When a small hematoma spreads along the myocardial fibers or epicardial tissues, CWH could form. Furthermore, the expanding hematoma could tear the surrounding microvessels, causing further expansion of the hematoma to a considerable size . Because it is difficult to elucidate the precise mechanism of CWH formation intraoperatively, CWH is sometimes considered as an intramyocardial dissecting hematoma or a subepicardial hematoma. According to the literature, CWH has been reported as a complication of acute myocardial infarction, and the mechanism is deemed to be ischemia-induced endothelial cell damage . In percutaneous coronary intervention, direct coronary artery injury and disruption of the interstitial and basal membrane from activated metalloproteinases during reperfusion is speculated to be the cause of CWH . Conversely, cardiac surgery-related CWH is a rare complication; however, it has been reported in mitral valve surgery, coronary artery bypass grafting, and ventricular septal defect repair [1,2,3]. Because of its rarity, its exact mechanism still remains unclear.
To the best of our knowledge, there have been no reports of CWH associated with thoracic aortic and aortic valvular surgery, as in our case. The possible mechanisms of CWH formation in our present case might include microvessel injury in the cardiac wall induced by (1) excessive traction of the tissue surrounding the right ventricular outflow tract (especially during aortic valve replacement or proximal aortic anastomosis); (2) mechanical damage to the heart externally due to forceps, suction tubes, etc.; (3) mechanical damage to the heart internally due to the Swan-Ganz catheter; and (4) inappropriate cardioplegia perfusion such as excessive perfusion pressure, inadequate myocardial protection, reperfusion injury, and a no-reflow phenomenon [2, 4]. Considering these mechanisms, it is not clear in any case; however, the surgeon should bear in mind the careful and gentle manipulation throughout the surgical maneuver.
The appropriate treatment of CWH during surgery remains controversial. Conservative treatments for hemodynamically stable cases have been described with favorable outcomes in recent years [2, 5]. However, CWH can sometimes be more lethal owing to adverse hemodynamic effects of the hematoma (e.g., ventricular outflow tract stenosis and coronary artery compression), arrhythmias, and bleeding from epicardial rupture, in which case surgical treatment, including removal of the hematoma and hemostatic procedures, should be performed urgently [2, 6]. In fact, surgical removal of CWH is difficult in most cases, and conservative treatment, such as compression hemostasis, early termination of CPB, and blood transfusion, is therefore inevitable. A successful non-surgical hemostatic procedure has been reported , and we believe that this procedure is reasonable for use in hemostasis because the site of CWH and the surrounding tissue may be fragile owing to inflammation.
Despite very large hematoma in our present case, radical hematoma removal was not required because there was no hemodynamic deterioration. Fortunately, we successfully controlled hematoma expansion and achieved hemostasis by non-surgical repair using manual compression with hemostatic agents combined with early weaning of CPB and transfusion. In such cases, the hematoma status should be monitored postoperatively by echocardiography, computed tomography, or cardiac magnetic resonance [1, 2, 5] because CWH may grow after surgery, especially in patients receiving anticoagulation .
In conclusion, cardiovascular surgeons should be fully aware that CWH can occur during cardiac surgery. It is important that we deal with this lethal complication at the earliest if a CWH is suspected or observed during cardiac surgery. Additionally, a combination of the immediate termination of CPB and non-surgical hemostatic procedures may be effective for this complication.