• Users Online: 76
  • Print this page
  • Email this page


 
 Table of Contents  
REVIEW ARTICLE
Year : 2022  |  Volume : 10  |  Issue : 1  |  Page : 26-34

Anesthetic management of intraoperative rupture of intracranial aneurysms


1 Department of Anaesthesiology, SMS Medical College, Jaipur, Rajasthan, India
2 Department of Anaesthesiology, Nalanda Medical College and Hospital, Patna, Bihar, India

Date of Submission21-Aug-2022
Date of Decision23-Aug-2022
Date of Acceptance25-Aug-2022
Date of Web Publication22-Sep-2022

Correspondence Address:
Dr. Harpreet Kaur
Department of Anaesthesiology, SMS Medical College, Jaipur, Rajasthan
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jcvs.jcvs_19_22

Rights and Permissions
  Abstract 


Intraoperative rupture of cerebral aneurysm is still the most commonly encountered fearsome complication that leads to subarachnoid hemorrhage and can be life threatening. Despite the advances in medical equipment and procedures, its incidence has not changed much in the past two decades. This article aims at reviewing the existing literature and describes the challenges faced by the diagnostician, surgeons, and anesthesiologists. It delineates the preoperative and perioperative factors that influence the rupture of cerebral aneurysm intraoperatively and further sketches the management of the same. A series of 129 articles related with the topic were searched from PubMed, Cochran, and Google databases to review the factors affecting the intraoperative rupture and its management. These factors were then collaborated and reported in this article to provide concise information on the topic that can direct the improvement in patient outcomes and management. This review concludes that thorough knowledge of the pathophysiology of intraoperative cerebral rupture and identifying the risk factors is the mainstay in better patient outcome. The management of this fearsome complication demands a synergistic approach from the surgeon, neuroradiologist, and the anesthesiologists.

Keywords: Anaesthesia, aneurysm, intraoperative, neuroanaesthesia


How to cite this article:
Kaur H, Kaur H. Anesthetic management of intraoperative rupture of intracranial aneurysms. J Cerebrovasc Sci 2022;10:26-34

How to cite this URL:
Kaur H, Kaur H. Anesthetic management of intraoperative rupture of intracranial aneurysms. J Cerebrovasc Sci [serial online] 2022 [cited 2022 Oct 4];10:26-34. Available from: http://www.jcvs.com/text.asp?2022/10/1/26/356700




  Introduction Top


Intraoperative aneurysm rupture leading to subarachnoid hemorrhage (SAH) is one of the most feared neurological complications. It leads to significant morbidity and unfavorable outcomes.[1],[2],[3]

While comparing the outcomes of open surgical repair and endovascular repair procedures, poorer outcomes have been reported in the surgical procedures. The higher morbidity in open surgical procedures is due to surgery rather than rebleeding. Despite the medical advances, aneurysm rupture has been reported to be the most commonly reported intraoperative complication.[4]

Upon epidemiological analysis done by various studies, it has been found that more than eighty percent of nontraumatic SAH are caused by intracranial aneurysmal rupture.[4] Other causes of spontaneous SAH include other vascular lesions, inflammation, tumors, and drug or substance use.[1],[4]

According to the existing literature, estimated incidence of SAH is 9.1/100,000/year worldwide. However, in some countries, notably, Japan and Finland, the incidence of nontraumatic SAH is higher, which is around 15–17/100,000/year.[5],[6]

Unruptured cerebral aneurysms have an incidence of around 3%–4% as per various angiographic and prospective autopsy studies. The mean age group affected in SAH is around 50–60 years with a female predominance of 1.6 times over males.[5]

The incidence of unruptured aneurysms has been increasing globally; Intra-Operative Rupture (IOR) of aneurysms still remains a dreaded and most commonly encountered complication.[7],[8],[9] Reported incidence from retrospective case series during microvascular surgeries is described to be between 7% and 40%,[10],[11],[12],[13],[14],[15] while it has been reported to be between 2% and 4.5% with endovascular procedures.[16],[17] The wide variation in the incidence of IOR with microsurgery could be due to wide variations in the definition of IOR. Some authors consider only major intraoperative ruptures (MIOR), while others include even the trivial or minor bleeding which have no effect on the patient outcome. A systematic review conducted by Muirhead et al., reported that different definitions account for the differences in rupture rates.[4] According to the study conducted by Hsu et al., MIOR is defined as aneurysmal rupture during brain retraction, aneurysm dissection, or clipping. These require further vigorous management to control the hemorrhage including hypotension, local packing, suctioning, and temporary clipping.[18] Minor or trivial intraoperative ruptures are those that occur during clip application and stop after approximation of the clip.[18] Chandler et al. have defined IOR as bleeding that changes the course of microsurgical procedure and it does not include minor bleeding that can be easily controlled surgically.[19] In spite of major advancements in microvascular surgeries and endovascular procedures, rupture of aneurysms is associated with high mortality rates of around one-third and severe disability in nearly one-sixth of the patients.[20]

A study conducted in the United States of America over 2 years (1996–1998) with a follow-up of 5 years included 1010 patients aimed at reporting the predictors of intraprocedural rupture (IPR) during coiling and clipping. According to this study, IPR occurred in 14.6% of the total cases, of which 19% were categorized under the clipped group and 5% in the coiled group. In the clipped group, 31% of patients with IPR had periprocedural death or disability as compared to 18% with no IPR. The coiled group in this study reported that 63% of patients had periprocedural death or disability. This study also called the Cerebral Aneurysm Rerupture After Treatment (CARAT) study is one of the largest cohort studies that studied the clinical implications of IPR.[10]


  Perioperative Factors Associated with Aneurysmal Rupture Top


According to literature, the risk of rupture of previously unruptured aneurysms is low 0.5%/year.[21] However, the prevalence of unruptured aneurysms is estimated to be around 0.65%–3.2% worldwide.[4]


  Preoperative Factors Top


Demographics such as age, sex, and family history as well as pathological causes like size of the aneurysm, shape, location, presence of co morbid conditions, and surgical or neuroradiological procedure are linked with perioperative cerebral aneurysm rupture.[7],[22] Asian and African races have been found to be independent predictors of rupture while coiling the aneurysm.[10] Similarly, genetics and family history has been found to be a major factor in the formation and rupture of an aneurysm.[23],[24] The prevalence of aneurysm is 9.5% in those with a positive family history as reported by the European Stroke Organisation.[25] The risk of SAH increases with a history of polycystic kidney disease.[7]

