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

## TL;DR

A patient with metastatic colorectal cancer and chronic lactic acidosis experienced a severe spike due to metformin toxicity and sepsis, which was successfully treated with kidney support therapy.

## Contribution

This case highlights the importance of identifying reversible causes of lactic acidosis in cancer patients with baseline elevations.

## Key findings

- Lactic acidosis was multifactorial, involving baseline liver metastases, sepsis, and metformin toxicity.
- CRRT led to rapid lactate clearance and clinical improvement.
- Early recognition of medication toxicity and renal dysfunction was critical for recovery.

## 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.