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Lactic acidosis involves the accumulation of lactic acid in the body, with type A linked to poor tissue perfusion and type B associated with underlying diseases or medications. Recognizing these distinctions is crucial for tailored treatment strategies. Numerous drugs have been identified as potential contributors to lactic acidosis, with metformin, a widely utilized medication, being notably recognized in this context. We present a case of severe lactic acidosis resulting from metformin misuse.
A 39-year-old woman with childhood history of Acute Lymphocytic Leukemia, non-proteinuric CKD stage 3b of unclear etiology, Avoidant Restrictive Food Intake Disorder (ARFID), multiple recurrent electrolyte and divalent ions deficiencies (hypokalemia, hypocalcemia, hypomagnesemia, hypophosphatemia), autoimmune cerebellitis treated with steroids, presented to emergency department for severe abdominal pain and vomiting with no associated diarrhea of 1 week duration. Her vital signs were stable upon presentation with BP 130/78, P=123, RR= 22, spo2=98%). Arterial Blood Gas (ABG) showed severe acidemia with pH of 6.6, bicarbonate of 1 mmoL, pCO2=10.3 mmHg. Her anion gap was 46, Cr 1.8 mg/dl which was close to her baseline values. Further tests revealed a significantly elevated lactate level of 22.1 (normal range 0.55 - 2.20 mmoL ) and elevated ketones level 50.6 (0.0- 5.0 mg/dL) thought to be due to starvation ketoacidosis. The rest of her laboratory results can be found in (Table 1). Patient received 200 meq of NaHCO3 and was started on IV fluids containing sodium bicarbonate. A progressive improvement in her metabolic acidosis was noted with values normalizing within 6 hours without requiring renal replacement therapy. (table 2)
Test
Result
Unit
WBC
21000
per cc.mm
Hemoglobin
12.8
mg/dL
Platelets
411000
BUN
65
Creatinine
1.8
Sodium
153
mmol/L
Potassium
3.3
Chloride
103
Carbon dioxide
4
Anion gap
46
Phosphorus
8.9
Calcium
9.7
Magnesium
1.9
Alkaline phosphatase
67
IU/L
AST
21
ALT
24
Gamma glutamyl transferase
13
Bilirubin total
0.3
Lipase
567
Glucose
100
Table 1: laboratory results on day of presentation
A CT angiography of the abdomen revealed no evidence of mesenteric ischemia. No drugs known to cause lactic acidosis were identified upon review of her prescribed medications. However, in the context of her history of an eating disorder, a prior suicidal attempt and CKD, metformin-induced lactic acidosis was considered. A serum level of metformin came back at 24.8 mg/L (normal 0.10-1.3, toxic=5-10 mg/L, fatal > 60 mg/L). Subsequently, a search of the patient's residence by family members revealed an empty metformin pill box. The patient later admitted to self-administering metformin as a mean for weight loss, prompted by an escalating fear of weight gain following the initiation of steroids approximately 1.5 months earlier for the treatment of her autoimmune cerebellitis. Coordination of care with her psychiatrist was intensified as a result of this life-threatening instance.
ABG
T 0 hours
T 2 hours
T 6 hours
T 10 hours
pH
6.64
6.94
7.43
7.59
(7.35-7.45)
PCO2
10.2
12.2
15
(35- 45 mmHg)
Bicarbonate, calculated
(22-26 mmol/L)
1
3
10
14
sO2 %
97.6
99.3
98.9
98.6
Lactate
22.1
23.4
14.9
7.9
Table 2: Arterial Blood Gas values
Remarkably, approximately 9 months later, patient presented with similar picture but with less severe metabolic acidosis. Metformin was again detected in her serum at a level of 10.0 mg/L.
Metformin, while generally safe when used as prescribed, can lead to life-threatening complications when misused, especially in the context of an eating disorder. It should be suspected in any patient with known eating disorder presenting with metabolic acidosis. Timely recognition and intervention are essential to improve outcomes in such cases.