Patient who developed heparin-induced thrombocytopenia type II after 24 years on hemodialysis

• Published in: Acta medica Croatica Vol. 66 Suppl 2; pp. 68 - 71
• Main Authors: Gavranić, Bruna Brunetta, Basić-Jukić, Nikolina, Kes, Petar
• Format: Journal Article
• Language: Croatian
• Published: Croatia 01.10.2012
• Subjects: Aged; Antibodies - blood; Anticoagulants - adverse effects; Female; Heparin - adverse effects; Heparin - immunology; Humans; Kidney Failure, Chronic - therapy; Renal Dialysis; Thrombocytopenia - chemically induced; Thrombocytopenia - immunology
• ISSN: 1330-0164

Heparin-induced thrombocytopenia type II (HIT) is a clinicopathologic syndrome in which one or more clinical events are temporally related to heparin administration and caused by HIT antibodies. There are at least five different types of clinical events that are associated with HIT: thrombocytopenia; thrombosis; skin necrosis at heparin injection site, venous limb gangrene; and an acute systemic reaction that occurs 5-30 min after intravenous bolus of heparin. HIT typically presents 5-14 days after initiation of heparin therapy, later onset is unusual. Heparin is a routine anticoagulant in hemodialysis but administration is different than in surgical and other medical population. Doses are lower and administered every other day, yet hemodialysis patients receive heparin for years. Relationship between dialysis vintage and HIT-antibody positivity has been analyzed in two studies. In national survey of HIT in hemodialysis population of the United Kingdom mean time between starting hemodialysis and development of HIT was 61 days (5-390 days). Japanese authors also found greatest incidence of HIT antibody positivity in patients who were on hemodialysis for less than 1 year, none of patients on hemodialysis for more than 10 years was HIT-antibody positive. We present a case of 70-years old female who developed HIT after 24 years of hemodialysis and exposure to heparin. First 22 years she was receiving unfractionated heparin for anticoagulation during hemodialysis sessions. Afterwards her therapy was changed to low molecular weight heparin. Last 12 years she has tunneled cuffed catheter which was also filled with unfractionated heparin. She had a history of severe renal osteodistrophy and severe aortal valve stenosis, hypothyreosis, thrombosis of both subclavian veins and partial colon resection due to mesenterial artery thrombosis. Her thrombocyte count was low, but despite extensive work-up which included HIT antibody detection, no cause could be identified. She started complaining of flushing, dyspnea and chest pain that developed several minutes after start of hemodialysis and stopped spontaneously during or after hemodialysis. Symptoms were attributed to her heart disease and she was hospitalized for cardiac reevaluation. Thrombosis of right superficial and commune femoral vein was diagnosed as well as further worsening of thrombocytopenia. HIT antibodies were assessed again and they were positive. Anticoagulation during hemodialysis was changed to fondaparinux and catheter filling to citrate. Afterwards symptoms during hemodialysis disappeared and thrombocyte count recovered. HIT type II is a rare but potentially fatal syndrome that can develop years after start of heparin therapy. To our knowledge, this is the patient with longest hemodialysis vintage and newly diagnosed HIT. This is also the first case of patient on hemodialysis that developed HIT in Croatia published to date.