Magnesium for the prevention and treatment of acute mountain sickness.

Magnesium is a physiological N-methyl-D-aspartate (NMDA) antagonist. The NMDA receptor may be involved in the pathogenesis of acute mountain sickness (AMS). In the present study, healthy subjects were randomized to receive either 400 mg of oral magnesium citrate (16 mmol) or matching placebo every 8 h for 5 days (prevention trial). Subjects then climbed to 4559 m in approx. 24 h and stayed there for 48 h. A Lake Louise Score <3 at any time was defined as the absence of AMS, whereas a score >6 (with ataxia, headache and nausea) was defined as a prevention failure. In a subsequent trial (treatment trial), subjects with a Lake Louise Score >6 (with ataxia, headache and/or nausea) were randomized to receive either 4 g of intravenous magnesium sulphate (16 mmol) or matching placebo. A decrease in the score >50% within 60 min was regarded as a treatment success. Dichotomous data were analysed using relative risk (RR) or odds ratio (OR), and continuous data using Student's t test or Wilcoxon's rank-sum test. In the prevention trial, data from 61 subjects (30 receiving magnesium and 31 placebo) were analysed. With oral magnesium, 20% of subjects had no AMS compared with 16.1% in the placebo group [RR (95% CI), 1.2 (0.4-3.6); where CI is confidence interval]. With magnesium, 40% were prevention failures compared with 35.5% in the placebo group [RR (95% CI), 1.13 (0.59-2.15)]. The mean time to failure and severity of AMS was similar between the two groups. With magnesium, 38.2% had loose stools compared with 11.8% in placebo group [RR (95% CI), 3.25 (1.18-8.97)]. In the treatment trial, 12 subjects received magnesium and 13 received the placebo. With intravenous magnesium, 25% were regarded as treatment successes compared with none in the placebo group [OR (95% CI), 9.71 (0.91-103.4)]. With magnesium, mean (+/- S.D.) scores decreased from 11.6 +/- 1.7 before treatment to 9.0 +/- 3.5 after treatment (P=0.009); scores remained unchanged in the placebo group. With magnesium, 75% of subjects experienced a transient flushing compared with 7.7% in the placebo group [RR (95% CI), 0.05 (0.01-0.25)]. In conclusion, oral magnesium does not prevent AMS. In subjects with established AMS, intravenous magnesium reduces the severity of symptoms to some extent, but this effect is of no clinical importance.

Fetal bradycardia due to intrathecal opioids for labour analgesia: a systematic review.

OBJECTIVE: To evaluate fetal and maternal adverse effects of intrathecal opioid analgesia during labour. DATA SOURCES: A systematic search was performed, in Medline, Embase, the Cochrane Library, bibliographies, and personal contact with authors, in any language, up to February 2001. STUDY: selection Full reports on randomised comparisons of any analgesia with intrathecal opioid (experimental group) with any non-intrathecal opioid regimen (control group) during labour. DATA EXTRACTION: Dichotomous data from 24 trials (3513 women). RESULTS: With intrathecal opioids, there was a significant increase in the risk of fetal bradycardia: odds ratio 1.8 (95% confidence interval 1.0 to 3.1), number-needed-to-harm 28. The risk of caesarean section due to fetal heart rate abnormalities was similar (6.0% versus 7.8%). The incidence of pruritus was significantly higher with intrathecal opioids: relative risk 29.6 (95% CI 13.6 to 64.6), number-needed-to-harm 1.7. CONCLUSIONS: Intrathecal opioids for labour increase the risk of fetal bradycardia and maternal pruritus. The risk of subsequent caesarean section is not increased.