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Critically ill patients with shock and disseminated intravascular coagulation (DIC) can develop ischemic limb injury affecting the lower and sometimes the upper extremities. Arterial pulses are usually maintained in symmetrical peripheral gangrene (SPG) as microthrombosis explains injury to acral (distal extremity) tissues. The strikingly symmetrical nature of the tissue injury, affecting 2 or 4 limbs, corresponds to the systemic nature of DIC and diminished peripheral blood flow in shock states. As some patients receive vasopressors, clinicians may attribute limb necrosis to the adverse effects of these agents. However, this raises the important question as to why only a minority of critically ill patients with shock, DIC, and vasopressor use develop SPG. A recent case series found that >90% of patients with SPG have preceding acute ischemic hepatitis (shock liver), indicating that severe acquired deficiency of the natural anticoagulants, protein C and antithrombin, in the setting of the procoagulant milieu of DIC, plausibly explains ischemic limb injury through markedly disturbed procoagulant-anticoagulant balance. In this paper, I review 20 case reports of SPG patients identified through a search strategy that included the term “vasopressors.” Strikingly, analysis of the 20 cases showed a characteristic delay (median, 3 d) between onset of hypotension (and initiation of vasopressors) and onset of critical limb ischemia. This delay between the start of vasopressor therapy and onset of limb ischemic necrosis argues against vasopressors playing a key role in ischemic limb injury, and points rather to a time-dependent decrease in hepatically synthesized natural anticoagulants as being a crucial factor explaining acral microthrombosis in SPG.