A 79-year-old, hypertensive, diabetic, male patient with a thoracic aortic aneurysm and aortic valve stenosis was scheduled for total aortic arch replacement and simultaneous aortic valve replacement. Following sternal entry, CPB was established by right axillary and femoral arterial cannulation with bicaval cannulation. After aortic cross-clamping, myocardial protection was achieved with antegrade, retrograde, and selective cold blood cardioplegia without any technical problem. The aortic valve was replaced with a 21-mm bioprosthesis (Inspiris Resilia, Edwards Life Sciences, Irvine, CA). Subsequent total aortic arch replacement was performed under antegrade selective cerebral perfusion with moderate hypothermic circulatory arrest. After aortic declamping, a small point of oozing hemorrhage was identified on the epicardial surface of the right ventricular outflow tract. The oozing was controlled by hemostatic agent application, followed by the reconstruction of the arch vessels. The surgical maneuver was completed without any technical difficulty; however, we noticed the progressively expanding hematoma at the right ventricular surface to the size of a Japanese rice ball measuring 50 × 50 mm (Fig. ). The hematoma was hard, and the epicardial surface was dark red and notably swollen with multiple oozing ruptures. There was no evidence of ST-T changes on electrocardiogram. No cardiac wall motion abnormalities were observed on transesophageal echocardiography. Because of the rapid growth of the hematoma, we decided that early discontinuation of CPB and protamine administration should be mandatory. After termination of CPB, followed by the administration of protamine and fresh frozen plasma/platelet transfusion, manual compression with hemostatic agents such as Surgicel (Ethicon, Somerville, NJ, USA) and Tachosil (CSL Behring, Tokyo, Japan) were applied for 15 min. Thereafter, hemostasis was achieved on the epicardial surface, and the hematoma did not expand further without hemodynamic deterioration. The patient showed uneventful postoperative course. Postoperative computed tomography showed hematoma absorption, and transthoracic echocardiography revealed normal ventricular function of both the right and left ventricles. He is doing well 1 year after surgery.
A 1-month-old boy weighing 3.1 kg was admitted to repair a VSD and atrial septal defect (ASD). The patient was born at 34 weeks, weighing 1.7 kg, and was admitted to the neonatal intensive care unit (ICU). There were no congenital anomalies found except large VSD and ASD in the routine neonatal check. Clinicians decided to perform correction surgery after the patient gained weight. Preoperative medication included diuretics, and there was no abnormal finding in laboratory data, chest radiography, and brain sonography.\nBefore surgery, transthoracic echocardiography revealed a huge (8 mm) perimembranous VSD with trabecular and outlet extensions, and a 2.5-mm secundum ASD. A bidirectional shunt was found through the VSD with interventricular septal flattening and right ventricular enlargement, attesting to severe pulmonary hypertension.\nSurgical correction was performed with cardiopulmonary bypass (CPB) at moderate hypothermia (30’C) after 100U/kg of heparin was administered. Activated clotting time was maintained above 450 s throughout the CPB. The VSD was closed with glutaraldehyde-fixed auto-pericardium and 7-0 Prolene sutures through a transatrial approach. The total CPB time and aorta cross-clamp time were 118 and 68 min, respectively, and the patient was successfully weaned from cardiopulmonary bypass under inotropic support, including dopamine and milrinone. Post-CPB TEE revealed no VSD leakage and good ventricular function with mild interventricular septal flattening.\nHowever, approximately 40 min later, two anechoic masses were found within the interventricular septum (Fig. , Additional file : Video S1). Low-velocity flow color Doppler echocardiography showed no communication between the ventricles and anechoic masses (Fig. , Additional file : Video S2). The larger mass was 1.51 1.48 cm, and interventricular septal hematomas were suspected (Fig. ). The attending surgeon and pediatric cardiologist were immediately notified of these echocardiography findings. The swollen interventricular septum compressed both the right and left ventricles. However, there were no significant mitral stenosis, tricuspid stenosis, and both right and left ventricular outflow tract obstruction. As there was no hemodynamic instability such as arrhythmia or hypotension, and the sternum was already closed, the surgeon decided to observe the patient. The size of hematomas and vital signs did not show any change during 30 min of observation. Therefore, expecting spontaneous resolution of the hematomas, a decision was made not to perform surgical exploration and incisional drainage. The patient was transferred to the ICU, and no specific treatment for hematoma was provided.\nOn postoperative day (POD) 4, follow-up transthoracic echocardiography revealed that thrombi were filling the hematomas (Fig. , Additional file : Video S3). Both ventricular functions were good, with an ejection fraction of 61%, and the interventricular septum thickness was reduced by 5.5 mm. There was no significant hemodynamic instability during the ICU stay. Follow-up echocardiography on POD 14 revealed cystic lesions in the apical ventricular septum, and on POD 40 (Fig. , Additional file : Video S4), there was no lesion in the interventricular septum, indicating complete resolution of the hematomas.