The incidence of SAH is 1.6 times higher in females as compared to males with occurrence in the fifth decade predominantly followed by regression in incidence in the later decades.[5],[6] Age has been shown to be an important factor in determining IOR with higher preponderance in elderly patients.[26],[27] However, in a retrospective study conducted by Lakicevic et al., male gender has been implicated to be having more chances of rupture as compared to females.[28]

Another important risk factor concerned with rupture of aneurysm is its location. As per existing literature, aneurysms are formed most commonly in the middle cerebral artery (MCA) followed by the internal carotid artery (ICA), whereas the risk of rupture is higher in anterior and posterior communicating arteries (AcoA and PCoA, respectively) and giant aneurysms of basilar artery.[12],[14],[29] The incidence of rupture is higher in posterior circulation, large and symptomatic aneurysms as quoted by a Japanese publication, whereas an American study concluded that most of the ruptured aneurysms are located in the anterior circulation.[30],[31]

Size of the aneurysm has also been implicated as a major cause of its rupture. International Study of Unruptured Intracranial Aneurysms has shown that larger aneurysms, those located in posterior circulation, and previous history of rupture have more chances of IOR.[24] Another large study showed that in addition to age of the patient, location and size of aneurysm are the main factors influencing the outcome of surgical clipping or endovascular coiling.[32] Sluzewski et al. have shown that aneurysm size is a major factor in IOR, smaller the size, lesser the chances of rupture.[33] Juvela et al. have also described the size of the aneurysm as an important predictor for rupture.[26] A study published in the New England Journal of Medicine quotes eleven times higher rates of rupture in aneurysms more than 10 mm in diameter (0.5%/year) in contrast to those with diameter <10 mm (0.05%/year). In giant aneurysms (>25 mm), rate was 6%/year.[34]

Complement activation and inflammatory tissue damage inside the aneurysmal vessel wall has been studied to be an important mechanism. Interplay of several biochemical mechanisms has been studied in the phenomenon of IOR. Variation in endothelial nitric oxide synthetase due to genetic modulations has also been implicated in the aneurysmal SAH.[35],[36] High catecholamine levels in cerebrospinal fluid (CSF) and serum S100 levels are associated with poor outcomes.[37],[38]

Predictors of aneurysmal growth may include diameter of 10 mm or more and location at basilar artery, ICA, or bifurcations.[39] Some aneurysms at rare locations which pose a great threat of rupture and are difficult to manage include intrasellar aneurysms, which mimic pituitary tumors, pericallosal aneurysms, and blood blister type of aneurysms.[40],[41],[42],[43],[44],[45] SAH related to nocturnal ruptures of aneurysms has also been found to be an independent risk factor for cerebral ischemia.[46] Aneurysms located at arterial bifurcations have wall shear stress acting at point of stress. However, in contrast, some studies have also reported contrast that aneurysms at junctions of PCoA as well as ICA do not have higher risk of rupture.[47],[48]

Patient related co morbidities like coronary artery disease (CAD) are an important risk factor for IOR. Smoking, hyperlipidemia, and hypertension also alter the vascular fragility which are known risk factors for CAD.[37] Therefore, CAD may lead to cardiac as well as cerebrovascular devastations during aneurysm surgery, thus making thorough cardiac evaluation important preoperatively.

Cigarette smoking has been found to be an important independent risk factor by various case–control and cohort studies worldwide. 40% of SAH cases have been attributed to smoking.[49],[50],[51],[52] In a prospective study, smoking and female sex have been found to be most significant factors in aneurysm formation and growth. Chronic obstructive pulmonary disease (COPD) has been found to be associated to IOR and cigarette smoking is the major cause of COPD. COPD patients have smoking related inflammatory changes along with biochemical changes like alpha-1 antitrypsin deficiency and high levels of matrix metalloproteinases, thus leading to a fragile vessel wall. Furthermore, loss of vascular smooth muscle, lesser collagen synthesis, and breakdown of extracellular matrix are other contributory factors. COPD also increases the resistance of airways causing a high transmural pressure gradient (TMPG) across the closed cranium.[51] The CARAT study also shows COPD to be major risk factor.[10] Faster growth rate of the aneurysm also increases the chances of rupture.[53]

Alcohol abuse has been studied by various researchers as one of the contributing factors to rupture of cerebral aneurysms and has been shown to be an independent risk factor of SAH in both males and females.[49],[50],[51] Ruigrok et al. have concluded that more than 300 g of alcohol consumption/week may lead to 20% more chances of SAH, while alcohol consumption between 100g and 299 g/week increases the chances of SAH by 11%.[52]

Rupture can be precipitated by sudden blood pressure or intracranial pressure (ICP) fluctuations.[4] Hypertension is, thus, one of the most important risk factors for formation and rupture of intracranial aneurysms.[53],[54] Poorly controlled hypertensives are at a high risk of aneurysm rupture. An increase in blood pressure increases the TMPG in the aneurysmal wall and also alters the vessel wall thickness. According to two case–control studies, the prevalence of hypertension is more in SAH patients than general population (20%–45%), yet after taking into account risk factors like age, gender, history of smoking and alcohol consumption, hypertension has not been shown to be a single significant risk factor.[51] However, general consensus of authors after combining the results of all case–control and cohort studies is to consider hypertension as a risk factor.[49] Researchers are also of the view that even though hypertensives do not show aneurysm growth more than normotensives, still hypertensive patients who use antihypertensive medication have a lower risk of aneurysm formation.[25]

Hypertension has been found to be more prevalent in multiple aneurysms and also makes a significant risk factor for the formation of new aneurysms and enlargement of the existing ones.[55]

Thus strict control of hypertension may improve the prognosis in cerebral aneurysm patients.[56] At the same time, cerebral vasospasm following rupture and hypotension as a measure to control it intraoperatively may lead to delayed ischemic neurological deficits.[57] Whereas, studies show that intraoperative hypotension or hypertension during aneurysm occlusion does not have any significant effect on the neurological outcome.[58]

This topic, thus, remains controversial, although studies recommend a strict control of systemic, diastolic, and mean arterial blood pressure.

