Hematologic malignancies rarely present with lactic acidosis (LA) as the predominant feature. The exact pathogenesis of LA in these patients is not yet clear, but recent reviews of the literature indicate an extremely poor prognosis. We discuss below the case of an elderly patient with lactic acidosis as the presenting aspect of a lymphoma that was diagnosed via pleural fluid analysis.
An 86 year-old Hispanic male was admitted to our ICU for suspected fluid overload and cardiac conduction abnormalities. The patient had a history of diabetes mellitus, hypertension and peptic ulcer disease and presented to the emergency department with severe shortness of breath on exertion, leg swelling, orthopnea and abdominal distension. He also complained of 3 episodes of night sweats over 2 weeks, but denied weight loss or fever. The initial chest x-ray revealed bilateral effusions, while initial labs showed a normal CBC, hyperkalemia (potassium of 5.9 mmol/L), renal insufficiency (BUN of 48 mg/dL and creatinine of 2.36 mg/dL) and anion gap metabolic acidosis. The initial lactic acid was elevated at 6.1 mg/dL, and remained elevated for 48 hours. The patient had no peritoneal signs, had never been hypotensive in hospital, was not on metformin and had normal liver enzymes. A 2D cardiac echo showed an ejection fraction of 70% with no evidence of diastolic or valvular dysfunction.The presence of LA in the absence of a typical source raised concerns for occult ischemia, especially mesenteric ischemia. A CT scan of abdomen and pelvis showed diffuse signs of peritoneal inflammation without a focus. Small, irregular kidneys and a slightly thickened sigmoid colon were seen, as was fat stranding throughout the abdomen, but no abscess, mass or enlarged nodes were visualized. Gastroenterology consultation was obtained, and colonoscopy to further evaluate for ischemic colitis was recommended. The patient’s dyspnea persisted and a thoracentesis was performed for palliation and diagnosis. Thoracentesis yielded 600cc of straw colored, mildly turbid fluid. The fluid characteristics were: WBC of 6940 with 86% monocytic predominance, pH of 7.0, LDH of 18649, and a negative Gram stain and culture. The fluid was sent for cytology and flow cytometry. While awaiting pleural fluid analysis, the patient came back positive for ANA and anti-centromere antibodies. Despite having no history consistent with scleroderma, an autoimmune pathology linking the pleuritis, nephritis, conduction abnormality and peritonitis was considered.This theory was supplanted when the results of flow cytometry demonstrated a diffuse large B-cell lymphoma, finally providing our diagnosis. The colonoscopy was performed and a rectal mass was identified and biopsied. This mass was identified by pathology as an adenocarcinoma –a second primary tumor unrelated to the LA or presenting symptoms. The patient was referred to hematology/oncology for treatment options.
Our patient presented with LA of unclear etiology. Our initial workup focused on the typical causes of LA: sepsis/hypotension, local ischemia, drug effects, and liver failure. We found a number of lab and imaging abnormalities, yet none explained the persistent acidosis. Despite the normal CBC and minimal constitutional symptoms we continued to pursue the possibility of hematological malignancy. Though LA is rarely seen in lymphoma, and is even more rarely seen as a presenting feature, we continued to pursue this diagnosis in an attempt to unify the myriad pathologies we uncovered. Our persistence led us from a rare manifestation to a definitive diagnosis via pleural fluid analysis.
Though our understanding of the cause of LA in hematologic malignancy is limited and the prognosis almost universally poor, only by recognizing that such rare entities exist can we expand our ability to diagnose these diseases.
Brian Rice, No Financial Disclosure Information; No Product/Research Disclosure Information