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Ann Thorac Surg 2000;69:766-768
© 2000 The Society of Thoracic Surgeons


Original Articles

Conservative surgical treatment of valvular injury after blunt chest trauma

James Halstead, MB, BChira, Amir-Reza Hosseinpour, FRCSa, Francis C. Wells, FRCSa

a Department of Cardiothoracic Surgery, Papworth Hospital, Cambridge, England, UK

Address reprint requests to Dr Halstead, 4 Cherry Grove, Cutgate, Rochdale, Lancs, OL11 5YT, England


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Comment
 References
 
Background. Blunt injury to the cardiac valves leads to progressive ventricular failure often requiring surgical management. Most frequently, prosthetic replacement is the chosen management.

Methods. Three consecutive patients presenting to one surgeon with blunt traumatic valve lesions formed the study group.

Results. At operation, the valvular pathology was assessed, and reparative techniques were used to correct the defects. All the patients had an excellent outcome at follow-up periods of 2 to 3 years.

Conclusions. Conservative operation to repair traumatic valve lesions is feasible and has potential advantages over replacement.


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Comment
 References
 
Blunt thoracic trauma is a common reason for presentation to the emergency services, especially following road traffic accidents. Myocardial contusion is a frequent sequelae. However, acute valvular dysfunction following blunt chest trauma is a rare event. We present a series of 3 such cases, affecting the aortic, tricuspid and mitral valves respectively. Currently there is no consensus as to the best management strategies for these patients [1, 2], although valve replacement is the most common outcome [3, 4]. In each case of our series the native valve was successfully conserved through reconstructive operation performed by one surgeon (F. C. W.).


    Patients and methods
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 Abstract
 Introduction
 Patients and methods
 Comment
 References
 
Patient 1
A 19-year-old man, involved in a road traffic accident on April 4, 1996, sustained fractures of his left femur, left talus, left olecranon, and both first ribs, together with cerebral and pulmonary contusions. After initial resuscitation, his femoral and olecranal fractures were internally fixed. Systolic and diastolic murmurs were subsequently heard when the patient was back on the ward, shortly before an episode of pulmonary edema. Transthoracic echocardiography revealed a markedly regurgitant aortic valve. He was referred to the above regional center for consideration of surgical management. The decision was made to proceed to surgical repair due to circulatory instability.

On opening the pericardium there was no bruising of the aorta, but the heart was volume loaded and hyperdynamic. After establishing cardiopulmonary bypass and cardioplegic arrest, the aorta was opened. The aortic valve was bicuspid with the left and right coronary cusps being fused. The right coronary cusp was detached from the commissure down to below the nidus of this leaflet. It was freely prolapsing into the left ventricular outflow tract. The leaflet was sutured back to the annulus with two running 5-0 Prolene (Ethicon, Edinburgh, England) sutures. The commissural attachment was further secured with a separate pericardial pledgetted 5-0 Prolene suture. The aorta was closed with two running 4-0 Prolene sutures.

The patient was easily weaned from cardiopulmonary bypass. A transoesophageal echocardiogram was performed on the table, which showed a competent aortic valve. He remained cardiovascularly stable in the postoperative period, and was transferred back to the referring hospital for the management of his fractures and neurologic follow-up. He was seen in the clinic 3 months later, by which time he had made a good recovery and no longer had any murmur. Repeat echocardiography revealed mild aortic regurgitation with good left ventricular function. There has been no recurrence of symptoms and most recent transthoracic echocardiogram (1999) revealed persistence of mild aortic regurgitation with normal left ventricular end-diastolic dimensions.

Patient 2
A 19-year-old man, involved in a head-on road traffic accident on April 13, 1996, sustained multiple injuries, including chest wall bruising and a fractured skull. Over the course of the following few weeks he made a good recovery. He later noticed exertional dyspnea and anginal chest pain with palpitations. On examination he had a regular pulse of 90 bpm, a raised jugular venous pulse, a laterally displaced apex beat, a loud pansystolic murmur heard best at the left lower sternal edge, and a palpable pulsatile liver. With the clinical diagnosis of tricuspid regurgitation, he was referred for right heart catheterization, which confirmed gross incompetence. The decision was made to proceed to operation to repair the valve.