Sudden rupture of aneurysm can also occur during induction of anesthesia in about 1%–2% of cases with a mortality rate of around 75%.[59],[60] Tsementzis et al. have reported that 8 patients out of 404 had an acute aneurysmal rupture during induction of anesthesia or while coughing and bucking during intubation, indicating sympathetic stimulation while airway manipulation.[59] Perioperatively, hypertension can occur during induction, intubation, positioning of patient, application of Mayfield pins on skull, pain at any time during local anaesthetic infiltration along the line of incision, during skin incision, periosteal flap dissection, opening of dura, coughing, or bucking anytime perioperatively, and extubation due to sympathetic surge. This increase in aneurysmal transmural pressure may lead to sudden rupture.[9],[61]

Preoperative neurological status of the patient is an essential determinant of IOR and patient outcome. A previously ruptured aneurysm has a higher risk of IOR as compared to a previously unruptured aneurysm.[12],[15]Preoperative Glasgow coma score is also an independent statistically significant predictor of major intraoperative rupture.[18] Evaluation of preoperative Hunt and Hess Grades (HH Grades) have shown that patients with HH Grades I and II have favorable outcome in 72.2% cases without IOR and 71.1% cases that had IOR. However, patients with HH Grades III and IV showed favorable outcomes in only 34.6% of cases without IOR and 23.1% of cases with IOR. Poor Fischer Grades (III and IV) are also associated with poor neurological outcomes postoperatively.[13] Schramm and Cedzich have stated that IOR affects the final outcome only if it occurs prematurely, while anesthetic induction or opening of dura.[14]

ICP is usually raised in patients with poor HH Grades. Sudden lowering of ICP may raise TMPG suddenly, leading to IOR.[62] Rapid large bolus of mannitol, excessive hyperventilation, rapid drainage of CSF via lumbar drains, or ventriculostomy catheters may cause IOR.[61] However, no substantial data is available to support the relation between ICP and IOR.[62] According to studies, application of Valsalva maneuver and positive end expiratory pressure may also lead to changes in aneurysmal transmural pressure.[61]

Timing of surgery after SAH in cases of already ruptured aneurysms has been found to be another factor involved in IOR. As stated by a study, incidence of IOR was three times greater in patients operated within 1st 3 weeks after SAH than in patients operated later (P < 0.05). Another study echoes similar results, in which 77 patients out of 222 who underwent surgery within 72 h of SAH had IOR in 40.2% cases, while the rate of rupture was 20.7% in the 145 patients who underwent operation after 72 h. However, mortality and severe morbidity after surgery was 2.6% in early surgery group, while it was 7.6% in late surgery group.[14]

Many variables are related to aneurysmal rupture during microvascular clipping or endovascular coiling. According to a study by Batjer and Samson, IOR of aneurysm is expected at three points. First is during the initial phase of surgery during craniotomy, dural opening, hematoma removal, and brain retraction (incidence of 7% and mortality 75%). Second stage is during blunt or sharp dissection (48% incidence). Third phase is during clip placement (incidence of 45%).[60] Inagawa concluded in the study that 9% intraoperative rupture occurs due to procedure itself, which is usually during dissection of aneurysm or dissection of adherent artery or clip application.[63] Posterior inferior cerebellar artery, ACoA, and PCoA are more likely to rupture intraoperatively as stated by another study.[64]

Experience of surgeon also plays a vital role in the IOR of aneurysm. Hsu et al. have conducted a multivariate analysis of 538 microsurgical clipping cases. They quoted that surgical experience is an independent predictor of MIOR. Experienced neurosurgeons encountered lesser number of MIOR (8%) as compared to novice surgeons (16%). Also, in cases of MIOR, the outcome was poorer in the hands of novice neurosurgeons by 1.9 fold. MIOR cases managed by experienced neurosurgeons had better prognosis than those by inexperienced neurosurgeons (poor outcome 22% vs. 60%).[18] Various other studies also have concordant results.[11],[15] In contrast some authors have reported that MIOR has no relation with surgical experience.[10],[65]

Management of very small aneurysm is challenging both surgically and endovascularly especially during endovascular embolization.[66] Iatrogenic rupture with coiling have been reported by Rasulić et al. in <4 mm and by Lakićević et al. in <2 mm aneurysms.[67] The advantage of surgical intervention being the immediate access to the proximal and distal vessels and removal of blood from operative site.[68] It has also been quoted that IOR during endovascular coiling has a poorer outcome due to lack of direct exposure.[59] Cloft and Kallmes. conducted a metaanalysis and found that IOR rate was 2.7%, with a rate of rupture of 4.1% in previously ruptured aneurysms.[69] Greater fragility and subsequent IOR of smaller aneurysms could be due to larger surface area of previous rupture, causing coils to damage the weakened site. Additionally, presence of daughter aneurysms may be an added risk factor.[17] Various mechanisms of rupture during coiling include guidewire or microcatheter perforation, high pressure contrast injection into the aneurysm leading to high transmural pressure.[70] Careless handling of guidewire or catheter such that catheter potential energy propels it forward leading to perforation of the aneurysm. Also wedging of catheter between deposited coils and aneurysm wall, overpacking and oversizing of coils could lead to rupture. In case of use of balloon assisted coiling, balloon inflation across the neck of aneurysm may lead to rupture.[71] CLARITY trial has studied endovascular management of aneurysms. According to this trial IOR is related more to patients of <65 years age, hypertensives and MCA aneurysms.[72] Another study revealed that there are five times more chances of rupture in already ruptured small aneurysms and balloon assisted hemostasis has better outcome.[73]

Usually surgery is warranted for younger age group and embolization for elderly patients. One study states that minimization of temporary occlusion and use of intraoperative angiography has improved the surgical outcome.[74] IOR and temporary occlusion for more than 20 min have been found to be independent predictors of perioperative stroke.[75]

The contributory factors may be excessive CSF drainage, hypertension causing hemodynamic stress and trauma during surgical manipulation.[76] Recurrence of aneurysm and subsequent SAH from residual necks after clipping[77] and incomplete occlusion after coiling may lead to chances of re rupture.[4]


  Postoperative Factors Top


Diagnosis of intraprocedure rupture

Clinically, unexplained sudden hypertension and bradycardia may indicate an IOR during coiling or clipping procedures.[59] Sudden high ICP and herniation could cause blown pupil, arrhythmias, and ischemia on neurophysiological monitoring (NPM)[58] Surgeon may notice increase in ooze from scalp incision or unexpected brain bulge.[59] According to authors, in case of an unexpected tense brain, IOR should be kept as a differential diagnosis[78] During coiling, dye extravasations or prolonged contrast dye transit time may be noticed. High ICP could lead to flow arrest or flow reversal of external carotid artery.[79] Postoperatively, delayed consciousness, sudden deterioration of neurological status, changes in hemodynamics, seizures, or focal neurological deficits are usual signs of IOR.[80]

NPM is helpful in identifying this crisis. Electroencephalography (EEG) may also show decrease in the power spectrum with weak alpha and beta frequencies and predominance or loss of low frequency components. EEG is a sensitive indicator of brain ischemia showing burst suppressions and finally complete electrical silence.[81]

