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Ann Thorac Surg 1996;61:1024-1029
© 1996 The Society of Thoracic Surgeons

Current Reviews

Mitral Valve Injury After Blunt Chest Trauma

Monica L. McDonald, MD, Thomas A. Orszulak, MD, Michael P. Bannon, MD, Scott P. Zietlow, MD

Sections of Cardiovascular Surgery and Critical Care Medicine, Mayo Clinic, Mayo Foundation, Rochester, Minnesota


   Abstract
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Introduction
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Isolated mitral valve injury after blunt chest trauma is a very rare event. This disruption, causing sudden and severe mitral regurgitation, will rapidly lead to congestive heart failure and death unless operatively corrected. A high index of suspicion coupled with appropriate diagnostic tests will provide the diagnosis and allow operative correction. We report a patient who survived this injury and review all previous reports of blunt traumatic disruption of the mitral valve.


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A 42-year-old man was injured when his ``parked'' but slow-moving truck rolled back and pinned him at chest level against a parked flatbed truck. He was found awake at the scene after an unknown period of time and complained of left chest pain. En route to the hospital, the patient was noted to have a systolic blood pressure of 130 mm Hg, a pulse rate of 140 beats/min, distended neck veins, and decreased breath sounds on the left side. On arrival in the emergency room, his systolic blood pressure was 130 mm Hg, pulse was regular at a rate of 130 beats/min, and respirations were 40 breaths/min. Physical examination revealed labored breathing, decreased breath sounds on his left side, and subcutaneous crepitus. The cardiac sounds were normal without rub, murmur, or gallop. A 36F chest tube was placed immediately in the left thoracic cavity in the midaxillary line. Other physical findings included paradoxic chest movements on the left. Upper and lower extremity pulses were intact and symmetric. Electrocardiogram confirmed a sinus tachycardia at a rate of 119 with low-voltage QRS. The chest roentgenogram demonstrated multiple left-rib fractures and an infiltrate in the left lung, the left chest tube, subcutaneous emphysema, and a tiny left apical pneumothorax. The right lung was normal. Laboratory data revealed a hemoglobin level of 15.6 g/dL, hematocrit of 45.6%, potassium level of 4.1 mEq/L, creatine kinase level of 661 U/L, creatine kinase MB fraction of 95.2 ng/mL, relative index of 14.4%, and lactate level of 2.5 mmol/L. Results of initial arterial blood gas analysis on 15 L nonrebreather mask were as follows: pH, 7.30; carbon dioxide tension, 45 mm Hg; oxygen tension, 56 mm Hg; base excess, -4; and oxygen saturation, 82%. The patient was then intubated and given 100% oxygen; repeat arterial blood gas results revealed a pH of 7.37, carbon dioxide tension of 41 mm Hg, oxygen tension of 71 mm Hg, base excess of -1, and oxygen saturation of 91%.

A bedside diagnostic peritoneal lavage was negative. Because of the degree of trauma, the patient underwent a full thoracic aortogram, which was normal. This was followed with a two-dimensional transthoracic echocardiogram with color-flow Doppler echocardiography. The study was limited because of the chest trauma. The view from the parasternal window primarily showed normal left ventricular size and function. The ejection fraction was approximately 0.70. The right ventricle did not appear enlarged; the right ventricular walls were not hypokinetic. There was no important pericardial effusion seen and no evidence of cardiac contusion.

Although hemodynamically stable throughout these evaluations, the patient began to have episodes of hypotension with systolic blood pressure drops into the 80s despite adequate volume resuscitation. A Swan-Ganz catheter was placed and initial readings demonstrated a pulmonary artery wedge pressure of 20 mm Hg, although it was difficult to obtain an accurate wedge tracing. Pulmonary artery systolic pressure was 46/28 mm Hg, with a mean of 36 mm Hg. The cardiac index was 1.97 L•min-1•m-2, systemic vascular resistance index 1,872 dynes•s/cm5•m2, pulmonary vascular resistance index 651 dynes•s/cm5•m2, and extraction ratio 49%. Severe myocardial contusion was deemed the cause of his poor cardiac output despite his previously normal echocardiogram. A dopamine infusion was begun to enhance the cardiac index. His course was further marked by intermittent episodes of oxygen desaturation, which prompted a bronchoscopy study to assess the airway. Thick copious secretions were removed from the glottus, but the remaining tracheobronchial tree was normal. It then became necessary to supplement and increase inotropic support for deteriorating hemodynamic status. Levophed (Winthrop Pharmaceuticals, New York, NY) was added to the dopamine infusion for hypotension and a cardiac index of 2.0 L/min. Creatine kinase enzyme levels during this period had risen to 4,390 U/L; MB fraction, 134.9 ng/mL; relative index, 3.1, and lactate level, 4.0 mmol/L. An electrocardiogram showed new ST elevation in leads V1 through V5.

