Anaesthesia and Intensive Care最新文献

In the second half of the nineteenth century and up to the First World War, anaesthetic practice in Scotland differed markedly from that in England. Chloroform was invariably used in Scotland with apparent disregard for reports of deaths under its influence. By contrast, in England concern about chloroform deaths, which were subject to inquests there, led to ether often being chosen instead. This article examines the different interpretations and handling of chloroform deaths in the two countries, drawing on the medical journals of the period and archived documents. Quite symmetrical claims were made. Whereas in England the danger of chloroform was perceived to be an inherent property of the agent itself, in Scotland the blame was thrown on a timid method of administration. The interpretation in Scotland was supported by a network of doctors who promoted chloroform as effective, safe and easy to administer; manufacturers who had monopoly of its manufacture; and legal practitioners who were uninterested in investigating anaesthetic deaths. Although the reporting of anaesthetic deaths was flawed in England, underreporting was far worse in Scotland. The fear of anaesthetic deaths in England allowed the seeds of specialisation in anaesthesia to germinate, whereas in Scotland the downplaying of anaesthetic risk obviated the notion of such specialisation.

James Young Simpson's Notice of a New Anaesthetic Agent is a rare pamphlet of which three copies have hitherto been documented. Two of the three known copies were inscribed by Simpson with the words 'proof copy'. A fourth copy of the pamphlet, also inscribed with the words 'proof copy', has been identified. Although regarded by Simpson as a proof copy, there is previously unreported evidence that the pamphlet was advertised by the publisher on 12 November 1847, published on 13 November 1847, and sold on that day by booksellers in Edinburgh. Thus, the Notice pamphlet was the first published report of the use of chloroform as an anaesthetic agent. The pamphlet was issued 2 or 3 days before the well-known revised edition bearing the title Account of a New Anaesthetic Agent, and one week before the publication of Simpson's papers on chloroform in The Lancet and the Medical Times.

The study objective was to determine the incidence of complications from induced hypertension used to treat delayed cerebral ischaemia (DCI) complicating aneurysmal subarachnoid haemorrhage (aSAH). Induced hypertension (IH) was defined as the use of vasopressors to achieve a supraphysiological systolic blood pressure target. A single-centre retrospective, observational cohort study was undertaken at the Royal Adelaide Hospital intensive care unit. Data are presented as predominantly median (interquartile range (IQR)). All patients admitted with a diagnosis of aSAH between 1 April 2020 and 1 April 2022 were included and analysed according to whether they did or did not receive vasopressors for IH. A total of 109 patients were included, of which 29 (27%) received vasopressors for IH (median age 58 (IQR 52-65) years, 65% female) and 80 did not receive IH (median age 55 (IQR 49-71) years, 62% female). Clinical DCI or radiological evidence of vasospasm were present in all patients given IH and in 16% of non-IH patients. Patients in the IH group had more ischaemic electrocardiogram (ECG) changes (17.2% vs 2.5%, P = 0.01), urine output (4807 (IQR 3186-5720) ml/day vs 2125 (IQR 1650-2760) ml/day, P < 0.001), fluid administration (4895 (IQR 3555-5999) ml/day vs 2704 (IQR 2300-3403) ml/day, P < 0.001) and intravenous potassium replacement (13 (IQR 5-24) mmol/day vs 5 (IQR 0-13) mmol/day, P = 0.001) than those in the non-IH group. IH was also associated with a greater incidence of hyponatraemia (58% vs 34%, P = 0.02). IH was not associated with arrhythmias or rebleeding. Mortality rates were 17% vs 20% (P > 0.9) in the IH and non-IH groups respectively. In conclusion, IH for the treatment of DCI following aSAH was associated with an increased rate of ischaemic ECG changes, increased urine output and hyponatraemia. However, in the IH group there was no increased rate of rebleeding, and 48% of the IH patients had an improvement in their neurological function following commencement of treatment.

