, clipping: 67.9%). !BRAT 67.Initiated at Barrow Neurologic Institute in 2002. Designed to ref lect “real-world ”practi- ces of ruptured aneurysm treatment in North America. Randomly assigned in an alternate fashionevery patient with SAH who agreed to participate. A large number of patients allocated to Table 87.2 Methodological shortcomings of ISAT 1. only 20% of 9559 patients presenting with SAH were randomized a a) selection could introduce biasb) more nonrandomized patients underwent MS than EDCc) guidelines not provided for which patients to consider for EDC2. most study centers were located in Europe, Australia & Canada3. the expertise of the surgeons and the interventionalists were not reported and were not necessarilycomparable4. the following features are not entirely representative of SAH patients at largea) 80% of patients were in good clinical condition (H&H grade 1 or 2)b) 93% of aneurysms were !10 mm diameter c) 97% were in the anterior circulation5. rebleeding rate: after EDC (2.4%) or MS (1.0%) was high for both groups, and the difference could be moresignificant beyond the 1-year follow-up providedamost SAH patients were referred specifically for MS or EDC. The only patients who were randomized were thosefor whom a panel decided it was not clear which procedure would be superior. Outcomes were not provided fornon-randomized patients Subarachnoid Hemorrhage and Aneurysms 1458 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 endovascular treatment crossed over to the surgical arm because patients could be enrolled regard- less of whether the aneurysm was amenable to both treatment modalities (75 crossed over from coil to surgery; 4 crossed over from surgery to coil). Proportion of patients with a poor outcome (i.e., mRS > 2) was 33.7% in the surgical group versus 23.2% in the endovascular group (p=0.02, intention- to-treat analysis). An “as-treated ”analysis yielded similar results (33.9 vs. 20.4%, p=0.01). There were 2 episodes of rebleeding following treatment —one assigned to and treated with clipping and the other assigned to coil, but treated with surgical clipping. Twelve patients (2.9%) required retreatment during the initial hospitalization (9 surgical and 3 coil patients). Overall, during the 1st year, therewas a significant increased probability of retreatment in patients actually treated with coiling com- pared with those actually treated by clipping (10.6% of coil vs. 4.49% of surgical patients, p=0.03).At 3 years, 72there was no significant di "erence in poor outcome between coiling (30%) and clip - ping (35.8%). Subgroup analysis: there were no di "erences in mRS scores between treatment groups at any time point among patients with anterior circulation aneurysms (83%). However, among poste-rior circulation aneurysms (17%), mRS scores were significantly better after endovascular manage-ment than after surgical treatment at every time point. Of note, with the exception of basilar tip aneurysms, the randomization of the posterior circulation aneurysms was unexpectedly skewed (large majority of SCA and PICA were clipped, whereas majority of PCA, vertebral, and basilar werecoiled). The lack of anatomical parity between the treatment groups makes it di !cult to draw strong conclusions. In addition, the degree of aneurysm obliteration (87 vs. 52%), rate of aneurysm recur-rence, and rate of retreatment (5 vs. 13%) were significantly better in the group treated with clippingas compared to coiling. However, no rebleeding occurrences were documented in the 2nd or 3rd yearof BRAT. !Meta-analyses. Lanzino et al 73conducted a meta-analsysis on the 3 prospective controlled stud- ies (Finnish, ISAT, BRAT). Pooled data showed poor outcome at 1 year to be lower in the embolizationgroup and no di "erence in mortality between groups; rebleeding rates within the first month were higher in coiled patients. However, the results were largely skewed by ISAT data.Li et al 74conducted a meta-analysis on the 4 RCTs (see above) and 23 observational studies. The result of the RCT analysis with regard to poor outcome at 1 year paralleled that by Lanzino et al. However, there was no di "erence in poor outcome between groups in the nonrandomized con- trolled trial analysis. Additional subgroup analysis showed a higher incidence of rebleeding after coiling (!2–3 vs. 1%), corresponding to a better complete occlusion rate of clipping (84 vs. 66.5%). Procedural complication rates and 1-year mortality did not di "er significantly between the groups. !Vasospasm. Whether coiling or clipping has an independent correlation with symptomatic vaso- spasm is debatable. One meta-analysis 75suggested a trend toward less symptomatic vasospasm after