Case Presentation: A 68-year-old man presented with dyspnea, wheezing and productive cough. He was hypoxemic and a chest radiograph revealed a left lower lobe infiltrate and he was admitted with a Chronic Obstructive Pulmonary Disease exacerbation and pneumonia. His troponin was mildly elevated and he was started on a heparin infusion. The intravenous line infusing heparin infiltrated in his left arm and was moved to his right arm, and again infiltrated. The next day he developed bilateral upper extremity painful purple patches and heparin was stopped. The following day the patient’s upper extremities had turned black and began to blister. He was transferred to our hospital for Dermatology consultation who noted bilateral upper extremity purpuric patches with reitform purpura, and hemorrhagic bullae on the patient’s bilateral upper extremities. No other skin or mucus membranes were involved. The patient had not been hospitalized for over twelve years and had no other heparin exposures. His platelets decreased from 236×109/L to 102×109/L therefore heparin induced thrombocytopenia (HIT) antibody was obtained but was within normal limits at 0.34. Protein S was 107% and protein C was 151%. Skin biopsy revealed erythrocyte extravasation without vascular inflammation. There was no vasculitis seen. These findings together were more consistent with heparin skin necrosis.
Discussion: The most common etiology of heparin skin necrosis is heparin dependent antibodies to heparin with or without thrombocytopenia (heparin induced thrombocytopenia). However, heparin skin necrosis can also occur from an Arthrus-type reaction; from incorrect injection or infusion; and from fat deposition. Skin lesions frequently appear five to ten days after exposure, but can occur earlier with previous heparin exposure. The lesions usually appear at the site of injection but can occur further away. This patient’s heparin infusion infiltrated into his bilateral upper extremities: the location of his skin necrosis. The initial appearance may be mistaken for a localized allergic reaction but will progress to necrosis. Lesions form heparin skin necrosis however, are not pruritic. The treatment is to discontinue heparin immediately. Non-heparin anticoagulants other than warfarin are safe to use if anti-coagulation is needed.
Conclusions: The differential diagnosis for the patient with new onset palpable purpura includes leukocytoclastic vasculitis from infection or medication, cryoglobulin-associated necrosis, and antiphospholipid syndrome. Heparin induced skin necrosis needs to be higher on the differential diagnosis list when skin lesions are associated with the site of heparin injection or infusion. While HIT is the more commonly considered side effect from heparin, the clinician should be able to recognize heparin skin necrosis by it’s timing and location to heparin injection or infusion; as well as lack of puritis.