Successful treatment of heparin-induced thrombocytopenia after tricuspid valve replacement: A case report

Objective: In this regard, we would like to present a case from our practice with heparin-induced thrombocytopenia developed after tricuspid valve surgery. Case presentation: A 41-year-old patient was admitted with a diagnosis of congenital heart disease: Ebstein anomaly, atrial septal defect, tricuspid regurgitation grade II – III and congestive heart failure. Her laboratory tests were unremarkable. She underwent tricuspid valve replacement surgery. On the 4th day after operation she developed sign of encephalopathy, discoloration of skin, hematomas all over the body, bradycardia 35 beats/min and atrioventricular (AV) block 2nd degree. She was transferred to intensive care unit and temporary pacemaker was inserted. Blood tests demonstrated marked reduction in hemoglobin levels (Hg – 91 and 78 g/l), red blood count to 3.0 and 2.53×1012/l, drop in hematocrit to 27.3 and 24.7%, thrombocytopenia (59×109 /l), leukocytosis, lymphopenia, and hyperfibrinogenemia. Morphology of erythrocytes showed signs of anisocytosis, polychromatophilia. Her biochemistry tests indicated kidney and liver dysfunction (increase in creatinine, bilirubin, transaminases). She was consulted by hematologist and vascular surgeon and diagnosis of disseminated intravascular coagulation was done. Her vascular ultrasound of peripheral vessels was normal. She received treatment including fresh frozen plasma and blood transfusions, anticoagulant, antibiotics, spironolactone, torasemide, and medicines for improving liver and kidney function. She showed improvement of condition on day 12, the blood parameters returned to normal, echocardiography demonstrated improvement in ejection fraction and normal size heart chambers. However, bradycardia and AV block sustained, therefore dual-chamber permanent pacemaker was implanted. Patients was discharged in satisfactory condition. Conclusion Because both unfractionated heparin and low molecular weight heparins are widely used in medicine, all physicians should be aware of the life-threatening complication of heparin treatment, HIT. Platelet counts should be monitored for 3 to 5 days in patients receiving heparin. Also, patients with Ebstein anomaly should be examined before surgery more comprehensively, including coagulation tests, hemostasis system, bleeding time, determination of factor antigens. In the case of HIT type 2, immediately discontinue heparin therapy and replace it with an alternative anticoagulant. If a patient who had experienced HIT type 2 and requires future cardiac surgery, direct thrombin inhibitors should be prescribed.

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Publication Details

Journal
Heart Vessels and Transplantation
Published
2025-03-08
DOI
https://doi.org/10.24969/hvt.2024.548
Citations
1
Primary Topic
Heparin-Induced Thrombocytopenia and Thrombosis
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article
Field-Weighted Citation Impact
2.01
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article

Successful treatment of heparin-induced thrombocytopenia after tricuspid valve replacement: A case report

Zhamalbek Ashimov, Zhanybek Gaibyldaev, Aida K. Kurmanbekova
1 citations
Heart Vessels and Transplantation
Heparin-Induced Thrombocytopenia and Thrombosis
2.01
article

Successful treatment of heparin-induced thrombocytopenia after tricuspid valve replacement: A case report

Zhamalbek Ashimov, Zhanybek Gaibyldaev, Aida K. Kurmanbekova
article en
1 citations

Abstract

Objective: In this regard, we would like to present a case from our practice with heparin-induced thrombocytopenia developed after tricuspid valve surgery. Case presentation: A 41-year-old patient was admitted with a diagnosis of congenital heart disease: Ebstein anomaly, atrial septal defect, tricuspid regurgitation grade II – III and congestive heart failure. Her laboratory tests were unremarkable. She underwent tricuspid valve replacement surgery. On the 4th day after operation she developed sign of encephalopathy, discoloration of skin, hematomas all over the body, bradycardia 35 beats/min and atrioventricular (AV) block 2nd degree. She was transferred to intensive care unit and temporary pacemaker was inserted. Blood tests demonstrated marked reduction in hemoglobin levels (Hg – 91 and 78 g/l), red blood count to 3.0 and 2.53×1012/l, drop in hematocrit to 27.3 and 24.7%, thrombocytopenia (59×109 /l), leukocytosis, lymphopenia, and hyperfibrinogenemia. Morphology of erythrocytes showed signs of anisocytosis, polychromatophilia. Her biochemistry tests indicated kidney and liver dysfunction (increase in creatinine, bilirubin, transaminases). She was consulted by hematologist and vascular surgeon and diagnosis of disseminated intravascular coagulation was done. Her vascular ultrasound of peripheral vessels was normal. She received treatment including fresh frozen plasma and blood transfusions, anticoagulant, antibiotics, spironolactone, torasemide, and medicines for improving liver and kidney function. She showed improvement of condition on day 12, the blood parameters returned to normal, echocardiography demonstrated improvement in ejection fraction and normal size heart chambers. However, bradycardia and AV block sustained, therefore dual-chamber permanent pacemaker was implanted. Patients was discharged in satisfactory condition. Conclusion Because both unfractionated heparin and low molecular weight heparins are widely used in medicine, all physicians should be aware of the life-threatening complication of heparin treatment, HIT. Platelet counts should be monitored for 3 to 5 days in patients receiving heparin. Also, patients with Ebstein anomaly should be examined before surgery more comprehensively, including coagulation tests, hemostasis system, bleeding time, determination of factor antigens. In the case of HIT type 2, immediately discontinue heparin therapy and replace it with an alternative anticoagulant. If a patient who had experienced HIT type 2 and requires future cardiac surgery, direct thrombin inhibitors should be prescribed.

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