**Part 5**

**Special Issues** 

196 Venous Thrombosis – Principles and Practice

[75] Khorana AA, Streiff MB, Farge D, Mandala M, Debourdeau P, Cajfinger F, Marty M,

[76] Guyatt G, Schünemann HJ, Cook D, Jaeschke R, Pauker S. Applying the grades of

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Falanga A, Lyman GH. Venous Thromboembolism Prophylaxis and Treatment in Cancer: A Consensus Statement of Major Guidelines Panels and Call to Action. J

recommendation for antithrombotic and thrombolytic therapy: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. 2004 Sep;126(3

**11** 

*USA* 

**Heparin-Induced Thrombocytopenia** 

Heparin-induced thrombocytopenia (HIT) is an immune-mediated response to heparin administration that causes thrombocytopenia and a prothrombotic state. Heparin is the most commonly used anticoagulant drug for the prevention and treatment of thromboembolic diseases in hospitalized patients. Heparin exists in two main forms, pure unfractionated heparin (UFH) and low molecular weight heparin (LMWH), which is derived from UFH. Though HIT is relatively rare, occurring in less than 5% of patients receiving UFH and less than 1% of patients receiving LMWH, it has the potential to cause significant morbidity and mortality. The main complication of HIT is thrombosis, most commonly deep vein thrombosis (DVT) or pulmonary embolism (PE). More rarely HIT can manifest as occlusion of a limb artery, acute myocardial infarct, stroke, a systemic reaction or skin necrosis. In the current chapter the topic of HIT will be reviewed in terms of its

*S-B is a 48-year-old male who was admitted to the orthopedics service for surgical repair of a right acetabular fracture resulting from a fall. He had no significant past medical history. His course was complicated by an ileus. He was given enoxaparin for thromboprophylaxis starting on day 2 of admission. During his hospital stay, he developed a pulmonary embolus and atrial fibrillation and the dose of enoxaparin was increased. An IVC filter was also placed. His platelet count dropped from 278K/uL on admission to a low of 88K/uL on hospital day 10. HIT antibody was positive. Enoxaparin was discontinued and lepirudin was started. Platelet count began improving by the next day and was 190K/uL two days after starting lepirudin. He was transitioned to warfarin. A PICC line was placed* 

*Several days later, the patient suddenly developed shortness of breath, chest pain, nausea and fever of 102°F. His heart rate increased to 130; he was normotensive. An arterial blood gas revealed metabolic acidosis and hypoxemia; his lactate level was elevated. Chest x-ray showed no infiltrates and a CT pulmonary angiogram (CTPA) was negative for infiltrates, pulmonary emboli and other pathology. EKG showed sinus tachycardia. Antibiotics were begun for possible sepsis. Platelet count was found to be 114K/uL compared to 231K/uL the previous day. Review of his chart revealed that the patient had received heparin flushes of his PICC line as part of a standing protocol. Heparin flushes were discontinued and lepirudin was restarted. Over the next several hours his fever, tachycardia, and hypoxemia improved. His lactate level normalized and platelets rose to 160K/uL by the following* 

**1. Introduction** 

pathophysiology, diagnosis, and treatment.

*for parenteral nutrition as his ileus had not resolved.* 

*morning. All cultures were negative and antibiotics were discontinued.* 

**1.1** *Clinical Vignette: Patient S-B* 

Kelly L. Cervellione and Craig A. Thurm *Jamaica Hospital Medical Center, Jamaica, New York,* 