Evoked potentials (EP) show decrease in amplitude and increased latency. Somatosensory EPs (SSEPs) are considered to be more significant than motor EP or brainstem EP. However, EEG and EP monitoring may be affected by anesthetics, temperature and hemodynamic status leading to erroneous interpretations.[82] During use of induced cerebral protection while temporary clipping, metabolic demand of neural tissue decreases and burst suppression is employed. This could lead to missing out of ischemic events on EEG. During this time of burst suppression, SSEP although not very sensitive to detect brain ischemia, may be helpful by the way of careful examination of the territory. It has been found to be helpful in 93% of the cases.[83] Intraoperative use of transcranial Doppler, cerebral oximetry, and intraoperative imaging like CT, MRI, and angiography has been found to be useful to diagnose IOR.[84],[85]

Management of IOR during surgical clipping

Before dural opening, various goals of management include ICP reduction and neuroprotection. Rapid lowering of ICP is not advocated, since ICP may have a protective tamponade effect which is beneficial to stop the bleeding. Gradual ICP reduction may be done using intravenous (IV) anesthetics like IV propofol or thiopentone sodium, moderate hyperventilation, and hypothermia.[86] IV anesthetics reduce the cerebral metabolic rate as well as ICP. Hypothermia has been quoted to have neuroprotective effects by lowering cerebral metabolism. It has free radical scavenging and membrane stabilizing effects. Different studies have variable views regarding induced hypothermia. Recent studies suggest use of mild hypothermia (32–35°) in good grade patients, but no benefit has been shown in poor grade patients.[87],[88] Its role during IOR is still controversial.

Hyperventilation may help lower the ICP but vasoconstriction induced by hyperventilation may worsen the brain ischemia. Short periods of moderate hyperventilation may be safe.[86]

Hemodynamic goals include lowering of blood pressure by 20% from baseline during IOR.[59],[61],[86] Aggressive treatment of blood pressure may lead to secondary ischemia. Prompt surgical clipping improves the outcome.[59] Various techniques may be implemented to blunt sympathetic stimulation to achieve hemodynamic stability to avoid rupture or re bleed. These include use of IV lignocaine, esmolol, or labetalol to reduce stimulation during airway manipulation. Local anesthetic infiltration at the site of incision and pin sites reduces stimulation while pinning and bone flap creation. Prophylactic propofol bolus or use of continuous infusion of short acting opioids like remifentanil or bolus of short acting opioid is also helpful to maintain cerebral perfusion pressure, ICP, and MAP.[86]

Other management goals include reducing the cerebral metabolism and lowering the abruptly increased ICP by ventricular drainage.[71] Use of iv anesthetics, controlling of blood pressure, and moderate hyperventilation can be started immediately.[61],[86] Urgent ventriculostomy or craniotomy may be the last resorts.[79]

After dural opening, induced hypotension with lowering of mean arterial pressure to 50 mmHg has been advocated by various authors. This helps improve surgical exposure and easy clipping of soft aneurysm neck.[59],[86] However, MAP of 50 mmHg may be difficult to achieve and could also lead to worsening of cerebral ischemia.[86] This is more so in situation of an IOR, where cerebral autoregulation is already impaired.[89] Thus, normotension, normovolemia, euglycemia, and proper electrolyte balance are advocated.[61],[86] Blood may be needed to be transfused in this situation.[90] During this phase, when dura is open, awareness or sudden movement under anesthesia must be avoided.[86] Neuromuscular monitoring is helpful. Temporary occlusion by clip application in case of IOR is imperative but difficult. This may be facilitated by transient circulatory arrest using adenosine.[91],[92] Adenosine induced flow arrest transiently may improve aneurysmal neck visualization. It is recommended to be started at a dose of 0.3–0.4 mg/kg to achieve profound hypotension for 45 s, along with remifentanil, low-dose volatile anesthetics, and propofol infusion.[91] Use of ventricular pacing for transient flow arrest has been found to be safe and effective during IOR.[93] The authors have recommended temporary interruption of arterial flow as a routine method for aneurysm clipping.[11]

During embolization, management includes reversal of heparin using protamine sulfate. Further continuing the packing with coils usually stops hemorrhage if bleeding is due to coil herniation.[11] Willinsky and terBrugge. have advocated leaving the microcatheter in situ, in case of perforation with it and introducing new catheter.[94]

Neuroprotection

Various neuroprotective mechanisms include hypothermia, hyperoxygenation, avoiding hyperthermia, maintaining euglycemia, hemodilution, hypervolemia, and hypertension. Other neuroprotective agents include calcium channel blockers, antifibrinolytic drugs, magnesium, anesthetic agents, and erythropoietin.[95],[96] Intraoperative hypothermia for aneurysmal surgery trial has stated that these neuroprotective drugs and mechanisms have no protective effects in the outcome.[97] Nitrous oxide used during anesthesia may also affect short term outcomes negatively, while no effect has been seen on long term outcomes.[97] However, during an episode of IOR, cerebral metabolic rate as well as blood pressure may be reduced using Propofol or thiopentone. Barbiturates have been found to have protective effects other than above.[98] Use of volatile anesthetics is recommended during IOR by authors, while their use during embolization should be avoided due to their effect in increasing cerebral blood volume and hence ICP.

Surgical management includes temporary occlusion of aneurysm in order to assist proper clipping and also decreases the chances of IOR. It has been seen that extra axial SAH or intraventricular hemorrhage have better outcomes then intraparenchymal hemorrhage[99] IOR is best prevented than treated. Various techniques include adequate exposure, proximal control, sharp dissection, and temporary clipping. Ruptures could also be prevented if small aneurysms <3 mm are not treated endovascularly.[67]


  Conclusion Top


Our review concludes that thorough knowledge of the pathophysiology of intraoperative cerebral rupture and identifying the risk factors is the mainstay in better patient outcome. The management of this fearsome complication demands a synergistic approach from the surgeon, neuroradiologist, and the anesthesiologists.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Siddiq F, Chaudhry SA, Tummala RP, Suri MF, Qureshi AI. Factors and outcomes associated with early and delayed aneurysm treatment in subarachnoid hemorrhage patients in the United States. Neurosurgery 2012;71:670-7.  Back to cited text no. 1
    
2.
McDonald RJ, McDonald JS, Bida JP, Kallmes DF, Cloft HJ. Subarachnoid hemorrhage incidence in the United States does not vary with season or temperature. AJNR Am J Neuroradiol 2012;33:1663-8.  Back to cited text no. 2
    