coiling as compared to clipping. However, the analysis had multiple limitations —the two treatment groups were not comparable (age, clinical grade, aneurysm location); there were di "erences in study design and definitions of vasospasm; and there was a lack of angiographic diagnosis of vasospasm. In the Chinese RCT (above) symptomatic vasospasm and consequent cerebral infarction were more common in the clipping group. Li et al 74found vasospasm was more common after clipping (48.8 vs. 43.1%); however, ischemic infarction did not di "er significantly. Treatment choice may also alter the spasm pattern: on one study, 76patients who underwent clipping developed localized vasospasm around the rupture site, whereas those treated with coiling demonstrated progressive distal vaso-spasm over time (possibly related to treatment-specific e"ects on CSF circulation). !Shunt-dependent hydrocephalus. One study showed a lower incidence of shunt-dependent hydrocephalus in the surgical treatment group (19.9 vs. 47.1%), 77but many others have failed to show this relationship. 74,78,79,80,81,82,83,84,85,86 A suggestion that fenestration of the lamina terminalis at the time of surgery may decrease shunt-dependent chronic hydrocephalus was refuted by a meta-analysis 87of 11 non-randomized studies (hydrocephalus rates of 10% with fenestration com - pared to 15% without). !Seizures. A literature review 88of seizures after aSAH reported a rate of !2% following either neu- rosurgical clipping or endovascular coiling. In contrast, ISAT showed endovascular intervention hadlower seizure rates (13.3% to 3.3%) compared to surgical clipping (2.2 –5.2%) in the first year. Assuch, there is no consensus as to whether treatment modality independently impacts seizure and/or epi-lepsy occurrence. !Factors toconsider (clipping vs. coiling) "health care environment / equipment available"skill set and experience of the neurosurgeon and interventionalist SAH from Cerebral Aneurysm Rupture 1459 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 #greater annual numbers of aneurysms treated by individual practitioners were significantlyrelated to decrease in morbidity 89 "anatomy and location of the aneurysm#favorable dome/neck ratio versus wide neck aneurysms#MCA aneurysms may be di !cult to coil because of a branch near the neck #basilar apex: favors coiling#associated IPH/SDH: surgery allows both evacuation of hemorrhage and treatment of aneurysm#symptoms due to mass e"ect: clipping 90,91 may be better than coiling. In 13 patients with PComA aneurysms and oculomotor nerve (3rd nerve) palsy (ONP ), 6 of 7 patients clipped vs. 2 of 6 with coiling recovered completely. 32Partial ONP improved with either treatment, but com- plete ONP recovered in 3 of 4 patients clipped vs. 0 of 3 coiled 32 "patient age#younger age: lower risk of surgery, and lower lifetime risk of recurrence than with coiling "clinical state/comorbidities#good outcome seen in 63% clip vs. 46% coil in poor-grade (WFNS IV/V) patients (contrary tofindings in practice guidelines 92); therefore, microsurgery and endovascular treatment, when selected primarily according to angiographic features, were equally likely to achieve goodoutcome 93 #patients on anticoagulation (e.g., Plavix) favor endovascular treatment Practice guideline: Aneurysm treatment decisions Level C 92: Treatment decisions should be multidisciplinary (made by experienced cerebrovascular and endovascular specialists) based on characteristics of the patient and aneurysm.Level C92: Microsurgical clipping may receive increased consideration in patients presenting with large (> 50 ml) intraparenchymal hematomas and middle cerebral artery aneurysms (!Fig. 85.1). Level C92: Endovascular coiling may receive increased consideration in the elderly (> 70 yo), in those presenting with poor-grade WFNS classification (IV/V) aSAH, and in those with aneurysms ofthe basilar apexLevel B 92: For patients with ruptured aneurysms judged to be technically amenable to both endo- vascular coiling and neurosurgical clipping, endovascular coiling should be considered Unruptured intracranial aneurysms Aswith ruptured aneurysms, there is controversy over the best treatment method for unruptured intracranial aneurysms (IUAs), and additional uncertainty surrounds the question of which IUAsneed to be treated (vs. observed). Darsaut et al 94found that practitioners do not agree regarding management of IUAs, even when they share a background in the same specialty, similar capabilitiesin aneurysm management, or years of practice.There are no prospective randomized studies of treatment interventions vs. conservative man-agement, 95or studies comparing treatment options to each other. Most data are either from personal series or are retrospective. !Surgical clipping. One summary of 260 patients (including a retrospective multicenter analysis) shows no surgical mortality, and morbidity of 0–10.3% (6.5% major and 8% minor morbidity in the multicenter study). 