Practical viewpoints on the diagnosis and management of heparin-induced thrombocytopenia

• Published in: Seminars in thrombosis and hemostasis Vol. 37; no. 3; p. 328
• Main Authors: Lassila, Riitta, Antovic, Jovan P, Armstrong, Elina, Baghaei, Fariba, Dalsgaard-Nielsen, Joern, Hillarp, Andreas, Holme, Paul A, Holmström, Margareta, Johnsson, Hans, Joutsi-Korhonen, Lotta, Sandset, Per Morten
• Format: Journal Article
• Language: English
• Published: United States 01-04-2011
• Subjects: Aged; Anticoagulants - therapeutic use; Cardiac Catheterization - methods; Cardiac Surgical Procedures - methods; Chondroitin Sulfates - therapeutic use; Dermatan Sulfate - therapeutic use; Female; Heparin - adverse effects; Heparin, Low-Molecular-Weight - therapeutic use; Heparitin Sulfate - therapeutic use; Hirudins; Humans; Male; Peptide Fragments - therapeutic use; Pipecolic Acids - therapeutic use; Recombinant Proteins - therapeutic use; Thrombocytopenia - chemically induced; Thrombocytopenia - diagnosis; Thrombocytopenia - drug therapy; Vascular Surgical Procedures - methods; Vitamin K - antagonists & inhibitors; Young Adult
• ISSN: 1098-9064
• DOI: 10.1055/s-0031-1274516

Heparin-induced thrombocytopenia (HIT, type II) is an immune-mediated disorder due to antibodies formed against heparin-platelet factor 4 complexes, usually appearing at days 5 to 14 after initiation of heparin. It is important to recognize HIT because heparin prophylaxis or treatment paradoxically associates with new venous and/or arterial thrombosis. Early clinical suspicion and diagnosis together with proper pharmacotherapy and close laboratory monitoring are the cornerstones for successful management. This includes monitoring of Thrombocytopenia, its Timing to heparin administration, appearance of new Thrombosis or resistance to treatment, and differential diagnosis by exclusion of o Ther causes (the 4T's). Specific attention should be paid to the absence or presence of thrombosis and to tailoring thromboprophylaxis or anticoagulant therapy with a nonheparin alternative. Even in the absence of HIT-associated thrombosis, an active policy for prolonged thromboprophylaxis is demanded. Rapid and reliable assays should be developed for diagnosis and anticoagulation monitoring to secure safe management with nonheparins. Semiquantitative testing for on-call hours should be available and later confirmed as clinically needed. Alternative therapeutic options are available, but because their use is infrequent, experienced coagulation treatment centers should provide guidance in the treatment and in laboratory monitoring. Most of the evidence in HIT is grade IC, and thus the best evidence is provided by clinical experience. New anticoagulants and platelet inhibitors may offer future alternatives in the management of HIT, but the current treatment options provide the best experience and benefit. The joint clinical and laboratory guidelines provided in this article along with two practical case scenarios were prepared by a Nordic expert panel. They will be valuable for hematologists and colleagues who do not routinely encounter HIT.