SESSION TITLE: Monday Medical Student/Resident Case Report Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/21/2019 02:30 PM - 03:15 PM INTRODUCTION: Heparin-induced Thrombocytopenia (HIT) is an immunoglobulin-mediated response against platelet factor 4-heparin complexes leading to thrombotic events carrying a mortality rate of 5-10%. HIT with pulmonary embolism (PE) although rare, is the most common life-threatening event occurring in 25% of all HIT cases. Treatment is controversial as heparin products are contraindicated and no best practices have been described. We present a case of a middle-age man with recent exposure to heparin presenting with syncope. CASE PRESENTATION: A 54 year-old male with type 2 diabetes and a recent hospitalization 10 days prior for diabetic ketoacidosis receiving prophylactic heparin presented for syncope. On arrival he was normotensive but tachycardic and hypoxemic. Laboratory studies revealed thrombocytopenia to 90k, a drop from baseline 150k, which was confirmed by repeat testing. Troponin and BNP were elevated. Electrocardiogram revealed sinus tachycardia and S1Q3T3 pattern. Given concern for submassive PE patient was started on a heparin drip since confirmatory computer tomography angiography could not be performed due to renal failure. Cardiology was consulted for possible catheter directed tissue plasminogen activator or thrombectomy, however both these interventions were unavailable at our institution. Given suspicion of HIT patient was switched from heparin to argatroban drip. Ventilation/perfusion scan demonstrated high probability of bilateral PE and transthoracic echocardiogram revealed right heart strain. Dopplers confirmed popliteal and left brachial vein thrombosis. Patient’s platelet count improved after discontinuation of heparin products to 140k. Platelet factor 4 and serotonin release assay were both positive. The patient was eventually transitioned to warfarin to be continued for 3 months and then re-evaluated. DISCUSSION: Treatment of submassive and massive PE in patients with HIT remains controversial. Several modalities of treatment have been described in the literature with varied success including non-heparin anticoagulation like argatroban, thrombolytic agents, catheter-based thrombus aspiration, and surgical embolectomy. Multiple cases using direct thrombin inhibitors like danaparoid, bivalirudin, lepirudin and argatroban have been reported however given argatroban is hepatically cleared, it tends to be used the most. Hemodynamic stability continues to be the prime factor when deciding between parenteral anticoagulation versus more invasive techniques. In the setting of HIT-associated PE with significant hemodynamic compromise, non-heparin anticoagulation with catheter-directed thrombolysis has been used with good outcomes. CONCLUSIONS: HIT associated PE is a rare phenomenon, however, when it occurs there are available treatment options. Although no clear study has demonstrated superiority, treatment primarily depends on hemodynamic stability and institutional resources. Reference #1: Mark Prince, Tim Wenham. “Heparin-induced thrombocytopenia” Postgraduate Medical Journal, Volume 94, Issue 1114 Reference #2: Hourmouzis, Z., et al. (2015). "Pulmonary embolism and heparin-induced thrombocytopenia successfully treated with tissue plasminogen activator and argatroban.” Am J Emerg Med 33(5): 739 e735-736 Reference #3: Warkentin TE, Kelton JG. “A 14-year study of heparin-induced thrombocytopenia” Am J Med. 1996;101(5):502 DISCLOSURES: No relevant relationships by Ayesha Azmeen, source=Web Response No relevant relationships by Anil Magge, source=Web Response no disclosure on file for Viraj Modi; No relevant relationships by Mario Perez, source=Web Response