Can acute overdose of metformin lead to lactic acidosis?

Wills, Brandon K.; Bryant, Sean M.; Buckley, Peter; Seo, B. S.

doi:10.1016/j.ajem.2009.04.012

Cited by 51 publications

(48 citation statements)

References 13 publications

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“…According to poison control centers LA is seen in 3.5% of metformin users, and only 16% of these exposures are due to intentional mono-overdoses with metformin [4]. In most cases serum metformin concentrations are not mentioned [4] [5]. In our case we do not only describe the plasma metformin concentration and plasma lactate at presentation, we also measured concentrations after dialysis, providing valuable information for future research.…”

Section: Discussionmentioning

confidence: 98%

“…The serum ethanol level in our patient was <0.1 g/L and there was no evidence of ingestion of products containing toxic alcohols. The elevated osmolgap may be explained by extreme hypotension [10] but is has also been previously described in metformin intoxications [4].…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

“…Presumably, the lactate production was higher than the clearance with haemodialysis, possibly due to a co-existing type A LA due to hypotension. In addition, glucose-infusion may have contributed to the initial worsening of lactatemia since increased metabolism of intracellular glucose may lead to an increase of lactate production [2] [4]. There is evidence that in severe cases with high plasma metformin concentrations, the time of dialysis must be prolonged to ensure clearance of lactate from the intracellular space [5] [6].…”

Section: Discussionmentioning

confidence: 99%

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Metformin Intoxication: A Case of a Combination of Severe Hypoglycaemia and Severe Lactic Acidosis (LA)

Agterhuis¹,

Freling²,

Henstra³

et al. 2015

JDM

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Metformin is a worldwide used and effective antihyperglycemic agent. It is generally well tolerated but contra-indicated in severe renal dysfunction. Metformin does not cause hypoglycaemia, however this case describes hypoglycaemia after an overdose. Another well-known, but rare and potentially life-threatening complication of metformin is the occurrence of LA, the so-called metformin-associated lactic acidosis (MALA). The severe consequences of an overdose of metformin, as well as the pathophysiologic mechanisms and the clinical consequences of LA in combination with severe hypoglycaemia are described in this report. Early recognition and swift clinical intervention is of paramount importance in case of auto-intoxication with metformin to prevent a lethal outcome.

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Metformin Intoxication: A Case of a Combination of Severe Hypoglycaemia and Severe Lactic Acidosis (LA)

Agterhuis¹,

Freling²,

Henstra³

et al. 2015

JDM

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“…In one case of acute metformin overdose, significant hyperglycemia was described; however, in that case, it was profound and progressive [47]. An acute overdose of metformin can cause a severe lactic acidosis [48][49][50][51]. In such cases, a depressed level of consciousness may occur following several hours of lucidity, although typically it is in the setting of cardiovascular instability [47,[52][53][54][55][56].…”

Section: Could This Be Metformin-associated Lactic Acidosis?mentioning

confidence: 99%

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

Villano

O'Connell

et al. 2015

J. Med. Toxicol.

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A 28-year-old man was brought to the Emergency Department (ED) for evaluation of a depressed level of consciousness that developed while in jail. Sixteen hours previously, he had been arrested on charges of murder. The patient's mental status was reported as normal at the time of arrest, and it had remained so during several hours of interrogation and during the booking process at jail. Following interrogation, the patient was placed into a cell with no other inmates. During the jail intake process, the patient had not reported any history of medical problems nor was he prescribed with any medications. Paramedics arrived to find him unresponsive, but maintaining airway reflexes and hemodynamically stable. They measured a blood glucose of 300 mg/dL and noted one episode of blood-tinged emesis during transport to the ED. No seizure activity was witnessed.On arrival to the ED, vital signs were: heart rate 132/min, blood pressure 129/74 mmHg, temperature 35.3°C (95.5°F), respiratory rate 24/min, and 100 % oxygen saturation on 15 l/ min of oxygen delivered by non-rebreather face mask.Physical examination was notable for a depressed level of consciousness. His eyes remained closed to pain, he withdrew all extremities equally to pain, and he was non-verbal. He had no signs of trauma, and his pupils were normal in size and reactive. Rapid sequence tracheal intubation was performed for airway protection. An electrocardiogram was normal except for sinus tachycardia at a rate of 111/min. An initial peripherally drawn arterial blood gas obtained immediately after intubation revealed: pH 6.97, pCO 2 40 mmHg, pO 2 215 mmHg. A computed tomography scan of the brain was normal. Initial blood chemistry panel was significant for a serum bicarbonate of 7 mEq/L, glucose of 362 mg/dL, and a normal potassium, blood urea nitrogen (BUN), creatinine, and calcium. The initial serum anion gap was 34 mEq/L. Measured serum osmolality was 320 mOsm/kg, yielding an osmol gap of 9 mOsm/kg (using formula of [2(Na)+BUN/2.8+glu-cose/18] for calculated serum osmolarity). Initial lactate was 156.5 mg/dL (normal reference range 4.5-19.8 mg/dL) and beta-hydroxybutyrate (βHB) 2.9 mg/dL (normal reference range 0.0-2.8 mg/dL). Initial liver panel included an aspartate aminotransferase (AST) of 64 U/L, alanine aminotransferase (ALT) of 27 U/L, and bilirubin of 0.4 mg/dL. Prothrombin time was 13.1 s (reference range 9.7-12.5), and lipase was normal at 25 U/L. Initial creatinine phosphokinase (CK) was slightly elevated at 373 U/L (0-175). Urinalysis was positive for small ketones and crystals were not present. Measurements of acetone and acetoacetate were not performed. Serum ethanol and salicylate levels were undetectable, and a urine drug of abuse panel by immunoassay was negative for amphetamines as a class, barbiturates as a class, benzodiazepines as a class, benzoylecgonine (cocaine metabolite), methadone, opiates as class, oxycodone, phencyclidine, and tetrahydrocannabinoids. Iron concentration was normal at 87 mcg/dL.Over the first hour of management,...

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Metformin and other biguanides: pharmacology and therapeutic usage

Samson

Garber

2015

International Textbook of Diabetes Mellitus

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Can acute overdose of metformin lead to lactic acidosis?

Cited by 51 publications

References 13 publications

Metformin Intoxication: A Case of a Combination of Severe Hypoglycaemia and Severe Lactic Acidosis (LA)

Metformin Intoxication: A Case of a Combination of Severe Hypoglycaemia and Severe Lactic Acidosis (LA)

Case Files from the University of California San Diego Health System Fellowship Coma and Severe Acidosis: Remember to Consider Acetaminophen

Metformin and other biguanides: pharmacology and therapeutic usage

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