3.
van der Kolk NM, Algra A, Rinkel GJ. Risk of aneurysm rupture at intracranial arterial bifurcations. Cerebrovasc Dis 2010;30:29-35.  Back to cited text no. 3
    
4.
Muirhead WR, Grover PJ, Toma AK, Stoyanov D, Marcus HJ, Murphy M. Adverse intraoperative events during surgical repair of ruptured cerebral aneurysms: A systematic review. Neurosurg Rev 2021;44:1273-85.  Back to cited text no. 4
    
5.
de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ. Incidence of subarachnoid haemorrhage: A systematic review with emphasis on region, age, gender and time trends. J Neurol Neurosurg Psychiatry 2007;78:1365-72.  Back to cited text no. 5
    
6.
Numminen H, Kotila M, Waltimo O, Aho K, Kaste M. Declining incidence and mortality rates of stroke in Finland from 1972 to 1991. Results of three population-based stroke registers. Stroke 1996;27:1487-91.  Back to cited text no. 6
    
7.
Vlak MH, Algra A, Brandenburg R, Rinkel GJ. Prevalence of unruptured intracranial aneurysms, with emphasis on sex, age, comorbidity, country, and time period: A systematic review and meta-analysis. Lancet Neurol 2011;10:626-36.  Back to cited text no. 7
    
8.
Brown RD. Unruptured intracranial aneurysms. Semin Neurol 2010;30:537-44.  Back to cited text no. 8
    
9.
Bederson JB, Connolly ES Jr., Batjer HH, Dacey RG, Dion JE, Diringer MN, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: A statement for healthcare professionals from a special writing group of the Stroke Council, American Heart Association. Stroke 2009;40:994-1025.  Back to cited text no. 9
    
10.
Elijovich L, Higashida RT, Lawton MT, Duckwiler G, Giannotta S, Johnston SC, et al. Predictors and outcomes of intraprocedural rupture in patients treated for ruptured intracranial aneurysms: The CARAT study. Stroke 2008;39:1501-6.  Back to cited text no. 10
    
11.
Fridriksson S, Säveland H, Jakobsson KE, Edner G, Zygmunt S, Brandt L, et al. Intraoperative complications in aneurysm surgery: A prospective national study. J Neurosurg 2002;96:515-22.  Back to cited text no. 11
    
12.
Leipzig TJ, Morgan J, Horner TG, Payner T, Redelman K, Johnson CS. Analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. Neurosurgery 2005;56:455-68.  Back to cited text no. 12
    
13.
Sandalcioglu IE, Schoch B, Regel JP, Wanke I, Gasser T, Forsting M, et al. Does intraoperative aneurysm rupture influence outcome? Analysis of 169 patients. Clin Neurol Neurosurg 2004;106:88-92.  Back to cited text no. 13
    
14.
Schramm J, Cedzich C. Outcome and management of intraoperative aneurysm rupture. Surg Neurol 1993;40:26-30.  Back to cited text no. 14
    
15.
Wong JM, Ziewacz JE, Ho AL, Panchmatia JR, Kim AH, Bader AM, et al. Patterns in neurosurgical adverse events: Open cerebrovascular neurosurgery. Neurosurg Focus 2012;33:E15.  Back to cited text no. 15
    
16.
Li MH, Gao BL, Fang C, Cheng YS, Li YD, Wang J, et al. Prevention and management of intraprocedural rupture of intracranial aneurysm with detachable coils during embolization. Neuroradiology 2006;48:907-15.  Back to cited text no. 16
    
17.
Doerfler A, Wanke I, Egelhof T, Dietrich U, Asgari S, Stolke D, et al. Aneurysmal rupture during embolization with Guglielmi detachable coils: Causes, management, and outcome. AJNR Am J Neuroradiol 2001;22:1825-32.  Back to cited text no. 17
    
18.
Hsu CE, Lin TK, Lee MH, Lee ST, Chang CN, Lin CL, et al. The impact of surgical experience on major intraoperative aneurysm rupture and their consequences on outcome: A multivariate analysis of 538 microsurgical clipping cases. PLoS One 2016;11:e0151805.  Back to cited text no. 18
    
19.
Chandler JP, Getch CC, Batjer HH. Intraoperative aneurysm rupture and complication avoidance. Neurosurg Clin N Am 1998;9:861-8.  Back to cited text no. 19
    
20.
Inagawa T. Trends in incidence and case fatality rates of aneurysmal subarachnoid hemorrhage in Izumo City, Japan, between 1980-1989 and 1990-1998. Stroke 2001;32:1499-507.  Back to cited text no. 20
    
21.
Weir B, Disney L, Karrison T. Sizes of ruptured and unruptured aneurysms in relation to their sites and the ages of patients. J Neurosurg 2002;96:64-70.  Back to cited text no. 21
    
22.
Smith GA, Dagostino P, Maltenfort MG, Dumont AS, Ratliff JK. Geographic variation and regional trends in adoption of endovascular techniques for cerebral aneurysms. J Neurosurg 2011;114:1768-77.  Back to cited text no. 22
    
23.
Ruigrok YM, Rinkel GJ, Algra A, Raaymakers TW, Van Gijn J. Characteristics of intracranial aneurysms in patients with familial subarachnoid hemorrhage. Neurology 2004;62:891-4.  Back to cited text no. 23
    
24.
Mackey J, Brown RD Jr., Moomaw CJ, Sauerbeck L, Hornung R, Gandhi D, et al. Unruptured intracranial aneurysms in the Familial Intracranial Aneurysm and International Study of Unruptured Intracranial Aneurysms cohorts: Differences in multiplicity and location. J Neurosurg 2012;117:60-4.  Back to cited text no. 24
    
25.
Wang PS, Longstreth WT Jr., Koepsell TD. Subarachnoid hemorrhage and family history. A population-based case-control study. Arch Neurol 1995;52:202-4.  Back to cited text no. 25
    
26.
Juvela S. Prehemorrhage risk factors for fatal intracranial aneurysm rupture. Stroke 2003;34:1852-7.  Back to cited text no. 26
    
27.
Koffijberg H, Buskens E, Granath F, Adami J, Ekbom A, Rinkel GJ, et al. Subarachnoid haemorrhage in Sweden 1987-2002: Regional incidence and case fatality rates. J Neurol Neurosurg Psychiatry 2008;79:294-9.  Back to cited text no. 27
    
28.
Rüptürünü İA. Factors influencing intraoperative rupture of intracranial aneurysms. Turk Neurosurg 2015;25:858-65.  Back to cited text no. 28
    
