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Diarrhoea and Vomiting Leading to Metformin Associated Lactic Acidosis: A Case Report
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A3372 - Diarrhoea and Vomiting Leading to Metformin Associated Lactic Acidosis: A Case Report
Author Block: C. Ferguson; Intensive Care Unit, Ulster Hosptital, Dundonald, United Kingdom.
Introduction
Metformin is commonly used in the treatment in type 2 diabetes mellitus, and reduces the rate of complications and risk of death. A theoretical complication of treatment with Metformin is lactic acidosis. This report highlights a case of severe lactic acidosis due to Metformin accumulation in acute kidney injury.
Case Report
A 70 year old man presented with a four day history of diarrhea and vomiting. He had continued to take his regular medication through his illness which included Metformin, Digoxin, Furosemide, Apixaban, Simvastatin, Nicorandil, Amiodarone, Citalopram and Bisoprolol.
On initial assessment he was drowsy, tachypneic, hypotensive and bradycardic. Clinically he was dehydrated with dry mucus membranes and reduced skin turgor. There was no residual urine in the bladder on catheterisation.
Initial investigations showed acute kidney injury (Urea 30 and Creatinine 363) and profound raised anion gap metabolic acidosis (pH 6.9, HCO3 3.7, BE -27.2, pCO2 2.3) Serum lactate was > 15.
Early management with fluid resuscitation using crystalloid failed and he remained hypotensive (60/30), anuric and drowsy.
Working diagnosis was multiorgan failure due to severe lactic acidosis secondary to Metformin accumulation in the setting of acute kidney injury. He was admitted to the intensive care unit where he received supportive therapy including intubation and ventilation, vasopressors and continuous renal replacement therapy (CRRT).
Initial noradrenaline requirement was 0.9mcg/kg/min, which was weaned off over the first 36 hours. His metabolic disturbance improved rapidly on CRRT, at 2 hours base deficit had improved to -17 and lactate had fallen to 8. After 36 hours acid base balance had normalized. CRRT was stopped on day 3. He was extubated to minimal supplemental oxygen via high flow nasal specs on day three and discharged from ICU on day 4. He was eventually discharged from hospital back to his own home having made a full recovery.
Discussion
Accumulation of Metformin in renal failure can lead to profound lactic acidosis. Despite a dramatic initial clinical presentation and scoring systems predicting high mortality in this case, the patient made a rapid and full recovery. Metformin Associated Lactic Acidosis should be considered when patients present with lactic acidosis on a background of Metformin ingestion. Recognition of this is important because outlook can be favourable with early supportive treatment including CRRT to aid drug clearance. Misdiagnosis of other conditions such as sepsis or bowel ischaemia could lead to inappropriately high estimates of mortality and suboptimal treatment.
Author Block: C. Ferguson; Intensive Care Unit, Ulster Hosptital, Dundonald, United Kingdom.
Introduction
Metformin is commonly used in the treatment in type 2 diabetes mellitus, and reduces the rate of complications and risk of death. A theoretical complication of treatment with Metformin is lactic acidosis. This report highlights a case of severe lactic acidosis due to Metformin accumulation in acute kidney injury.
Case Report
A 70 year old man presented with a four day history of diarrhea and vomiting. He had continued to take his regular medication through his illness which included Metformin, Digoxin, Furosemide, Apixaban, Simvastatin, Nicorandil, Amiodarone, Citalopram and Bisoprolol.
On initial assessment he was drowsy, tachypneic, hypotensive and bradycardic. Clinically he was dehydrated with dry mucus membranes and reduced skin turgor. There was no residual urine in the bladder on catheterisation.
Initial investigations showed acute kidney injury (Urea 30 and Creatinine 363) and profound raised anion gap metabolic acidosis (pH 6.9, HCO3 3.7, BE -27.2, pCO2 2.3) Serum lactate was > 15.
Early management with fluid resuscitation using crystalloid failed and he remained hypotensive (60/30), anuric and drowsy.
Working diagnosis was multiorgan failure due to severe lactic acidosis secondary to Metformin accumulation in the setting of acute kidney injury. He was admitted to the intensive care unit where he received supportive therapy including intubation and ventilation, vasopressors and continuous renal replacement therapy (CRRT).
Initial noradrenaline requirement was 0.9mcg/kg/min, which was weaned off over the first 36 hours. His metabolic disturbance improved rapidly on CRRT, at 2 hours base deficit had improved to -17 and lactate had fallen to 8. After 36 hours acid base balance had normalized. CRRT was stopped on day 3. He was extubated to minimal supplemental oxygen via high flow nasal specs on day three and discharged from ICU on day 4. He was eventually discharged from hospital back to his own home having made a full recovery.
Discussion
Accumulation of Metformin in renal failure can lead to profound lactic acidosis. Despite a dramatic initial clinical presentation and scoring systems predicting high mortality in this case, the patient made a rapid and full recovery. Metformin Associated Lactic Acidosis should be considered when patients present with lactic acidosis on a background of Metformin ingestion. Recognition of this is important because outlook can be favourable with early supportive treatment including CRRT to aid drug clearance. Misdiagnosis of other conditions such as sepsis or bowel ischaemia could lead to inappropriately high estimates of mortality and suboptimal treatment.
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