5Findings from one meta-analysis of 733 patients who underwent surgical clip - ping showed a mortality rate of 1% and major morbidity rate of 4%. 96A larger meta-analysis of 2,460 patients revealed mortality and morbidity rates of 2.6% and 10.9%, respectively. 97 The ISUIA investigators found surgical mortality to be 2.3% at 30 days, and 3.8% at 1 year. 98Addi- tionally, they found a combined morbidity and mortality at 1 year of 12.6% for those without pre- vious hemorrhage and 10.1% for those with previous subarachnoid hemorrhage from anotheraneurysm. For patients treated with surgical clipping, morbidity and mortality were greatest inthose with aneurysms that were large or in the posterior circulation, and in patients older than age50. In comparison, the combined morbidity and mortality forthe 451 patients treated with an endo- vascular procedure was 9.1% at 30 days and 9.5% at 1 year. Predictors of adverse outcome included aneurysm size and posterior circulation aneurysms. Additionally, the presence of calcification (inde-pendent of aneurysm size) has been shown to increase the likelihood of poor outcome. 99 Subarachnoid Hemorrhage and Aneurysms 1460 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 !Comparison of clipping to coil embolization. Early retrospective studies have shown a lower incidence of in-hospital death and discharge to skilled nursing facilities with endovascular therapycompared to those treated surgically. 100,101 A recent retrospective study conducted at a single center showed early outcome and lower complication rate favoring clipping, but the results did not remainsignificant long-term. 102A meta-analysis 103showed that clipping resulted in significantly higher dis- ability as compared to coiling (OR 2.38 –2.83). However, subgroup analysis by outcome-measure- ment time revealed clipping to be associated with greater risk of disability in the short-term (< 6months) but not in the long-term (> 6 months). In addition, mortality (in-hospital and overall), hem-orrhage, and infarction were no di "erent between groups. Despite inclusion of a large number of studies and patients, it is very challenging to draw any conclusion from the meta-analysis, as all the studies were observational (i.e., low levels of evidence), and the analysis did not stratify outcomesbased on size and/or location of aneurysms.Lawson et al 104 compared natural history rupture risk to national treatment risk for coiling and clipping (taken from the Nationwide Inpatient Sample from 2002 –2008). Overall mortality rate for clipping and coiling was 2.66% and 2.17%, respectively. Poor outcome was significantly greater for clipping (4.75%) versus coiling (2.16%). Data regarding the homogeneity of the two groups regarding aneurysm size or location was not available. Treatment risk curves were generated and compared against natural history actuarial risk curves calculated from four prominent studies. 9,105,106,107 Over- all, the analysis demonstrated rationale for clipping small, unruptured aneurysms in patients < 61 – 70 years and coiling small unruptured aneurysms in patients < 70 –80 years. Additional studies have focused on the e"ect of age on outcomes. Mahaney et al 108showed that procedural and in-hospital morbidity and mortality increased with age in patients treated with sur-gery, but remained relatively constant with endovascular treatment. Poor neurological outcomefrom aneurysm or procedure-related morbidity and mortality did not di "er between management groups for patients 65 years old and younger, but was significantly higher in the surgical group for patients older than 65 years. Surgery appeared to show a surgical benefit in patients < 50 years oldat 1 year. Others have suggested an overall benefit of endovascular treatment over surgical clipping, which becomes more pronounced with age. 109 !Cost. Several studies have compared total hospital costs for treatment of unruptured aneurysms with mixed results. Halkes et al 110and Hoh et al 111found endovascular treatment to be associated with higher total hospital costs. A later study by Hoh et al 112found that on a national level, surgical clipping was associated with higher costs. A long-term outcome study 113showed that clipping was associated with higher initial costs, but overall costs at 2 and 5 years were similar to coiling (due tohigher number of follow-up angiograms and outpatient costs). More recently, total hospital cost was shown to be lower forclipping, despite higher fixed-direct and fixed-indirect costs. 