Background: Volatile anaesthetics are known to cause drug-induced liver injury, a hepatotoxic reaction characterised by antibodies to trifluoroacetylated lipid and protein adducts and cytochrome p450 2E1. The incidence of volatile anaesthetic druginduced liver injury from older agents has been described, but modern agents have not been prospectively studied. Aim:To determine prospectively the incidence of volatile anaesthetic drug-induced liver injury from sevoflurane and desflurane.Methods: Adult surgical patients with a predicted post-operative stay of at least 4 days were recruited. If volatile anaesthetic was administered, liver biochemistry was performed regularly. Medications, observations and other investigations were documented. Patients with abnormal liver biochemistry were classified as likely volatile anaesthetic drug-induced liver injury or not based on clinical assessment, Roussel Uclaf Causality Assessment Method score, and the absence of other likely pathology. Some patients were also tested for antibodies to both trifluoroacetylated lipid and protein adducts, and cytochrome p450 2E1. Results:A total of 209 patients were recruited, of which 121 were included for analysis. Post-operative liver biochemistry was abnormal in 62 patients (51.2%); further classified as not volatile anaesthetic drug-induced liver injury in 47 cases (38.8%), and likely volatile anaesthetic-drug induced liver injury in 15 cases (12.4%). Of the likely volatile anaesthetic drug-induced liver injury patients, only one had severe disease with alanine transaminase greater than five times the upper limit of normal, while four cases had moderate disease with alanine transaminase greater than three times the upper limit of normal. Thus, the incidence of clinically significant volatile anaesthetic drug-induced liver injury was 4.1%. No risk factors were identified. Conclusions:Volatile anaesthetic drug-induced liver injury from modern agents seems to be as common (4.1%) as previously reported with older agents (3%), and may identify patients at risk of severe acute liver injury with subsequent re-exposure.

BackgroundHepatic encephalopathy is a confusional state associated with cirrhosis. Serum ammonia levels are neither sensitive nor specific for the diagnosis.AimsWe audited the ordering location and hospital unit whilst assessing the impact on management at a major Australian tertiary centre.MethodsWe conducted a single‐centre retrospective chart review of the ordering of serum ammonia levels between 1 March 2019 and 29 February 2020 at The Royal Melbourne Hospital, a tertiary‐referral centre in Melbourne, Victoria. Demographic, medication and pathology results, including serum ammonia measurements, were collected. The main outcomes assessed were ordering location, sensitivity, specificity and impact on management.ResultsA total of 1007 serum ammonia tests were ordered in 425 patients. Nearly all ammonia ordering was by non‐gastroenterologists, 24.2% by the intensive care unit, 23.1% by general medicine and 19.5% by the emergency department (ED). Only 21.6% of patients had a history of cirrhosis, with hepatic encephalopathy diagnosed in 13.6%. On subgroup analysis, 217 ammonia tests were performed in 92 patients with cirrhosis. Cirrhotic patients were older (64 vs 59 years, P = 0.012) and had higher median ammonia levels (64.46 vs 59 μmol/L, P < 0.001) compared with non‐cirrhotic patients. In cirrhotic patients, the sensitivity and specificity for serum ammonia and diagnosis of hepatic encephalopathy were 75% and 52.3% respectively.ConclusionWe affirm the poor utility of serum ammonia levels for guiding management of hepatic encephalopathy within the Australian context. ED and general medical units account for the majority of test ordering within the hospital. Understanding where ordering occurs provides a target for targeted education.

Background and aims Little is known regarding the epidemiology and outcomes of patients with primary sclerosing cholangitis (PSC) in Australia. We, therefore, evaluated the epidemiology and clinical outcomes of PSC in a large cohort of Australian patients and compared these to the general population. Methods We conducted a multicentre, retrospective cohort study of PSC patients at nine tertiary liver centers across three Australian states, including two liver transplant centers. Results A total of 413 PSC patients with 3,285 person-years of follow-up were included. Three hundred and seventy-one (90%) patients had large duct PSC and 294 (71%) had associated inflammatory bowel disease. A total of 168 (41%) patients developed cirrhosis (including 34 at the time of PSC diagnosis) after a median of 15.8 (95% CI 12.4, NA) years. The composite endpoint of death or liver transplantation occurred in 49 (12%) and 78 (19%) patients, respectively, with a median transplant-free survival of 13.4 (95% CI 12.2–15) years. Compared to the general population, PSC accounted for a 240-fold increased risk of development of cholangiocarcinoma (CCA) and CCA-related death. CCA risk was increased with older age of PSC diagnosis, presence of dominant stricture and colectomy. Compared to same-aged counterparts in the general population, PSC patients who were diagnosed at an older age or with longer disease duration had reduced relative survival. Conclusion In this large retrospective cohort study of PSC patients in Australia, increased age and time from diagnosis was associated with increased mortality and morbidity particularly from CCA and development of cirrhosis, necessitating need for liver transplant.

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