On opening the pericardium it was found that the right ventricle and atrium were distended, hyperdynamic, and overloaded. After the institution of cardiopulmonary bypass and cardioplegic arrest, the right atrium was opened. The anterior and septal leaflets of the tricuspid valve were completely prolapsed into the right atrium since their papillary muscle support had ruptured. These ruptured papillary muscles were reattached with interrupted 5-0 Prolene sutures over Teflon (Impra Inc, a subsidiary of C. R. Bard, Tempe, AZ) and pericardial pledgets. On testing, the valve appeared much more competent, but there was some annular dilatation as a result of the chronic regurgitation. A size 33 Carpentier-Edwards tricuspid annuloplasty ring was therefore sewn in, and on testing the valve was completely competent. The atrium was closed with two running 3-0 Prolene sutures and the patient weaned from cardiopulmonary bypass easily. Transoesophageal echocardiography was performed on table, which showed that the tricuspid valve was completely competent.

His postoperative course was uneventful, and an echocardiogram performed on the fifth postoperative day showed no tricuspid regurgitation with good leaflet excursion. He was discharged home the following day. Subsequent review in clinic 6 weeks later showed him to have made a full recovery, he was in sinus rhythm and had no murmur. A recent echocardiography study showed no tricuspid regurgitation.

Patient 3
A 29-year-old man was involved in a motorcycle accident during a race on April 13, 1997. He was hit in the left side of his ribs by another rider, who had been thrown from his own bike. He sustained multiple rib fractures and pulmonary contusion. His initial management included endotracheal intubation and ventilation. However, subsequent to weaning from the ventilator, he was noted to be short of breath. On auscultation a significant pansystolic murmur was heard. Echocardiography demonstrated significant mitral regurgitation. The decision was made to operate, with the intention of repairing the valve, if possible.

After induction, transoesophageal echocardiography was undertaken, confirming severe mitral regurgitation, together with an echogenic mass prolapsing into the left atrium. This mass was presumed to be the papillary muscle, although it did not appear to be suspended by chordae. When the pericardium was opened, extensive adhesions were found, probably as a result of a resolved hemopericardium. There was a rent in the pericardium, through which the apex of the heart had herniated. After the institution of cardiopulmonary bypass and cardioplegic arrest, the left atrium was opened. The findings were dramatic. The posteromedial papillary muscle had torn out of the left ventricular wall and twisted itself several times through the chordae. This had shortened the chordae significantly giving rise to the echocardiographic appearances of no attaching chordae. In addition, a small primary cord from this papillary muscle, which had been attached to the commissural area, was noted to be ruptured. The papillary muscle was untwisted (there were 5 rotations through the chordae) and was sutured back into the ventricular wall with a 4-0 pledgetted Prolene suture. Next, a new cord was constructed with Gore-Tex (W. L. Gore & Assoc, Flagstaff, AZ) connecting the papillary muscle to the commissure where the original cord had been attached. On testing, there still seemed to be a leak and thus a size 28 Carpentier-Edwards annuloplasty ring was inserted. This allowed the anatomy of the prolapsed commissural area to be seen more clearly. The previous stitch was removed, and a small imbrucation stitch was placed at the commissure, which appeared to control the leak. The rest of the valve appeared totally competent on testing.

The atrium was closed, and the patient weaned off bypass easily. His postoperative course was uneventful, and an echocardiogram on the sixth postoperative day showed only trivial to mild mitral regurgitation with good leaflet excursion. He was discharged to home the next day, and was seen in clinic 6 weeks later, at which time he was asymptomatic. There has been no clinical or echocardiographic evidence of progression of the mitral reflux during follow-up.


