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.
Background: Degenerative cervical myelopathy is a spinal disorder resulting in progressive spinal cord compression and consequent neurological deficits that can be assessed and tracked using the modified Japanese Orthopedic Association (mJOA) questionnaire. However, it is difficult to predict which patients will recover neurological function after surgery, making it difficult for clinicians to set reliable postoperative patient expectations. Methods: Sixty-eight operative myelopathy patients (50 male, 14 female) consented to complete the mJOA questionnaire both preoperatively and 6-months postoperatively. Fifteen of these patients had mild, twenty-three had moderate, and thirty had severe preoperative disease. Results: We found that in mild myelopathy, sensation and strength recover in similar proportions. In moderate myelopathy, a greater proportion of patients recover in each domain except for sensation. Recovery in severe myelopathy was comparable to moderate disease, but showed more dramatic recovery in sensation and sphincter function. Conclusions: This study shows that the severity of myelopathic disease influences the pattern of postoperative recovery. Though limited in sample size, the recovery patterns identified above are an important first step in recognizing myelopathy as a disease that patients experience heterogeneously both pre- and post-operatively. Our results will aid clinicians in goals-of-surgery discussions and assist with managing postoperative patient expectations.
Background: Degenerative cervical myelopathy is characterized by progressive compression of the spinal cord resulting in debilitating loss of dexterity, independent ambulation, and sphincter control. Diffusion tensor imaging (DTI) has shown that, compared to healthy controls, myelopathy patients have decreased integrity of the corticospinal tracts and corpus callosum (Bernabeu-Sanz et al, 2020). Methods: Twenty-six myelopathy patients consented to cerebral diffusion tensor imaging (3 Tesla, 32 directions, b=1000) preoperatively, as well as 6-weeks, 12-weeks, and 6-months postoperatively. Average mean diffusivity (MD), fractional anisotropy (FA), radial diffusivity (RD), and axial diffusivity (AD) were measured in the corticospinal tracts, forceps major, and forceps minor. Results: Both MD and RD decreased from 6-12 weeks postoperatively in the right corticospinal tract. The forceps major of the corpus callosum showed an initial postoperative increase in MD followed by a subsequent increase in FA and decrease in RD 3-6 months postoperatively. The AD of the forceps major increased both immediately and 3-6 months postoperatively. Conclusions: Changes in microstructural integrity of the corticospinal tract and forceps major over the postoperative recovery period suggest a pattern of recovery in myelopathy patients. This study is the first to report postoperative DTI changes in myelopathy-relevant white matter tracts in the brain.
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