A 38-year-old woman presented with dyspnea and fatigue for 1 week. Physical examination was unremarkable. Laboratory tests were unrevealing. Chest X-ray showed dextrocardia and a right lung mass measuring 5×4 cm (Fig. 1). Computed tomography (CT) of the chest revealed an accessory lobe of the liver extending into the chest cavity through a defect in the posterior right hemi-diaphragm, and the right pulmonary vein draining into the infradiaphragmatic inferior vena cava (IVC) instead of the left atrium (Fig. 2), consistent with Scimitar syndrome.
Critically ill patients are known to have a variety of electrolyte abnormalities. Lactic acidosis can frequently be seen secondary to shock states and is usually treated with aggressive volume resuscitation. Interestingly, hypophosphatemia is a potential cause of resistant lactic acidosis, which may not be as commonly identified or considered. We present a case of a 42-year-old man admitted twice over a span of 6 months with an elevated lactate level that did not resolve with volume resuscitation. It was ultimately determined that his lactic acidosis was due to hypophosphatemia after ruling out other potential causes. Phosphate replacement therapy resulted in the normalization of his lactate. In the literature, multiple theories have indicated the association of hypophosphatemia with lactic acidosis though no prior cases exist supporting a direct relationship. In this case, we set forth to evaluate the complicated relationship between all of these factors and to highlight the importance of early detection and treatment of hypophosphatemia, which may be beneficial in treating lactic acidosis.
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