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Ann Thorac Surg 2009;87:1289-1290. doi:10.1016/j.athoracsur.2008.08.041
© 2009 The Society of Thoracic Surgeons

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Case Reports

Repair of Mitral Valve and Left Atrioventricular Disruption Caused by Blunt Chest Trauma

A. David Slater, MDa,*, Sujata Subramanian, MDa, Jiapeng Huang, MD, PhDb, Michael Bouvette, MDb, Sebastian Pagni, MDa, Robert D. Dowling, MDa

a Department of Surgery, University of Louisville, Louisville, Kentucky
b Department of Anesthesiology & Perioperative Medicine, University of Louisville, Louisville, Kentucky

Accepted for publication August 18, 2008.

* Address correspondence to Dr Slater, Department of Surgery, University of Louisville, 201 Abraham Flexner Way, Suite 1200, Louisville, KY 40202 (Email: dslater{at}ucsamd.com).


    Abstract
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We describe a case of acute cardiac failure in a patient involved in a motor vehicle accident. A diagnosis of acute mitral regurgitation and left atrioventricular disruption was made with transesophageal echocardiography. Successful repair was performed using the mitral valve leaflets to patch the disruption followed by valve replacement.


    Introduction
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Intracardiac injury resulting from blunt trauma is uncommon. Atrioventricular disruption usually results from intraoperative injury and is associated with high mortality.

A 64-year-old woman was the restrained driver in a motor vehicle accident. In the emergency room, her vital signs were stable with a blood pressure of 138/54, pulse rate of 80 beats/minute, oxyhemoglobin saturation of 100% on 2 L nasal cannula, and a Glasgow Coma Scale score of 15. Cardiac examination was normal and the electrocardiogram showed nonspecific ST segment elevation changes. Her past medical history was significant for hypertension with no history of cardiac disease. Her injuries included multiple rib fractures, a left hemothorax, pulmonary contusion, splenic laceration, and complex pelvic fracture.

Thirty-six hours after admission, acute respiratory distress with decreased oxygen saturations and hypotension developed in the patient. A chest roentgenogram revealed increased left pleural effusion and an electrocardiogram suggested inferior wall infarction with right bundle branch block. Cardiac enzymes were mildly elevated with creatine kinase of 2,447 units, creatine kinase-MB fraction of 20.1, and troponin of 1.11 nanograms/ml. She was intubated and required an PIO2 of 1.0 to maintain O2 saturation above 90%. Pulmonary artery catheter readings revealed pulmonary artery pressure of 58/26 mm Hg, pulmonary capillary wedge pressure of 18 mm Hg, cardiac output of 3.39 L/min, and a cardiac index of 1.68 L/min/m2.

Transesophageal echocardiography was obtained and demonstrated severe mitral regurgitation, rupture of the P1 segment of the mitral valve and a type III partial disruption of the left ventricle (LV) beneath the mitral valve annulus. Severe tricuspid regurgitation and severe right ventricular dysfunction with elevated right ventricular and pulmonary artery pressures were noted. The patient was stabilized with intropic support and intra-aortic balloon pump placement. Her creatinine level rose to 3.6 mg/dL by post-injury day 8; however, her cardiac index improved to 2.8 L/min/m2 and the FIO2 was weaned to 0.4. Her neurologic status improved and she was believed to be a candidate for operative therapy. Cardiac catheterization showed normal coronary arteries. Intraoperative transesophageal echocardiography showed a 1.17-cm pseudoaneurysm of the LV just below the level of mitral annulus, prolapse of the P1 segment of the posterior leaflet, severe right ventricular dysfunction, and severe tricuspid regurgitation without structural abnormality of the tricuspid valve (Fig 1).


Figure 1
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Fig 1. Flail posterior leaflet type III partial left ventricular disruption.

 
A median sternotomy incision was performed, and cardiopulmonary bypass was initiated with aortic and bi-caval cannulation. The left atrium was opened through the interatrial groove. The posterior leaflet was torn to the junction of the P1 and P2 scallop with rupture of the chordae to P1. A defect in the LV wall was noted just inferior to the posterior annulus measuring approximately 3 cm in length and 1 cm in width. This was not suitable for primary repair because of the necrosis of the LV muscle and the extent of the defect.