114This is a func- tion of much higher variable costs (i.e., the cost of coils and devices) overcoming any substantial costreduction due to shorter length of stay in patients treated endovascularly. !Miscellaneous. Oculomotor nerve palsy: Complete recovery of oculomotor nerve palsy associated with PComA aneurysms is more common with surgical clipping than with endovascular treatment(87 % vs. 44%). 115 Pregnancy: No studies have directly compared clipping versus coiling. Clipping may be preferred by some 116; see pregnancy and SAH (p. 1425). 87.8 Timing of aneurysm surgery 87.8.1 Background Historically, there was controversy between so-called “early surgery ”(generally, but not precisely defined as #48–96 hrs post-SAH) and “late surgery ”(usually "10–14 days post-SAH). The current consensus is that there should be intervention for a ruptured aneurysm (clipping or coiling) as promptly as possible to secure the aneurysm and prevent rebleeding. In a review of all patients withSAH treated by clipping or coiling in the Nationwide Inpatient Sample between 2002 –2010, treat- ment at non-teaching hospitals and older age (> 80 yo) were associated with delays in time to aneur- ysm clipping, but these associations were not seen when endovascular treatment was performed. 117 Increased time to procedure (> 3 days) was significantly associated with an increased likelihood of moderate to severe neurological deficit. Ultra-early (< 24 h after SAH) coiling of ruptured aneurysmshas also been associated with improved clinical outcomes (mRS 0–2) compared to coiling at > 24 hours in poor-grade SAH patients (Hunt and Hess (H&H) grade IV/V). 118 This does not rule out a selection bias, however. Additionally, the increased morbidity and mortality associated with surgical SAH from Cerebral Aneurysm Rupture 1461 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 intervention on patients who present subacutely with evidence of vasospasm on imaging, may bebetter suited forendovascular intervention. Early surgery advocated forthe following reasons: 1. if successful, virtually eliminates the risk of rebleeding, which occurs most frequently in theperiod immediately following SAH (p. 1437)2. facilitates treatment of vasospasm which peaks in incidence between days 6–8 post-SAH (never seen before day 3) by allowing induction of arterial hypertension and volume expansion withoutdanger of aneurysmal rupture3. allows lavage to remove potentially vasospasmogenic agents from contact with vessels, includinguse of thrombolytic agents (p. 1444)4. although operative mortality is higher, overall patient mortality is lower 119 Arguments against early surgery in favor of late surgery include1. inf lammation and brain edema are most severe immediately following SAHa) this necessitates more brain retractionb) at the same time this softens the brain, making retraction more di !cult (retractors have more tendency to lacerate the more friable brain) 2. the presence of solid clot that has not had time to lyse impedes surgery3. the risk of intraoperative rupture is higher with early surgery 4. incidence of vasospasm possibly increased after early surgery from mechanotrauma to vessels Factors that favor choosing early surgery include:1. good medical condition of patient2. good neurologic condition of patient (H&H grade #3) 3. large amounts of subarachnoid blood, increasing the likelihood and severity of subsequent vaso-spasm (p. 1447), !Table 86.2. Having the aneurysm clipped permits use of hyperdynamic ther- apy for vasospasm 4. conditions that complicate management in face of unclipped aneurysm: e.g., unstable blood pres-sure; frequent and/or intractable seizures5. large clot with mass e"ect associated with SAH 6. early rebleeding, especially multiple rebleeds7. indications of imminent rebleeding (see below) Factors that favor choosing delayed surgery (10 –14 days post-SAH) include: 1. poor medical condition and/or advanced age of patient (age may not be a separate factor relatedto outcome, when patients are stratified by H&H grade 120) 2. poor neurologic condition of patient (H&H grade "4):controversial . Some say the risk of rebleed- ing and its mortality argues for early surgery even in bad-grade patients, 121since denying sur- gery on clinical grounds may result in withholding treatment from some patients who would dowell (54% of H&H grade IV and 24% of H&H grade V patients had favorable outcome in one ser- ies120). Some data show no di "erence in surgical complications in good- and bad-grade patients with anterior circulation aneurysms 122 3. aneurysms di !cult to clip because