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Ann Thorac Surg 1996;61:992-993
© 1996 The Society of Thoracic Surgeons

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Case Report

Traumatic Tricuspid Regurgitation With Cyanosis: Diagnosis by Transesophageal Echocardiography

Departments of Surgery and Medicine, University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School, New Brunswick, New Jersey

Accepted for publication September 18, 1995.

	Abstract

Top Footnotes Abstract Introduction Comment References

 
This case report demonstrates the utility of transesophageal echocardiography in the rapid diagnosis of a cardiac injury from blunt thoracic trauma. Initial transesophageal echocardiography identified a flail tricuspid valve leaflet and regurgitation in a patient with jugular venous distention and hemodynamic instability. Progressive hypoxemia prompted repeat transesophageal echocardiography with contrast enhancement, which revealed opening of the foramen ovale and a right-to-left interatrial shunt. Operative repair of the lesion was lifesaving.

	Introduction

Top Footnotes Abstract Introduction Comment References

 
Here we describe a patient who sustained blunt trauma and was seen with persistent jugular venous distention associated with hemodynamic instability. The diagnosis of tricuspid valve regurgitation (TVR) was made during the first hour using transesophageal echocardiography (TEE). Six days later, acute, critical hypoxemia developed. Repeat TEE with contrast enhancement revealed opening of the foramen ovale and a right-to-left interatrial shunt. Operative repair of the lesion was lifesaving, and a rapid recovery followed.

A 35-year-old female driver who was not wearing a seat belt was involved in a highway rollover crash and was transported to a Level I Trauma Center. Initial vital signs included normal sinus rhythm, heart rate of 76 beats/min, and systolic blood pressure of 92 mm Hg. Bilateral jugular venous distention was evident. No murmurs were noted initially. Diagnostic peritoneal lavage was negative. Because of persistent hypotension, TEE was performed and demonstrated a flail tricuspid valve leaflet caused by a ruptured papillary muscle.

The first 5 hospital days were marked by relative respiratory and hemodynamic stability while the patient was on mechanical ventilation but no inotropic agents. On day 6, progressive hypoxemia developed with a partial pressure of arterial oxygen of 61 mm Hg on an inspired oxygen fraction of 0.6. Hemodynamic data included the following: central venous pressure of 22 mm Hg; pulmonary artery wedge pressure of 13 mm Hg; and cardiac index of 3.2 L•min^-1•m^-2. There was no evidence of pulmonary congestion on chest radiograph. Repeat TEE revealed a patent foramen ovale and a right-to-left interatrial shunt (Fig 1).

View larger version (81K): [in this window] [in a new window]   Fig 1. . Transesophageal echocardiogram illustrating ruptured tricuspid papillary muscle head (solid arrow) in the right atrium (RA) during systole. A patent foramen ovale (hollow arrow) is also evident. (LA = left atrium; TV = tricuspid valve ring.)

Another TEE with intravenous contrast enhancement revealed a major shunt of contrast solution from the right atrium into the left atrium. The proximal ascending aorta was briefly but completely opacified by contrast medium. These findings led to emergent operation. Operative findings included a patent foramen ovale and flail anterior and septal leaflets of the tricuspid valve because of a ruptured papillary muscle. Reimplantation of the ruptured papillary muscle, De Vega annuloplasty, and closure of the patent foramen ovale were performed. After repair, TEE confirmed competence of the tricuspid valve with no evidence of regurgitation or interatrial shunt.

There was rapid improvement in the postoperative period. By 20 hours postoperatively, the inspired oxygen fraction requirement was only 0.4, with arterial blood gas pH 7.45, partial pressure of arterial carbon dioxide of 42 mm Hg, partial pressure of arterial oxygen of 115 mm Hg, and arterial oxygen saturation of 98%. By 36 hours, the patient was weaned from all inotropic support. Hemodynamic data revealed a central venous pressure of 14 mm Hg, a pulmonary artery wedge pressure of 17 mm Hg, and a cardiac index of 4.1 L•min^-1•m^-2. She was eventually extubated and was discharged to rehabilitation on postoperative day 23.

	Comment

Top Footnotes Abstract Introduction Comment References

 
Nine cases of acquired right-to-left interatrial shunt resulting from traumatic TVR have been reported [1–3]. The condition was ultimately diagnosed by cardiac catheterization. In our patient, the diagnosis of TVR was initially made by TEE.

There is a broad spectrum of cardiac injuries that have been attributed to blunt thoracic trauma. These injuries include myocardial contusion, valvular disruption, and chamber rupture. Presentation may be subtle and hemodynamically insignificant, acute and life-threatening, or delayed with progressive deterioration.