    Comment
 Top
 Abstract
 Introduction
 Patients and methods
 Comment
 References
 
Blunt thoracic injury should always raise the suspicion of damage to the ribs, sternum, thoracic viscera, or spinal column. When cardiac injury is suspected, clinical examination may reveal the signs of aortic incompetence, pericardial effusion, right or left ventricular heaves, apical displacement or thrills, and the presence of murmurs.

Chest radiography may reveal cardiac chamber enlargement, left ventricular failure, or a left pleural cap associated with mediastinal bleeding (which may have a cardiac origin), in addition to trauma to other structures. The electrocardiogram may show a sustained dysrhythmia, Q waves, ST segment and T wave abnormalities, or the presence of frequent ectopic beats. Blood tests may reveal an elevated concentration of creatinine kinase. These should raise suspicion, but specificity is low, hence echocardiography is the investigation of choice, preferably through the transoesophageal route, as it gives good resolution images of all four chambers of the heart and aorta [5]. It is also inexpensive, rapid, and relatively safe.

The most common injury after blunt chest trauma is myocardial contusion, which itself is probably underdiagnosed [6]. Septal and free wall ruptures of all four chambers have been well described. Postmortem series suggest that the right ventricle is most commonly ruptured, while coronary artery disruption is said to be rare [7]. Similarly, the postmortem series and paucity of published series suggest that acute valvular dysfunction is very rare [8, 9].

Mitral insufficiency following nonpenetrating cardiac injury is usually the result of papillary muscle rupture [3], other causes being papillary muscle dysfunction, chordal rupture, or leaflet disruption [10]. Papillary rupture can be partial occurring through one of the heads, or complete through the muscle body [11]. In this latter case especially, severe left ventricular failure ensues and surgical management is usually essential. The presentation can be delayed, perhaps due to eventual rupture of a necrotic papillary muscle contused in the initial trauma. Damage to the mitral valvular apparatus is said to occur in early systole during isovolumetric contraction, when the force delivered by an impact grossly elevates the left ventricular pressure [12]. As with our patient, mitral repair is possible in a proportion of cases. It was first reported in a 7-year-old boy whose anterior leaflet had been torn, with rupture of the attached chordae, when he was struck by a car [10]. Where possible it should certainly be attempted, given the risks of anticoagulation, reoperation, endocarditis, and thromboembolism associated with prosthetic valve implantation. The reparative technique utilized naturally depends on the operative appearance of the mitral valve and its subvalvular apparatus. Direct injury to the mitral valve leaflets may be amenable to direct suturing, possibly with annuloplasty ring insertion. Ruptured chordae have been directly sutured to the free ventricular wall, excised together with the concomitant flail mitral scallop, or replaced with autologous fascia lata graft or artificial material [13]. Ruptured papillary muscles are often reimplanted into the left ventricular wall, provided that it has not itself been seriously contused.

Traumatic insufficiency of the tricuspid valve arises approximately as frequently as the mitral valve [7], and leads to right ventricular dysfunction. However, the lesion is often better tolerated due to the lower pressures in the right heart, and indeed patients often come to operation years after the insult [4]. The pathology is almost always an anterior leaflet prolapse due to chordal or papillary muscle rupture with annular dilatation [14]. Best management strategies for these patients remain controversial, ranging from medical therapy to early surgical intervention. However, significant tricuspid regurgitation is an abnormal state and in our opinion should not be tolerated in an otherwise fit individual. Moreover, there is no consensus over whether to attempt repair or to replace the valve [1416]. We believe that reparative techniques can often effectively correct the defect, even in patients presenting years later [17], and should be the primary aim of surgical management.

