Use of recombinant hirudin in heparin-induced thrombocytopenia and thrombosis (HITT) and renal failure - A case report

Citation
S. Whelen et Me. Carr, Use of recombinant hirudin in heparin-induced thrombocytopenia and thrombosis (HITT) and renal failure - A case report, ANGIOLOGY, 52(10), 2001, pp. 711-715
Citations number
21
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
ANGIOLOGY
ISSN journal
00033197 → ACNP
Volume
52
Issue
10
Year of publication
2001
Pages
711 - 715
Database
ISI
SICI code
0003-3197(200110)52:10<711:UORHIH>2.0.ZU;2-1
Abstract
Treatment of critically ill patients who have heparin-induced thrombocytope nia and thrombosis (HITT) and also renal failure is a challenge. Recombinan t hirudin (Refludan, Hoechst Marion Roussel) is a direct thrombin inhibitor indicated for anticoagulation in HITT and approved by the United States Fo od and Drug Administration. Because this drug is renally cleared, a single dose of hirudin may induce prolonged (up to one week) unpredictable anticoa gulation in patients with renal insufficiency. There are a few case reports of patients with renal failure and suspected heparin-induced thrombocytope nia (HIT) in which patients were anticoagulated with Refludan for catheter thrombosis. There is no literature on the therapeutic use of Refludan to tr eat HITT in patients with diffuse thrombosis and renal failure. The authors report the case of a 44-year-old female dialysis patient with HITT and ext ensive life-threatening thrombosis. The patient developed common iliac vein occlusion extending to the right atrium with progressive right internal ju gular vein thrombus developing while on heparin. Her platelet count dropped to 60,000/muL. She was lethargic and hemodynamically unstable. Refludan wa s initially given as a bolus of 0.2 mg/kg (total, 12 mg) at a 50% dose redu ction based on the patient's ideal body weight. This dose was based on the published pharmacokinetics of Refludan in patients with renal failure. Only 2 additional boluses of 6 mg and 3 mg were needed to extend the duration o f therapeutic anticoagulation (measured by PTT) to 140 hours. The patient i mproved both clinically and radiographically after the treatment with Reflu dan. There were no additional thromboembolic events or bleeding complicatio ns. The platelets returned to normal within a few days. The patient was tra nsitioned to coumadin and discharged from the hospital. She remains stable at 1-year follow-up.