A 55-year-old woman comes to the office due to right leg swelling and tenderness. She has a history of ovarian cancer and is currently undergoing chemotherapy. A duplex venous ultrasound of the right lower extremity shows thrombosis of the right popliteal vein. The patient is sent home with subcutaneous enoxaparin. A week later, the patient returns to the office for a follow-up appointment. Laboratory results are as follows: This patient's current condition predisposes her to which of the following?

Question

A 55-year-old woman comes to the office due to right leg swelling and tenderness.  She has a history of ovarian cancer and is currently undergoing chemotherapy.  A duplex venous ultrasound of the right lower extremity shows thrombosis of the right popliteal vein.  The patient is sent home with subcutaneous enoxaparin.  A week later, the patient returns to the office for a follow-up appointment.  Laboratory results are as follows:  This patient's current condition predisposes her to which of the following?

Quizplus · Accepted Answer

Explanation: 11ec25c8_d41b_0482_bc81_27a2f13f0ab8_MD0003_00 This patient was initiated on low molecular weight heparin (enoxaparin) due to an acute deep venous thrombosis. A week later, laboratory studies show a significant reduction in platelet count, suggesting type 2 heparin-induced thrombocytopenia (HIT). A drop in platelets by >50% or a new thrombus within 5-10 days of heparin initiation should raise suspicion for HIT (HIT may manifest sooner in patients previously exposed to heparin). Heparin induces a conformational change to a platelet surface protein (platelet factor 4 [PF4]), which creates a neoantigen. In patients with HIT, the immune system responds by forming an IgG autoantibody (HIT antibody). HIT antibodies then coat the surface of platelets, causing: Thrombocytopenia - the reticuloendothelial system (largely the spleen) removes HIT antibody-coated platelets, causing mild to moderate thrombocytopenia (mean nadirs of 60,000/mm³). Severe thrombocytopenia (<20,000/mm³) is uncommon. Thrombus - HIT antibodies activate platelets, resulting in platelet aggregation and the release of procoagulant factors. This puts patients at very high risk (as high as 50%) for arterial and venous thrombus. Venous thrombosis in the leg veins, cardiac vessels, and skin (at the site of heparin injection) is common. Arterial thrombosis may occur in the heart, limbs, or central nervous system. If HIT is suspected, all heparin products should be discontinued immediately and anticoagulation should be initiated with a non-heparin medication (eg, argatroban, fondaparinux). Diagnosis is confirmed by functional assay (eg, serotonin-release assay [gold standard]) or high-titer immunoassay of the blood. (Choice A) Acute interstitial nephritis (AIN) presents with renal dysfunction and is typically caused by medications, autoimmune disorders (eg, systemic lupus erythematosus), or infections. Heparin is not commonly associated with AIN. (Choice C) Coronary vasospasm is caused by hyperreactivity of the coronary vessels and may result in anginal symptoms. Patients with HIT are at risk for venous and arterial thrombus in the coronary vessels (not vasospasm). (Choice D) Hemarthrosis is usually due to trauma (most common), vascular damage, or coagulopathy (eg, hemophilia). It is uncommon for HIT to cause bleeding issues. (Choice E) Mycotic aneurysms are bacterial infections of the vascular wall that tend to occur after trauma or with preexisting aneurysm. Deep venous thrombosis typically does not put patients at increased risk for a mycotic aneurysm. Educational objective: Heparin-induced thrombocytopenia (HIT) is an immune-mediated process that causes thrombocytopenia several days after initiation of heparin therapy. HIT is highly thrombogenic and patients must be placed on alternate forms of anticoagulation due to the risk for arterial and venous clots. References: Heparin-induced thrombocytopenia: an update. (http://www.ncbi.nlm.nih.gov/pubmed/22399304)

A 55-Year-Old Woman Comes to the Office Due to Right