Ann Thorac Surg 1998;66:1811-1814
© 1998 The Society of Thoracic Surgeons
Case Reports
Traumatic tricuspid valve regurgitation and cerebral emboli
Ali A. Khaki, MDa,
Albert Starr, MDa
a Providence St Vincent Hospital, Portland, Oregon, USA
Accepted for publication April 30, 1998.
Address reprint requests to Dr Khaki, Oregon Medical Laser Center, 9205 SW Barnes Rd, Portland, OR 97225
e-mail: (ali_khaki{at}phsor.org)
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Abstract
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We report a case of traumatic tricuspid valve regurgitation and late presentation with transient ischemic attacks caused by the presence of a right-to-left shunt through a small atrial septal defect.
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Introduction
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A 28-year-old man presented at Providence St. Vincent Hospital in Portland, Oregon, with transient numbness, tingling in his left arm, and inability to speak. This lasted only for few minutes. During careful history taking, he recalled similar episodes over the year before his admission. He had a motorcycle accident 6 years earlier with chest contusion, multiple fractures, and a ruptured spleen. A murmur also was noticed. Echocardiography was done and showed tricuspid regurgitation as a result of the trauma, but it was of no clinical significance at that time. He was treated for other injuries, but the valvular injury was left alone. After the accident he remained well, until he reported the new neurologic events. His exercise tolerance, however, had slightly decreased over the last 6 years but not enough for him to seek medical advice.
On this admission his preoperative chest radiograph showed no evidence of right ventricular enlargement or cardiomegaly (Fig 1). Magnetic resonance imaging scan of the head showed foci of old infarcts in the cortical and subcortical areas. Transthoracic echocardiography demonstrated severe tricuspid regurgitation. This was confirmed by cardiac catheterization, which showed a small atrial septal defect and demonstrated normal right heart pressures. Intraoperative transesophageal echocardiography revealed ruptured chordae, with a prolapsed anterior leaflet of the tricuspid valve in systole. There was a significant jet of reverse flow toward the interatrial septum (Fig 2). The results of screening for deep venous thrombosis as a source of emboli were negative.
During the operation, the septal leaflet of the tricuspid valve was completely normal; however, the posterior leaflet showed mild prolapse. The anterior leaflet was greatly enlarged and prolapsed, and a 15-mm tear was found in the middle. There was no thickening, and the entire valve was thin and delicate. The tricuspid valve was repaired by direct suture of the leaflet tear. Then three areas of the leaflet were tacked down to the wall of the right ventricle by raising a papillary muscle in each of these areas from its bed and attaching it to the free margin [1]. A 32-mm Carpentier-Edwards annuloplasty ring (Baxter Healthcare, Irvine, CA) was then placed. There was a small atrial septal defect, which was closed by direct suture.
Postoperative transesophageal echocardiography showed a satisfactory repair of the valve with only small residual regurgitation (Fig 3), and the atrial septal defect was tightly closed. The period after the operation was uneventful, and the patient was followed up for 4 years. He is now symptom free and has no limitation to his activities.
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Comment
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A case of traumatic tricuspid regurgitation after nonpenetrating chest trauma was reported in 1829 by Williams [2]. Tricuspid valve injury in blunt chest trauma is the third most common injury, after injury to the aortic and mitral valves [3]. The sharp increase in the incidence of motor vehicle accidents in the past decades has led to more frequent reports of these injuries. Tricuspid valve involvement in blunt chest trauma is very rare. The total reported cases of such injury so far are approximately 100 [4].
The anterior tricuspid leaflet and the subvalvular mechanism, because of their location, are more vulnerable to injury than the other two leaflets [5, 6]. A sudden increase in the intraventricular pressure can result in the disruption of the leaflet and its structures, such as the chordae or papillary muscle, or can cause a tear in the leaflet itself. Rupture of the chordae is the most commonly reported injury in the tricuspid valve, followed by rupture of the papillary muscle. Leaflet tears are very rare [7, 8]. The usual hemodynamic stability with tricuspid valve regurgitation in the early posttraumatic period draws the attention to the management of the associated injuries that occurred simultaneously. Opinions differ regarding surgical intervention of the valve at a later date. In most of the reported cases of traumatic tricuspid regurgitation, the patient sought medical advice many years after the injury, when the ventricular functions had deteriorated and caused shortness of breath and dyspnea [3, 4, 6].
With the improved diagnostic aids and techniques, early surgical intervention, after complete recovery from other associated injuries, results in better outcome. The geometry of the right ventricle and the anatomy of the tricuspid valve make valvular repair a much more appropriate procedure than replacement, especially with improved surgical skills. Several reports in the past have mentioned traumatic tricuspid regurgitation associated with an atrial septal defect, but those patients presented with dyspnea or cyanosis.
In our patient the main complaint was the transient ischemic attacks. Fortunately, there was complete recovery with no residual neurologic deficit. There was no noticeable right ventricular dysfunction over the 6-year period after the injury. The presence of the tricuspid valve prolapse and the regurgitant jet may have created flow turbulence and a possible source of emboli.
We conclude that early tricuspid valve repair and closure of the atrial septal defect are highly recommended for tricuspid valve injury with the presence of a septal defect to avoid the possibility of a major neurologic insult.
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References
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