IN 1917 Rous and Robertson1 suggested that fragmentation was the normal fate of the effete erythrocyte at the end of its life-span. More recently it has become recognized that erythrocytes may undergo fragmentation earlier if they are subjected to excessive trauma within the circulation. The most striking example of this form of hemolysis has been the erythrocyte fragmentation that may result from a malfunctioning prosthetic heart valve2 or incomplete repair of an intracardiac defect.3 The hemolysis will cease, and the erythrocyte fragments disappear from the peripheral blood once the intracardiac defect is successfully repaired or the malfunctioning prosthetic valve is . . .