As should be evident from the case reports, epidemiology studies, and animal data, the primary mode of cocaine action is vasoconstriction, whether it occurs on the maternal side or the fetal side of the placenta. Attempts to characterize the fetal effects of cocaine exposure during pregnancy in order to formulate a "fetal cocaine syndrome" has revealed a wide spectrum of fetal effects. Therefore, a well-defined "fetal cocaine syndrome" does not exist. In fact, most fetal defects may be related to vasoconstriction, hypertension, and infarcts at any time during gestation and in any structure. Even the issues of SIDS and seizures may be the result of clinically undetectable vasospasm or hemorrhages. Traditional dogma dictates that a teratogen interferes with normal development of a structure such that the structure is missing, malformed, or dysfunctional. Moreover, since individual structures are formed at specific times during development, these structures are vulnerable to injury at these "time windows." Classical teratogens exert their damaging effects during the organogenesis period. For cocaine, however, exposure during any period in gestation may place any organ or structure at potential risk for damage. While repeated exposures during pregnancy may increase the risk of cocaine-induced damage, it appears that even a single exposure may produce infarction, edema, and tissue necrosis. The site of damage may be related to the tissue level of cocaine and the weakness of the blood vessels at that site. Subsequent loss of vascular supply and tissue necrosis produce fetal damage that is beyond capacity for repair.