29.
UCAS Japan Investigators, Morita A, Kirino T, Hashi K, Aoki N, Fukuhara S, et al. The natural course of unruptured cerebral aneurysms in a Japanese cohort. N Engl J Med 2012;366:2474-82.  Back to cited text no. 29
    
30.
Morita A, Fujiwara S, Hashi K, Ohtsu H, Kirino T. Risk of rupture associated with intact cerebral aneurysms in the Japanese population: A systematic review of the literature from Japan. J Neurosurg 2005;102:601-6.  Back to cited text no. 30
    
31.
Winn HR, Jane JA Sr., Taylor J, Kaiser D, Britz GW. Prevalence of asymptomatic incidental aneurysms: Review of 4568 arteriograms. J Neurosurg 2002;96:43-9.  Back to cited text no. 31
    
32.
Wiebers DO, Whisnant JP, Huston J 3rd, Meissner I, Brown RD Jr., Piepgras DG, et al. Unruptured intracranial aneurysms: Natural history, clinical outcome, and risks of surgical and endovascular treatment. Lancet 2003;362:103-10.  Back to cited text no. 32
    
33.
Sluzewski M, Bosch JA, van Rooij WJ, Nijssen PC, Wijnalda D. Rupture of intracranial aneurysms during treatment with Guglielmi detachable coils: Incidence, outcome, and risk factors. J Neurosurg 2001;94:238-40.  Back to cited text no. 33
    
34.
Lakićević N, Vujotić L, Radulović D, Cvrkota I, Samardžić M. Factors influencing intraoperative rupture of intracranial aneurysms. Turk Neurosurg 2015;25:858-85.  Back to cited text no. 34
    
35.
Khurana VG, Meissner I, Sohni YR, Bamlet WR, McClelland RL, Cunningham JM, et al. The presence of tandem endothelial nitric oxide synthase gene polymorphisms identifying brain aneurysms more prone to rupture. J Neurosurg 2005;102:526-31.  Back to cited text no. 35
    
36.
Tulamo R, Frösen J, Paetau A, Seitsonen S, Hernesniemi J, Niemelä M, et al. Lack of complement inhibitors in the outer intracranial artery aneurysm wall associates with complement terminal pathway activation. Am J Pathol 2010;177:3224-32.  Back to cited text no. 36
    
37.
Moussouttas M, Huynh TT, Khoury J, Lai EW, Dombrowski K, Pello S, et al. Cerebrospinal fluid catecholamine levels as predictors of outcome in subarachnoid hemorrhage. Cerebrovasc Dis 2012;33:173-81.  Back to cited text no. 37
    
38.
Shim JH, Yoon SM, Bae HG, Yun IG, Shim JJ, Lee KS, et al. Which treatment modality is more injurious to the brain in patients with subarachnoid hemorrhage? Degree of brain damage assessed by serum S100 protein after aneurysm clipping or coiling. Cerebrovasc Dis 2012;34:38-47.  Back to cited text no. 38
    
39.
Matsubara S, Hadeishi H, Suzuki A, Yasui N, Nishimura H. Incidence and risk factors for the growth of unruptured cerebral aneurysms: Observation using serial computerized tomography angiography. J Neurosurg 2004;101:908-14.  Back to cited text no. 39
    
40.
Hanak BW, Zada G, Nayar VV, Thiex R, Du R, Day AL, et al. Cerebral aneurysms with intrasellar extension: A systematic review of clinical, anatomical, and treatment characteristics. J Neurosurg 2012;116:164-78.  Back to cited text no. 40
    
41.
Nguyen TN, Raymond J, Roy D, Chagnon M, Weill A, Iancu-Gontard D, et al. Endovascular treatment of pericallosal aneurysms. J Neurosurg 2007;107:973-6.  Back to cited text no. 41
    
42.
Kamijo K, Matsui T. Acute extracranial-intracranial bypass using a radial artery graft along with trapping of a ruptured blood blister-like aneurysm of the internal carotid artery. Clinical article. J Neurosurg 2010;113:781-5.  Back to cited text no. 42
    
43.
Schaller B. Extracranial-intracranial bypass to reduce the risk of ischemic stroke in intracranial aneurysms of the anterior cerebral circulation: A systematic review. J Stroke Cerebrovasc Dis 2008;17:287-98.  Back to cited text no. 43
    
44.
Schaller B, Lyrer P. Anticoagulation of an unruptured, thrombosed giant intracranial aneurysm without hemorrhage or recanalization in the long-term follow-up. Eur J Neurol 2003;10:331-2.  Back to cited text no. 44
    
45.
Hauck EF, Wohlfeld B, Welch BG, White JA, Samson D. Clipping of very large or giant unruptured intracranial aneurysms in the anterior circulation: An outcome study. J Neurosurg 2008;109:1012-8.  Back to cited text no. 45
    
46.
Juvela S, Siironen J, Varis J, Poussa K, Porras M. Risk factors for ischemic lesions following aneurysmal subarachnoid hemorrhage. J Neurosurg 2005;102:194-201.  Back to cited text no. 46
    
47.
He W, Hauptman J, Pasupuleti L, Setton A, Farrow MG, Kasper L, et al. True posterior communicating artery aneurysms: Are they more prone to rupture? A biomorphometric analysis. J Neurosurg 2010;112:611-5.  Back to cited text no. 47
    
48.
Omodaka S, Sugiyama S, Inoue T, Funamoto K, Fujimura M, Shimizu H, et al. Local hemodynamics at the rupture point of cerebral aneurysms determined by computational fluid dynamics analysis. Cerebrovasc Dis 2012;34:121-9.  Back to cited text no. 48
    
49.
Feigin VL, Rinkel GJ, Lawes CM, Algra A, Bennett DA, van Gijn J, et al. Risk factors for subarachnoid hemorrhage: An updated systematic review of epidemiological studies. Stroke 2005;36:2773-80.  Back to cited text no. 49
    
50.
Kissela BM, Sauerbeck L, Woo D, Khoury J, Carrozzella J, Pancioli A, et al. Subarachnoid hemorrhage: A preventable disease with a heritable component. Stroke 2002;33:1321-6.  Back to cited text no. 50
    
51.
Juvela S, Hillbom M, Numminen H, Koskinen P. Cigarette smoking and alcohol consumption as risk factors for aneurysmal subarachnoid hemorrhage. Stroke 1993;24:639-46.  Back to cited text no. 51
    
52.
Ruigrok YM, Buskens E, Rinkel GJ. Attributable risk of common and rare determinants of subarachnoid hemorrhage. Stroke 2001;32:1173-5.  Back to cited text no. 52
    