Impact trauma is said to rupture the aortic valve most frequently [18], but there are far fewer reports of repair or replacement in the literature, possibly due to the catastrophic nature of these injuries, specifically associated coronary artery disruption and aortic rupture. Incompetence usually results from cusp tears or avulsion of the valve from its annulus. Aortic valvular disruption, as a lone traumatic cardiac lesion, often occurs, as in our case, in a congenitally bicuspid valve [7]. Aortic valve replacement is the most common outcome for these patients, although successful repair of these injuries has been reported [19, 20].

As our series and the literature illustrate, surgical reconstruction of cardiac valves damaged in blunt trauma is a feasible and durable option in many cases. Repaired valves do not necessitate treatment with monitored anticoagulant therapy, and may carry a lower risk of endocarditis and thromboembolism. In the absence of absolute contraindications to operative intervention, the various surgical options for treatment should be considered in all cases of valve trauma.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Comment
 References
 

  1. Al Kasab S., Westaby S., Al Zaibag M.A., Habbab M., Gunawardena K.A., Al Fagih M.R. Traumatic papillary muscle dysfunction. Eur Heart J 1988;9:1030-1033.[Abstract/Free Full Text]
  2. Pellegrini R.V., Copeland C.E., DiMarco R.F., et al. Blunt rupture of both atrioventricular valves. Ann Thorac Surg 1986;42:471-472.[Abstract]
  3. McDonald M.L., Orszulak T.A., Bannon M.P., Zietlow S.P. Mitral valve injury after blunt chest trauma. Ann Thorac Surg 1996;61:1024-1029.[Abstract/Free Full Text]
  4. Van Son J.A.M., Danielson G.K., Schaff H.V., Miller F.A., Jr Traumatic tricuspid valve insufficiency. J Thorac Cardiovasc Surg 1994;108:893-898.[Abstract/Free Full Text]
  5. Weiss R.L., Brier J.A., O’Conner W., Ross S. The usefulness of transoesophageal echocardiography in diagnosing cardiac contusions. Chest 1996;109:73-77.[Abstract/Free Full Text]
  6. Westaby S. Cardiac trauma. Current Opin Cardiol 1986;1:292-295.
  7. Parmley L.F., Manion W.C., Mattingly T.W. Nonpenetrating traumatic injury of the heart. Circulation 1958;18:371-396.[Medline]
  8. Warburg E. Myocardial and pericardial lesions due to non-penetrating injury. Br Heart J 1940;2:271-280.
  9. Parmley L.F., Mattingly T.W., Manion W.C., Jahnke E.J. Nonpenetrating injury of the aorta. Circulation 1958;17:1086-1101.[Medline]
  10. McLaughlin J.S., Cowley R.A., Smith G., Matheson N.A. Mitral valve disease from blunt trauma. J Thorac Cardiovasc Surg 1964;48:261-283.
  11. Cuadros C.L., Hutchinson J.E., Mogtader A.H. Laceration of a mitral papillary muscle and the aortic root as a result of blunt chest trauma. J Thorac Cardiovasc Surg 1984;88:134-140.[Abstract]
  12. Devineni R., McKenzie F.N. Acute mitral insufficiency resulting from blunt chest trauma. J Thorac Cardiovasc Surg 1983;85:797-798.[Medline]
  13. Zussa C., Frater R.W.M., Polesel E., Galloni M., Valfre C. Artificial mitral valve chordae. Ann Thorac Surg 1990;50:367-373.[Abstract]
  14. Maisano F., Lorusso R., Sandrelli L., et al. Valve repair for traumatic tricuspid regurgitation. Eur J Cardiothorac Surg 1996;10:867-873.[Abstract]
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  16. Ataka K., Ota T., Okada M., Okada K., Minami Y., Yoshimura N. Traumatic tricuspid regurgitation. J Japanese Assoc Thorac Surg 1993;41:2383-2388.
  17. Yasuura K., Matsuura A., Maseki T., et al. Successful repair of tricuspid regurgitation 46 years after causal blunt trauma. Scand J Thorac Cardiovasc Surg 1996;30:105-108.[Medline]
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Accepted for publication August 16, 1999.




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