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Ann Thorac Surg 2007;83:2207-2210
© 2007 The Society of Thoracic Surgeons
a Department of Surgery, Good Samaritan Hospital, Cincinnati, Ohio
b Divisions of General and Cardiothoracic Surgery, Broward General Medical Center, and affiliation with Nova Southeastern College of Osteopathic Medicine, Department of Surgery, Ft Lauderdale, Florida
Accepted for publication December 27, 2006.
* Address correspondence to Dr Thors, c/o Amy Engel, Hatton Institute Floor 11J, Good Samaritan Hospital, 375 Dixmyth Ave, Cincinnati, OH 45220 (Email: amy_engel{at}trihealth.com).
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Introduction |
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Many of the first documented cases of atrial septal rupture were retrospective from autopsy studies. Atrial septal rupture injuries have been reported in less than 5% of blunt chest trauma [11, 12]. In this article, we report a patient who presented after a motor vehicle accident with dyspnea and left-sided chest discomfort. He was hemodynamically stable with refractory hypoxemia. This patient was diagnosed and successfully treated surgically for atrial septal rupture with right-to-left shunt, flail tricuspid valve with papillary muscle rupture, and complete heart block.
A 20-year-old man presented to the trauma center after a motor vehicle accident in which he was an unrestrained passenger. On arrival by ambulance, the patient was awake and alert, complaining of left-sided chest pain. He also had some bruising on his legs and minor lacerations and abrasions over his body. There was no evidence of fractures to the long bones, ribs, or skull, and no major hemorrhaging sites. The patient remained hemodynamically stable throughout the assessment. He was hypoxemic, with an initial saturated oxygen level of 81% on a non-rebreather mask. The Glasgow coma scale remained at 15.
A chest roentgenogram revealed a normal mediastinum with no evidence of hemothorax or pneumothorax. Some mild infiltrate was present, consistent with pulmonary contusion. A quad-screen ultrasound revealed no intraabdominal or pericardial fluid collections. Cervical spine and pelvis roentgenograms revealed no occult fracture. An electrocardiogram (ECG) revealed sinus tachycardia of 147 beats/min, incomplete right bundle branch block, and possible inferior wall infarction (Fig 1). The patient remained hypoxemic and was intubated.
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Examination of the atrioventricular valves found moderate-to-severe 3+ to 4+ tricuspid regurgitation, with flail tricuspid leaflets and ruptured papillary muscles. The right atrium was not distended, and the Doppler regurgitant flow jet was quickly dissipated. At this point, with intracardiac shunting a possibility, the patient underwent a repeat echocardiography with a microbubble contrast study. The bubble study revealed a large atrioseptal defect with right-to-left shunting (Fig 2).
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During the operation, the right atrium was isolated and an atriotomy was performed. At the initial inspection, there was an obvious traumatic atrial septal tear with complete disruption of the atrial septal wall. Further inspection revealed it to extend from the anterior limbus to the edge of the coronary sinus laterally along the tendon of Todaro and the inferior vena cava orifice. Inspection of the tricuspid valve revealed multiple papillary muscle ruptures with flail anterior and posterior leaflets. The inner surface of the right ventricle revealed multiple papillary muscle ruptures extending from the septum and moderator band to the lateral wall of the ventricle. The tricuspid valve was determined to be unsalvageable, so the annulus was trimmed and sized for valve replacement.
Discontinuation of the temporary ventricular pacemakers revealed the patient to be in complete heart block with an idioventricular rhythm. Suspecting an injury to the conduction tract during the valvular repair, a DDDR pacemaker (dual-chamber paced, dual-chamber sensed, dual response, rate-modulated device) was inserted, and anesthesia was terminated. The patient was taken to the cardiovascular intensive care unit in critical but much improved condition.
The patient was extubated on the postoperative day 11. After successfully completing a course of physical therapy, tolerating his diet well, and having a stable cardiopulmonary status, the patient was discharged home on postoperative day 16.
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Comment |
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ASDs with right-to-left shunting secondary to nonpenetrating chest trauma are a rare occurrence. Survival from traumatic atrial septal defect, including flail tricuspid valvulopathy and complete heart block, is an even further rarity. Despite extensive reports of myocardial sequelae after blunt chest trauma, there is a paucity of information pertaining to this specific injury.
