She died 72 hours after being admitted.Ī 76-year-old woman with history of type 2 diabetes mellitus, dyslipidaemia, and depressive disorder. However, the patient remained in a coma, with low-voltage EEG. Her analytical tests then improved: plasma creatinine (Cr): 1.2mg/dl and serum bicarbonate: 22mEq/l. Haemodialysis was performed with bicarbonate solution. A lumbar puncture was performed, and the result was compatible with pneumococcal meningitis. Vasoactive drugs and antibiotics were administered. She was transferred to the intensive care unit (ICU) and underwent orotracheal intubation with mechanical ventilation. The chest X-ray revealed infiltration in the left base. The arterial blood gas test showed pH: 7.03 bicarbonate: 10mEq/l and plasma lactic acid: 14mmol/l (Table 1). Analytical tests showed plasma creatinine: 1.79mg/dl glycaemia: 215mg/dl and prothrombin activity: 7%. In the emergency department she was hypotensive, poorly perfused, and comatose (Glasgow coma score 6/15). Her general health started to deteriorate, with vomiting and decreased level of consciousness. Two days before being admitted she was taking ibuprofen (600mg/8hr) due to bone pain. She was being treated with metformin (850mg/8hr), glipizide (5mg/day), lercanidipine (10mg/day), lisinopril and hydrochlorothiazide (20/12.5mg/day), acenocoumarol and occasionally ibuprofen. We describe 5 patients with severe metformin-induced lactic acidosis, analysing the influence that kidney disease could have on its pathogenesis and evolution, as well as the role that extrarenal depuration techniques can have on its treatment.Ī 78-year-old woman with history of high blood pressure, type 2 diabetes mellitus, generalised osteoarthritis, congestive heart failure (class II on the New York Heart Association) and chronic atrial fibrillation. Therefore, it is contraindicated in patients with chronic kidney disease. However, a small percentage of patients may suffer a severe complication: metformin-induced lactic acidosis, 3-5 especially subjects with comorbidities, mainly liver, heart and severe kidney diseases.
Its most frequent secondary effects are gastrointestinal, such as diarrhoea, abdominal pain and vomiting. 2 It is well absorbed through oral administration and it is mainly excreted through the kidney, which is why it can accumulate in cases of renal function deterioration. 1 Studies such as the UKPDS also show that it reduces morbidity and mortality in patients with type 2 diabetes. It can reduce fasting and postprandial glycaemia and haemoglobin A 1C (HbA 1C), with weight loss and an improved lipid profile. 1 It is a glycaemia-lowering agent that promotes glucose entering the tissues and reduces hepatic gluconeogenesis and glucose synthesis. Metformin is the main biguanide, widely used in diabetes mellitus treatment.
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