Interventricular septal hematoma detected by transesophageal echocardiography after congenital heart surgery in an infant: a case report

Background Interventricular septal hematoma is an extremely rare complication following congenital heart surgery. During cardiac surgery, interventricular septal hematomas can be detected only by intraoperative transesophageal echocardiography. Here, we report an interesting case of interventricular septal hematoma that was accidentally found in an infant following ventricular septal defect (VSD) closure. Case presentation Transesophageal echocardiography images were acquired from a 1-month-old boy after surgical repair of a large (6.5 mm) perimembranous outlet VSD with interventricular septal flattening. Surgical correction was performed with auto-pericardium and 7–0 Prolene sutures. The patient was successfully weaned from cardiopulmonary bypass, and transesophageal echocardiography showed no VSD leakage and good ventricular function. However, approximately 30 min later, two anechoic masses were found within the interventricular septum, which were suspected to be interventricular septal hematomas; the larger mass measured 1.51 \documentclass[12pt]{minimal} \usepackage{amsmath} \usepackage{wasysym} \usepackage{amsfonts} \usepackage{amssymb} \usepackage{amsbsy} \usepackage{mathrsfs} \usepackage{upgreek} \setlength{\oddsidemargin}{-69pt} \begin{document}$$\times $$\end{document}× 1.48 cm. The swollen interventricular septum showed decreased contractility and compressed both the right and left ventricles. However, there was no change in the size of hematomas or a significant hemodynamic instability for 30 min of observation. Therefore, expecting spontaneous resolution of the hematomas, the interventricular septum was not explored, and the patient was removed from cardiopulmonary bypass. On postoperative day 4, follow-up transthoracic echocardiography revealed thrombi filling the hematomas. The patient was discharged on postoperative day 15 and followed up with regular echocardiographic evaluations. Conclusions We describe a unique case of interventricular septal hematoma after VSD closure. Surgical manipulation of perimembranous VSD and injury of the septal perforating artery may contribute to the development of an interventricular septal hematoma. Moreover, conservative treatment and serial echocardiographic evaluation generally show gradual hematoma resolution in hemodynamically stable patients. Pediatric cardiac anesthesiologists should be aware of this rare complication after VSD repair. Supplementary Information The online version contains supplementary material available at 10.1186/s40001-021-00552-4.

wound infection, or seizures can still occur [2]. Interventricular septal hematoma is an extremely rare complication after congenital heart surgery, which can be life-threatening [3,4]. In adults, interventricular septal hematoma is associated with a high mortality rate of more than 80% [5]. In contrast, the reported survival rate of pediatric patients is higher than that of adults [3].
We report a case of interventricular septal hematomas that were accidentally detected on transesophageal echocardiography (TEE) after surgical correction of VSD in an infant.

Case presentation
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.
Before 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.
Surgical 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 autopericardium 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.
However, approximately 40 min later, two anechoic masses were found within the interventricular septum ( Fig. 1, Additional file 1: Video S1). Low-velocity flow color Doppler echocardiography showed no communication between the ventricles and anechoic masses ( Fig. 2, Additional file 2: Video S2). The larger mass was 1.51 × 1.48 cm, and interventricular septal hematomas were suspected (Fig. 3). 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.
On postoperative day (POD) 4, follow-up transthoracic echocardiography revealed that thrombi were filling the hematomas (Fig. 4, Additional file 3: 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. 5, Additional file 4: Video S4), there was no lesion in the interventricular septum, indicating complete resolution of the hematomas.

Discussion and conclusions
This case report described a large interventricular septal hematoma that was newly detected using TEE after VSD repair in an infant. The patient was transferred to the ICU without surgical intervention, and follow-up echocardiography showed that all hematomas were absorbed without residual intramural lesions.
Most cases of interventricular septal hematomas occurred after the closure of perimembranous VSD [4], as in this present case. Surgical injury of the septal perforating artery during VSD closure is suggested to be a contributing factor for the development of ventricular septal hemorrhage [4,6]. The septal perforating branch passes toward the base of the medial papillary muscle and outlet septum of the right ventricle (RV) from the superior interventricular artery. In a perimembranous VSD, the septal perforating arteries are near the anterior-superior margin of VSD [7,8] (Fig. 6). Although there might be some variations in coronary arteries, the surgeon should be careful not to place the suture deep in the myocardium, particularly during the closure of the anterior margin of VSD, to prevent injury of the first or the second septal perforating branch.
Surgical trauma and other factors can contribute to the development of intramural hematomas [3]. High-perfusion pressure during cardioplegia and high preoperative RV pressure are other risk factors for myocardial hemorrhages [3,9,10]. Suteu et al. reported a case of spontaneous interventricular septal hematoma in an infant with pulmonary atresia with an intact ventricular septum following RV outflow tract reconstruction [3]. The severely increased RV pressure might lead to impaired RV perfusion, development of a myocardial lesion, and intramural hematoma after CPB weaning [3]. Regardless of the cause, the small hematoma due to disruption of the coronary circulation in patients anticoagulated for CPB has the potential to enlarge [11]. A large myocardial hematoma could be associated with decreased ventricular function, myocardial ischemia, or conduction abnormalities, leading to lethal arrhythmias [4,12,13]. Some cases of intraventricular septal hematoma showed hemodynamic instability with tachycardia, arrhythmia, ST changes in electrocardiogram [4,7], or both ventricular outflow tract obstruction [13].
Treatment of myocardial hematoma should be determined based on several factors such as hemodynamic instability, cause and extent of hematoma, or speed of progression [14]. Prompt surgical drainage is required when there is hemodynamic instability or a mechanical complication such as a myocardial defect [14,15].
In adult patients, intramyocardial hematoma has been described following myocardial infarction or cardiac catheterization [14,16,17]. A previous review article demonstrated that intramyocardial hematoma following myocardial infarction could be successfully treated by surgical intervention, while only 10% of patients who received medical treatment survived [15]. In contrast, the reported treatment for interventricular septal hematoma is different in pediatric patients. According to a case report by Drago et al., hemodynamic instability with global septal kinesia and left ventricular outflow tract obstruction occurred due to huge septal hematoma just below the VSD patch in an infant,