A 59-year-old woman with history of chronic kidney disease stage 4 was admitted to the hospital for further management of shortness of breath. She complained of worsening leg swelling and progressive orthopnea. Diagnostic studies showed significantly elevated creatinine and chest X-ray was remarkable for pulmonary edema. Patient was managed for fluid overload secondary to acute on chronic kidney injury, and was started on high dose furosemide. She did not show any response to diuresis and eventually required urgent dialysis. On day 6 of hospitalization, patient developed a diffuse erythematous rash on her back associated with itching. Her platelet count was found to be low at 96,000 from a baseline of 259,000. Given the recent exposure to heparin during dialysis along with a significant drop in her platelet count, the rash was though to be a clinical manifestation of heparin-induced thrombocytopenia. Her 4T score was 7 and thus, further work up for HIT was pursued. Lab work showed Heparin-PF4 antibody optical density of 0.439 and Heparin-PF4 AB inhibitor of 102%. Serotonin release assay was positive. These findings were consistent with a diagnosis of heparin-induced thrombocytopenia. Patient was started on argatroban. In a few days, her rash completely resolved and her platelet counts recovered. She was later discharged to home on warfarin.
Discussion:
Heparin induced thrombocytopenia (HIT) is a life-threatening complication of heparin exposure. HIT results from an autoantibody directed against endogenous platelet factor-4 complex. This antibody activates platelets and can cause serious arterial and venous thrombosis. Other clinical manifestations include skin necrosis and non-necrotic erythematous skin lesions. Non-necrotic erythematous skin lesions secondary to HIT are rare, and can precede the thrombosis. This rash when present in association with thrombocytopenia and recent heparin exposure should raise the suspicion for HIT. Our patient received heparin during dialysis, had thrombocytopenia and later developed a non-necrotic skin rash that led to the testing for HIT. With prompt diagnosis and treatment, patient’s rash and thrombocytopenia resolved.
Conclusions:
Non-necrotic erythematous rash is a rare clinical manifestation of heparin-induced thrombocytopenia. The rash can precede the thrombotic events and thus, physicians should have a high degree of clinical suspicion to diagnose HIT in patients with rash and new onset thrombocytopenia. To prevent further morbidity and mortality, all heparin products should be held and these patients should be treated with non-heparin anticoagulants until the diagnosis is confirmed.