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Our interest in the metabolism of hemoglobin in patients with thermal injury was stimulated by early observations that (a) in spite of multiple whole blood transfusions anemia often developed rapidly in the first 96 hours after injury, and (b) in the protracted convalescence of a patient with only a small burn, moderate anemia inevitably ensued. The latter was exceptionally refractory to all except replacement therapy. With these two facts in mind we have undertaken our present study of the burn patient in an attempt to answer the following questions: (1) to what extent does hemolysis occur, and (2) Previous work on the same general problem has already been presented by Moore, Peacock, Blakeley, and Cope (1), who demonstrated an increased excretion of urobilinogen in the urine of four patients and an increased excretion in the feces in one patient. Similarly, the British workers, Anderson and Semeonoff (2), described increased excretion of urinary urobilinogen. Others have pointed out the potentiality of increased osmotic fragility and plasma hemolysis (3, 4) early in the post-burn period as well as agglutination and "sludging" of the red cells (5) in the peripheral circulation removed from the site of the injury.

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