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Neurology India, Vol. 59, No. 1, January-February, 2011, pp. 1-3 Editorial Neurosurgery and nitrous oxide: Not time yet for the last laugh? GS Umamaheswara Rao National Institute of Mental Health and Neurosciences (NIMHANS), Bangalore, India Date of Submission: 11-Oct-2010 Code Number: ni11001 PMID: 21339649 Traditionally, nitrous oxide (N 2 O) has been an integral component of general anesthesia. However, in recent years, evidence on complications associated with N 2 O has raised arguments against the use of N 2 O in anesthesia, particularly for patients with cerebral pathology. In this issue of Neurology India, Singh et al. [1] challenge the need to withhold N 2 O from anesthesia for brain tumour surgery by demonstrating that N 2 O did not significantly influence the duration of intensive care stay or mortality. The study raises a debate on the propriety of using N 2 O during neurosurgery. By contributing to the depth of anesthesia, [2] N 2 O decreases the need for the primary anesthetic agent, and thus helps in rapid awakening of the patient, which facilitates immediate post-operative neurological examination. Arguments for avoiding N 2 O in anesthesia, in general, are based on its adverse effects: (1) Potential to interfere with vitamin B 12 and folate metabolism, leading to megaloblastic anemia; [3] (2) expansion of the volume of gas-filled cavities (eg, pneumothorax, distended bowel); [4] and (3) post-operative nausea and vomiting (PONV). [5] The ENIGMA trial, [6] comprising 2,050 patients, showed that avoidance of N 2 O during anesthesia decreased the incidence of major post-operative complications such as severe PONV, wound infection, pneumonia, and atelectasis. The hospital stay was not significantly affected by N 2 O; however, among the patients admitted to the intensive care unit (ICU), the probability of discharge from ICU, on any given day, was higher in the N 2 O-free group. There are additional concerns also for using N 2 O in neurosurgery. Studies have documented increase in cerebral blood flow (CBF), [7] cerebral blood volume (CBV), and cerebral metabolism. [8] Background anesthetic and the degree of ventilation seem to influence the magnitude of these changes. Intravenous anesthetic agents like propofol [9] and hyperventilation [10] limit the increase in CBF and CBV. N 2 O-induced PONV may confound post-operative vomiting caused by raised intracranial pressure (ICP) due to acute intracranial complications (eg, post-operative hematoma). Venous air embolism during neurosurgery, with the patient in a sitting position and post-operative tension pneumocephalus due to subdural air collection during craniotomy may be accentuated by N 2 O. [11] N 2 O can decrease the amplitude of cerebral electrophysiological signals, [12],[13] dissuading its use when crucial electrophysiological monitoring is required. It has been implicated in the reversal of neuronal protection offered by thiopentone in experimental cerebral injury. [14] N 2 O interferes with homocysteine metabolism by oxidising the cobalt atom in vitamin B 12 , which, in turn, leads to defects of neuronal myelination. [15],[16] Neurological manifestations such as numbness, decreased deep tendon reflexes, cognitive dysfunction with histological evidence of neuronal mitochondrial swelling, vacuolation, and apoptosis have been reported. [17] N 2 O has also been implicated as a cause of post-operative dementia and cognitive deficits. [18],[19] By increasing serum homocysteine concentration, N 2 O may increase platelet aggregation, cause vasoconstriction, and impair endothelial function. [20] Do all the aforementioned effects of N 2 O influence the outcome of neurosurgery? Two recent publications address this issue, both of which are posthoc analyses of the Intra-operative Hypothermia for Aneurysm Surgery trial (IHAST) data. [21] The first study [22] analysed the effect of N 2 O on neurologic and neuropsychological function after intracranial aneurysm surgery. Of the 1,000 patients studied, 373 received N 2 O. N 2 O did not influence the development of delayed ischaemic neurological deficit (DIND). Outcomes at three months, as assessed by Glasgow Outcome Scale (GOS), National Institutes of Health (NIH) stroke scale, Rankin Disability Score, Barthel Index and neuropsychological testing, were similar between the groups. The authors speculate on the cause for the lack of difference between the groups: First, the study is posthoc in nature. Second, many of the patients may not have suffered ischemia that could have been influenced by N 2 O. In a subsequent study, [23] where only patients subjected to temporary vascular occlusion intraoperatively were included, N 2 O increased the risk of DIND [odds ratio (OR) = 1.78; 95% confidence interval (CI) = 1.08-2.95, P = 0.025). However, at three months, there was no difference in the neurological outcome scores. The data suggest that N 2 O may influence the short-term, if not the long-term neurological morbidity. Although Singh et al [1] . showed that there was no effect of N 2 O on post-operative ICU stay or mortality, the data obtained are not reassuring with regard to the use of N 2 O during craniotomy. The major limitation is the grossly inadequate sample size. The study data do not have any measure of raised ICP or cerebral ischemia in the study population. The subjects of the study being elective brain tumour patients, who would have been substantially optimised with pre-operative ICP control measures, the possibility of finding adverse influence of any therapeutic intervention is low. An adequately powered outcome trial, where raised ICP or cerebral ischemia is objectively quantified, is required to address the issue. The issue of using ICU stay and survival rates as the primary outcome measures of clinical interventions of low, but not negligible, risk also needs to be further debated. References
Copyright 2011 - Neurology India |
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