Blood transfusions reduce the mortality associated with such conditions as major trauma, major surgery, and myelotoxic chemotherapy and, as such, have revolutionized medical care. With the exception of acute hemolytic transfusion reactions, the practice of blood transfusion was once considered to be relatively risk-free. It is now clear that blood transfusions are associated with short- and long-term side effects, including the transmission of infectious agents, transfusion-related immunomodulation (TRIM), and proinflammatory stimulation of the innate immune system (Table 166-1) (1–3). As an interface between circulating blood and underlying tissue, the endothelium is preferentially exposed to cellular and noncellular mediators contained within blood products. Thus, transfusion may result in phenotypic alteration of the endothelium.

INFECTIOUS AGENTS

Owing to marked improvements in screening assays (particularly nucleic acid amplification–based protocols), transfusion-transmitted viral infections rarely occur today. However, it is important to recognize that pathogenic viruses from other parts of the world may undergo a change in their natural range of distribution, and thus become introduced into the United States, as illustrated by the recent reports of West Nile Virus (4). Many viruses and viral proteins, most notably cytomegalovirus (CMV) and the Tat proteins from human immunodeficiency virus (HIV)-1, have been shown to interact directly with the endothelial cell (EC) membrane, resulting in increased surface expression of adhesion molecules and the synthesis and release of chemokines (5,6). The resulting proinflammatory phenotype may lead to the firm adhesion of granulocytes, polymorphonuclear neutrophil (PMN)- mediated acute lung injury (ALI), or other tissue damage (5,6).