Colchicine overdose
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Extra pontine myelinolysis and other toxicities: case report A 34-year-old man developed nausea, vomiting, hyponatraemia, shock, medulla oblongata sheath lysis and extra pontine myelinolysis (EPM) following acute poisoning and overdose of colchicine for acute attack of gout. Additionally, sodium supplementation also contributed to the EPM. The man was admitted with a 8-day history of intermittent nausea, vomiting and extremities weakness accompanied by shock for 3h. Eight days ago, he took 20 tablets of oral colchicine 0.5 mg/tablet, one tablet per hour because of an acute attack of gout. Subsequently, he developed nausea, vomiting and weakness of extremities. Three hours before the admission, his BP dropped to 85/60mm Hg, and he visited to the hospital. He had a history of gout for more than 3 years and was intermittently treated with colchicine. At admission, physical examination showed body temperature 36.7°C, BP 103/58mm Hg (treated with dopamine), pulse rate 96 beats/min and RR 17 breaths/min. He had clear consciousness, muscle strength of upper limbs was grade 5 and of lower limb was grade 4+. The serum sodium ion concentration of venous blood was 111 mmol/L. He was diagnosed with acute colchicine poisoning and overdose leading to hyponatremia (electrolyte imbalance) and shock. The man received symptomatic and supportive treatment including rehydration, correction of electrolyte imbalance with sodium supplementation and anti-shock therapy. On day 2, re-examination revealed that the serum sodium ion concentration was 124 mmol/L. He also developed lethargy; hence, sodium supplementation was continued. On day 3, the serum sodium ion concentration was 129 mmol/L. His serum sodium increased by >10 mmol/L within 24h after the admission, and he developed dyskinesia due to rapid correction of hyponatraemia by sodium supplementation. He then presented with a slurred speech and was unable to stand up. A repeat physical examination revealed that both the pupils were equal in size, eyes could move in all directions, frontal lines on both sides were equal, proximal muscle strength of both upper limbs was grade 1, distal muscle strength of both the upper and lower limbs was grade 0 with normal muscle tension and positive bilateral Babinski sign. A head MRI and diffusion examination showed abnormal signals in the medulla oblongata, which was considered to be medulla oblongata sheath lysis. He was diagnosed with medulla oblongata sheath lysis as part of EPM. Hence, hormone therapy was started immediately. On day 4 after the admission, his BP returned to 147/83mm Hg, and vasopressor was stopped. He was treated with methylprednisolone with an improvement. Because of medulla oblongata lesion, the enhanced head MRI was performed; however, no abnormal enhancement in lesions were observed, which ruled out the inflammation and tumour, indicating medulla oblongata sheath lysis. His symptoms improved significantly and the hormone therapy was stopped. After 27 days, muscle strength of the left upper limb recovered to grade 5, mu
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