Ann Thorac Surg 1999;68:563-564
© 1999 The Society of Thoracic Surgeons
Case Reports
Right ventricular thrombosis early after bidirectional Glenn shunt
Kazuhito Imanaka, MDa,
Shinichi Takamoto, MDa,
Arata Murakami, MDa,
Yukihiro Kaneko, MDa
a Department of Cardiothoracic Surgery, University of Tokyo, Tokyo, Japan
Address reprint requests to Dr Imanaka, First Department of Surgery, Saitama Medical School, 38 Morohongo, Moroyama-machi, Iruma-Gun, Saitama 350-0495, Japan
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Abstract
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Thrombosis in the right ventricle occurred early after b idirectional superior cavopulmonary shunt in 2 patients with pulmonary atresia with intact ventricular septum and major right ventricular coronary artery communication, and perioperative brain infarction occurred in 1 patient. Clinicians should be aware of the hazards of this potentially lethal complication, and transfusion of platelets and fresh plasma should be minimized. Although the hemodynamic state is good, echocardiography should be performed frequently and strict anticoagulation should be started as early as possible.
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Introduction
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Thrombosis in the right ventricle (RV) is potentially lethal for patients with pulmonary atresia with intact ventricular septum (PA-IVS) and major right ventricular coronary artery communication (RVCC), because fatal thromboembolism may occur through the RVCC or through tricuspid regurgitation and atrial septal defect. This occurred early after bidirectional superior cavopulmonary shunt (BSCPS) in 2 patients with PA-IVS and major RVCC. They had undergone a right modified Blalock-Taussig shunt in early infancy, and BSCPS was the next palliation. BSCPS was performed under mildly hypothermic cardiopulmonary bypass with the heart beating.
Patient 1 was a 21-month-old girl. She had undergone successful balloon atrial septostomy at the age of 2 weeks. Patient 2 was an 8-month-old boy. He underwent concomitant atrial septal defect enlargement. In both patients, homologous fresh-frozen plasma was transfused during and early after BSCPS. Level of fibrinogen was elevated above 400 mg/dL at postoperative day 2. The postoperative hemodynamic state was good and there was no evidence of infection. A fairly mobile, high-echoic mass about 15 mm in diameter, considered to be a thrombus, was found in the RV on surveillance echocardiography 9 days after BSCPS (Fig 1). Because of perioperative brain infarction, patient 1 was continued to be closely observed without administration of anticoagulant to avoid inducing hemorrhage in the infarcted area of the brain. Serial echocardiographic study showed moderate shrinkage, but persistence, of the mass. In patient 2, the mass grew in size and a new one developed despite administration of ticlopidine hydrochloride. Levels of fibrin degenerative protein, thrombin-antithrombin complex, and D-dimer were significantly elevated. Therefore, administration of warfarin sodium and heparin was started. The international normalized ratio was maintained around 1.30. The mass shrunk and disappeared 6 days later (Fig 2), and did not reappear after cessation of heparinization. No thromboembolism or electrocardiographic change occurred.
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Fig 1. High-echoic masses in the RV were found 9 days after surgery in both patients. These masses were thought to be thrombi. (A) Patient 1; (B) patient 2.
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Fig 2. Shrinkage and disappearance of the mass in patient 2. During conservative treatment with anticoagulant, the mass tended to be smaller and disappeared 6 days later. (A) Initial; (B) 3 days later; (C) 6 days later.
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Comment
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Judging from clinical courses, the RV masses in both patients were considered to be thrombi, although this was not confirmed histologically. Thrombus in the RV is life threatening for patients with PA-IVS and RVCC, and may have caused the brain infarction in patient 1. If untreated, a growing RV thrombus may extend into the RVCC and the coronary arteries [1]. Cavopulmonary thrombosis after BSCPS has been reported mostly in hemodynamically suboptimal patients [2]. One of the most striking aspects in our 2 patients was that another dangerous thrombosis occurred while the hemodynamic state was good, and this was unexpected before surveillance echocardiography.
To our knowledge, thrombosis in the RV after BSCPS has not been described previously. However, it is particularly likely to develop in patients with PA-IVS. BSCPS reduces venous return to the right atrium considerably. Inflow volume into the RV is markedly decreased in patients with PA-IVS because their RV is almost a dead end and the tricuspid valve is stenotic. Smooth flow from the right atrium to the left atrium also reduces the inflow volume into the RV, and their RV has dense trabeculations and is poorly contractile. In addition to these circumstances, polycythemia and a hypercoagulable state [3] may also contribute to thrombosis. Excessive perioperative supplementation of platelet or coagulation factors is quite unfavorable.
The management of RV thrombosis is difficult. Thrombosis is likely to recur after surgical removal, because most of the factors mentioned above remain after reoperation. In the early postoperative period, thrombolytic therapy may induce bleeding or fragmentation of the fresh thrombus, which can be fatal. Therefore, we selected a conservative treatment [4]. In patient 1, however, anticoagulation might add the risk of hemorrhagic brain infarction and was not safe. It is not always easy to be optimally treated. Prevention is important.
Clinicians should be aware of the hazards of perioperative thrombosis in the RV after BSCPS in patients with PA-IVS. Even if the hemodynamic state is good, echocardiography should be performed frequently [5]. To prevent thrombosis not only around the anastomosis but also in the RV, transfusion of platelets and fresh plasma should be minimized. Furthermore, strict anticoagulation should be started as early as possible and should be managed appropriately.
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References
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Accepted for publication January 6, 1999.
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Abstract
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