53.
Juvela S, Poussa K, Porras M. Factors affecting formation and growth of intracranial aneurysms: A long-term follow-up study. Stroke 2001;32:485-91.  Back to cited text no. 53
    
54.
Nahed BV, DiLuna ML, Morgan T, Ocal E, Hawkins AA, Ozduman K, et al. Hypertension, age, and location predict rupture of small intracranial aneurysms. Neurosurgery 2005;57:676-83.  Back to cited text no. 54
    
55.
Wermer MJ, van der Schaaf IC, Velthuis BK, Algra A, Buskens E, Rinkel GJ, et al. Follow-up screening after subarachnoid haemorrhage: Frequency and determinants of new aneurysms and enlargement of existing aneurysms. Brain 2005;128:2421-9.  Back to cited text no. 55
    
56.
Kim J, Kim JH, Lee HS, Suh SH, Lee KY. Association between longitudinal blood pressure and prognosis after treatment of cerebral aneurysm: A nationwide population-based cohort study. PLoS One 2021;16:e0252042.  Back to cited text no. 56
    
57.
Thongrong C, Kasemsiri P, Duangthongphon P, Kitkhuandee A. Appropriate blood pressure in cerebral aneurysm clipping for prevention of delayed ischemic neurologic deficits. Anesthesiol Res Pract 2020;2020:6539456.  Back to cited text no. 57
    
58.
Akkermans A, van Waes JA, Peelen LM, Rinkel GJ, van Klei WA. Blood pressure and end-tidal carbon dioxide ranges during aneurysm occlusion and neurologic outcome after an aneurysmal subarachnoid hemorrhage. Anesthesiology 2019;130:92-105.  Back to cited text no. 58
    
59.
Tsementzis SA, Hitchcock ER. Outcome from “rescue clipping” of ruptured intracranial aneurysms during induction anaesthesia and endotracheal intubation. J Neurol Neurosurg Psychiatry 1985;48:160-3.  Back to cited text no. 59
    
60.
Batjer H, Samson D. Intraoperative aneurysmal rupture: Incidence, outcome, and suggestions for surgical management. Neurosurgery 1986;18:701-7.  Back to cited text no. 60
    
61.
Connolly ES Jr., Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: A guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke 2012;43:1711-37.  Back to cited text no. 61
    
62.
Heuer GG, Smith MJ, Elliott JP, Winn HR, LeRoux PD. Relationship between intracranial pressure and other clinical variables in patients with aneurysmal subarachnoid hemorrhage. J Neurosurg 2004;101:408-16.  Back to cited text no. 62
    
63.
Inagawa T. Dissection from fundus to neck for ruptured anterior and middle cerebral artery aneurysms at the acute surgery. Acta Neurochir (Wien) 1999;141:563-70.  Back to cited text no. 63
    
64.
Leipzig TJ, Morgan J, Horner TG, Payner T, Redelman K, Johnson CS. Analysis of intraoperative rupture in the surgical treatment of 1694 saccular aneurysms. Neurosurgery 2005;56:455-68.  Back to cited text no. 64
    
65.
Lawton MT, Du R. Effect of the neurosurgeon's surgical experience on outcomes from intraoperative aneurysmal rupture. Neurosurgery 2005;57:9-15.  Back to cited text no. 65
    
66.
Russell SM, Lin K, Hahn SA, Jafar JJ. Smaller cerebral aneurysms producing more extensive subarachnoid hemorrhage following rupture: A radiological investigation and discussion of theoretical determinants. J Neurosurg 2003;99:248-53.  Back to cited text no. 66
    
67.
Lakićević N, Prstojević B, Rasulić L, Vujotić L, Vukašinović I, Miličić B, et al. Intraoperative aneurysmal rupture: Clinical outcome following open surgery or endovascular treatment. Acta Clin Croat 2015;54:285-94.  Back to cited text no. 67
    
68.
Levy E, Koebbe CJ, Horowitz MB, Jungreis CA, Pride GL, Dutton K, et al. Rupture of intracranial aneurysms during endovascular coiling: Management and outcomes. Neurosurgery 2001;49:807-11.  Back to cited text no. 68
    
69.
Cloft HJ, Kallmes DF. Cerebral aneurysm perforations complicating therapy with Guglielmi detachable coils: A meta-analysis. AJNR Am J Neuroradiol 2002;23:1706-9.  Back to cited text no. 69
    
70.
Choi SS, Jeon SJ. Comprehension of two modalities: Endovascular coiling and microsurgical clipping in treatment of intracranial aneurysms. Neurointervention 2010;5:1-7.  Back to cited text no. 70
    
71.
Levy E, Koebbe CJ, Horowitz MB, Dutton K. Rupture of intracranial aneurysms during endovascular coiling: Management and outcome. Neurosurgery 2001;49:807-13.  Back to cited text no. 71
    
72.
Pierot L, Cognard C, Anxionnat R, Ricolfi F, CLARITY Investigators. Ruptured intracranial aneurysms: Factors affecting the rate and outcome of endovascular treatment complications in a series of 782 patients (CLARITY study). Radiology 2010;256:916-23.  Back to cited text no. 72
    
73.
Gil A, Vega P, Murias E, Cuellar H. Balloon-assisted extrasaccular coil embolization technique for the treatment of very small cerebral aneurysms. J Neurosurg 2010;112:585-8.  Back to cited text no. 73
    
74.
Schaller B, Lyrer P. Focal neurological deficits following spontaneous thrombosis of unruptured giant aneurysms. Eur Neurol 2002;47:175-82.  Back to cited text no. 74
    
75.
Ogilvy CS, Carter BS, Kaplan S, Rich C, Crowell RM. Temporary vessel occlusion for aneurysm surgery: Risk factors for stroke in patients protected by induced hypothermia and hypertension and intravenous mannitol administration. J Neurosurg 1996;84:785-91.  Back to cited text no. 75
    
76.
Hashimoto Y, Horita Y, Imaizumi T, Niwa J. Postoperative rupture of an untreated aneurysm on the 3rd day after subarachnoid hemorrhage surgery. Neurol Med Chir (Tokyo) 2005;45:249-52.  Back to cited text no. 76
    
77.
Pouratian N, Oskouian RJ Jr., Jensen ME, Kassell NF, Dumont AS. Endovascular management of unruptured intracranial aneurysms. J Neurol Neurosurg Psychiatry 2006;77:572-8.  Back to cited text no. 77
    
78.
Pickard JD, Lovick AH, Read DH. Evidence for brain engorgement as the initial cause of brain swelling following intraoperative aneurysm rupture in man after subarachnoid haemorrhage. Acta Physiol Scand Suppl 1986;552:94-5.  Back to cited text no. 78
    
