Critically sick individuals with shock and disseminated intravascular coagulation (DIC) can suffer ischemic limb damage in the lower and, in certain cases, upper limbs. As micro thrombosis explains harm to acral tissues, arterial pulses are frequently preserved in symmetrical peripheral gangrene (SPG). The apparent symmetry of the tissue damage, which affects two or four limbs, correlates to the systemic character of DIC and decreased peripheral blood flow in shock states. Because some patients are given vasopressors, doctors may attribute limb necrosis to these drugs’ side effects.

However, this begs the question of why only a small percentage of critically sick patients with shock, DIC, and vasopressor usage develop SPG. A recent case series discovered that more than 90% of patients with SPG have prior acute ischemic hepatitis, implying that severe acquired deficiency of the natural anticoagulants, protein C and antithrombin, in the setting of the procoagulant milieu of DIC, may explain ischemic limb injury through markedly disturbed procoagulant-anticoagulant balance. Researchers looked at 20 case studies of SPG patients that were found using a search method that contained the word “vasopressors.”

Surprisingly, an examination of the 20 cases revealed a distinct delay between the development of hypotension and the beginning of critical limb ischemia. This time lag between the initiation of vasopressor therapy and the onset of limb ischemic necrosis argues against vasopressors playing a role in ischemic limb injury and instead points to a time-dependent decrease in hepatically synthesized natural anticoagulants as a key factor explaining acral micro thrombosis in SPG.