The salvaged blood syndrome: a sequel to mechanochemical activation of platelets and leukocytes?

Disseminated intravascular coagulopathy (DIC) and/or increased vascular permeability in the lungs (ARDS) or systemic circulation (anasarca) has been seen in an occasional patient following the administration of washed autologous red cells. We have found that platelets and leukocytes, activated by the process of salvage, can contaminate such red cell suspensions. Apparently, activation begins with the mechanical deposition of platelets on the centrifuge bowl wall during the cell-concentration phase of blood salvage if there has been substantial prior dilution of the salvaged blood with saline. Electron microscopy of the deposit reveals activated, degranulated platelets lining the inner surface of the bowl. There is a preferential "homing" of specific leukocyte types to local regions of the deposit. On the basis of morphological evidence, we hypothesize that these mechanically activated platelets release leukoattractant substances, including arachidonate-rich phospholipids which trigger the oxidative burst enzymatic pathway in exposed phagocytic cells. These cells, when reinfused, cause increased vascular permeability. This presents clinically as ARDS or anasarca, whereas DIC results from reinfused platelet phospholipid plus accompanying cellular debris.