Tricuspid valve rupture may involve leaflets, chordae tendineae, or papillary muscles. Isolated papillary muscle rupture of the tricuspid valve is rare [3]. The usual symptoms of TVR include fatigue, peripheral edema, and dyspnea. Physical findings include jugular venous distention and a pansystolic murmur heard at the lower left sternal border. The electrocardiogram usually shows right bundle-branch block. Cardiac catheterization or a pulmonary artery catheter should reveal giant V waves in the right atrium [4, 5].

Traumatic TVR is usually not discovered during the initial evaluation of trauma patients. The lesion is often clinically subtle and initially well tolerated hemodynamically [6]. Patients have development of slow but progressive fatigability and dyspnea. Presentation may be delayed weeks to years. Of the previously reported cases of traumatic TVR with right-to-left shunt, approximately half were discovered 10 to 25 years after injury [1].

In our patient, the proposed mechanism of injury begins with forceful compression of the right ventricle, transient outflow obstruction, and a sudden increase in right ventricular pressure. This results in rupture of the papillary muscle, TVR, elevated right atrial pressures, and progressive right atrial dilatation [5]. As right atrial pressure overcomes left atrial pressure (central venous pressure > pulmonary artery wedge pressure), opening of the foramen ovale results in a right-to-left shunt, thereby producing an acquired cyanotic heart syndrome.

Transesophageal echocardiography provides a safe method for visualization of the heart, mediastinum, and most of the thoracic aorta. It is a sensitive study for detection of cardiac injury, eg, regional wall motion abnormalities, valvular dysfunction, septal defects, pericardial tamponade, and aortic disruption [7]. The method provides enhanced resolution of the heart and great vessels compared with surface echocardiography and is not limited by chest wall dressings, monitoring devices, or a ventilator.

Transesophageal echocardiography with contrast enhancement using microbubbles provides additional diagnostic information [8]. The technique in our patient involved 5% dextrose solution passed between two syringes on a stopcock manifold. Intravenous injection of this contrast solution results in opacification of the right cardiac chambers. Appearance of contrast solution in the left heart is indicative of a shunt.

In summary, this case report emphasizes the utility of TEE in the rapid and efficient diagnosis of cardiac injury from blunt thoracic trauma, not only at initial presentation but also at follow-up for acute clinical deterioration.

	Footnotes

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Address reprint requests to Dr Boyarsky, Department of Surgery, MEB 439, UMDNJ–Robert Wood Johnson Medical School, One Robert Wood Johnson Place-CN19, New Brunswick, NJ 08903–0019.

	References

Top Footnotes Abstract Introduction Comment References

 

1. Bardy GH, Talano JV, Meyers S, Lesch M. Acquired cyanotic heart disease secondary to traumatic tricuspid regurgitation: case report with a review of the literature. Am J Cardiol 1979;44:1401–6.[Medline]
2. Jacob L, Bonnet F, Pavie A, et al. Severe hypoxemia revealing traumatic tricuspid regurgitation with right-to-left intracardiac shunt. J Trauma 1985;25:659–61.[Medline]
3. Linka A, Ritter M, Turina M, Jenni R. Acute tricuspid papillary muscle rupture following blunt chest trauma. Am Heart J 1992;124:799–802.[Medline]
4. Osborn JR, Jones RC, Jahnke EJ. Traumatic tricuspid insufficiency: hemodynamic data and surgical treatment. Circulation 1964;30:217–22.[Abstract/Free Full Text]
5. Liedtke AJ, DeMuth WE Jr. Nonpenetrating cardiac injuries: a collective review. Am Heart J 1973;86:687–97.[Medline]
6. Gayet C, Pierre B, Delahaye J, Champsaur G, Andre-Fouet X, Rueff P. Traumatic tricuspid insufficiency: an underdiagnosed disease. Chest 1987;92:429–32.[Abstract/Free Full Text]
7. Shapiro MJ, Yanofsky SD, Trapp J, et al. Cardiovascular evaluation in blunt thoracic trauma using transesophageal echocardiography (TEE). J Trauma 1991;31:835–40.[Medline]
8. Chang G, Shindler OI. Negative contrast effect in atrial septal defect. Prim Cardiol 1992;18:29–32.

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Peter M. Scholz Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Chiu, W. C. Articles by Boyarsky, A. H. Search for Related Content PubMed PubMed Citation Articles by Chiu, W. C. Articles by Boyarsky, A. H.