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Heparin-Induced Thrombocytopenia After Mitral Valve Replacement

Background: Heparin-induced thrombocytopenia (HIT) is a rare autoimmune reaction that involves a decrease in platelet count following heparin exposure and can be associated with life-threatening thrombosis. Because of their prolonged heparin exposure, patients undergoing cardiac surgery are at risk...

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Autores principales: Tugulan, Carmen, Chang, Donald D., Bates, Michael J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Academic Division of Ochsner Clinic Foundation 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8238100/
https://www.ncbi.nlm.nih.gov/pubmed/34239383
http://dx.doi.org/10.31486/toj.20.0007
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author Tugulan, Carmen
Chang, Donald D.
Bates, Michael J.
author_facet Tugulan, Carmen
Chang, Donald D.
Bates, Michael J.
author_sort Tugulan, Carmen
collection PubMed
description Background: Heparin-induced thrombocytopenia (HIT) is a rare autoimmune reaction that involves a decrease in platelet count following heparin exposure and can be associated with life-threatening thrombosis. Because of their prolonged heparin exposure, patients undergoing cardiac surgery are at risk of HIT, with an incidence of 0.1% to 3%. Case Report: A 65-year-old male with severe mitral regurgitation and preoperative ejection fraction of 20% to 25% underwent mitral valve bioprosthetic replacement with coronary artery bypass graft surgery. Heparin anticoagulation was started on postoperative day (POD) 1. Respiratory failure resulted in prolonged mechanical ventilation and heparinization without the ability to initiate warfarin. While the patient was on heparin, his platelet count declined on POD 2 and then steadily increased to above the preoperative level on POD 7. On POD 10, the patient's platelet count dramatically decreased, and on POD 13 he developed acute common femoral artery occlusion necessitating embolectomy. Intraoperative transesophageal echocardiography revealed heavy thrombus burden across the mitral bioprosthesis. HIT was confirmed with a positive heparin-induced platelet antibody and serotonin release assay. Heparin was stopped and argatroban initiated. The patient underwent reoperative bioprosthetic mitral valve replacement on POD 18 using bivalirudin intraoperatively. Despite resolution of HIT, the patient developed sepsis and died on POD 59. Conclusion: The diagnosis of HIT is challenging in patients who undergo cardiopulmonary bypass. Platelet counts often decrease 40% to 60% during the first 72 hours postoperatively, and the frequency of nonspecific anti–platelet factor 4/heparin antibody formation is high. These findings can mask early signs of HIT and delay diagnosis.
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spelling pubmed-82381002021-07-07 Heparin-Induced Thrombocytopenia After Mitral Valve Replacement Tugulan, Carmen Chang, Donald D. Bates, Michael J. Ochsner J Case Reports and Clinical Observations Background: Heparin-induced thrombocytopenia (HIT) is a rare autoimmune reaction that involves a decrease in platelet count following heparin exposure and can be associated with life-threatening thrombosis. Because of their prolonged heparin exposure, patients undergoing cardiac surgery are at risk of HIT, with an incidence of 0.1% to 3%. Case Report: A 65-year-old male with severe mitral regurgitation and preoperative ejection fraction of 20% to 25% underwent mitral valve bioprosthetic replacement with coronary artery bypass graft surgery. Heparin anticoagulation was started on postoperative day (POD) 1. Respiratory failure resulted in prolonged mechanical ventilation and heparinization without the ability to initiate warfarin. While the patient was on heparin, his platelet count declined on POD 2 and then steadily increased to above the preoperative level on POD 7. On POD 10, the patient's platelet count dramatically decreased, and on POD 13 he developed acute common femoral artery occlusion necessitating embolectomy. Intraoperative transesophageal echocardiography revealed heavy thrombus burden across the mitral bioprosthesis. HIT was confirmed with a positive heparin-induced platelet antibody and serotonin release assay. Heparin was stopped and argatroban initiated. The patient underwent reoperative bioprosthetic mitral valve replacement on POD 18 using bivalirudin intraoperatively. Despite resolution of HIT, the patient developed sepsis and died on POD 59. Conclusion: The diagnosis of HIT is challenging in patients who undergo cardiopulmonary bypass. Platelet counts often decrease 40% to 60% during the first 72 hours postoperatively, and the frequency of nonspecific anti–platelet factor 4/heparin antibody formation is high. These findings can mask early signs of HIT and delay diagnosis. Academic Division of Ochsner Clinic Foundation 2021 2021 /pmc/articles/PMC8238100/ /pubmed/34239383 http://dx.doi.org/10.31486/toj.20.0007 Text en ©2021 by the author(s); Creative Commons Attribution License (CC BY) https://creativecommons.org/licenses/by/4.0/©2021 by the author(s); licensee Ochsner Journal, Ochsner Clinic Foundation, New Orleans, LA. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (creativecommons.org/licenses/by/4.0/legalcode) that permits unrestricted use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Case Reports and Clinical Observations
Tugulan, Carmen
Chang, Donald D.
Bates, Michael J.
Heparin-Induced Thrombocytopenia After Mitral Valve Replacement
title Heparin-Induced Thrombocytopenia After Mitral Valve Replacement
title_full Heparin-Induced Thrombocytopenia After Mitral Valve Replacement
title_fullStr Heparin-Induced Thrombocytopenia After Mitral Valve Replacement
title_full_unstemmed Heparin-Induced Thrombocytopenia After Mitral Valve Replacement
title_short Heparin-Induced Thrombocytopenia After Mitral Valve Replacement
title_sort heparin-induced thrombocytopenia after mitral valve replacement
topic Case Reports and Clinical Observations
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8238100/
https://www.ncbi.nlm.nih.gov/pubmed/34239383
http://dx.doi.org/10.31486/toj.20.0007
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