79.
Sharma DP, Singh D, Jagetia A, Singh H, Tandon M, Ganjoo P. Intra procedure rupture of intracranial aneurysm during endovascular coiling: Neurosurgeons' experience and review of the literature. Neurol India 2011;59:690-5.  Back to cited text no. 79
[PUBMED]  [Full text]  
80.
Mahaney KB, Todd MM, Bayman EO, Torner JC, IHAST Investigators. Acute postoperative neurological deterioration associated with surgery for ruptured intracranial aneurysm: Incidence, predictors, and outcomes. J Neurosurg 2012;116:1267-78.  Back to cited text no. 80
    
81.
Bacigaluppi S, Fontanella M, Manninen P, Ducati A, Tredici G, Gentili F. Monitoring techniques for prevention of procedure-related ischemic damage in aneurysm surgery. World Neurosurg 2012;78:276-88.  Back to cited text no. 81
    
82.
Schick U, Döhnert J, Meyer JJ, Vitzthum HE. Effects of temporary clips on somatosensory evoked potentials in aneurysm surgery. Neurocrit Care 2005;2:141-9.  Back to cited text no. 82
    
83.
Krayenbühl N, Sarnthein J, Oinas M, Erdem E, Krisht AF. MRI-validation of SEP monitoring for ischemic events during microsurgical clipping of intracranial aneurysms. Clin Neurophysiol 2011;122:1878-82.  Back to cited text no. 83
    
84.
Park J, Woo H, Kim GC. Diagnostic usefulness of intraoperative ultrasonography for unexpected severe brain swelling in ultra-early surgery for ruptured intracranial aneurysms. Acta Neurochir (Wien) 2012;154:1869-75.  Back to cited text no. 84
    
85.
Schnell O, Morhard D, Holtmannspötter M, Reiser M, Tonn JC, Schichor C. Near-infrared indocyanine green videoangiography (ICGVA) and intraoperative computed tomography (iCT): Are they complementary or competitive imaging techniques in aneurysm surgery? Acta Neurochir (Wien) 2012;154:1861-8.  Back to cited text no. 85
    
86.
Priebe HJ. Aneurysmal subarachnoid haemorrhage and the anaesthetist. Br J Anaesth 2007;99:102-18.  Back to cited text no. 86
    
87.
Zhao ZX, Wu C, He M. A systematic review of clinical outcomes, perioperative data and selective adverse events related to mild hypothermia in intracranial aneurysm surgery. Clin Neurol Neurosurg 2012;114:827-32.  Back to cited text no. 87
    
88.
Li LR, You C, Chaudhary B. Intraoperative mild hypothermia for postoperative neurological deficits in intracranial aneurysm patients. Cochrane Database of Systematic Reviews. 2012;(2):CD008445.  Back to cited text no. 88
    
89.
Cossu M, Gennaro S, Rossi A, Balestrero MA, Cella F, Viale GL. Autoregulation of cortical blood flow during surgery for ruptured intracranial aneurysms. J Neurosurg Sci 1999;43:99-105.  Back to cited text no. 89
    
90.
Le Roux PD, Elliott JP, Winn HR. Blood transfusion during aneurysm surgery. Neurosurgery 2001;49:1068-74.  Back to cited text no. 90
    
91.
Bendok BR, Gupta DK, Rahme RJ, Eddleman CS, Adel JG, Sherma AK, et al. Adenosine for temporary flow arrest during intracranial aneurysm surgery: A single-center retrospective review. Neurosurgery 2011;69:815-20.  Back to cited text no. 91
    
92.
Luostarinen T, Takala RS, Niemi TT, Katila AJ, Niemelä M, Hernesniemi J, et al. Adenosine-induced cardiac arrest during intraoperative cerebral aneurysm rupture. World Neurosurg 2010;73:79-83.  Back to cited text no. 92
    
93.
Saldien V, Menovsky T, Rommens M, Van der Steen G, Van Loock K, Vermeersch G, et al. Rapid ventricular pacing for flow arrest during cerebrovascular surgery: Revival of an old concept. Neurosurgery 2012;70:270-5.  Back to cited text no. 93
    
94.
Willinsky R, terBrugge K. Use of a second microcatheter in the management of a perforation during endovascular treatment of a cerebral aneurysm. AJNR Am J Neuroradiol 2000;21:1537-9.  Back to cited text no. 94
    
95.
Frietsch T, Kirsch JR. Strategies of neuroprotection for intracranial aneurysms. Best Pract Res Clin Anaesthesiol 2004;18:595-630.  Back to cited text no. 95
    
96.
Hill MD, Martin RH, Mikulis D, Wong JH, Silver FL, Terbrugge KG, et al. Safety and efficacy of NA-1 in patients with iatrogenic stroke after endovascular aneurysm repair (ENACT): A phase 2, randomised, double-blind, placebo-controlled trial. Lancet Neurol 2012;11:942-50.  Back to cited text no. 96
    
97.
Hindman BJ, Bayman EO, Pfisterer WK, Torner JC, Todd MM, IHAST Investigators. No association between intraoperative hypothermia or supplemental protective drug and neurologic outcomes in patients undergoing temporary clipping during cerebral aneurysm surgery: Findings from the Intraoperative Hypothermia for Aneurysm Surgery Trial. Anesthesiology 2010;112:86-101.  Back to cited text no. 97
    
98.
Pasternak JJ, McGregor DG, Lanier WL, Schroeder DR, Rusy DA, Hindman B, et al. Effect of nitrous oxide use on long-term neurologic and neuropsychological outcome in patients who received temporary proximal artery occlusion during cerebral aneurysm clipping surgery. Anesthesiology 2009;110:563-73.  Back to cited text no. 98
    
99.
Chowdhury T, Petropolis A, Wilkinson M, Schaller B, Sandu N, Cappellani RB. Controversies in the anesthetic management of intraoperative rupture of intracranial aneurysm. Anesthesiol Res Pract 2014;2014:595837.  Back to cited text no. 99
    




 

Top
 
 
  Search
 
Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
Access Statistics
Email Alert *
Add to My List *
* Registration required (free)

 
  In this article
Abstract
Introduction
Perioperative Fa...
Preoperative Factors
Postoperative Fa...
Conclusion
References

 Article Access Statistics
    Viewed12    
    Printed0    
    Emailed0    
    PDF Downloaded0    
    Comments [Add]    

Recommend this journal


[TAG2]
[TAG3]
[TAG4]