Multiple extremity gangrene developed in five patients as a complication of dopamine therapy. The clinical conditions were (1) penetrating chest trauma requiring pneumonectomy with postoperative sepsis, (2) cardiac arrest with aspiration pneumonia, (3) lymphoma with sepsis, (4) Klebsiella pneumonia, and (5) myocardial infarction. The development of acrocyanosis leading to gangrene occurred at dopamine dosages of 5.1 to 10.2 micrograms/kg/min. The alpha-adrenergic vasoconstriction effects of dopamine would not be expected from the doses employed in these patients. Thus, other factors beside pure alpha vasoconstriction are responsible for tissue necrosis after the use of dopamine. We believe that the embolic complications of disseminated intravascular coagulation and hypovolemia are serious risk factors in the development of dopamine gangrene. Peripheral vasoconstriction from dopamine, even at low doses, may set the stage for thrombotic complications of disseminated intravascular coagulation and lead to tissue damage. In laboratory models of disseminated intravascular coagulation, an alpha-adrenergic drug is required to produce peripheral ischemic tissue damage. Treatment of tissue ischemia related to dopamine depends on early recognition of acrocyanosis. Phentolamine, an alpha blocker, has been recommended for treating dopamine ischemia, either through local instillation into ischemic tissues or intravenous infusion. We recommend a high index of suspicion for, and early treatment of, underlying consumptive coagulopathy in all patients requiring dopamine.