Repair of the defect was performed as follows: the anterior leaflet of the mitral valve was detached from the annulus and divided in the middle. The posteromedial half was fashioned to create a button and reattached to the annulus at the level of the posterior commissure. The anterolateral half of the leaflet was rotated posteriorly and sutured to the torn portion of the P1 segment with 5-0 polypropylene to form a patch that was secured to the ventricular myocardium around the ruptured area using 5-0 polypropylene. Then 2-0 pledgeted Ethibond sutures (Ethicon, Somerville, NJ) were placed circumferentially around the mitral valve annulus from the atrial side, except in the area of the leaflet patch where the pledgets were placed from the ventricular side, incorporating the leaflet patch (Fig 2). A 29-mm St. Jude Biocor prosthesis (St. Jude Medical, Minneapolis, MN) was used to replace the mitral valve to avoid the necessity of postoperative anticoagulation. The tricuspid valve was approached through the right atrium; it was structurally intact with evidence of annular dilatation. A 28-mm Edwards MC 3 ring (Edwards Lifesciences, Irvine, CA) was placed. The patient was taken off bypass without difficulty. Intraoperative transesophageal echocardiography post-repair showed good LV function with no mitral regurgitation or tricuspid regurgitation, no paravalvular leak, and closure of the LV pseudoaneurysm.


Figure 2
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Fig 2. Repair of disruption and valve replacement.

 
Postoperatively, the patient did require a brief duration of dialysis support, but eventually made a full neurologic and renal recovery and was thereafter discharged from the hospital on postoperative day 27.


    Comment
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Posterior LV wall disruption is rare, and it is usually a complication of mitral valve replacement, posterior wall infarction, or both [1]. A type III partial wall disruption without rupture resulting from blunt trauma developed in our patient. Type III ruptures are now rare because of the prevalence of mitral valve repair versus replacement, knowledge of proper techniques for elevation of the heart after mitral valve replacement, and design modifications of mitral valve prostheses [1]. Intracardiac valve injury from blunt chest trauma is rare [2]. The mechanism is a sudden increase in intracardiac pressure during late diastole or during the isovolumetric contraction phase of the cardiac cycle [3]. Mitral apparatus injury may be caused by papillary muscle rupture, chordae tendinea rupture, or leaflet tears [4]. As in our case, an initial asymptomatic stage with subsequent development of congestive heart failure has been reported previously with mitral valve injury [2]. Transesophageal echocardiography is the procedure of choice for the diagnosis of this condition because it is accurate and can be readily performed at the bedside in critically ill patients who may have chest dressings and tubes [5].

Urgent surgery is the treatment of choice for severe acute mitral insufficiency and for ventricular pseudoaneurysm. Complete atrioventricular disruption after mitral valve replacement requires immediate repair with cardiopulmonary bypass. Successful repair of disruption or pseudoaneurysm usually requires placement of a pericardial patch to cover the defect with sutures through the patch for the prosthetic valve [1]. Small pseudoaneurysms beneath the annulus have been repaired by dividing the posterior leaflet, closure of the defect, and reattachment of the leaflet without valve replacement [6].

In this case, surgery was delayed because the patient was initially unresponsive and she responded hemodynamically with insertion of the intra-aortic balloon pump. The defect was too large with borders containing contused myocardium to allow direct closure. We were also concerned about potential damage to the posterior papillary muscle and elected to replace the valve.

We describe a technique for successful repair of traumatic left atrioventricular disruption and mitral valve rupture using native mitral valve tissue. This approach allowed for chordal sparing and successful mitral valve replacement.


    References
 Top
 Abstract
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 Comment
 References
 

  1. Zacharias A. Repair of spontaneous rupture of the posterior wall of the left ventricle after mitral valve replacement: operative techniques Thorac Cardiovasc Surg 2003;8:36-41.
  2. Kan C-D, Yang Y-J. Traumatic aortic and mitral valve injury following blunt chest injury with a variable clinical course Heart 2005;91:568-570.[Abstract/Free Full Text]
  3. Banning AP, Pillai R. Non-penetrating cardiac and aortic trauma Heart 1997;78:226-229.[Free Full Text]
  4. Bernabeu E, Mestres CA, Lama-Osorio Pm, et al. Acute aortic and mitral valve regurgitation following blunt chest trauma Int Cardiovasc Thorac Surg 2004;3:198-200.[Abstract/Free Full Text]
  5. Selzer A, Kelly JJ, et al. The syndrome of mitral insufficiency due to isolated rupture of the chordae tendinae Am J Med 1967;43:822-836.[Medline]
  6. Halstead J, Hosseinpour AR, Wells FC. Conservative surgical treatment of valvular injury after blunt chest trauma Ann Thorac Surg 2000;69:766-768.[Abstract/Free Full Text]




This Article
Right arrow Abstract Freely available
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Right arrow Email this article to a friend
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Right arrow Author home page(s):
A. David Slater
Sujata Subramanian
Michael Bouvette
Sebastian Pagni
Robert D. Dowling
Right arrow Permission Requests
Citing Articles
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Google Scholar
Right arrow Articles by Slater, A. D.
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Right arrow Articles by Slater, A. D.
Right arrow Articles by Dowling, R. D.
Related Collections
Right arrow Valve disease


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