Ann Thorac Surg 2000;69:1261-1263
© 2000 The Society of Thoracic Surgeons
CASE REPORTS
Redo without transfusion in a patient with idiopathic thrombocytopenic purpura
Toshiya Koyanagi, MDa,
Shunei Kyo, MDa,
Eiji Hirooka, MDa,
Isamu Koyama, MDa,
Ryozo Omoto, MDa
a Department of Surgery, Saitama Medical School, Saitama, Japan
Address reprint requests to Dr Koyanagi, Sakakibara Memorial Hospital, 2-5-4, Yoyogi, Shibuya, Tokyo 151-0053, Japan
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Abstract
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Mitral valve replacement was able to be carried out at redo operation requiring neither allogeneic platelet nor blood transfusion in a patient with idiopathic thrombocytopenic purpura, by means of preoperative high-dose intravenous 
-globulin, autologous blood predonation, use of a centrifugal pump, heparin-coated extracorporeal circuits, and simultaneous splenectomy.
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Introduction
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Although 23 patients with idiopathic thrombocytopenic purpura (ITP) who safely underwent a cardiac surgical procedure have been reported, platelets were transfused in 87% (20 of 23) of the cases [1]. We report the case of a patient with ITP who underwent redo mitral valve operation without transfusion.
A 59-year-old man was admitted with a history of increasing shortness of breath on effort and orthopnea as well as edema of the lower legs. He had been diagnosed with mitral stenosis due to rheumatic disease and therefore underwent closed mitral commissurotomy through a left thoracotomy at the age of 21 years. He had no history of blood transfusion at that time. An echocardiogram showed commissural and subvalvular fusion, leaflet thickening, and decreased motion of the posteromedial leaflet, requiring a redo operation. He had been noted to have thrombocytopenia for 4 years, but had no history of bruising or bleeding manifestations. Platelet count was 38,000/mm3 on admission. Coagulation screen (prothrombin time, activated partial thromboplastin time, and thrombin time) was normal. The bone marrow contained an increased number of megakaryocytes. Antiplatelet antibodies were not detected, but platelet-associated IgG (PAIgG) level was elevated markedly to 53.8 ng/107 cells (normal value 9.0 to 25.0 ng/101 cells). He received high-dose -globulin (375 mg · kg-1 · day-1; Venilon-I, Kaketsuken-Teijin Inc, Kumamoto, Japan) intravenously for 5 days until the day before the operation. As a result, the platelet count increased to 128,000/mm3 just before the operation. Moreover, autologous blood predonation was scheduled; 800 mL of blood was collected within 2 weeks before the operation, whereas recombinant human erythropoietin (Epogin, Chugai Inc, Tokyo, Japan) was administered intravenously every other day. The hematocrit level was 41.7% before preoperative donation, and then 32.5% just before operation. He underwent mitral valve replacement using a St. Jude Medical valve prosthesis (St. Jude Medical, St. Paul, MN) size 29 mm through a midline sternotomy. Cardiopulmonary bypass grafting was established with a centrifugal pump (Terumo Inc, Tokyo, Japan) and heparin-coated extracorporeal circuits (Terumo Inc). Heparin (250 units/kg) was given and the activated coagulation time was maintained over 400 seconds during the extracorporeal circulation. After neutralization of heparin with protamine sulfate, splenectomy was additionally carried out through a left laparotomy. Although the lowest platelet count was 63,000/mm3 during cardiopulmonary bypass, the platelet count returned to 94,000/mm3 at the end of the operation. The postoperative course was uneventful. The total blood loss within the initial 24 hours was 305 mL and then the chest tubes were removed. The minimum hematocrit level was 27.5% postoperatively. The platelet count increased markedly postoperatively and reached maximum on the 12th postoperative day (482,000/mm3) and then was normalized by 4 weeks after the operation. PAIgG decreased to a normal value. Oral anticoagulant therapy with warfarin and dipyridamole was given immediately after the operation. Neither allogeneic platelet nor blood transfusion was necessary throughout the whole perioperative course.
