• Ryan K Dean, Rogin Subedi, Dalvir Gill, and Amitpal Nat.
• Department of Medicine, SUNY Upstate Medical University, 750 East Adams Street, Syracuse, NY 13210, United States. Electronic address: deanr@upstate.edu.
• Am J Emerg Med. 2017 Aug 1; 35 (8): 1214.e5-1214.e6.

AbstractLactic acidosis is a common metabolic acidosis characterized by increased serum lactate and is usually associated with a decreased blood pH. Lactic acidosis has many different causes but has been differentiated into type A, hypoxic causes, and type B, non-hypoxic causes. Tissue hypoxia, type A, is the most common cause, usually secondary to processes such as sepsis and multi-organ failure. Type A must be differentiated from type B in the correct clinical setting as treatments are vastly different. Type B causes may include drug side-effects, toxins, enzymatic defects, inherited or acquired, any of which may lead to overproduction or underutilization of lactate. However, as most clinicians are more familiar, and likely more initially concerned with hypoxic etiologies, evaluation is directed toward finding the source of hypoperfusion or hypoxia, and thus generally leading to a delay in discovering a type B cause (or mixed type A and type B). Here we describe a case of lactic acidosis in the setting of thiamine deficiency thought to be secondary to advanced lung cancer. The purpose of this paper is to bring awareness to the clinician to consider other causes of lactic acidosis when evaluating a patient.Copyright © 2017 Elsevier Inc. All rights reserved.

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