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Ann Thorac Surg 2008;86:1054-1055. doi:10.1016/j.athoracsur.2007.12.063
© 2008 The Society of Thoracic Surgeons

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Correspondence

Postoperative Complications After Cardiac Surgery and HIT: A Word of Caution

Federico Pappalardo, MDa, Andreas Greinacher, MDb, Sixten Selleng, MDb

a Department of Cardiovascular Anesthesia and Intensive Care, San Raffaele Hospital, Via Olgettina 60, Milan, 20132 Italy
b Institut für Immunologie und Transfusionsmedizin, Abteilung Transfusionsmedizin, Ernst-Moritz-Arndt-Universität Greifswald, Sauerbruchstrasse, 17475 Greifswald

(Email: pappalardo.federico{at}hsr.it; greinach{at}uni-greifswald.de; sixten.selleng{at}uni-greifswald.de).

To the Editor:

The article by Kerendi and colleagues [1] draws attention to post-cardiac surgery patients who present with thrombocytopenia and who also test positive for anti-Platelet Factor4/heparin antibodies. The authors used a commercially available enzyme-immunoassay (EIA) and found patients testing positive in this assay have an enhanced risk for thromboembolic complications, renal failure, and mortality as compared with antibody negative patients.

However, the study needs some comments, addressing the diagnosis of heparin-induced thrombocytopenia (HIT). We have concerns that "thrombocytopenia (<100 x 109/L), which did not begin to rise after the second postoperative day" fulfills the criterion of at least an intermediate pre-test probability of HIT. HIT usually manifests between the fifth and tenth postoperative day after cardiopulmonary bypass (CPB), even in case of heparin exposure before CPB [2]. Especially after CPB, platelet counts often do not raise before day 3. It is therefore likely that a considerable number of patients in the study of Kerendi and colleagues [1] had a low pre-test probability. Interpretation of a positive anti-PF4/heparin EIA is problematic in these patients, as only about 50% of antibodies reacting in commercial EIAs are likely to cause clinical HIT [3]. The clinically relevant antibodies are of the immunoglobulin G class and cause platelet activation in functional assays. Using a positive EIA for "diagnosis" of HIT without consideration of clinical circumstances bears the risk to grossly overdiagnose HIT. Recent studies estimated this risk to be as high as 100% (ie, only half of the patients really have HIT [3]).

Such an overdiagnosis with inappropriate discontinuation of heparin and initiation of nonheparin anticoagulation is potentially harmful. The risk of major bleeding is about 0.7% to 1% per treatment day [3], and this might be even higher in patients in whom thrombocytopenia is caused by other reasons than HIT. Furthermore, an incorrect diagnosis of HIT has a high impact on future patient management as most physicians will hesitate to re-expose a patient who has HIT with heparin.

Overdiagnosis of HIT can be reduced by testing only those patients with at least an intermediate pre-test probability. Commercially available EIAs are excellent to rule out HIT, as they have a high negative predictive value. However, EIA positive patients require further testing by a functional assay [4, 5].


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 References
 

  1. Kerendi F, Thourani VH, Puskas JD, et al. Impact of heparin-induced thrombocytopenia on postoperative outcomes after cardiac surgery Ann Thorac Surg 2007;84:1548-1555.[Abstract/Free Full Text]
  2. Lillo-Le Louet A, Boutouyrie P, Alhenc-Gelas M, et al. Diagnostic score for heparin-induced thrombocytopenia after cardiopulmonary bypass J Thromb Haemost 2004;2:1882-1888.[Medline]
  3. Lo GK, Sigouin CS, Warkentin TE. What is the potential for overdiagnosis of heparin-induced thrombocytopenia? Am J Hematol 2007;82:1037-1043.[Medline]
  4. Greinacher A, Warkentin TE. Treatment of heparin-induced thrombocytopenia: an overviewIn: Warkentin TE, Greinacher A, editors. Heparin-induced thrombocytopenia. New York: Informa Healthcare; 2007. pp. 283-317.
  5. Greinacher A, Juhl D, Strobel U, et al. Heparin-induced thrombocytopenia: a prospective study on the incidence, platelet-activating capacity and clinical significance of anti-PF4/heparin antibodies of the IgG, IgM, and IgA classes J Thromb Haemost 2007;5:1666-1673.[Medline]

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Faraz Kerendi, Vinod H. Thourani, John D. Puskas, Robert A. Guyton, and Omar M. Lattouf
Ann. Thorac. Surg. 2008 86: 1055. [Extract] [Full Text] [PDF]



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F. Kerendi, V. H. Thourani, J. D. Puskas, R. A. Guyton, and O. M. Lattouf
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Ann. Thorac. Surg., September 1, 2008; 86(3): 1055 - 1055.
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