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Comment
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ITP is an autoimmune coagulation disorder characterized by a decreased number of circulating platelets and a shortened platelet life span. Platelet count is very low, often 50,000/mm3 or less [2]. Corticosteroids, immunosuppressive drugs, -globulin, and Danazol are recommended as medical treatment for ITP. Although successful cardiac operations have been reported in patients with ITP, large quantities of platelets, or blood transfusions were necessary in the postoperative period [1]. Therefore, intensive perioperative management should be planned for patients with ITP in an attempt to avoid the depletion of platelets. Corticosteroids and immunosuppressive therapy seem to be unsuitable due to postoperative infectious complications. High-dose intravenous -globulin therapy is recognized to be very effective in patients with ITP [3]. The mechanisms are thought to be (1) reticuloendothelial Fc receptor blockade, (2) decrease in autoantibody synthesis, (3) protection of platelets or megakaryocytes from platelet antibody, and (4) clearance of persistent viral infection by infusion of specific antibody. Consequently, "intact" type -globulin with Fc fragment is selected. We used S-sulfonated human immunoglobulin. Platelet counts usually increase 5 to 7 days after administration of high-dose -globulin and then are restored to the previous level within 1 month [4]. Autologous blood predonation is commonly performed to avoid homologous blood transfusion during cardiac operation. The total amount of autologous blood, 800 mL, was able to be collected safely even in a patient with ITP, using recombinant human erythropoietin. Heparin coating improves biocompatibility by reducing both complement activation and platelet loss on the surface of the extracorporeal circuits [5]. The spleen contributes to the production of antiplatelet antibodies, the sequestration and removal of coated platelets, and, more controversially, may have some suppressive effect on either the maturation or release of platelets from the bone marrow. Remission rate of ITP by means of splenectomy is reported to be more than 70%. Response to splenectomy typically occurs within several days. Caution should be paid to the possibility of an excessive increase in platelets immediately after the operation, because the effects of both high-dose -globulin and splenectomy may cause a marked increase.
Although 23 patients with ITP who safely underwent a cardiac surgical procedure have been reported, no platelets were transfused in 3 patients. All 3 patients received preoperative treatment with intravenous immunoglobulin but no prophylactic splenectomy. In 1 patient, therapy with prednisolone was added in an attempt to obtain remission before operation, though this regimen resulted in only small, transient increases in the platelet count. We achieved mitral valve replacement in a patient with ITP at redo operation using neither allogeneic platelet nor blood transfusion throughout the whole perioperative course, by means of preoperative high-dose intravenous -globulin, autologous blood predonation, use of a centrifugal pump, heparin-coated extracorporeal circuits, and simultaneous splenectomy.
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References
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Mathew T.C., Vasudevan R., Leb L., et al. Coronary artery bypass grafting in immune thrombocytopenic purpura. Ann Thorac Surg 1997;64:1059-1062.[Abstract/Free Full Text]
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Maronas J.M., Llamas P., Caffarena J.M. Mitral valve replacement and splenectomy in a patient with chronic idiopathic thrombocytopenic purpura. Thorac Cardiovasc Surg 1982;30:407-408.[Medline]
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Mori Y., Hadama T., Takasaki H., et al. Aortic valve replacement and splenectomy in a patient with chronic idiopathic thrombocytopenic purpura—preoperative management with high-dose -globulin. Heart Vessel 1991;6:121-124.[Medline]
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Tanaka S., Ishihara S., Hara S., Niinami H. Aortic valve replacement in a patient with chronic idiopathic thrombocytopenic purpura. J Jpn Assoc Thorac Surg 1994;42:297-301.
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Videm V., Mollnes T.M., Garred P., Svennevig J.L. Biocompatibility of extracorporeal circulation. In vitro comparison of heparin-coated and uncoated oxygenator circuits. J Thorac Cardiovasc Surg 1991;101:654-660.[Abstract]
Accepted for publication September 2, 1999.
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[Abstract]
[Full Text]
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Abstract
Introduction
