Where Is the Lactate Coming From? An Unusual Presentation of Persistent Lactic Acidosis
Abstract
Persistent lactic acidosis in patients with metastatic colorectal cancer is uncommon and often attributed to impaired hepatic clearance from liver metastases. Acute worsening, however, may signal reversible metabolic derangements, including medication-related toxicity. A 64-year-old male with type 2 diabetes mellitus, hypertension, and metastatic colorectal cancer to the liver presented with weakness, lethargy, and inability to tolerate oral intake for three days. His baseline lactate was persistently elevated (5-7 mmol/L) over six months. On presentation, he was hypotensive [blood pressure (BP) 82/41 mmHg], tachycardic [heart rate (HR) 122 bpm], febrile (101°F), and drowsy. Labs showed acute kidney injury (AKI) (Cr 2.7 mg/dL), hyperkalemia [Potassium (K) 6.1 mmol/L], severe metabolic acidosis (bicarbonate 4 mmol/L), transaminitis [aspartate aminotransferase (AST) 424, alanine transaminase (ALT) 576], and lactate 18 mmol/L. Complete blood count showed a white blood cell (WBC) count of 19,000/µL. Computed tomography (CT) of the abdomen revealed the known 7 cm colorectal mass with multiple hepatic metastases, moderate ascites, and no obstruction or ischemia. Despite aggressive intravenous (IV) fluids and vasopressors, lactate rose to 20 mmol/L, and urine output remained negligible. Medication review revealed metformin use, raising suspicion for metformin-associated lactic acidosis (MALA) in the setting of AKI. Nephrology consultation was obtained, and continuous renal…
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