of large size, or di !cult location necessitating a lax brain dur- ing surgery (e.g., di !cult basilar bifurcation or mid-basilar artery aneurysms, giant aneurysms) 4. significant cerebral edema seen on CT 5. the presence of active vasospasm 87.8.2 Conclusions Practice guideline: Timing of intervention for ruptured aneurysm Level B 92: Surgical clipping or endovascular coiling of a ruptured aneursym causing aSAH should be performed as early as feasible in the majority of patients to reduce the risk of rebleeding. Subarachnoid Hemorrhage and Aneurysms 1462 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 87.8.3 Imminent aneurysm rupture Findings that may herald impending aneurysm rupture and may therefore increase the need for expedient intervention include:1. progressing cranial nerve palsy e.g., development of 3rd nerve palsy with PComA aneurysm; tra- ditionally regarded as an indication forurgent treatment (p. 1454) 2. increase in aneurysm size on repeat angiography3. beating aneurysm sign 123: pulsatile changes in aneurysm size between cuts or slices on imaging (may be seen on angiography, MRA, or CTA) 87.9 General technical considerations of aneurysm surgery 87.9.1 General information The goal of aneurysm surgery is to prevent rupture or further enlargement of the aneurysm, whileat the same time preserving all normal vessels and minimizing injury to brain tissue and cranialnerves. This is usually accomplished by excluding the aneurysm from the circulation with a clipacross its neck. Placing the clip too low on the aneurysm neck may occlude the parent vessel, whiletoo distal placement may leave a so-called “aneurysmal rest, ”which is not benign since it may enlarge (see below).See Intraoperative aneurysm rupture (p. 1466) for general measures to reduce the risk of this complication during surgery. 87.9.2 Aneurysmal rest When a portion of the aneurysm neck is not occluded by a surgical clip, it is referred to as an aneur-ysmal rest. A “dog-ear ”occurs when a clip is angled to leave part of the neck at one end, and obliter- ates the neck at the other. Rests are not innocuous, even if only 1–2 mm, because they may later expand and possibly rupture years later, especially in younger patients. 124The incidence of rebleed- ing was 3.7% in one study, with an annual risk of 0.4 –0.8% during the observation period of 4–13 yrs. 125 Patients should be followed with serial angiography, and any increase in size should be treated by reoperation or endovascular techniques if possible. Booking the case: Craniotomy for aneurysm Also see defaults & disclaimers (p. 25).1. position: (depends on location of aneurysm), radiolucent head-holder2. intraoperative angiography (optional)3. equipment: microscope (with ICG capability if used)4. blood: type and cross 2 U PRBC5. post-op: ICU6. consent (in lay terms for the patient —not all-inclusive): a) procedure: surgery through the skull to place a permanent clip on the base of the aneurysmto prevent future bleeding, intraoperative angiogram, possible placement of external (ventric-ular) drain, possible lumbar drainb) alternatives: nonsurgical management, endovascular treatment only for aneurysms that arecandidatesc) complications: usual craniotomy complications (p. 25) plus (the following are not really compli - cations of surgery but are possible developments) post-op vasospasm, hydrocephalus, forma-tion of new aneurysms 87.9.3 Surgical exposure General information Toavoid excessive brain retraction, surgical exposure requires su !cient bony removal and adequate brain relaxation (see below). SAH from Cerebral Aneurysm Rupture 1463 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 Brain relaxation More critical for ACoA and basilar tipthan for easier-to-reach aneurysms such as PComA or MCA …. Techniques include:1. hyperventilation2. CSF drainage: provides brain relaxation and a field dry of CSF, and removes blood & blood break-down products along with the CSF. !CSF drainage before opening the dura is associated with an increased risk of aneurysmal rebleeding (p. 1437)a) ventriculostomy: risks include seizures, bleeding from catheter insertion, infection (ventricu-litis, meningitis), possible increased risk of vasospasm"placed pre-op in cases of acute post-SAH hydrocephalus (p. 1426)"placed intra-op b) lumbar spinal drainage (see below)c) intraoperative drainage of CSF from cisterns3. diuretics: mannitol and/or furosemide. Although proof is lacking, lowering ICP by this or anymeans may theoretically increase the risk of rebleeding 126 Lumbar spinal drainage See section 110.4.May be inserted with Tuohy needle following induction of anesthesia (to minimize BP elevation),prior to final positioning. CSF