Heparin-Induced Thrombocytopenia in a Patient With Pulmonary Embolism and Bilateral Deep Venous Thrombosis: A Case Report

The main non-bleeding complication arising from exposure to heparin is heparin-induced thrombocytopenia (HIT). Type I HIT is a non-immune-mediated mild decrease in platelet count, which mostly does not need treatment, and type II HIT is an immune-mediated, severe decrease in platelet count characterized by a significant risk of thrombotic complications requiring immediate treatment. HIT type II is a serious condition that can threaten life due to an immune and thrombotic response that continues to pose diagnostic and management challenges. Due to ineffective alternatives to heparin in certain typical and recurring situations, the disease burden remains unchanged in the U.S. HIT occurs in about 20,000 cases annually, representing one in every 1,500 hospital admissions. For patients diagnosed with pulmonary embolism (PE), heparin is often employed as an anticoagulant; however, the emergence of HIT in these cases complicates both the treatment plan and management approach. This case illustrates a patient who was diagnosed with a PE and received heparin therapy. Shortly after starting treatment, the patient experienced thrombocytopenia, a key indicator of HIT. A 73-year-old male, while on admission, was noticed to have left upper extremity swelling and increased shortness of breath. A CT chest pulmonary angiogram revealed a positive for acute pulmonary artery embolus in the right lower lobar branch pulmonary artery. Vascular Laboratory (VL) left upper extremity duplex revealed acute occlusive deep venous thrombosis (DVT) of the left jugular, subclavian, axillary, and brachial veins and superficial vein thrombosis in basilic and cephalic veins. The patient received an IV heparin bolus and continued on heparin infusion. The platelet count on initiating the heparin drip was 145 K/μL. On hospital day 5, the patient's platelet count dropped to 98 K/μL.The 4Ts for HIT score calculated was 7 points, meaning high probability, and heparin-induced platelet (HIP) antibody was ordered, and heparin drip was discontinued. Argatroban infusion was started. The Hematologist evaluated the patient and stated that the clinical findings were consistent with HIT. The HIP antibody (screening test) resulted positive, and the patient's optical density (O.D) was elevated to 0.536. Later on, the patient was noted to have right upper extremity swelling, and VL duplex upper extremity right veins showed acute occlusive DVT involving the right subclavian vein, axillary vein, brachial vein, and internal jugular vein, and a drop in platelet count to 54 K/μL. The unfractionated heparin (UFH) serotonin release assay, which is the confirmatory test for HIT, resulted positive result. Argatroban dose was increased to the maximum of the therapeutic range, aiming for a partial thromboplastin time of 70-80, as the patient continued to experience thromboses. This led to the recovery of platelets, discontinuation of Argatroban, and transition of the patient to Eliquis.

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A 73-year-old man with pulmonary embolism and deep venous thrombosis developed heparin-induced thrombocytopenia (4Ts score 7, positive serotonin release assay) on heparin therapy; he was switched to argatroban, platelets recovered, and he was transitioned to apixaban.

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