Cardiothoracic surgery was consulted immediately and cardiology was consulted to confirm the findings. Meanwhile, the diagnostic peritoneal lavage was clinically con-sidered to be borderline positive for blood, and subsequent laboratory analysis demonstrated 450,000 erythrocytes/mL (positive is considered above 100,000). After discussion between the cardiothoracic and general surgical teams, it was determined that the injuries of highest priority were the flail AV valves. Thus, with the general surgical team on standby, in case of significant intraabdominal bleeding, the patient underwent full cardiopulmonary bypass (CPB) for replacement of the MV and TV. To this moment the patient was resuscitated with 5.5 L crystalloid solution and 4 U packed red blood cells (PRBC). An arterial catheter and a second 16-gauge peripheral IV catheter were inserted. Anesthesia was maintained with 0.5%–0.7% isoflurane in addition to fentanyl and versed boluses. The circuit used for the CPB was a Medtronic custom perfusion pack: closed, heparin coated with leukocyte depleting filter. Heparin 16,000 U was given to keep the activated clotting time more than 400 seconds. Myocardial protection was assured with cold cardioplegia to keep the heart temperature <15°C. The duration of the aortic cross-clamp was 143 and CPB time was 217 min. One L crystalloid solution, 4 U fresh-frozen plasma, 2 U of platelets, and 1 U of PRBC were administered in addition to the retransfusion from the cell saver. Intraoperative findings confirmed the TEE diagnosis: the anterolateral papillary muscle was found to be avulsed from the myocardium with a flail mitral anterior leaflet. There was bruising of the right ventricle and the septal papillary muscle was completely avulsed from the right ventricular septum with a flail TV. There was also a significant laceration of the posterior pericardium extending from the apex of the pericardium posteriorly on the left side to above the left superior pulmonary vein. The nature of the injuries and the extent of the bruising precluded primary repair as an option. The MV was replaced with a 31 mm St. Jude extended cuff prosthesis and the TV was replaced with a 33 mm regular Master Series extended cuff prosthesis. Although there was good contractile function of the left ventricle, poor right ventricular function required inotropic support with milrinone and epinephrine to wean the patient from CPB. TEE on postoperative day (POD) 1 demonstrated a severely hypokinetic right ventricle that showed improvement on the follow-up echocardiograms at POD 7, POD 9, and POD 19. Because of the inability to navigate a pulmonary artery catheter through the prosthetic TV, cardiac outputs were determined by a noninvasive cardiac output monitor (Novametrix NICO®, Respironics Inc., Wallingford, CT) during the early postoperative course. A postoperative brain/face computed tomography (CT) scan revealed a hemorrhagic contusion in the left inferior frontal lobe measuring 1.9 × 1 cm and minimally displaced nasal bone fractures. The brain lesion appeared stable with some surrounding edema but no significant mass effect and was followed to resolution by POD 14. Abdominal CT showed a hemoperitoneum, which was later identified as originating from a small contained splenic laceration that did not require surgical intervention. The patient was tracheally extubated on POD 5 and returned to the OR POD 9 for repair of his left acetabular fracture. Anticoagulation was withheld until the resolution of the hemorrhagic brain contusion. Before discharge Coumadin therapy was started. On POD 23 the patient was discharged. On discharge the patient did not have any motor or sensory deficits. There was some antegrade amnesia for the first days after the accident as well as mild impairment in short-term memory and concentration. Pathologic diagnosis of the intraoperative specimen was valves with focal myxoid degeneration and papillary muscles with focal fibrosis.
Surviving the rupture of the both AV valves in blunt thoracic trauma is an uncommon event, making the diagnosis unlikely. We found only three similar cases in the literature (5–7) and one report in an autopsy series (8). The actual frequency of this type of cardiac injury is not known (9) and may be under-appreciated as a result of prehospital or early postadmission mortality and missed diagnoses.
Some authors have concluded that only patients with blunt chest trauma who develop cardiac complications benefit from echocardiography and that TEE is of value only when the transthoracic echocardiographic examination (TTE) is suboptimal or aortic injury is suspected (10). Others recommend that TEE should be routinely performed in all victims of violent deceleration collisions regardless of the presenting mediastinal profile on supine chest radiograph (1,11) or at least considered in the cases suspicious for heart injury (12).
The diagnostic superiority of the TEE has been established when compared to TTE (13–15), angiography (16) and helical CT (17). Most authors agree that TEE is an ideal tool to diagnose cardiac and aortic injury in the patient with blunt chest trauma because it provides high quality images of the heart and thoracic aorta and can be safely and rapidly performed in the emergency department, OR, or intensive care unit (18–20).
We conclude that this patient’s case not only presents an example of a rare consequence of blunt chest trauma but also adds further evidence to support the important utility of screening TEE in trauma. Because of the rushed emergent nature in which this unstable trauma patient presented to the OR with these surreptitious cardiac injuries present, it is almost certain that this patient’s outcome would have been fatal had a screening intraoperative TEE not been performed. We hope that this report will serve to reinforce to other anesthesiologists the possibility of similar intracardiac pathology in severely traumatized patients.
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