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- W2023707812 abstract "Heparin-induced thrombocytopenia (HIT) is a well-recognized syndrome characterized by a decrease in platelet count to less than the lower limit of normal, or greater than 50% from the patient's baseline, after re-exposure to heparin. Two categories of HIT have been delineated: a benign form, type I, and the immune-mediated form known as type II. Type II HIT is associated with an increased risk for potentially catastrophic thrombosis. When thrombosis occurs in the setting of HIT, it is termed “heparin-induced thrombocytopenia with thrombosis.”1Warkentin T.E. Greinacher A. Heparin-induced thrombocytopenia: Recognition, Treatment and Prevention. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.Chest. 2004; 126: 311S-337SCrossref PubMed Scopus (756) Google Scholar The pathologic mechanism of type II HIT is antibody-induced platelet activation, leading to platelet loss (thrombocytopenia) and platelet aggregation (thrombosis). The principal antigen is a complex of heparin and platelet factor 4 (PF4). Platelet α-granules are the storage sites of PF4. The activation of platelets by heparin triggers the release of PF4 into circulation.2Amiral J. Meyer D. Heparin-dependent antigens in heparin-induced thrombocytopenia.in: Warkentin T.E. Greinacher A. Heparin-Induced Thrombocytopenia. ed 3. Marcel Dekker Inc, New York, NY2004: 137-148Google Scholar Up to 80% of patients who develop HIT produce an immunoglobulin G antibody against the heparin-PF4 complex.3Kelton J.G. The pathophysiology of heparin-induced thrombocytopenia: Biological basis for treatment.Chest. 2005; 172: 9S-20SCrossref Scopus (85) Google Scholar This HIT antibody binds to the platelet surface via the heparin-PF4 complex. The Fc portion of the HIT antibody binds the platelet Fc receptor activating the platelet. Activated platelets release additional PF4 leading to a cycle of heparin-induced platelet activation. The presence of heparin is a prerequisite for HIT antibody platelet binding.2Amiral J. Meyer D. Heparin-dependent antigens in heparin-induced thrombocytopenia.in: Warkentin T.E. Greinacher A. Heparin-Induced Thrombocytopenia. ed 3. Marcel Dekker Inc, New York, NY2004: 137-148Google Scholar It has been shown that up to 8% of heparinized patients will develop HIT type II without becoming thrombocytopenic.4Kappers-Klunne M.C. Boon D.M. Hop W.C. et al.Heparin-induced thrombocytopenia and thrombosis: A prospective analysis of the incidence in patients with heart and cerebrovascular diseases.Br J Haematol. 1997; 96: 442-446Crossref PubMed Scopus (85) Google Scholar One percent to 5% of patients on heparin will experience HIT with thrombocytopenia,5Warkentin T.E. Levine M.N. Hirsh J. et al.Heparin-induced thrombocytopenia in patients treated with low-molecular-weight heparin or unfractionated heparin.N Engl J Med. 1995; 332: 1330-1335Crossref PubMed Scopus (2147) Google Scholar and, of those, at least one third will manifest a venous and/or arterial thrombosis.6Demasi R. Bode A.P. Knupp C. et al.Heparin-induced thrombocytopenia.Am Surg. 1994; 60: 26-29PubMed Google Scholar Investigators have shown an increased likelihood of HIT-associated thrombosis at sites of endothelial injury that occur with vascular interventions. Present on the surface of the endothelium are heparin-like heparan sulfate molecules.7Shorten G. Comunale M. Johnson R. Management of cardiopulmonary bypass in a patient with heparin-induced thrombocytopenia using prostaglandin E1 and aspirin.J Cardiothorac Vasc Anesth. 1994; 8: 556-558Abstract Full Text PDF PubMed Scopus (22) Google Scholar The HIT antibody-PF4 complex binds to heparan sulfate on the endothelial surface forming a larger complex that induces tissue factor expression on the endothelium, thus contributing to the procoagulant state.8Schmidt B.P. Adelman B. Heparin-associated thrombocytopenia: A critical review and pooled analysis.Am J Med Sci. 1993; 305: 208-215Crossref PubMed Scopus (151) Google Scholar The numbers of patients receiving unfractionated heparin (UFH) and low–molecular-weight heparin (LMWH) therapy before vascular surgery, cardiac surgery, cardiac catheterization, and as prophylaxis for deep venous thrombosis continue to rise. The incidences of HIT related to UFH and LMWH are 3% to 5% and <1%, respectively.9Martel N. Lee J. Wells P.S. Risk for heparin-induced thrombocytopenia with unfractionated and low-molecular-weight heparin thromboprophylaxis: A meta-analysis.Blood. 