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A 41-year-old man with a continuous- flow left ventricular assist device presented for evaluation of dysphagia and dark urine. He was found to have a significantly elevated L-lactate dehydrogenaseand an elevated plasma free hemoglobin consistent with intravascular hemolysis.After the hemolysis ceased,both the black urine and dysphagia resolved spontaneously.Transient esophageal dysfunction,as a manifestation of gastrointestinal dysmotility,is known to occur in the setting of hemolysis.Paroxysmal nocturnal hemoglobinuria is another recognized cause of massive hemolysis with gastrointestinal dysmotility occurring in25%-35%of patients during a paroxysm.Intravascular hemolysis increases plasma free hemoglobin,which scavenges nitric oxide(NO),an important second messenger for smooth muscle cell relaxation.The decrease in NO can lead to esophageal spasm and resultant dysphagia.In our patient the resolution of hemolysis resulted in resolution of dysphagia.
A 41-year-old man with a continuous-flow left ventricular assist device presented for evaluation of dysphagia and dark urine. He was found to have a significantly elevated L-lactate dehydrogenase and an elevated plasma free hemoglobin consistent with intravascular hemolysis. After the hemolysis ceased, both the black urine and dysphagia resolved spontaneously. Transient esophageal dysfunction, as a manifestation of gastrointestinal dysmotility, is known to occur in the setting of hemolysis. Paloxysmal nocturnal hemoglobinuria is another recognized cause of massive hemolysis with gastrointestinal dysmotility occurring in 25% -35 % of patients during a paroxysm. Intravascular hemolysis increases plasma free hemoglobin, which scavenges nitric oxide (NO), an important second messenger for smooth muscle cell relaxation. decrease in NO can lead to esophageal spasm and resultant dysphagia. In our patient the resolution of hemolysis resulted in resolution of dysphagia.