is gradually withdrawn by the anesthesiologist only after the dura is opened (to minimize chances of intraoperative aneurysmal bleeding); usually a total of 30 –50 cc are removed in !10 cc aliquots. Risks include 127: aneurysmal rebleeding (#0.3%), back pain (10%, may be chronic in 0.6%), catheter malfunction preventing CSF drainage (< 5%), catheter fracture or laceration resulting in retainedcatheter tipin the spinal subarachnoid space, post-op CSF fistula, spinal H/A (may be di !cult to dis- tinguish from post-craniotomy H/A), infection, neuropathy (from nerve root impingement with nee-dle), epidural hematoma (spinal and/or intracranial). Cerebral protection during surgery Pathophysiology of cerebral ischemiaThe cerebral metabolic rate of oxygen consumption (CMRO 2) (p. 1537) arises from neurons utilizing energy for two functions: 1) maintenance of cell integrity (homeostasis) which normally accounts for !40% of energy consumption, and 2) conduction of electrical impulses. Occlusion of an artery produces a central core of ischemic tissue where the CMRO 2is not met. The oxygen deficiency pre- cludes aerobic glycolysis and oxidative phosphorylation. ATP production declines and cell homeosta- sis cannot be maintained, and within minutes irreversible cell death occurs; a so-called cerebralinfarction. Surrounding this central core is the penumbra, where collateral f low (usually through leptomeningeal vessels) provides marginal oxygenation which may impair cellular function withoutimmediate irreversible damage. Cells in the penumbra may remain viable for hours. Cerebral protection by increasing the ischemic tolerance of the CNS1. drugs that mitigate the toxic e"ects of ischemia without reducing CMRO 2 a) calcium channel blockers: nimodipine, nicardipine, f lunarizineb) free radical scavengers: superoxide dismutase, dimethylthiourea, lazaroids, barbiturates, Vita-min Cc) mannitol: although not a cerebral protectant per se, it may help re-establish blood f low to compromised parenchyma by improving the microvascular perfusion by transiently increas-ing CBV and decreasing blood viscosity 2. reduction of CMRO 2 a) by reducing the electrical activity of neurons: titrating these agents to a isoelectric EEGreduces CMRO 2by up to a maximum of !50% "barbiturates: in addition to reducing CMRO 2, they also redistribute blood flow to ischemic cortex, quench free radicals, and stabilize cell membranes. For dosing of thiopental, seebelow"isof lurane (p. 109): shorter acting and less myocardial depression than with barbiturates b) by reducing the maintenance energy of neurons: no drugs developed to date can accomplishthis, only hypothermia has any e"ect on this. Below mild hypothermia, extracerebral e"ects must be monitored (p. 1051) Subarachnoid Hemorrhage and Aneurysms 1464 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 "mild hypothermia (core temperatures down to 33 °C): in a multicenter RCT, 128mild hypo - thermia was demonstrated to be safe, but did not improve the neurological outcome after craniotomy among good-grade (Hunt and Hess I–III) patients with aSAH "moderate hypothermia: 32.5 –33 °C has been used forhead injury "deep hypothermia to 18 °C permits the brain to tolerate up to 1 hour of circulatory arrest"profound hypothermia to < 10 °C allows several hours of complete ischemia (the clinicalusefulness of this has not been substantiated) Adjunctive cerebral protection techniques used in aneurysm surgery1. systemic hypotensiona) usually used during final approach to aneurysm and during manipulation of aneurysm for clipapplicationb) theoretical goals"to reduce turgor of aneurysm facilitating clip closure, especially with atherosclerotic neck"to decrease transmural pressure (p. 1427) to reduce the risk of intraoperative rupture c) one retrospective study 129suggests that a decrease in MAP > 50% is associated with poor out- come. However, after adjustment for age, this association was no longer statistically signifi- cant. Because of the potential danger of hypoxic injury to brain and other organs (includingareas of impaired autoregulation as well as normal areas), some surgeons avoid this method 2.