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A case of multi‐organ failure

Colchicine is a commonly used drug in the treatment of gout. Gastrointestinal side effects such as nausea, vomiting and diarrhoea are commonly associated with colchicine but more severe adverse effects are uncommon. We report a case of colchicine toxicity, which resulted in multi-organ failure, bone marrow suppression and death. This clinical message highlights the important lessons learnt from this case and summarises the clinical features and management of colchicine toxicity. Colchicine is a commonly used drug in the treatment of gout. Gastrointestinal side effects such as nausea, vomiting and diarrhoea are commonly associated with colchicine but more severe adverse effects are uncommon. We report a case of colchicine toxicity, which resulted in multi-organ failure, bone marrow suppression and death. A 65-year-old patient was admitted to hospital with 12 days history of watery diarrhoea and vomiting. Two days prior to onset of diarrhoea, he was started on colchicine by his general practitioner for the treatment of an attack of suspected acute gouty affecting the left big toe. He consumed 1.5 mg of colchicine a day for 2 weeks prior to admission. The patient was known to have gout for the last 5 years and had previous attacks of gout affecting the toes. There was no significant past medical history, apart from gout, or family history of note. He was not taking any regular medications prior to his current illness. The patient denied any alcohol intake on admission. However, later during the admission his daughter revealed a history of moderately excessive alcohol intake of 30 units a week approximately. On admission, he was drowsy but responsive with a Glasgow coma scale of 15/15. Clinical examination revealed a blood pressure of 110/70 and heart rate of 110 beats/ min and tachypnoea. Jugular venous pressure was low. There was no evidence of jaundice, clubbing, cyanosis, oedema or lymphadenopathy. There was no evidence of chronic gouty arthropathy or tophi. Abdominal, cardiac and respiratory examination revealed no further abnormalities. Chest and abdominal X-rays were unremarkable. An electrocardiograph showed sinus tachycardia. Urinalysis showed evidence of microscopic haematuria and proteinuria. Initial investigations showed evidence of acute renal failure, leucopenia, neutropenia, thrombocytopenia, hypocalcaemia, hyperphosphataemia, metabolic acidosis and abnormal clotting. These results are summarised in Table 1. There were no previous blood test results recorded for this patient to compare with prior to this admission. Colchicine was stopped and the patient was resuscitated with intravenous fluids. Broad-spectrum antibiotics (imipenem, ciprofloxacin and fluconazole) and granulocyte colony-stimulating factor (GCSF) were started for neutropenia. Further investigations were carried out. Urinary total protein was 0.98 g/l, no urinary free light chains, lactate 7.5 mmol/l [normal range (NR) 0.3–1.3] and troponin T 0.5 lg/l (NR < 0.01). D-dimer levels were raised and fibrinogen levels were normal throughout the admission. Blood film did not show any evidence of haemolysis. Anti-nuclear, antismooth muscle, anti-mitochondria, anti-glomerular basement membrane and anti-neutrophil cytoplasmic antibodies were negative. There was no growth on urine, blood or stool cultures. Hepatitis B surface antigen and hepatitis C antibody were both negative. Abdominal/renal ultrasound was unremarkable and kidney size was 10 cm bilaterally. The patient’s clinical condition continued to deteriorate despite some improvement in renal function with hydration. He received intravenous fluids replacement guided by central venous pressure monitoring, electrolytes supplements, antibiotics, GCSF and platelet, blood and fresh frozen plasma (FFP) transfusions (see Figure 1). He developed abdominal distension secondary to intestinal pseudoobstruction. On day 5, he had upper gastrointestinal bleeding and endoscopy showed severe oesophageal ulceration that was treated with intravenous omeprazole infusion. The patient then started to develop respiratory distress and hypoxia with inspiratory crackles on examination. Chest X-ray (CXR) was unremarkable. He was transferred to the intensive care unit where he received continuous positive airway pressure respiratory support and also inotropic support for hypotension. On day 7 the patient developed asystole and died. Post-mortem examination showed the presence of complicated atheroma in the aorta and the left descending coronary artery was reduced to 20% of normal. There was also evidence of pulmonary oedema and bilateral pleural effusions. Gastrointestinal system examination revealed fatty liver and oesophageal ulceration.