Benzodiazepinones/oxycodone/paroxetine overdose
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Various toxicities following intentional multiple drug overdose: case report A 55-year-old woman developed drug intoxication in the form of cardiac arrest, hyperkalaemia, sepsis with Escherichia coli and Staphylococcus aureus infections, septic-shock, aspiration pneumonia and hypoxaemia leading to distributive shock, ocular clonus, bilateral Babinski signs, hyperthermia, serotonin syndrome, prolonged coma with absent brainstem reflexes, respiratory depression, superficial ulcerative lesions in the distal oesophagus and stomach leading to upper GI bleeding, anaemia, thrombocytopenia, leukopenia and coagulopathy following intentional overdose of paroxetine, temazepam, oxazepam and oxycodone. The woman, who had a short history of depression, was found at home following an intentional drug overdose with ingestion of paroxetine 1600mg, temazepam 120mg, oxazepam 80mg, oxycodone 75mg and mecoprop [2-methyl-4-chlorophenoxypropionic acid]. On arrival to the emergency medical services, she was found to be pulseless, and an ECG showed a sinus bradycardia, which was consistent with pulseless electrical activity. The woman received advanced life support for 2 minutes, leading to return of spontaneous circulation. While in the emergency department, she was comatose (E1M1V1). She was intubated, and an ECG revealed a broad complex tachycardia. Lab tests showed severe respiratory acidosis and hyperkalaemia. Following insertion of a nasogastric tube, she received activated charcoal. The hyperkalaemia was treated with calcium chloride, insulin and glucose. Subsequently, she was moved to the ICU, wherein she received sodium bicarbonate to alkalise the urine and to increase the elimination of mecoprop. After a few hours of admission, she developed distributive shock, for which she was treated with IV fluids and norepinephrine. Bedside cardiac echo showed hyperdynamic left ventricle and kissing ventricles. She exhibited a lack of efficacy during treatment with norepinephrine and sodium bicarbonate. Blood cultures grew Escherichia coli, and sputum cultures grew Escherichia coli and Staphylococcus aureus. Also, she developed hyperthermia and an ocular clonus. Based on a suspected diagnosis of serotonin syndrome from paroxetine intoxication, she started receiving active cooling and dantrolene. Neurologically she showed E1M1Vtube on the Glasgow Coma Scale, and she received sedation briefly while she had been receiving dantrolene. In addition to coma, she had breathing stimulus, cough reflex and bilateral Babinski signs. She had respiratory depression, to which benzodiazepine (temazepam, oxazepam) and opioid (oxycodone) intoxication contributed. Electroencephalogram showed a burst-suppression pattern, without epileptic state. The distributive shock persisted, and therefore, she started receiving off-label soya-oil-emulsion [lipid emulsion; intralipid] to enhance redistribution and elimination of toxic compounds. Also, she received amoxicillin/clavulanic acid for possible aspiration pneumonia. Following initial signs of stabilisation, h
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