Pulmonary embolism caused by delayed heparin-induced thrombocytopenia in a patient who received prophylactic LMWH.

BACKGROUND: Heparin induced thrombocytopenia (HIT) is a serious complication associated with heparin use. HIT usually develops between 5-14 days after starting heparin. Delayed-onset HIT can still occur 9-45 days after heparin had been discontinued. In patients with delayed HIT, the patient might be admitted to the hospital for new thrombosis and reexposure to heparin further worsens the patient's condition. CASE REPORT: Our patient is a 71-year old female readmitted for worsening dyspnea 2 weeks after she was discharged from the hospital. On her previous hospitalization, she was diagnosed with bronchiolitis obliterans organizing pneumonia (BOOP). She had received prophylactic doses of LMWH. Dyspnea was initially thought to be secondary to CHF exacerbation secondary to atrial fibrillation with rapid ventricular response. She was started on a heparin. However, the patient's clinical condition deteriorated and she needed to be intubated. Her platelet counts also decreased rapidly. After CT angiography of the chest showed pulmonary embolism, HIT was strongly considered. All forms of heparin were discontinued and argatroban was started. However, the patient did not improve and she subsequently expired on the 7(th) hospital day. Heparin-induced antibodies came back positive that same day. CONCLUSIONS: HIT is an immune-mediated disorder characterized by formation of antibodies against heparin-platelet factor 4 complex. The major clinical presentation of HIT is arterial and venous thrombosis. Once HIT is suspected, immediate cessation of any form of heparin is needed. Alternative anticoagulation must be started. Early treatment decreases the incidence of new thrombosis and stroke, and improves survival and cost savings.

Coumadin-induced skin necrosis in a 64 year-old female despite LMWH bridging therapy.

BACKGROUND: Coumadin is the standard oral anticoagulant used in a variety of clinical conditions. Coumadin inhibits the vitamin-K dependent gamma-carboxylation of coagulation factors II, VII, IX, X and the anticoagulant proteins C and S. Rarely, skin necrosis occurs when the resultant initial procoagulant state in the first few days of starting coumadin leads to thrombosis and formation of blood clots tin the dermal capillaries. This in turn causes skin necrosis due to interruption in blood supply to the skin. CASE REPORT: We are presenting the case of a 64 year-old female admitted for acute respiratory distress secondary to newly-diagnosed pulmonary embolism. The patient was started on therapeutic doses of low molecular weight heparin (LMWH) and coumadin. After 5 days of treatment, the patient started complaining of pain and numbness in both upper extremities. Overnight, this rapidly progressed to manifest hemorrhagic bullae with necrotic areas. This was immediately recognized as coumadin-induced skin necrosis. Coumadin was stopped immediately. Vitamin K was administered and local wound care was provided. Therapeutic LMWH was continued. The skin lesions began to show improvement after 3 days. CONCLUSIONS: In coumadin-induced skin necrosis, the patient initially presents with pain and erythema, followed by petechial lesions which progress to become purpuric. Hemorrhagic bullae with necrosis and eschar formation may soon develop. Once it is suspected, coumadin should be stopped and the patient should be given Vitamin K and FFP to reverse the effects of coumadin.