(485) Catastrophic Presentation of Delayed HIT: When Argatroban Was Not Enough!

Introduction: Heparin induced thrombocytopenia(HIT) is commonly seen post cardiac surgery. Delayed onset HIT, a rarer form, manifests with thrombocytopenia 5 days after heparin cessation with severe thrombotic complications. Argatroban is the drug of choice, however in exceptional cases, resistance can be fatal, prompting a need for IVIG therapy to improve platelet counts and prevent repeat thrombotic events.

Description: A 59 year old lady exposed to heparin during CABG, presented to ED on POD15 with worsening leg swelling, breathlessness and melena. She was compliant with aspirin and plavix. She was hemodynamically stable with good oxygenation on room air, exhibiting tense edema of both lower extremities with preserved pulsations. Fecal guaiac test was positive. Platelet count was 99x10^3/cmm. D-dimer was 35200. PT/PTT was normal. Acute kidney injury was noted. Bilateral lower extremity dopplers confirmed deep venous thrombosis(DVT) in both lower extremities up to the groin. Decision was made to cautiously start heparin infusion due to risk of worsening GI bleed. Suspected cephalad thrombosis progression prompted renal venous doppler, revealing nearly complete thrombosed inferior vena cava, bilateral renal and common iliac vein thrombosis, confirmed by CT venogram. CTA chest showed PE to right main pulmonary artery. Within 12 hours of starting heparin, platelets dropped to 33x10^3/cmm. Calculated 4T score was 6, prompting a switch to argatroban drip. IR-guided venous thrombectomy was performed. HIT Ab titers were high. DIC ,TTP and hypercoagulopathy workup was negative. Platelets remained low for 3 days with a nadir of 27x10^3/cmm. Repeat dopplers confirmed recurrence of left leg DVT. After receiving two doses of IVIG, platelet counts improved. Eventually SRA came positive. A second venous thrombectomy was performed and patient was discharged on Eliquis and Plavix.

Discussion: Delayed onset HIT causes grave thrombotic complications due to highly pathologic Ab causing both heparin-dependent and independent platelet aggregation. The platelet drop after heparin exposure suggested preexistence of circulating Ab. We endorse discontinuing heparin without waiting for serological confirmation when clinicopathological suspicion is high. However in cases unresponsive to argatroban therapy, IVIG is indicated.