“focal ”hypotension: using temporary aneurysm clips (specially designed with low closing force to avoid intimal injury) placed on parent vessel (small perforators will not tolerate temporaryclips without injury)a) used in conjunction with methods of cerebral protection against ischemiab) may be combined with systemic hypertension to increase collateral f low c) the proximal ICA can tolerate an hour or more of occlusion in some cases, whereas the perfo-rator-bearing segments of the MCA and the basilar apex may tolerate clipping foronly a few minutesd)in addition to the risk of ischemia, there is the risk of intravascular thrombosis and subse- quent release of emboli upon removal of the clip 3. circulatory arrest, utilized in conjunction with deep hypothermiaa) candidates include patients with large aneurysms that contain significant atherosclerosisand/or thrombosis that impedes clip closure and a dome that is adherent to vital neuralstructures 4. blood glucose: intraoperative hyperglycemia has been associated with long-term decline in cog - nition and gross neurologic function 130and should be avoided Systematic approach to cerebral protectionSee reference. 131 The following factors may mandate the use of temporary clips (and associated techniques of cere-bral protection): giant aneurysm, calcified neck, thin/fragile dome, adherence of dome to criticalstructures, vital arterial branches near the aneurysm neck, intraoperative rupture. Aside from giantaneurysms, most of these factors may be di !cult to identify pre-op. Therefore, Solomon provides some degree of cerebral protection to all patients undergoing aneurysm surgery.1. spontaneous cooling is permitted during surgery, which usually results in a body temperature of34 °C by the time that dissection around the aneurysm begins2. if temporary clipping is utilizeda) if a long segment of the ICA is being trapped, administer 5,000 U IVheparin to prevent throm- bosis and subsequent embolib) < 5 mins temporary clip occlusion: no further interventionc) up to 10 or 15 mins occlusion: administer IVbrain protection anesthesia (e.g., thiopental, pro- pofol, and/or etomidate) and titrate to burst suppression (p. 249) on EEG"administration of IV brain protection anesthesia to burst suppression has been shown tosignificantly decrease infarction rate with temporary clipping within this time range 132 "intermittent reperfusion has been shown to be advantageous in some studies, 132while in others findings have been contradictory 133,134 d) > 20 mins occlusion: not tolerated (except possibly ICA proximal to PComA), terminate opera-tion if possible and plan repeat operation utilizing"deep hypothermic circulatory arrest (see above)"endovascular techniques"bypass grafting around the segment to be occluded SAH from Cerebral Aneurysm Rupture 1465 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 87.9.4 Intraoperative and postoperative angiography Due to the fact that unexpected findings (aneurysmal rest, unclipped aneurysm, or major vesselocclusion) were seen on 19% of post-op angiograms (the only predictive factor identified was a new post-op deficit, which signaled major vessel occlusion), the routine use of some confirmatory test isrecommended. May also be applied to AVM surgery. Options include: 1. post-op angiography 135: correctable problems identified with this option require a return to the operating room, and some potentially reversible deficits may be too late to recover by that time2. intraoperative optionsa) catheter angiography using traditional iodinated contrast and f luoroscopy. Requires use ofradiolucent headholder. Typically the introducer sheath is placed in the femoral artery at thetime of initial pre-op angio, and is left in place forintraoperative use. Requires the services of an angiographer if the surgeon does not do thisb) visualize the vessels during surgery (has largely supplanted intra-op catheter angiography)1. indocyanine green (ICG) 136,137,138 : can be visualized under normal light, or sometimes to better advantage when illuminated with near-infrared light. Use is restricted to surfacevessels. May be less reliable with giant or wide-neck aneurysms or with thick-walled athe-rosclerotic vessels.Adult dose: may give 25 mg diluted to 5 ml with sterile water as rapid IV bolus. PDRadvises do not exceed maximum of 2 mg/kg (adult or child).2. f luorescein video angiography 138 87.9.5 Some drugs useful in aneurysm surgery Drug info: Propofol (Diprivan®) May be used to achieve burst suppression 139with shorter duration of action than other barbiturates. Results are preliminary, further investigation is needed to demonstrate the degree of neuroprotec-tion. Has been reported at doses 170 mcg/kg/min for neuroprotection 140(if tolerated) but this may be risky. May also be used as a continuous drip for sedation (p. 140), and for ICP management(p. 1049). Reverses rapidly upon discontinuation (usually within 5 –10 minutes). Side e!ects: possible anaphylactic reaction with angioneurotic edema (angioedema) of the airways, 141see propofol infusion syndrome (p. 140). 87.9.6 Intraoperative aneurysm rupture Epidemiology Reported rates of intraoperative aneurysm rupture (IAR) range from !18% in the cooperative study (1963 –1978) 142to!36% in a pre-microscope series 143(NB: this series had an unexplained high IAR rate of 61% with the microscope) and 40% in a more recent series. 