Autoimmune Heparin-Induced Thrombocytopenia in a Patient With Decompensated Liver Cirrhosis

Saturday, January 21, 2023

10:00 AM – 11:00 AM PT

Location: Exhibit Hall - RST 09

First Author(s)

DD

Dana Darwish, MD

n/a
Dallas, Texas

Disclosure information not submitted.

Co-Author(s)

MP

Megha Patel, MD

Resident Physician
UT Southwestern Medical Center, United States

Disclosure information not submitted.
MB

Melissa Bellomy, MD

assistant Professor
UT Southwestern Medical Center, United States

Disclosure information not submitted.
KK

Kunal Karamchandani, MD, FCCP, FCCM

Associate Professor
University of Texas Southwestern Medical Center
Dallas, United States

Disclosure information not submitted.

INTRODUCTION: In patients with end stage liver disease (ESLD) presenting for liver transplant, heparin-induced thrombocytopenia (HIT) poses significant challenges. Due to the rarity of this condition, there is limited evidence on how to best manage HIT in this setting. We present the case of a patient with decompensated cirrhosis and acute renal failure who developed autoimmune heparin-induced thrombocytopenia while waiting for liver transplantation.

DESCRIPTION: 67-year-old female presented with decompensated non-alcoholic steato-hepatitis (NASH) cirrhosis for liver transplant evaluation. Upon admission to the intensive care unit (ICU), she developed septic shock complicated by renal failure and thrombocytopenia with extensive lower extremity deep vein thrombosis (DVT). Patient was only exposed to heparin via line flushes. Her HIT work-up was positive for PF-4 antibodies, and the diagnosis of HIT was confirmed with a serotonin release assay. Further work-up revealed a diagnosis of autoimmune HIT. Patient received 3 doses of intravenous Immunoglobulin (IVIG) and anticoagulation was initiated. Bivalirudin was contraindicated due to prolonged PTT in the setting of liver failure and a high risk of bleeding. Hence, Fondaparinux was chosen despite renal failure, long half-life, and lack of reversal. There was inadequate response to Fondaparinux, and Bivalirudin was eventually started and titrated to a goal PTT of 1.5-2x her current baseline level. Subsequently, she developed GI bleeding and Bivalirudin had to be stopped. Since she was not a candidate for plasma exchange (due to high titer of heparin/PF4 antibodies and the risk of counteracting with the IVIG), Bivalirudin was restarted at a lower PTT goal, and titrated up. No other bleeding episodes occurred, and platelets normalized. She was eventually transitioned to Apixiban, considering the challenges with warfarin in the setting of cirrhosis and was discharged home.

DISCUSSION: The management of autoimmune HIT is extremely challenging in patient with liver cirrhosis and acute renal failure with no clear guidelines on proper management. This case demonstrates the safe use of IVIG, in conjunction with bivalirudin with significant recovery in platelets and resolution of autoimmune HIT.