Loperamide overdose
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Loperamide overdose Various toxicities following drug intoxication: case report
A 79-year-old man developed cardiotoxicity, dehydration, drowsiness, hyperkalaemia, miosis, nausea, paresis, fine distal tremor and vomiting secondary to drug intoxication following an overdose loperamide for diarrhoea associated with ileostomy and short bowel syndrome. The man was admitted due to nausea, vomiting, paresis and fine distal tremor. It was reported that due to diarrhoea associated with ileostomy and short bowel syndrome, he increased loperamide intake and ingested a total of 276 tablets (552mg) in the last 4 days. Additionally, he was receiving treatment with nifedipine and levothyroxine sodium [levothyroxine] concomitantly. Subsequently, he was admitted. On admission, examination showed HR of 78 beats per minutes, RR of 16 rpm, oxygen saturation of 94% and BP of 114/78mm Hg. Also, tendency to drowsiness, miosis, dehydration, pulmonary fields without aggregates, poor general condition, rhythmic precordium, soft abdomen with functional ileostomy with 300cc output, extremities with oedema and normal peristalsis were observed. Laboratory investigation revealed urea 95 mg/dL, potassium of 8.8 meq/L, and creatinine 3.95 mg/dL. Blood gas analysis revealed pH of 7.31, partial pressure of carbon dioxide (pCO2) 47mm Hg, partial pressure of oxygen (pO2) 134mm Hg, bicarbonate (HCO3) of 23 mmol/L, and lactate level of 2.6 mmol/L. Electrocardiogram showed heart rate of 60 beats per minute, PR segment 0.24ms, lengthening of the QRS complex reached up to 440ms in V1, sinus rhythm, axis-60, QTc 480ms and right bundle branch block. These findings were consistent with cardiotoxicity. Based on these findings and clinical presentation it was concluded that an overdose loperamide caused loperamide intoxication, which resulted in cardiotoxicity, dehydration, drowsiness, hyperkalaemia, miosis, nausea, paresis, fine distal tremor and vomiting [duration of treatment to reactions onset not stated]. The man was treated with sodium-bicarbonate and subsequent infusion. Additionally, he received anti-hyperkalaemic measures and hydration without achieving improvement in the potassium concentrations. Thereafter, a haemodialysis session was performed, with a potassium check-up of 5.71 meq/L at the end. He had not required a new session of haemodialysis or another antiarrhythmic. In the control ECG, normalisation of the QRS complex (140ms), the PR segment (0.12ms), and a QTc of 400ms was observed. Subsequently, his condition improved, and normalisation of potassium and decreased tremor was observed. Later, his treatment with loperamide was discontinued, and he was treated with octreotide due to high ileostomy output. Moranchel-Garcia L, et al. Cardiotoxicity due to loperamida. [Spanish]. Medicina Interna de Mexico 36: 124-129, No. 1, Jan-Feb 2020. Available from: URL: http:// doi.org/10.24245/mim.v36i1.2901 [Spanish; summarised from a translation]
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