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.

No abstract

developed abdominal pain. Two days later he passed a melaena stool and was admitted to hospital. On admission his haemoglobin level had fallen to 8 5 g'dl and his prothrombin time was greater than 3 min. Extensive generalised haemorrhage into the tissues was revealed by the later appearance of Cullen's sign and bruising on the legs. Despite blood transfusion and correction of the prothrombin time with vitamin K he survived the haemorrhage only to succumb to intractable cardiac failure three weeks later. Permission for postmortem examination was not obtained. I am grateful to Miss H M Chadwick of Ames Co for a gift of Tek-chek quality control material.