A 62-year-old hospitalized woman is evaluated for worsening skin lesions. She was admitted 6 days ago for elective coronary artery bypass grafting due to extensive coronary artery disease. The surgery was uncomplicated, and the patient was extubated on hospital day 2. She has recovered well, but yesterday she noticed red patches on her abdomen that progressed to purple lesions today. The patient has a history of non-ST elevation myocardial infarction, type 2 diabetes mellitus, hypertension, and hyperlipidemia. She is receiving low-dose subcutaneous heparin for prophylaxis of deep venous thrombosis and has not received any oral anticoagulation. Temperature is 37.1 C (98.7 F), blood pressure is 130/82 mm Hg, and heart rate is 90/min. Cardiopulmonary examination reveals patchy rales and normal heart sounds. The sternal surgical site is healing well. Several large purple/black patches are seen in the periumbilical area, surrounded by erythema. Peripheral pulses are normal. Neurologic examination is unremarkable. Which of the following is the most likely cause of this patient's skin lesions?
Clinical features of type 2 heparin-induced thrombocytopenia | |
Clinical signs | Suspected with heparin exposure >5 days & any of the following:
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Diagnostic evaluation |
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Therapy |
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Heparin-induced thrombocytopenia (HIT) is a life-threatening complication of heparin therapy. Heparin induces a conformational change in a platelet surface protein (platelet factor 4), which exposes a neoantigen. In patients with HIT, HIT antibodies form in response to the neoantigen and bind to the surface of platelets, causing platelet aggregation, thrombocytopenia (or drop in platelets >50%), and a prothrombotic state. In patients receiving heparin subcutaneously (eg, enoxaparin), a classic thrombotic complication of HIT is skin necrosis at the abdominal injection site.
HIT is diagnosed by immunoassay (only if high titer) or functional assay (eg, serotonin release assay [gold standard]). Treatment involves immediately discontinuing all heparin products (including heparin flushes) and initiating an alternate anticoagulant (eg, argatroban, fondaparinux). If HIT is suspected, treatment should not be delayed for laboratory confirmation as the risk of venous and arterial thrombosis is as high as 50% in untreated HIT.
(Choice A) Warfarin is an oral anticoagulant that can cause an acquired protein C deficiency, which may manifest as skin necrosis. However, this patient has not received any oral anticoagulation. Warfarin is often used for chronic anticoagulation maintenance in HIT but not until argatroban or fondaparinux are initiated and platelets are >150,000/mm3.
(Choice C) Delayed hypersensitivity reactions typically cause skin erythema, vesicles, or bullae. More severe reactions are associated with systemic symptoms, such as fever. This patient has necrotic lesions likely at the site of her low-molecular-weight heparin injections, making HIT much more likely.
(Choice D) Cholesterol embolization can occur due to plaque embolization into small arteries following coronary angiography. Cholesterol embolization classically causes skin findings (eg, livedo reticularis [mottled erythema], gangrene, cyanosis) that most commonly affect the lower extremities. With necrotic lesions on the abdominal wall, HIT is much more likely.
(Choice E) Viral reactivation is common with herpes zoster. Lesions are typically unilateral, in a single dermatome, and quite painful. They tend to be vesicular, not necrotic.
Educational objective:
Heparin-induced thrombocytopenia (HIT) should be suspected in patients on heparin who develop thrombocytopenia or thrombotic complications. In patients receiving heparin subcutaneously (eg, enoxaparin), a classic thrombotic complication is skin necrosis at the abdominal injection site. HIT is treated by discontinuing all heparin products and initiating an alternate anticoagulant (eg, argatroban, fondaparinux).