144Although rupture rate may be higher in early surgery than with late surgery, 144other series found no di "erence. 145 Morbidity and mortality for patients experiencing significant IAR is!30–35% (vs. !10% in the absence of this complication), although IAR may primarily a"ect outcome when it occurs during induction of anesthesia or opening of dura. 144 See aneurysm rupture during coiling (p. 1924). Prevention of intraoperative rupture Presented as a list here to be incorporated into general operative techniques.1. prevent hypertension from catecholamine response to pain:a) ensure deep anesthesia during headholder pin placement and skin incisionb) consider local anesthetic (without epinephrine) in headholder pin-sites and along incisionline 2. minimize increases in transmural pressure: reduce MAP to slightly below baseline just prior to dural opening3. reduce shearing forces on aneurysm during dissection by minimizing brain retraction:a) radical removal of sphenoid wing forcircle of Willis aneurysms Subarachnoid Hemorrhage and Aneurysms 1466 87 https://ebooksmedicine.net/neurosurgery-book | 14.02.23 - 13:48 b) reduce brain volume by a number of mechanisms: diuretics (mannitol, furosemide), CSFdrainage through lumbar subarachnoid drain placed preoperatively and opened by the anes-thesiologist at the time of dural incision, hyperventilation 4. reduce risk of large tear in aneurysm fundus or neck: a) utilize sharp dissection in exposing aneurysm and in removing clot from around aneurysmb) whenever possible, completely mobilize and inspect aneurysm before attempting clipapplication Details of intraoperative rupture Rupture can occur during any of the three following stages of aneurysm surgery 146: 1. initial exposure (predissection)a) rare. Brain can become surprisingly tight even when bleeding seems to be into open subar-achnoid space. Usually carries poor prognosisb) possible causes:"vibration from bone work: dubious"increasing transmural pressure upon opening the dura"hypertension from catecholamine response to pain (see above) c) management tactics:"have anesthesiologist radically drop BP"control bleeding (with anterior circulation aneurysms) by placing temporary clip acrossICA as it exits from cavernous sinus, or if not possible then compress ICA in patient ’s neck through drapes"if necessary to gain control, resect portions of frontal or temporal lobe 2. dissection of the aneurysm: accounts forthe majority of IARs, two basic types: a) tears caused by blunt dissection"tends to be profuse, proximal to the neck, and di !cult to control "do not attempt definitive clipping unless adequate exposure has been achieved (which isusually not the case with these tears)"temporary clipping: this step is often necessary in this situation; after the temporary clip isin place return the MAP to normal and administer neuroprotective agent (e.g., propofol) "once the temporary clip is in place, it is better to take a few extra moments to improve the exposure and apply a well-placed permanent clip instead of hastily clipping and trying torestore circulation"microsutures may need to be placed to close any portion of the tear that extends onto theparent vessel b) laceration by sharp dissection"tend to be small, often distally on fundus, and usually easily controlled by a single suction"may respond to gentle tamponade with a small cottonoid"may shrink down with repeated low current strokes with the bipolar (avoid the temptationto use continuous high current) 3. clip application: bleeding at this point is usually due to eithera) inadequate exposure of aneurysm: clip blade may penetrate unseen lobe of aneurysm. Similarto tears caused by blunt dissection (see above). Bleeding worsens as clip blades becomeapproximated"prompt opening and removal of clip at the first hint of bleeding may minimize the extent ofthe tear"utilize 2 suckers to determine if definitive clipping can be done, or what is more common,to allow temporary clipping (see above) b) poor technical clip application: tends to abate as clip blades become approximated. Inspectthe blade tips forthe following: "to be certain that they span the breadth of the neck. If not, a second longer clip is usuallyapplied parallel to the first, which may then be advanced"to verify that they are closely approximated. If not, tandem clips may be necessary, andsometimes multiple clips are needed 87.9.7 Aneurysm recurrence after treatment Incompletely treated aneurysms may increase in size and/or bleed. This includes aneurysms that areclipped or coiled where there is still aneu