Despite all resuscitative efforts, hypotension and oliguria persisted, and a transesophageal echocardiogram was obtained to reassess myocardial contractility (Figs 1, 2GoGo). This identified a flail segment of the anterior mitral valve leaflet and a mass consistent with a ruptured papillary muscle head at the end of the flail segment. There was severe mitral regurgitation and a hyperdynamic left ventricle. Emergent cardiac operative consultation was obtained, and the patient was then taken directly to the operating room.



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  		Fig 1. . Transesophageal echocardiogram showing the left atrium (LA) and ventricle (LV) in systole. The arrow is illustrating the ruptured papillary muscle. Note the flail anterior mitral leaflet in the left atrium. (AL = anterior leaflet; PL = posterior leaflet.)

 


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  		Fig 2. . Transesophageal echocardiogram showing the left atrium (LA) and ventricle (LV) in diastole. The arrow denotes the ruptured papillary muscle of the left ventricle. (AL = anterior leaflet; PL = posterior leaflet.)

 
A transesophageal echocardiography probe was placed during induction for preoperative and postoperative valvular and left ventricular assessment. Under extracorporeal circulation, the patient underwent valve repair involving reattachment of the ruptured papillary muscle, which involved a portion of the papillary head, insertion of two artificial chordae, plication of the posteromedial commissure, and insertion of two thirds of a 27-mm Duran ring as a posterior mitral annuloplasty. His postoperative course was complicated by the traumatic respiratory insufficiency; the patient improved after intensive pulmonary support. He was discharged after 4 weeks in the hospital. Echocardiographic findings before discharge showed trivial mitral regurgitation and an ejection fraction of 0.56. Later contact with the patient at 6 months of follow-up found him to be fully recovered and at work.


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 Abstract
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References
 
The most common cardiac injury after chest trauma is myocardial contusion. This diagnosis may initially evade detection and may surface with the onset of troubling arrhythmias. Serial electrocardiograms and enzyme measurements have been the historic methods of diagnosis; however, more recently echocardiography, transthoracic (TTE) or transesophageal (TEE), has provided a real-time window for assessing myocardial injury and function.

In contrast, cardiac valve rupture is an exceptionally rare event. One must be aware of the possibility of an associated cardiac injury in any patient who sustains nonpenetrating thoracic trauma. The severity of the chest wall injury does not have a direct relation to the occurrence of cardiac trauma. When a cardiac valve is damaged, the aortic valve is more frequently involved, followed by the mitral and tricuspid, respectively [1]. Experiments have shown that intraventricular pressures of greater than 320 mm Hg are required to cause any form of cardiac wall or valve rupture [2]. Isolated tricuspid valve injury has been reported rarely and usually has less serious hemodynamic consequences than isolated injury of the mitral valve [3]. Aortic valve trauma might be explained by the simultaneous occurrence of blunt trauma and an instinctive Valsalva maneuver, which generates a great increase in systemic blood pressure and potential aortic leaflet rupture. Rupture of the mitral valve may occur when a rapid compressive force is applied at early systole, during the brief interval between closure of the mitral valve and opening of the aortic valve (isovolumic contraction) [4]. The rarity of mitral valve trauma was shown by Parmley and co-workers [5], who reviewed 546 autopsy cases of nonpenetrating cardiac injuries; they did not find a single case of isolated mitral valve lesion. The first case of traumatic rupture of a papillary muscle of the left ventricle was reported in 1936 by Glendy and White [6]. In 1964, McLaughlin and associates [7] reported the first successful repair of a mitral valve after blunt trauma when a 7-year-old boy presented with congestive heart failure 7 months after an accident. This first repair was accomplished by plication of the mitral annulus. A review of the literature yielded 23 reported cases of operative correction of mitral damage (Table 1Go). Of note, with the availability of echocardiography, the time from injury to presentation is now much shorter than in the earlier reported cases. This further highlights the need to have a high index of suspicion for this injury and to pursue diagnostic tests early in the patient's course.


