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Case Report |
AMANDA HOWARD-THOMPSON, PHARM.D., is Assistant Professor, College of Pharmacy, University of Tennessee (UT), Memphis; at the time of writing she was Internal Medicine Pharmacy Resident, Methodist University Hospital (MUH), Memphis. JUSTIN B. USERY, PHARM.D., is Internal Medicine Clinical Specialist and Assistant Professor, College of Pharmacy, UT; at the time of writing he was Internal Medicine Pharmacy Resident, MUH. BOB L. LOBO, PHARM.D., BCPS, is Assistant Director of Clinical Pharmacy, MUH, and Associate Professor, College of Pharmacy, UT. CHRISTOPHER K. FINCH, PHARM.D., BCPS, is Critical Care Clinical Specialist, Department of Pharmacy, MUH, and Associate Professor, College of Pharmacy, UT.
Address correspondence to Dr. Finch at the Department of Pharmacy, Methodist University Hospital, 1265 Union Avenue, Memphis, TN 38014 (finchc{at}methodisthealth.org).
Summary. A patient with a history of hypertension, heart failure, and myocardial infarction was admitted to the hospital after complaining of a two-day history of shortness of breath, diaphoresis, and chest pain. The patient underwent a cardiac catheterization and received several medications, including heparin. Suspicions of HIT occurred when her platelets began to decrease severely and she developed a left groin hematoma and a pseudoaneurysm. Lepirudin was initiated and a heparin platelet factor 4 (PF4) antibody test was performed. The results were negative and lepirudin was discontinued. She was rechallenged with unfractionated heparin (UFH) after surgery of the pseudoaneurysm, but her platelets began to decrease again. A second PF4 test was performed, the results of which were positive. The UFH treatment was discontinued. Warfarin was also initiated after surgery and the patients platelets rapidly increased after heparin was discontinued. She was discharged one week later. Three days after discharge, she was readmitted after complaining of severe pain and swelling of the fatty tissue of her right flank that began the day after she was discharged. Some blistering and necrosis were noted on the lesion. Histological sections showed focal thrombosis of vessels in the deep reticular dermis consistent with WISN. Local wound care was given to manage the WISN, lepirudin was initiated, and warfarin was discontinued and reinstated one week later at a low dosage.
Conclusion. A patient with HIT developed severe skin necrosis after initiation of warfarin therapy.
Index terms: Anticoagulants; Dosage; Heparin; Necrosis; Skin diseases; Thrombocytopenia; Toxicity; Warfarin
Purpose. A case of heparin-induced thrombocytopenia (HIT) complicated by warfarin-induced skin necrosis (WISN) is reported.
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