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Withdrawal syndrome and opioid toxicity: case report An approximately 60-year-old man developed seizure following the abrupt withdrawal of lorazepam. Later, he developed drenching diaphoresis, delirium, akathisia, agitation, psychosis, muscle rigidity, sinus tachycardia and dysphagia following misuse and withdrawal of diphenhydramine, and opioid toxicity manifesting as mild confusion, sedation and myoclonus during treatment with hydromorphone [not all dosages, routes, duration of treatments to reaction onset and outcomes stated]. The man was diagnosed with distal oesophageal carcinoma metastatic to bone and a large paraspinal mass. Subsequently, he was admitted to acute care with suboptimally controlled pain (current presentation). Systemic cancer therapy was not stated due to poor performance status, but palliative radiotherapy was offered. His medical history was significant for cocaine, benzodiazepine and diphenhydramine use disorders. He reported abstinence from cocaine since many years. Twelve months prior to the current presentation (at the age of approximately 60 years), he abruptly stopped his lorazepam therapy, and suffered a seizure. Thereafter, he successfully completed a slow taper of lorazepam. After that, he was detoxified from benzodiazepines; however, in the past 8 months, his family noted a gradual decline in his cognition including short-term memory loss and word-finding difficulties. At the time of current presentation, subtle signs of opioid toxicity including sedation, myoclonus and mild confusion were noted, which was consistent with rapidly escalating doses of oral hydromorphone at home for a 2 week period. His infectious workup was nonremarkable. Hence, the oral sustained-release hydromorphone was changed to fentanyl with adjuvant dexamethasone, and improvement was noted in his cognition and pain management within 36 hours. On day 2 of admission, radiotherapy was started. However, on hospitalisation day 3, he developed akathisia, generalized increased muscle tone, drenching diaphoresis, agitation, delirium and psychosis. Upon discussion with his family, it was revealed that he had been using diphenhydramine 500mg or more at night for >10 years as an anxiolytic and a sleep aid. Diphenhydramine had not been ordered at the time of admission. Hence, the symptoms were considered secondary to the abrupt cessation of diphenhydramine (acute drug withdrawal). Based on the sustained psychosis and the pronounced sympathetic nervous response, withdrawal from a much higher dose (500mg at night as reported by the family) was suspected. Based on previously published case reports, the man was started on IV diphenhydramine 50mg every 6 hours. Rapid improvement was noted in diaphoresis and muscle rigidity, which confirmed the suspected diphenhydramine withdrawal syndrome. Over the following 6 days, the dose of diphenhydramine was successfully tapered to one IV dose of 50mg diphenhydramine at night only. For attenuation of sympathetic nervous response such as sinus tachycardia and diaphoresis, he received