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  		Table 1. . Reported Cases of Traumatic Mitral Valve Repair
 
The initial clinical manifestations of mitral valve injury are variable and dynamic because of the high likelihood of associated cardiac contusion and the frequency of other combined chest injuries. Valvular injury may consist of papillary muscle rupture (the most common), chordae tendineae rupture, or laceration of the valve leaflet (least common) [8]. Papillary muscle rupture may occur as a complete or partial event. Each papillary muscle is supplied by a long central artery arising from an epicardial vessel, and, if damaged, the muscle tip may undergo progressive ischemia and subsequent infarction, resulting in the delayed rupture [9]. Alternatively, papillary muscles may have more than one head or be based on a broad flat structure such that only a portion of the head is damaged, limiting the degree of valvular incompetence by tethering the flail portion. Whether instantaneous or delayed, papillary muscle rupture may be of two types. The first is a complete rupture involving the entire muscle belly, and the second is a partial rupture that involves one or more apical heads [10]. When rupture of a papillary muscle has occurred, the severe mitral regurgitation and subsequent congestive heart failure may be present immediately or delayed, depending on the volume of regurgitation and the state of left ventricular function. With rupture of the chordae tendineae, the clinical picture again depends upon the extent of damage to the valvular apparatus, the degree of valvular regurgitation produced, and the competence of the left ventricle. The symptoms of cardiac injury may be fulminant or delayed and can occur hours, days, and even years after injury [11]. A cardiac injury that presents in a delayed fashion usually can be attributed to late rupture of an ischemic muscle. We believe that this was the scenario of events in our patient, given the initially negative evaluation for cardiac injury.

Clinical findings of mitral regurgitation include a harsh systolic murmur, an apical systolic thrill, and an electrocardiogram that reveals normal sinus rhythm [12, 13]. The murmur is usually loud and rough and commonly radiates toward the base rather than the axilla [14]. The hallmark holosystolic murmur of mitral regurgitation may be inaudible because of chest wall crepitation or the overlying sounds of direct lung injury. Alternatively, the degree of mitral regurgitation may be minimal at presentation because of a partial tear or disruption of the valve support apparatus, thereby delaying the onset and detection of important valve regurgitation. Diagnosis of acute mitral insufficiency at the bedside using Swan-Ganz catheterization data depends upon the ability to record elevated pulmonary capillary wedge pressure, pulmonary artery hypertension, dominant large V waves, and a marked reduction in the cardiac index [12]. The large V waves are due to the marked reflux of blood into a small, noncompliant left atrium. As discussed by Moore and colleagues [12], failure to recognize acute mitral insufficiency can occur when the pulmonary arterial and wedge pressures are similar (as is often seen in this condition), when one depends upon waveforms rather than mean pressure measurements for diagnostic inference, and when the condition is not suspected clinically. The presence of a large V wave can be misinterpreted to be a contaminated pulmonary artery tracing. An overdamped nondiagnostic pressure tracing may then result if the catheter tip is positioned against a vessel wall or if the balloon is overinflated in a small pulmonary artery. Clarification of the V wave through simultaneous pressure and electrocardiogram tracings will reveal the pulmonary artery peak occurring before or during the T wave, whereas the V wave occurs later during or after the T wave [15]. In retrospect, the patient in our report indeed may have had abnormal V waves that were originally attributed to a nonwedging catheter.

Echocardiography is an exceptional modality for the diagnosis of papillary muscle rupture, and the sonographic appearance of this lesion has been well described [16]. Originally, echocardiography was performed only on the surface of the chest (TTE). In trauma and other clinically difficult situations, the technical limitations of TTE include: poor access to available windows because of tenderness and the presence of operative dressings; air interference from pneumothorax, mechanical ventilation, or mediastinal emphysema; an inability to position the patient; and a large body habitus. More recently, transesophageal echocardiography (TEE) has increased the power of resolution of sonography and is superior to TTE for most intrathoracic pathologic processes, including papillary muscle rupture [17]. Our case may illustrate this phenomenon in that the initial TTE did not demonstrate an abnormality, but a TEE done 20 hours later did confirm the rupture. It is not possible to determine the precise timing of detachment of the papillary muscle. The muscle tear could have occurred as a delayed result of papillary muscle ischemia. Alternatively, the initial tear may have been small, but with time and the presence of a hyperdynamic cardiac state resulting in increased stress and tension, completion of the disruption to its final stage occurred.

