Blood cell abnormalities complicating the hypophosphatemia of hyperalimentation: erythrocyte and platelet ATP deficiency associated with hemolytic anemia and bleeding in hyperalimented dogs.

Abstract

Abstract Hemolytic anemia and bleeding diathesis may occur in starved dogs infused with solutions of amino acids and hypertonic glucose (hyperalimentation). Dogs, as well as patients, develop profound hypophosphatemia within 24 hours of infusion. Paralleling the decrease in serum P, red cell and platelet ATP levels fall. Red cells become spheroidal, dehydrated, poorly filterable, and entrapped by the spleen; concomitantly, their survival is shortened. These abnormalities are prevented or reversed if cellular ATP is maintained by supplementation of animals with phosphate in vivo or by brief incubation of depleted red cells with adenosine and phosphate in vitro. Associated with ATP depletion in platelets, clot retraction becomes faulty; thrombocytopenia also occurs, which results from a 5- to 10-fold decrease in platelet survival. Maintenance of serum P levels by phosphate supplementation of infusion solutions prevents these platelet abnormalities and the hemorrhagic diathesis. We conclude that hypophosphatemia in hyperalimented dogs critically affects red cell and platelet function and survival through depletion of cellular ATP. By extrapolation to humans, we suggest that serum P levels should be monitored and carefully maintained in hyperalimented individuals so as to preclude these complications.