Nitrous oxide (N₂O) is a greenhouse gas that is a significant contributor to the carbon dioxide-equivalent emissions of health services. We aimed to obtain information about N₂O usage and knowledge of its environmental effects among clinical staff at an Australian metropolitan public health network. We distributed an anonymised survey to doctors, nurses and midwives working in anaesthesia, birthing, adult and paediatric emergency medicine, and paediatrics. We analysed 403 of 1320 (31%) responses; 117 of 198 (59%) from anaesthesia, 102 of 368 (27%) from birthing, 137 of 643 (21%) from adult and paediatric emergency medicine and 40 of 111 (36%) from paediatrics. Descriptive statistics were used, and statistical analyses performed on questions regarding environmental knowledge. Of those who currently used N₂O, the majority indicated there were alternative therapies (184/239, 77%), which they would (137/239, 57%) or could (90/239, 38%) be willing to use. Approximately half (219/385, 57%) of respondents correctly identified N₂O as a greenhouse gas, but only 70/382 (18%) identified its global warming potential as hundreds of times that of carbon dioxide. Almost half (180/383, 47%) answered that N₂O is ozone depleting. For anaesthetists, 96% (45/47) knew that N₂O was a greenhouse gas, compared with 41% (32/79) of midwives. This survey demonstrated that frequency of use and reason for use of N₂O varies between clinical groups, and that a significant proportion of staff that use N₂O do not know its harmful environmental characteristics. Our results provide data to inform future research on interventions to minimise clinical use of N₂O, and suggest that educational programs should form part of these efforts.

Nebulised unfractionated heparin (UFH) might reduce time to ventilator separation in patients with COVID-19 by reducing virus infectivity, pulmonary coagulopathy, and inflammation, but clinical trial data are limited. Between 1 July 2020 and 23 March 2022, we conducted, at two hospitals in Victoria, Australia, a randomised, parallel-group, open-label, controlled trial of nebulised UFH. Eligible patients were aged 18 years or more, intubated, under intensive care unit management, had a P_aO₂ to F_IO₂ ratio of 300 or less, had acute opacities affecting at least one lung quadrant and attributed to COVID-19, and were polymerase chain reaction-positive for SARS-CoV-2 or had further testing planned. The target sample size was 270, however, the trial was stopped due to slow recruitment. There were 50 enrolments, all of whom were analysed. The median age was 55 (interquartile range (IQR) 46-64) years, 28 (56%) were males, and 46 (92%) had acute respiratory distress syndrome. Twenty-seven (54%) were randomised to nebulised heparin and 23 (46%) to standard care. Nebulised UFH was administered to the heparin group on 6 (IQR 4-10) days; median daily dose of 83 (IQR 75-88) kIU. The primary outcome, time to separation from invasive ventilation to day 28 adjusted for the competing risk of death, was not significantly different between groups but took numerically longer in the nebulised heparin group (12.0, standard deviation (SD) 10.4 days versus 7.4, SD 6.9 days; hazard ratio (HR) 0.56, 95% confidence interval (CI) 0.31 to 1.01, P = 0.052). One patient died by day 28 in each group, fewer than expected. Time to separation from invasive ventilation among survivors to day 28 occurred more quickly than expected in the standard care group and was, without correction for multiple comparisons, significantly slower in the heparin group (11.3, SD 10.0 days, n = 26 versus 6.4, SD 5.2 days, n = 22; HR 0.52, 95% CI 0.30 to 0.92, P = 0.024). Nebulised heparin did not reduce time to ventilator separation in intubated adult patients with COVID-19. The study is limited by the small sample size and potential for sampling bias. Further study is required.

Hypotension after non-cardiac surgery is common and associated with harm. Anaesthetists treat hypotension in the post-anaesthesia care unit (PACU) with intravenous (IV) fluids and vasopressor medications. Our aim was to determine the incidence of hypotension after these treatments. We conducted a single centre retrospective cohort study of all adult patients who were hypotensive (systolic blood pressure less than 90 mmHg) in the PACU after non-cardiac, non-obstetric surgery over a one-year period. The primary outcome was a composite of hypotension or vasopressor infusion in the 24 h after PACU discharge. During the study 459 patients were hypotensive in the PACU. No treatment was administered in 232 (51%) episodes, IV fluid alone was administered in 138 (30%) episodes, vasopressors alone were administered in 22 (5%) episodes, and both fluid and vasopressors were administered in 67 (14%) patients. A total of 167 patients (36%) met the primary outcome, of which 118 (25%) were hypotensive and 49 (11%) required vasopressor infusions. The treatment group was significantly associated with the primary outcome (P < 0.001), with 36 (15%) patients who received no treatment becoming hypotensive, compared with 67 (46%, P < 0.001) patients who received IV fluid alone, 12 (55%, P < 0.001) who received vasopressors alone and 52 (75%, P < 0.001) who received both IV fluid and vasopressors. Patients who were hypotensive in the PACU frequently developed later hypotension or required vasopressors in the 24 h after PACU discharge. Treatments delivered in the PACU had limited long-term effectiveness. Novel treatments to protect patients from subsequent hypotension are urgently needed.