Enoxaparin sodium/heparin

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Enoxaparin sodium/heparin Heparin induced thrombocytopenia and acute submassive pulmonary embolism : case report

A 69-year-old woman developed heparin-induced thrombocytopenia and acute submassive pulmonary embolism during anticoagulation treatment with heparin and enoxaparin-sodium [not all dosages and routes stated, time to reactions onset not stated]. The woman, who had a history of type II diabetes mellitus, hypertension, asthma, previous situational deep vein thrombosis (DVT) and pulmonary embolism (PE), underwent left total knee replacement. After the surgery, she was discharged to a rehabilitation centre with SC enoxaparin-sodium [enoxaparin] 30mg twice a day for DVT prophylaxis. After 1 week (while at the rehabilitation facility), she complained of acute shortness of breath, right leg pain, swelling and chest pain. Hence, she was taken to the emergency room (ER). On arrival to the ER, her BP was 145/103mm Hg, heart rate was 120 bpm and respiratory rate was 18 /minute. Her oxygen saturation was 94% on 5 litre of nasal cannula. Physical examination revealed bilateral lower extremity oedema from the upper thighs to calves with mild tenderness. ECG showed sinus tachycardia with S1Q3T3 pattern. CT scan of the chest showed a saddle PE, which was extending into the sub-segmental and segmental arteries of both the lungs. An increase in right to left ventricular ratio (>1) was detected with slight leftward septal deviation indicating right ventricular strain. Transthoracic echocardiography (TTE) showed an ejection fraction of 64% and moderate to severe right ventricle dysfunction with right ventricle systolic pressures of 60 mmHg, which was indicative of moderate pulmonary hypertension. Bilateral femoral and popliteal acute deep vein thrombosis was detected during venous duplex of the legs. In the ER (prior to receiving her laboratory results), she was started on weight-based IV unfractionated heparin and warfarin [coumadin] 5mg for PE and DVT. However, her complete blood count revealed platelet count of 23,000 /µL. Hence, heparin-induced thrombocytopenia (HIT) was suspected. The woman’s heparin therapy was discontinued. She was empirically started on argatroban, and she was transferred to another institution. The following day, anti-platelet factor-4/heparin antibody assay and serotonin-releasing assay (SRA) were positive with optical density of 2.524. After a single dose of warfarin, her international normalised ratio (INR) was 2.6. Also, in the setting of acute HIT with profound thrombocytopenia, there was a concern of warfarin-warfarin induced skin necrosis. Hence, to reverse the effect of warfarin, she received vitamin-K. On hospital day 3, she complained about worsening of shortness of breath, and she required 50% of fraction of inspired oxygen (FiO2) via a venturi mask. Thereafter, she also developed atrial fibrillation with a rapid ventricular rate of 148 bpm. Her BP was 108/60. Her therapy was switched from argatroban to bivalirudin (off label use), considering the institutional experience with bivali