Page 24 - Delaware Medical Journal - March 2018
P. 24
Metformin Induced Lactic Acidosis in a Patient with GIB
Shelby Catlett, MD; Christian Coletti, MD, MHCDS
This is a 58-year-old, Caucasian female with a history of diabetes on metformin who presented to the emergency department for GI bleeding and was found to have profound lactic acidosis. She was taken to the operating room due to concerns for mesenteric ischemia, however, intra-operatively had a normal appearing bowel. Her acidosis improved with hemodialysis and was thought to be due to metformin. This is an unusual case because, while the patient did have a slight increase in her creatinine, she was not in renal failure, and the underlying cause of her lactic acidosis was obscured by concomitant GI bleeding.
Introduction
Metformin is the most commonly prescribed oral antihyperglycemic therapy for type 2 diabetes, especially in those patients who also have dyslipidemia.1,2 It works by lowering fasting insulin
levels and enhancing insulin sensitivity;
it suppresses gluconeogenesis in the liver and causes greater peripheral glucose uptake and, therefore, improved glycemic control.3 Metformin inhibits mitochondria respiration in the liver, yielding elevated lactic acid levels in the blood.4 Metformin has a lower likelihood of causing a lactic acidosis than prior biguanide, such as phenformin (approximately 20 times less), but the phenomenon is still reported in approximately four cases per 100,000 person years.4,5,6 Traditionally, metformin has been contraindicated in those with risk of the development of metformin- associated lactic acidosis (MALA), and
is also thought to be more likely in those patients who develop acute kidney injury for any reason.3 When patients have
an elevated lactate level thought to be secondary to metformin, dialysis is typical treatment.7
CASE
diabetes on metformin and hyperlipidemia presented as a transfer from an outside facility for gastrointestinal (GI) bleeding. Prior to transfer, she had multiple episodes of bright red blood per rectum (BRBPR) and an episode of hematemesis. Her systolic blood pressures were low in the 70s mmHg with an initial hemoglobin (Hgb) of 5 G/dL. She received two units
of red blood cells, six units fresh frozen plasma, and 4L of isotonic crystalloid prior to transfer. Of note, her initial lactic acid was 12 mmol/L on presentation.
On arrival to our emergency department, her vital signs were stable and she was
in no acute distress. She had some mild bilateral lower abdominal and suprapubic tenderness. She did have a large, grossly bloody bowel movement on arrival.
She noted that she was feeling unwell the night prior to presentation and had an episode of syncope. She had felt the urge to move her bowels, however, was unsure if she had had blood in her stool at home. She denied any history of prior GI bleeding, excessive NSAID use, or alcohol consumption.
Past medical history was notable for hyperlipidemia and diabetes, for which she was on levemir and metformin. She had had recent knee surgery, but denied taking NSAIDs at home.
Diagnostic studies showed an initial
some mild lower abdominal tenderness on initial exam, however, was not peritonitic. Additional laboratory work revealed a now stable Hgb of 12.5 G/ Metabolic Panel (BMP) showed a critical creatinine (Cr) to 1.44 mg/dL with a decreased GFR of 37 and an anion gap of 32. She was also noted to have a critical
She was given cryoprecipitate and started on a bicarbonate drip given her also given piperacillin/ tazobactam empirically for her abdominal tenderness. She had a CT scan of her abdomen prior to transfer. These images were reviewed and showed diffuse bowel
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Del Med J | March 2018 | Vol. 90 | No. 3
Abstract