2005; 106: 2710-2715Crossref PubMed Scopus (637) Google Scholar Although the percentage of patients developing thrombotic events is as low as 0.3%, the absolute number of patients who are at risk for thromboembolic complications is substantial.5Warkentin T.E. Levine M.N. Hirsh J. et al.Heparin-induced thrombocytopenia in patients treated with low-molecular-weight heparin or unfractionated heparin.N Engl J Med. 1995; 332: 1330-1335Crossref PubMed Scopus (2147) Google Scholar, 6Demasi R. Bode A.P. Knupp C. et al.Heparin-induced thrombocytopenia.Am Surg. 1994; 60: 26-29PubMed Google Scholar The development of HIT with thrombotic complications has been reported in patients receiving intravenous heparin, subcutaneous heparin,10Fabris F. Ahmad S. Cella G. et al.Pathophysiology of heparin-induced thrombocytopenia Clinical and diagnostic implications—A review.Arch Pathol Lab Med. 2000; 124: 1657-1666PubMed Google Scholar and heparin flushes used to maintain intravenous catheters.11Kadidal V.V. Mayo D.J. Horne M.K. Heparin-induced thrombocytopenia (HIT) due to heparin flushes: A report of three cases.J Intern Med. 1999; 246: 325-329Crossref PubMed Scopus (76) Google Scholar, 12Heeger P.S. Backstrom J.T. Heparin flushes and thrombocytopenia.Ann Intern Med. 1986; 105: 143Crossref PubMed Scopus (72) Google Scholar Therapy for HIT requires the discontinuation of exposure to UFH and LMWH and the institution of alternative anticoagulation.1Warkentin T.E. Greinacher A. Heparin-induced thrombocytopenia: Recognition, Treatment and Prevention. The Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.Chest. 2004; 126: 311S-337SCrossref PubMed Scopus (756) Google Scholar, 13Lewis B.E. Wallis D.E. Berkowitz S.D. et al.Argatroban anticoagulant therapy in patients with heparin-induced thrombocytopenia.Circulation. 2001; 103: 1838-1843Crossref PubMed Scopus (642) Google Scholar The direct thrombin inhibitors lepirudin and argatroban are effective in reducing thrombosis and resolving HIT and are approved for the treatment of HIT.14Shotren G.D. Comunale M. Heparin-induced thrombocytopenia.J Cardiothorac Vasc Anesth. 1996; 10: 521-530Abstract Full Text PDF PubMed Scopus (36) Google Scholar The direct thrombin inhibitors must be continued until the platelet count recovers, and an overlap with warfarin to an international normalized ratio goal of 2 to 3 for a minimum of 4 days must be achieved to protect against thrombosis. A 77-year-old man with a history of HIT type II without thrombosis, aortic valve replacement, bilateral renal stents, right femoral aneurysm repair, a current left femoral aneurysm, hypertension, and coronary artery disease presented for open repair of a 5.7-cm abdominal aortic aneurysm. Endovascular repair of the AAA was not feasible because of previous vascular interventions. The diagnosis of HIT was made by positive tests for both HIT enzyme-linked immunosorbent assay and serotonin release assays. Preoperative anticoagulation initiated for prophylaxis against clots secondary to his heart valve was maintained with a continuous argatroban infusion. The infusion was titrated to maintain an activated partial thromboplastin time (aPTT) ratio between 1.5 and 3.0. The activated coagulation time (ACT) goal during surgery was >300 seconds (reference range, 105-167 seconds). Before aortic clamping, a 7.8-mg (0.1 mg/kg) intravenous bolus of argatroban was given to ensure adequate anticoagulation before aortic clamping. The ACT, measured 3 minutes after the bolus, was 522 seconds. After the aorta was clamped, suturing of the graft was begun, and inadvertent irrigation of the graft with a heparin-containing saline solution (10,000 U/L normal saline) was performed. Clots began to form both within the graft and the abdominal cavity. The platelet count was 76,000/mm3 (reference range, 150,000-450,000/mm3), and the ACT was 376 seconds when the clotting was first observed. Serial ACT levels obtained every 15 to 20 minutes for 60 minutes were 365, 324, 324, and 285. Laboratory values drawn when clotting began revealed an aPTT ratio >6.95, an international normalized ratio of 2.6, and a platelet count of 53,000/mm3. Upon recognition that a heparin-containing irrigation solution was being used and clot formation was occurring, the solution was discontinued. The abdominal cavity was then irrigated with normal saline, and the clots were suctioned. Only normal saline was used for the remainder of the procedure, and no further clotting was observed. The patient was transferred to the intensive care unit in which an argatroban infusion was resumed to prevent ongoing thromboses secondary to both pre-existing HIT and re-exposure to heparin. Postoperatively, he did not exhibit either bleeding or thrombosis. Inadvertent exposure to a heparin-containing irrigation solution, in this previously diagnosed HIT patient, resulted in thrombosis. Thrombosis occurred while the patient received therapeutic levels of the direct thrombin inhibitor argatroban as measured by the ACT and aPTT ratio. Furthermore, the ACT levels were prolonged before, during, and after clotting was observed. We propose that the presence of preformed HIT antibodies predisposed this patient to form clots when rechallenged with heparin. In a patient with suspected or known HIT, any form of heparin can precipitate thrombosis. We must now include heparin-containing irrigation solutions in the list of heparin preparations that may lead to thrombosis in HIT patients. This case shows the importance of avoiding all heparin in patients with a history of HIT or HIT with thrombosis." @default.
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- W2023707812 title "Intraoperative Thrombosis From a Heparin-Containing Irrigation Solution in a Patient With Heparin-Induced Thrombocytopenia" @default.
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