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J Thorac Cardiovasc Surg 2001;122:1028-1030
© 2001 The American Association for Thoracic Surgery
Brief Communications |
From Pediatric Cardiac Surgery, Pediatric Cardiology, Pediatric Anesthesia and Critical Care, and Clinical Coagulation Laboratory, The University of Chicago Children's Hospital, Chicago, Ill.
Received for publication March 22, 2001. Accepted for publication April 9, 2001. Address for reprints: Emile A. Bacha, MD, Congenital and Pediatric Cardiac Surgery, MC 5040, 5841 S Maryland Ave, University of Chicago Children's Hospital, Chicago, IL 60637 (E-mail: ebacha{at}surgery.bsd.uchicago.edu).
The arterial switch operation (ASO) for transposition of the great arteries (TGA) is currently performed with low morbidity and mortality.
1,2 Although thromboembolic events have been described with a number of other neonatal cardiac repairs, 3 they have not been commonly associated with the ASO. In this report we describe this complication, its recognition, and its management.
Clinical summary
A term newborn was diagnosed with D-TGA at an outside hospital and transported to our unit after he was intubated and started on prostaglandin infusion. On arrival, he was hypoxemic (saturation 50%) and in cardiogenic shock, with a pH of 6.91. An echocardiogram showed D-TGA with the circumflex coronary artery (LCX) arising from the right coronary artery (RCA), a patent ductus arteriosus, and an intact ventricular septum with a restrictive patent foramen ovale. Emergency balloon atrial septostomy was performed after initial resuscitation. The patient's condition slowly improved thereafter, but his preoperative course was further complicated by pulmonary sepsis. He was weaned from inotropic support and cleared his infection before surgical repair. Routine coagulation parameters were normal for age-adjusted values.
At age 12 days, an ASO was performed. Crossclamp time was 60 minutes, including 7 minutes of deep hypothermic circulatory arrest for closure of the atrial septostomy. High-dose aprotinin was used during bypass (loading dose, 170 mL/m2; infusion, 40 mL · m–2 · h–1) and stopped at the end of the procedure. A left atrial (LA) line was not placed. The patient left the operating room on infusions of dopamine at 5 µg · kg–1 · min–1 and 0.4 µg · kg–1 · min–1 milrinone. He recovered very smoothly until 7 hours postoperatively, when blood pressure and heart rate suddenly dropped. An electrocardiogram showed no changes from the immediate postoperative study. An echocardiogram showed isolated severe left ventricular dysfunction with strikingly preserved right ventricular function. Specific wall motion or coronary flow abnormalities could not be determined. The chest was therefore reopened in the intensive care unit for inspection of the myocardium and preparation for potential extracorporeal membrane oxygenator support. The myocardium was found to be pink throughout. A serum lactate level measured at this time was 6.6 mmol/L. Urine output remained brisk. A repeat echocardiogram showed no change. He was therefore taken to the catheterization laboratory, where an aortic angiogram showed a filling defect in the aortic root with no filling of the left coronary artery (LCA) and normal RCA/LCX flow (Figure 1). The patient was thus taken to the operating room, where the anteriorly located main pulmonary artery was divided to expose the ascending aorta. A large organized clot (Figure 2) was found in the aortic root with one end plugged into the LCA ostium. The clot was removed. Retrograde cardioplegia was given through the coronary sinus to flush out any debris. Because it was unclear whether the entire clot had been removed from the LCA, the left button was taken down, inspected, sucked out, and reanastomosed in the same location. The patient required 10 µg · kg–1 · min–1 dopamine and 0.6 µg · kg–1 · min–1 milrinone to be weaned from cardiopulmonary bypass (CPB). The LA pressure was 7 mm Hg. The electrocardiogram was normal. Histologic examination of the thrombus revealed a predominantly platelet-containing acute thrombus.
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Discussion
The ASO for simple D-TGA is an operation that can be performed with less than 5% mortality or morbidity. Although a review of all large published series of ASOs, some including over 1000 patients, failed to disclose documentation of coronary thromboembolic events, 1,2 the present case provides clear evidence that this complication can occur after the ASO.
Several risk factors might have contributed to clot formation. Profound circulatory collapse immediately postpartum, followed by a slow recovery complicated by sepsis, can predispose neonates toward abnormal clotting, especially when combined with CPB-induced coagulopathy. 3 A sustained consumptive coagulopathy after neonatal CPB has been well described. 3 The massively abnormal prothrombin time, partial thromboplastin time, and platelet counts after the second bypass run are indirect evidence that a consumptive coagulopathy could have been taking place. The use of aprotinin could also be incriminated. Although the use of a high-dose regimen during complex neonatal repairs has been shown to decrease blood loss, it has also been implicated in venous, but not arterial, thromboses. 4 It is also possible that this patient's complicated preoperative course predisposed him to have the subsequent embolic event. The fact that only minor alterations of routine coagulation parameters were found preoperatively does not exclude CPB-induced coagulopathy. A more comprehensive preoperative hematologic workup was not indicated and would have likely not altered the management. A further source of left-sided thromboembolism is the LA line. This patient did not have an LA line after the initial ASO.
Surgical experience dictates that coronary problems, such as kinking or external compression by pulmonary artery branches, for example, should be excluded first and foremost when postoperative complications arise after the ASO. The present case adds thromboembolism as a further cause for acute coronary hypoperfusion. The electrocardiogram and echocardiogram obtained acutely after the event were singularly unhelpful, as was surgical inspection of the myocardium. It is of interest that even retrospective review of the electrocardiogram obtained during the event showed no signs of ischemia, casting some doubt on the usual surgical practice of looking at electrocardiographic changes as a sign of coronary ischemia after ASO. 5 The fact that the LCX was originating from the RCA may have played a role in this because it was feeding the posterolateral portion of the left ventricle. Early catheterization is essential because it is the only available means of conclusively diagnosing a coronary problem in this setting.
In summary, a coronary embolic event should be suspected in a patient with acute-onset cardiogenic shock after an uncomplicated ASO, even if the electrocardiogram is normal. Prompt cardiac catheterization and operative removal is essential. Aprotinin administration might have played a role as a prothrombogenic agent.
References
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