Semin Thromb Hemost 2011; 37(3): 328-336
DOI: 10.1055/s-0031-1274516
© Thieme Medical Publishers

Practical Viewpoints on the Diagnosis and Management of Heparin-Induced Thrombocytopenia

Riitta Lassila1 , Jovan P. Antovic2 , Elina Armstrong1 , Fariba Baghaei3 , Joern Dalsgaard-Nielsen4 , Andreas Hillarp5 , Paul A. Holme6 , Margareta Holmström7 , Hans Johnsson7 , Lotta Joutsi-Korhonen1 , Per Morten Sandset6 , 8
  • 1Unit of Coagulation Disorders, Hematology and Clinical Chemistry Laboratory Services (HUSLAB), Helsinki University Central Hospital, Helsinki, Finland
  • 2Department of Molecular Medicine and Surgery, Karolinska Institute, Hematology, Clinical Chemistry Karolinska University Laboratory, Karolinska University Hospital, Stockholm, Sweden
  • 3Department of Internal Medicine, Coagulation Centre. Sahlgrenska University Hospital, Gothenburg, Sweden
  • 4Centre for Haemostasis and Thrombosis, Copenhagen University Hospital, Copenhagen, Denmark
  • 5Department of Clinical Chemistry, Lund University, University Hospital of Malmö, Sweden
  • 6Department of Hematology, Oslo University Hospital, Oslo, Norway
  • 7Department of Emergency Medicine, Karolinska Hospital, Solna, Stockholm, Sweden
  • 8Institute of Clinical Medicine, University of Oslo, Oslo, Norway
Further Information

Publication History

Publication Date:
31 March 2011 (online)

ABSTRACT

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 oTher 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.

REFERENCES

Riitta Lassila, M.D. , Ph.D. 

Unit of Coagulation Disorders

PoB 340, FI-00029HUS, Helsinki, Finland

Email: riitta.lassila@hus.fi