Page 25 - Delaware Medical Journal - March 2018
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CASE REPORT
Surgery, GI, and the medical ICU team were involved early in her care. Plan was initially for endoscopy, given concerns for an UGIB, however, this was held in the setting of profound acidosis. Repeat POC lactate after continued resuscitation was >20 mmol/L, with lab value returning at
Patient was taken to the OR for concerns for mesenteric ischemia given her
rising lactate in the setting of GIB, appropriate resuscitation, and worsening abdominal tenderness on exam. The entirety of her bowel was examined by the surgical team and no ischemic bowel was performed. She did then transiently require vasopressor support for low blood pressures, however was quickly weaned off and remained stable.
Nephrology was consulted and the decision was made to dialyze due to profound acidosis. Given the normal appearance
of bowel and slight increase in patient’s creatinine, the concern was for metformin induced lactic acidosis. The patient’s creatinine was not as elevated as one would expect for such an accumulation of metformin. On further questioning, patient has not taken any more metformin than prescribed, and had in fact missed several days. Patient’s lactate rapidly cleared after
to 5.7 and she required no further dialysis sessions. Of note, her Cr did improve to presentation. She had no further episodes of GI bleeding while hospitalized, and was discharged in stable condition with plans for outpatient endoscopy and colonoscopy.
DISCUSSION
Metformin is a frequently prescribed medication in type 2 diabetes. It is thought to reduce cardiovascular morbidity and
mortality when compared to other methods of treatment, however is contraindicated in patients at a higher risk of lactic acidosis. The FDA updated its recommendations
in April of 2016 to include the safe use of
Cochran did an extensive review of the literature looking at the incidence of fatal and non-fatal lactic acidosis in DMII patient on metformin.6 They found no difference in the incidence of lactic acidosis in patient on metformin vs. patients not on metformin. They found that the risk of lactic acidosis was 4.3 per 100,000 person-years in metformin users while it was 5.4 in the non- metformin group.
Richy et al. performed a retrospective cohort study from 2007-2012 looking at the incidence of lactic acidosis in type
2 DM patients on metformin.5 They 30-60), or severely reduced (GFR<30) renal function based on GFR. The study included 77,601 patients for a total of lactic acidosis events for an incidence of 10.7 per 100,000 patient years, with no fatalities. Twenty-three of the 35 patients had other conditions such as ischemic heart disease of ARF. Notably, the difference in incidence between levels of
Bodmer et al. performed a nested case- control analysis in the UK looking at
the risk of lactic acidosis, as well as hypoglycemia, in type 2 diabetics on an oral antihyperglycemic.3 Out of a total six with lactic acidosis associated with antihyperglycemic use. One was on metformin alone, four were on combined therapy with a sulfonylurea, and one
was on a sulfonylurea alone. All of the metformin users in their cohort also had
clinically prior to their development of a lactic acidosis.
Silvestre et al. published a series of two case reports looking at MALA. In each elevated. One patient had a Cr of 6 and the other had a Cr of 2.2. An additional case report was published by Weisberg, which reported a patient who presented with shortness of breath.10 This patient did have a history of severe dilated cardiomyopathy. What is notable about this case is that the in his Cr. His Cr at presentation was 1.36, with a baseline of 1.13. The patient had bicarbonate infusion and CRRT.
CONCLUSION
Metformin associated lactic acidosis is
a very uncommon phenomenon. It can
not metformin is the culprit, as patients presenting with an elevated lactate
often have exacerbations of underlying comorbidities which could also be to blame. Systemic reviews have shown
that metformin can be safely used in patients with a moderate degree of renal dysfunction, i.e. GFR >30. Our patient on presentation, however not to the degree one would typically associate with MALA. While her Cr was only 1.44, her GFR was 37. Outpatient labs from six months after her presentation showed a
Cr of 1.0 and a GFR of >60. The trend for the overall evaluation of renal dysfunction is trending towards the use of GFR as opposed to Cr, perhaps in future studies of lactic acidosis, the focus should be
on GFR as opposed to Cr. This patient’s
quickly diagnose due to her concomitant GI bleeding, which stabilized very shortly after presentation.
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