The numerous drugs to which the acutely ill are exposed place these patient
s at a significant risk of developing drug-induced thrombucytopenia. Such p
atients tend to have preexisting hemostatic defects that place them at addi
tional risk of complications as a result of the drug-induced thrombocytopen
ia. The clinical challenge is to provide rapid identification and removal o
f the offending agent before clinically significant bleeding or, in the cas
e of heparin, thrombosis results, Drug-induced thrombocytopenic disorders c
an be classified into three mechanisms: bone marrow suppression, immune-med
iated destruction, and platelet aggregation. Clinical characteristics. prel
iminary laboratory findings, and drug history specific to the mechanisms ca
n assist clinicians in rapidly isolating the causative drug.