The mechanisms of injury that have been proposed link the various intracardiac and extracardiac injuries sustained after significant chest trauma. These mechanisms have been the subject of many investigations [1–12, 14–23]. The central premise posits an acute force against a variable intracardiac volume inducing enough pressure change to overcome the compliance of a particular myocardial structure. The timing of the extrinsic force with the particular phase of the cardiac cycle remains an important independent variable of subsequent injury.
The complex injury pattern sustained by our patient can only be explained as multifactorial. One theory would be that the mediastinal compressive force occurred during isovolumetric contraction in which the ventricles were maximally displaced with end-diastolic volume against closed atrioventricular valves. This could potentially explain the rupture of the anterior and posterior tricuspid papillary muscles from the right ventricular trabeculae carnea.
The atrial wall has some built-in anatomic weakness, namely the fossa ovalis. It can be theorized that a blast-type force created the ASD secondary to a regurgitant flow jet created at the time of tricuspid valvular rupture. Furthermore, directly before impact, central venous pressure could have been markedly elevated secondary to a Valsalva maneuver. Hence, a high-velocity column of fluid entering an already high-pressure space could be sufficient to rupture the atrial septal wall [8].
Damage to the right heart structures are generally well compensated and some time can pass before the onset of acute distress [9]. This was clearly not the case in our patient. The difficulty oxygenating this patient remained the center of the diagnostic work-up. The differential diagnosis included lung contusion with intrapulmonary shunting, traumatic valvular failure, constrictive heart failure, and intracardiac shunting [14]. The refractory shunt mechanics, coupled with the inability to obtain a visible contrast bolus on chest CT, suggested an intracardiac right-to-left shunt.
The variability in presentation of patients with blunt chest trauma can range from someone in complete hemodynamic shock to someone who appears completely normal. Multiple external injuries can be a distraction for the more dangerous internal injuries, which can initially be overlooked [22]. A delay in the diagnosis of acute or evolving injury secondary to nonpenetrating chest trauma might be because no gold standard diagnostic test or diagnostic criteria exist for blunt chest trauma [2, 4, 10, 17, 22].
One reason for this disparity in diagnosis is because trauma physicians are not trying to make a definitive diagnosis initially, but rather are determining who is at increased risk for developing complications of blunt chest trauma such as valvular rupture, cardiac rupture, dysrhythmias, and ventricular dysfunction [2]. The fact remains that despite similarities in mechanism of injury and initial presentation, a cookie-cutter approach is difficult to apply to patients with blunt chest trauma. A working diagnosis then must rely on focused and individual diagnostic testing.
Initial diagnostic imaging, including chest roentgenogram, transthoracic echocardiogram (TTE), and transesophageal echocardiogram (TEE); ECG; and laboratory tests for cardiac enzymes, including cardiac troponin I (cTnI), creatine kinase-MB fraction, as well as baseline hematologic and chemistry values are agreed on as appropriate [1, 3–10, 16–19, 20–24]. Most other diagnostic testing and procedures depend on the patient’s complaints, physical exam, and hospital course.
Cardiac enzymes, including creatine phosphokinase isoenzyme MB fraction (CPK-MB), and cTnI, as well as ECG, are often used for patients with blunt chest trauma in addition to the mentioned tests. Of the two cardiac enzymes, cTnI has widely replaced CPK-MB in the diagnosis of myocardial injury [2]. All of the mentioned tests have documented usefulness in blunt chest injury, and coupled with the patient’s clinical presentation, monitored status, and the acuteness of the hospital course, a diagnosis should be reached. For example, as seen in our patient, the chest roentgenogram revealed pulmonary contusion, cTnI was elevated, ECG revealed sinus tachycardia with abnormal ST-T changes, and subsequent TTE and TEE established the diagnosis. So the question of the accepted diagnostic tests for blunt chest injury is, not are they useful, but which one should be used first? and what tests can reliably be used for observation and subsequent discharge of patients? Most researchers of this subject agree that it is a combination of all of the mentioned diagnostic tests as well as how the patient responds to treatment, with the realization that patient presentation and injury are extremely variable.
In conclusion, intracardiac rupture is a rare result of nonpenetrating chest trauma that must remain in the differential diagnosis. Patients with chest trauma, especially those who present with minor external signs of trauma, must be treated vigilantly with appropriate diagnostic testing. Abnormal values must be scrutinized and explained to prevent subacute presentations and injuries from being discharged prematurely. Diligent surgical triage must take place to properly prioritize the injuries that will require repair first, and those that can be medically compensated or delayed. Overall, our patient had a relatively benign course, and is expected to have a full recovery from his injuries.
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