During its approximately four-month lifespan, the human red blood cell (RBC) travels approximately 300 miles, making about 170,000 circuits through the heart, enduring cycles of osmotic swelling and shrinkage while traveling through the kidneys and lungs, and an equal number of deformations while passing through capillary beds [1,2]. It has been speculated that accumulated damage to the RBC, especially to its membrane, renders the aging RBC unfit to circulate, leading to its destruction, via mechanisms which are poorly understood.
The normal time of RBC senescent death in adults is approximately 110 to 120 days. Hemolysis is usually defined as a shortened survival of circulating RBCs to a value of less than 100 days.
This topic will review the mechanisms of normal RBC destruction and the methods used to measure RBC survival, which may be used in the evaluation of patients with suspected hemolysis . Approaches to the patient with hemolytic anemia and with anemia in general are presented elsewhere. (See "Approach to the diagnosis of hemolytic anemia in the adult" and "Approach to the adult patient with anemia".)
MECHANISMS OF RBC DESTRUCTION
In normal subjects, red blood cells (RBCs) are destroyed by two different mechanisms, one related to increasing RBC age (senescence) and the other to a random process which destroys intact RBCs, or portions of an intact RBC (eg, vesicles) independent of their age (random hemolysis). These two processes may not be fully independent of one another .
Senescence — Virtually all RBCs in normal subjects die of processes associated with "wear and tear" associated with prolonged circulation within the intravascular space. These processes include, but are not limited to :