Case Presentation: A 65-year-old man with a history of nasal polyps was admitted to the hospital with a lactate of 10 mmol/L (0.5-2.2 mmol/L). He reported drenching night sweats and a 10-pound weight loss over the last 2-3 months. He noted orthostatic and ambulatory dizziness, as well as left-sided tinnitus, sinus pain, and nosebleeds over the past 6 months. He had no fevers, chills, respiratory or gastrointestinal symptoms, or other areas of bleeding. He did not take metformin. Other than left-sided hearing loss, vital signs and physical exam were unremarkable. Laboratory evaluation demonstrated a pH of 7.34, lactate 10.3 mmol/L, a low serum bicarbonate with elevated anion gap, a white blood cell count of 4,200/mm3 (differential notable for mild basophilia and rare blasts), hemoglobin 9.7 g/dL (13.6-17.5 g/dL) with mean corpuscular volume 86 fL (80-100 fL), and platelets 117/mm3 (140-450/mm3). Given his lactate, he was given 2 liters of intravenous fluids and started on empiric antibiotics. Peripheral flow cytometry was notable for 1% myeloid blasts but otherwise had no evidence of a lymphoproliferative disease. He underwent CT of the chest, abdomen, and pelvis which showed multifocal splenic infarcts. He underwent a bone marrow biopsy revealing 1.1% myeloid blasts and a relative increase in natural killer (NK) cells but again no definitive evidence of lymphoproliferative disorder. His lactate increased to 16 with an associated pH of 7.27-7.29. Given his sinus symptoms, he underwent nasal endoscopy revealing a polypoid mass in the left nare. Sinus MRI showed a large solid mass with extensive local and multicompartmental invasion, as well as subcutaneous, perineural, and intracranial spread. Pathology confirmed NK/T-cell lymphoma, nasal type, which was also demonstrated after additional staining on his bone marrow. He began urgent chemotherapy, and his lactate normalized within 4 days.
Discussion: Type B lactic acidosis occurs when there is increased serum lactate without evidence of systemic hypoperfusion; causes include medications, malignancy, liver or kidney disease, diabetes mellitus, alcoholism, toxins, HIV infection, mitochondrial disorders, and thiamine deficiency. In particular, type B lactic acidosis secondary to malignancy is the result of impaired hepatic clearance, mitochondrial dysfunction, and preferential aerobic glycolysis (transformation of glucose to lactate to produce energy).1,2 Preferential utilization of aerobic glycolysis to metabolize glucose to lactate is also known as the Warburg effect.3 Clinically significant lactic acidosis primarily occurs in hematologic malignancies, including multiple myeloma, lymphomas, and leukemias.4 Lactic acidosis from NK/T-cell lymphoma, as in our patient, is extremely rare.5 Previous case reports have shown that cancer patients with lactic acidosis have a high mortality rate estimated at 80%.6,7 Use of sodium bicarbonate, hemofiltration, or hemodialysis can be used to temporize the pH in patients with severe lactic acidosis,8 but prompt chemotherapy is essential to reduce lactate levels.
Conclusions: Hospitalists frequently encounter patients with type B lactic acidosis and should maintain a high clinical suspicion for an occult hematologic malignancy when it is severe. Expedited diagnosis is critical to facilitate urgent chemotherapy for this potentially life-threatening oncologic emergency.