Case Presentation:

A 71‐year‐old man with stage IV chronic lymphocytic leukemia (CLL), hypertension, and diabetes mellitus was admitted to the hospital medicine service for the evaluation of 2 weeks of generalized weakness, anorexia, and mild abdominal pain. He was found to have a lactate level of 10.4. The medical team began to investigate the etiology of his severe lactic acidosis. The patient did not have fever, leukocytosis, or hypotension to suggest severe sepsis. Blood cultures, urine cultures, and a chest x‐ray were negative for infection. A CT of the chest, abdomen, and pelvis did not show any abscess or mesenteric ischemia but revealed hepatomegaly, splenomegaly, and diffuse bulky retroperitoneal and upper abdominal adenopathy consistent with CLL. Broad‐spectrum antibiotics and volume repletion with IV fluids had no effect on the patient's symptoms or lactic acidosis, and the patient rapidly deteriorated throughout the hospitalization. He became lethargic and severely thrombocytopenic, and his kidney function declined. The infectious disease service discontinued antibiotic treatment after all infectious workup was negative. The hematology/oncology service ruled out TTP and tumor lysis syndrome with a normal peripheral smear and electrolyte panel, respectively. It was thus thought that the constellation of symptoms and the persistently high lactic acid may be due to the CLL, which had not progressed since the last dose of chemotherapy 6 months earlier. The patient was transferred to the ICU and ultimately died after a DNR/DNI order was signed.

Discussion:

Lactic acidosis is the most common form of metabolic acidosis encountered in hospital medicine. It is most commonly associated with systemic hypoperfusion and resultant tissue ischemia (type A lactic acidosis). Malignancies, particularly hematologic malignancies, can rarely cause a severe lactic acidosis without any apparent systemic hypoperfusion (type B lactic acidosis). The pathogenesis of type B lactic acidosis in hematologic malignancies is unclear, although it is speculated to result from an increase in lactate production by cancer cells and a decrease in hepatic lactate utilization. Although type B lactic acidosis does not seem to correlate with tumor burden, nearly all of the reported cases describe the phenomenon in the setting of rapid cellular proliferation or acute leukemia. Only chemotherapy has been effective in correcting the acute lactic acidosis in a few patients. As such, it seems to portend a poor prognosis regardless of the treatment rendered. The aforementioned case of type B lactic acidosis is unique not only in its overall rarity in hematologic malignancies but more so in its presence in a chronic type.

Conclusions:

The purpose of discussing this case is to broaden the differential diagnosis of lactic acidosis in hospitalized patients who have hematologic malignancies without any evidence of systemic hypoperfusion.