In the Intraoperative Hypothermia for Aneurysm Surgery Trial, neither systemic hypothermia nor supplemental protective drug affected short- or long-term neurologic outcomes of patients undergoing temporary clipping.

Background Perioperative hypothermia has been reported to increase the occurrence of cardiovascular complications. By increasing sympathetic nervous system activity, perioperative hypothermia also has the potential to increase cardiac injury and dysfunction associated with subarachnoid hemorrhage. Methods The Intraoperative Hypothermia for Aneurysm Surgery Trial randomized patients undergoing cerebral aneurysm surgery to intraoperative hypothermia (n = 499, 33.3 ± 0.8°C) or normothermia (n = 501, 36.7 ± 0.5°C). Cardiovascular events (hypotension, arrhythmias, vasopressor use, myocardial infarction, etc.) were prospectively followed until 3 month follow-up and were compared between hypothermic and normothermic patients. A subset of 62 patients (hypothermia, n = 33; normothermia, n = 29) also had preoperative and postoperative (within 24 h) measurement of cardiac troponin-I and echocardiography to explore the association between perioperative hypothermia and subarachnoid hemorrhage-associated myocardial injury and left ventricular function. Results There was no difference between hypothermic and normothermic patients in the occurrence of any single cardiovascular event or in composite cardiovascular events. There was no difference in mortality (6%) between groups and there was only a single primary cardiovascular death (normothermia). There was no difference between hypothermic and normothermic patients in post- vs. preoperative left ventricular regional wall motion or ejection fraction. Compared with preoperative values, hypothermic patients had no postoperative increase in cardiac troponin-I (median change 0.00 μg/L) whereas normothermic patients had a small postoperative increase (median change + 0.01 μg/L, P = 0.038). Conclusion In patients undergoing cerebral aneurysm surgery, perioperative hypothermia was not associated with an increased occurrence of cardiovascular events.

Background We explored the relationship between nitrous oxide use and neurological and neuropsychological outcome in a population of patients likely to experience intraoperative cerebral ischemia: i.e., those who had temporary cerebral arterial occlusion during aneurysm clipping surgery. Methods A post hoc analysis of a subset of the data from the Intraoperative Hypothermia for Aneurysm Surgery Trial was conducted. Only subjects who had temporary arterial occlusion during surgery were included in the analysis. Metrics of short-term and long-term (i.e., 3 months post-surgery) outcome were evaluated via both univariate and multivariate logistic regression analysis. An odds ratio (OR) of greater than 1.0 denotes a worse outcome in patients receiving nitrous oxide. Results We evaluated 441 patients, of which 199 received nitrous oxide. Patients receiving nitrous oxide had a greater risk of delayed ischemic neurologic deficits (i.e., the clinical manifestation of vasospasm) (OR=1.78, 95% confidence interval [CI]=1.08–2.95, p=0.025). However, at 3 months after surgery, there was no difference in any metric of gross neurologic outcome: Glasgow Outcome Score (OR=0.67, CI=0.44–1.03, p=0.065), Rankin Score (OR=0.74, CI=0.47–1.16, p=0.192), National Institutes of Health Stroke Scale (OR=1.02, CI=0.66–1.56, p=0.937), or Barthel’s Index (OR=0.69, CI=0.38–1.25, p=0.22). The risk of impairment on at least one test of neuropsychological function was reduced in those who received nitrous oxide (OR=0.56, CI=0.36–0.89, p=0.013). Conclusion In our patient population, use of nitrous oxide was associated with an increased risk for the development of delayed ischemic neurologic deficits; however, there was no evidence of detriment to long-term gross neurologic or neuropsychological outcome.

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CARDIOTHORACIC ANESTHESIA, RESPIRATION AND AIRWAYPurpose: To present the case of an initially unexplained complication of sudden pulmonary edema in a patient during stenting of the carotid artery in the interventional neurology suite.Clinical Features: A 46-yr-old woman (ASA III) having an intracavernous carotid artery angioplasty and stenting procedure under neurolept anesthesia developed sudden pulmonary edema on completion of an otherwise uneventful stenting procedure. The patient responded well to initial management of pulmonary edema although the cause of the edema remained unclear. On retrospective examination of data and with the evolution of clinical signs it became apparent that the patient had suffered a subarachnoid hemorrhage which eventually resulted in her death.Conclusions: Clinical signs of intracerebral events may be slow to evolve. The cause of sudden pulmonary edema in patients undergoing an interventional neuroendovascular procedure is likely to be neurogenic in origin despite the initial lack of neurological signs. Éléments cliniques : Une femme de 46 ans (ASA III) admise pour une angioplastie du siphon carotidien et la pose d'un tuteur sous neuroleptanesthésie, a développé un oedème pulmonaire soudain à la fin de la pose du tuteur, par ailleurs sans incident. La patiente a bien réagi au traitement initial de l'oedème pulmonaire même si la cause en est restée obscure. À la suite d'un examen rétrospectif des données et de l'évolution des signes cliniques, il est devenu évident que la patiente a subi une hémorragie sous-arachnoïdienne qui a finalement causé sa mort. Conclusion :Les signes cliniques d'événements intracérébraux peuvent présenter une lente évolution. La cause d'un oedème pulmonaire soudain chez des patients qui subissent une intervention neuroendovasculaire peut être d'origine neurogène malgré l'absence initiale de signes neurologiques.