Summary This study investigated the effects of etomidate on endocrine responses to anaesthesia and surgery. Patients undergoing abdominal hysterectomy received standard anaesthetics of either etomidate for induction with etomidate infusion, or thiopentone and halo thane. Etomidate suppressed the secretion of cortisol and aldosterone for between 8 and 22 hours after the end of the etomidate infusion; 11‐deoxycortisol secretion was not suppressed during the etomidate infusion, but rose postoperatively; 17α‐hydroxyprogesterone suppression also lasted only as long as the etomidate infiion. There were no effects on plasma oestradiol, A CTH, or prolactin, but growth hormone concentrations were elevated in the etomidate group. Etomidate was concluded to have influenced adrenocortical function only, where it probably inhibits 11 β‐hydroxylation, 17 α‐hydroxylation and other intramitochondrial hydroxylation reactions. There were no clinical sequelae attributable to adrenocortical suppression. The relationship of chemical structure of etomidate and other phenylated imidazoles to inhibition of steroidogenesis is discussed.
One hundred and eighty-three patients were studied to examine the role of a number of risk factors in the development of silent ischaemia after general anaesthesia for general and vascular surgery. We collected evidence of cardiovascular risk factors using a binary questionnaire. The patients were monitored pre- and postoperatively using a Holter ECG monitor. Usable data were collected on 140 patients. Pre-operative silent myocardial ischaemia was found to be strongly associated with postoperative silent myocardial ischaemia (odds ratio: 10.8, 95% confidence intervals: 3.8-30.7). A history of hypertension, indicated by treatment with antihypertensive drugs, was associated with increased risk (odds ratio: 2.58, 95% confidence intervals: 1.12-5.96). A linear trend was found for risk associated with increasing admission systolic blood pressure (odds ratio: 1.20 for each 10-mmHg increase in systolic pressure, 95% confidence intervals: 1.01-1.42). An association between vascular surgery and postoperative silent myocardial ischaemia was also confirmed (odds ratio: 2.36, 95% confidence intervals: 1.1-5.1).
We performed a retrospective case-control study to investigate hypertension and admission blood pressure as risk factors for postoperative cardiovascular death. We identified records of 76 patients who had died of a cardiovascular cause within 30 days of anaesthesia and elective surgery and 76 matched controls. From the records of each patient (case and control) we recorded the admission blood pressure and details of any history of hypertension. A pre-operative history of hypertension was strongly associated with perioperative cardiovascular death (p < 0.001 with one degree of freedom: odds ratio 4.14, 95% confidence intervals 1.63-11.69). There was no association between systolic or diastolic pressure at admission for operation and perioperative cardiovascular death. The mean admission systolic pressure of the cases was 145.5 mmHg (range 90-250 mmHg) and that of the controls was 146.5 mmHg (range 100-200 mmHg). The mean admission diastolic pressure of the cases was 83.2 mmHg (range 60-130 mmHg), and that of the controls was 84.5 mmHg (range 60-110 mmHg).
Summary Ninety four patients undergoing transurethral resection of the prostate underwent Holter electrocardiographic monitoring pre‐and postoperatively. There was no difference in silent myocardial ischaemia incidence or load between the spinal (n = 60) ami the general anaesthesia (n = 34) groups. Ischaemic heart disease and a higher Detsky score both significantly increased the incidence of silent myocardial ischaemia but not the ischaemic load of those patients that actually demonstrated ischaemia. In this specific surgical population, not undergoing cardiac or vascular surgery, both ischaemic heart disease and cardiac risk scores are poor predictors of ischaemic load. Merely the presence of short duration silent myocardial ischaemia probably has little predictive value for postoperative adverse outcome.
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