This report describes two cases of central anticholinergic syndrome, the first after general anaesthesia and the other during a prolonged stay in the intensive care unit. The symptoms in both patients resolved soon after physostigmine administration. There was a delay in the diagnosis of central anticholinergic syndrome, which resulted in acute lung injury and unanticipated intensive care unit admission. It is suggested that in cases of abnormal mental recovery after anaesthesia or sedation, the diagnosis of central anticholinergic syndrome should be considered.

This report describes an association between hepatic encephalopathy and central anticholinergic syndrome(CAS). A 60-year-old anaemic woman was admitted unconscious and with a delayed reaction to pain but with no focal neurological deficits. She had signs of portal hypertension and a history of non-alcoholic liver cirrhosis grade Child B. Suspecting upper gastrointestinal bleeding, she was intubated for gastroduodenoscopy and a fibrin-covered ulcer was revealed. Raised intra-abdominal pressure resultingfrom ascites caused cardiopulmonary failure, which required mechanical ventilation for 24 h, but extubation was possible after drainage of the ascites and blood volume replacement therapy. However, her neurological state remained unchanged despite normal blood ammonia concentration and no sedation. CAS was considered and physostigmine injected with immediate effect. The patient opened her eyes immediately and was fully orientated to personal and medical history. We suggest that hepatic encephalopathy may trigger CAS, although the significance of physostigmine in the treatment of hepatic encephalopathy remains to be addressed by controlled investigations.

Two patients presented with very different signs of central anticholinergic syndrome following general anaesthesia for which they had received premedication with hyoscine. Both responded dramatically to 1 mg of intravenous (i.v.) physostigmine, which produced a rapid return to a normal level of consciousness. The aetiology of central anticholinergic syndrome is multi-factorial, but the diagnosis should be considered in all patients who demonstrate abnormal post-anaesthetic awakening. It is recommended that 1 mg of intravenous physostigmine is a safe and effective treatment for central anticholinergic syndrome, and that a supply of this important drug must be kept readily available in the recovery area of the operating theatre department.

The purpose of this prospective study was to identify the incidence of a distinct central anticholinergic syndrome following routine anaesthesia. For 2 months, all inpatients aged more than 15 years scheduled for elective procedures and cared for in the recovery room were investigated for symptoms of the syndrome. Patients with neuropsychiatric disease or other disorders that could alter consciousness were excluded. Prolonged action of anaesthetics or relaxants, respiratory depression and metabolic disorder were ruled out before making the diagnosis. Out of 962 patients (366 men, 596 women), 18 (4 men, 14 women) developed the syndrome. The difference between men and women was not statistically significant. Six out of 60 women developed the syndrome after a hysterectomy with or without adnectomy/oophorectomy, and this high incidence was significantly different from that observed after all other procedures in women (P = 0.003) or all other gynaecological procedures (P = 0.013). The reason for this is unknown. In six of the 18 cases, untreated prolonged somnolence lasted for more than 2 h. All patients woke up after an injection of physostigmine, but six of them relapsed into somnolence and needed a second, and in one case a third, injection. The findings of the study emorders phasize that, when there is delayed recovery from anaesthesia, the diagnosis of central anticholinergic syndrome should be considered if other accessible causes for that condition have been excluded.