What question did this study set out to answer?

To investigate the cause of persistent lactic acidosis in a patient with metastatic colorectal cancer and identify reversible factors.

February 28, 2026Cureus1 citationsOpen Access

Where Is the Lactate Coming From? An Unusual Presentation of Persistent Lactic Acidosis

WSWaleed SadiqRobert Wood Johnson University Hospital MWMadeeha Subhan Waleed

Key Points

To investigate the cause of persistent lactic acidosis in a patient with metastatic colorectal cancer and identify reversible factors.
Case presentation of a 64-year-old male with metastatic colorectal cancer and lactic acidosis.
Assessment of vital signs, laboratory findings, and imaging (CT scan).
Medication review leading to the suspicion of metformin-related lactic acidosis.
Initiation of continuous renal replacement therapy (CRRT) for treatment.
Baseline lactate levels were persistently elevated at 5-7 mmol/L for six months.
Upon presentation, lactate sharply increased to 18 mmol/L, complicated by acute kidney injury and metabolic acidosis.
Following CRRT, lactate decreased significantly to 6 mmol/L within 12 hours, and hemodynamics improved.

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 replacement therapy (CRRT) was initiated. Lactate declined to 12 mmol/L at four hours and 6 mmol/L at 12 hours. Hemodynamics improved, vasopressors were discontinued, urine output increased, and creatinine and bicarbonate normalized on day two. Eventually, the patient was successfully extubated, tolerated oral intake, and was discharged home after completing antibiotics. This case illustrates multifactorial lactic acidosis: baseline elevation from liver metastases, superimposed type A lactic acidosis from sepsis, and type B lactic acidosis from metformin accumulation. Early recognition and initiation of CRRT were critical for rapid lactate clearance and clinical recovery. In patients with baseline lactic acidosis due to metastatic liver disease, sudden lactate spikes should prompt evaluation for reversible causes, including renal dysfunction and medication toxicity. Multidisciplinary management and renal support can be lifesaving.

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