HIGH ANION GAP METABOLIC ACIDOSIS IN SEVERE DELIBERATE POISONING WITH METFORMIN – SUCCESSFUL TREATMENT WITH 2.5-HOUR CONVENTIONAL HEMODYALISIS
Journal
Journal of Morphological Sciences
Date Issued
2020
Author(s)
Petronijevik Z
Smokovski I
Abstract
Metformin-associated lactic acidosis is a rare, life-threatening condition with a high mortality
rate, that could occur both with therapeutic use and in metformin overdose. Clinical manifestations may
be nonspecific, with severe anion gap metabolic acidosis and elevated lactate levels being the most
prominent laboratory findings; hence, delaying the diagnosis and treatment. Renal replacement therapy
plays a key role in the treatment of severe metformin poisoning. We herewith present a case with
intentional metformin poisoning successfully treated with one session of hemodialysis in combination
with parenteral sodium bicarbonate therapy.
A 17-year-old non-diabetic woman ingested 25 grams of metformin in a suicide attempt. She
developed vomiting and diarrhoea and was brought to the local emergency unit, and shortly after
admittance she became nonresponsive. Glasgow coma scale was 7/15 (E2, V1, M4), glucose level was 3.4
mmol/L and blood pressure was 90/60 mmHg. The first arterial blood gas analysis demonstrated a severe
metabolic acidosis with high lactate level (pH = 6.778, BE -31.7, lactate 18 mmol/L, anion gap 39.8
mmol/L), and, subsequently, she developed a non-oliguric renal failure. Lactic acidosis was successfully
treated with a combination of a conventional 2.5-hour bicarbonate HD and early administration of
intravenous bicarbonate. The arterial pH steadily increased back to normal levels, lactic acidosis
improved and kidney function recovered completely.
It could be concluded that even a single session of timely applied conventional HD in
combination with parenteral administration of bicarbonates allows simultaneous drug removal, lactate
reduction and acid-base correction and should be a treatment of choice in hemodynamically stable
patients with severe metformin poisoning.
rate, that could occur both with therapeutic use and in metformin overdose. Clinical manifestations may
be nonspecific, with severe anion gap metabolic acidosis and elevated lactate levels being the most
prominent laboratory findings; hence, delaying the diagnosis and treatment. Renal replacement therapy
plays a key role in the treatment of severe metformin poisoning. We herewith present a case with
intentional metformin poisoning successfully treated with one session of hemodialysis in combination
with parenteral sodium bicarbonate therapy.
A 17-year-old non-diabetic woman ingested 25 grams of metformin in a suicide attempt. She
developed vomiting and diarrhoea and was brought to the local emergency unit, and shortly after
admittance she became nonresponsive. Glasgow coma scale was 7/15 (E2, V1, M4), glucose level was 3.4
mmol/L and blood pressure was 90/60 mmHg. The first arterial blood gas analysis demonstrated a severe
metabolic acidosis with high lactate level (pH = 6.778, BE -31.7, lactate 18 mmol/L, anion gap 39.8
mmol/L), and, subsequently, she developed a non-oliguric renal failure. Lactic acidosis was successfully
treated with a combination of a conventional 2.5-hour bicarbonate HD and early administration of
intravenous bicarbonate. The arterial pH steadily increased back to normal levels, lactic acidosis
improved and kidney function recovered completely.
It could be concluded that even a single session of timely applied conventional HD in
combination with parenteral administration of bicarbonates allows simultaneous drug removal, lactate
reduction and acid-base correction and should be a treatment of choice in hemodynamically stable
patients with severe metformin poisoning.
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