Several points are demonstrated by this case in relation to TEE. This procedure can be performed safely at the bedside, is available in most trauma centers and emergency rooms, and should be considered as an adjunctive diagnostic modality. It is unaffected by mechanical ventilation and does not depend upon patient position, and it is less influenced by body habitus. It is also important to realize the limits of TTE in the trauma patient and not hesitate to use the transesophageal approach. In addition, intraoperative TEE is a well-established procedure. It confirms the diagnosis and can reveal inadequacy of an attempted valve repair and the subsequent need for valve replacement. Finally, although it is used more frequently because of the cardiac nature of this case, intraoperative TEE can be performed in most operative procedures to assess pericardial diseases (ie, fluid tamponade) and, perhaps more important, to evaluate ventricular function.

Operation is usually considered for chronic mitral insufficiency only when disability has progressed substantially or there is progressive cardiac enlargement with other signs of hemodynamic or clinical deterioration. Posttraumatic valve insufficiency, on the other hand, should be corrected upon diagnosis because of its morbid sequelae when left to a natural course.

Operative treatment of traumatic papillary muscle rupture has generally relied on experience from postinfarct ischemic rupture. Historically and practically, this has resulted in valve replacement because of both papillary muscle and left ventricular wall involvement with necrosis. Traumatic rupture differs from ischemic rupture in that the injury or disruption is a focal rupture of the papillary muscle due to the high intraventricular pressure and resultant burst effect. With this injury, patients usually have an absence of diffuse ischemic myocardial damage.

The operative correction is dictated by the extent and location of damage and the interval from injury to operation [10]. Correction may require prosthetic valve replacement; however, with increasing experience with mitral valve repair, preservation of autogenous tissue is desirable and achievable [17]. Different techniques of reconstruction have been used for more than 20 years for ruptured chordae tendineae. McGoon [18] was the first to describe a surgical procedure to correct mitral insufficiency secondary to spontaneous valve rupture. He performed a leaflet plication in the region of the chordal disruption. The majority of patients with rupture of the chordae tendineae involving the mitral leaflet can be treated by excising the flail leaflet, approximating the leaflets with interrupted sutures, and inserting reinforcing support to restore the deformed annulus to its normal size and shape [19]. Other various methods of operative correction for ruptured chordae tendineae include primary repair of the disrupted chord by reattaching it to the ventricular wall, plastic repair using an autologous fascia lata graft, and replacement with a prosthetic valve [20]. There have been conflicting reports on the success of reconstruction of disrupted valves, and some authors have recommended total valve replacement for all cases of acute disruption of the mitral valve [13, 21, 22]. Despite reported success with mitral valve reconstruction for ischemic insufficiency [23], patients who present acutely often have a friable, necrotic papillary muscle, and reimplantation into the left ventricular wall may be ineffective when the left ventricle contracts. Sanders and colleagues [13] argued that placement of artificial chordae is indicated only if the left ventricular cavity is normal in size. Zussa and associates [24] advocated the use of artificial chordae and Gore-Tex (W.L. Gore & Assoc, Flagstaff, AZ) suture; again, this may be applicable when the ventricular wall is of good quality at the site where the papillary muscles would be reattached. In the Mayo Clinic experience with postinfarction papillary muscle rupture, 21 of 22 patients underwent valve replacement [25]. In the unstable patient, replacement of the valve was indicated, and the surgeons specifically tried to preserve the posterior leaflet chordal attachments and papillary muscle whenever possible. Preservation of these structures is important because of the papillary muscle-annular continuity to overall left ventricular function. Although debate continues, our patient plus 33% of the previous patients had repair with successful outcomes. This should encourage consideration of repair rather than automatic replacement.

Early diagnosis of traumatic mitral valve rupture can be achieved when the physician has a high index of suspicion for this injury. Repetitive examinations and diagnostic maneuvers should be used to identify pathologic processes and alter the unfavorable course of a puzzling trauma patient. With confirmation of the diagnosis, prompt operative treatment should be undertaken. Because of the limited experience with valve repair in the setting of traumatic mitral insufficiency, one needs to exhibit caution when considering valve reconstruction. The decision to perform reconstruction versus replacement must be individualized based on the patient's ventricular function and the extent of damage. Intraoperative examination of the mitral valve can determine whether reconstruction of the leaflets is possible. The outlook for these patients is generally excellent if their injury is recognized in a timely fashion.


   Footnotes
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Address reprint requests to Dr Orszulak, Mayo Clinic, 200 First St SW, Rochester, MN 55905.


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