Tricuspid Insufficiency

KENNETH JORGE JAMES WARREN

M. KESSLER,

MD,

MAJ,

MC*

E. FOIANINI, MD, LTC, MC E. DAVIA, MD, LTC, MC T. ANDERSON,

MD,

MAJ,

MC

KARL PFUETZE, MD, MAJ, MC THOMAS PINDER, MD, MAJ, MC MELVIN

D. CHEITLIN,

MD,

FACC,

COL,

MC Fort Campbell, Kentucky Washington, D. C.

Due To Nonpenetrating

Trauma

This case of tricuspid insufficiency due to nonpenetrating trauma involved a male patient who had received major chest trauma in an automobile accident, had a nonholosystolic murmur that increased slightly during inspiration on standing, and transient electrocardiographic findings of right bundle branch block. Unlike findings in previous cases, the right atrial V wave was not dominant and was less than 8 mm Hg. An echocardiogram indicating right ventricular volume overload was an essential diagnostic tool that led to cardiac catheterization and definitive diagnosis.

Tricuspid insufficiency as a rare result of penetrating1 and nonpenetrating2J trauma has been the subject of recent reports. We report this case of traumatic tricuspid insufficiency because of its nonspecific and occult clinical findings, an atypical catheterization finding and the key role that echocardiography played in the diagnosis. Case

From the Departments of Medicine and Surgery, U.S. Army Hospital, Fort Campbell, Kentucky, and the Cardiology Service, Walter Reed Army Medical Center, Washington, D.C. Manuscript accepted December 27, 1974. Present address and address for reprints: Kenneth M. Kessler, MD, Section of Cardiology, Temple University Health Sciences Center, 3400 N. Broad St., Philadelphia, Pa. 19140. l

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A 21 year old black man, on active duty with the Army, received major anterior chest and face trauma in an automobile accident on September 29, 1973. He had no known congenital heart disease, rheumatic fever, rheumatic heart disease or murmur before the accident. Clinical findings during his hospital course, first at Baptist Hospital, Nashville, Tenn. and later at the U.S. Army Hospital, Fort Campbell, Ky., included nondisplaced mandibular and sternal fractures, pulmonary infiltrates and effusions, fever with spontaneous resolution (without infection noted and without use of antibiotic agents), glucose-6-phosphate dehydrogenase deficiency and phlebitis of the left brachial vein, which was secondary to a central venous pressure line and resolved with phenylbutazone therapy. The cardiovascular course was complex. During the first 2 weeks of hospitalization, pericarditis was evidenced by a loud three component pericardial friction rub. Pericardial effusion was evidenced by an enlarged cardiac silhouette on X-ray examination and echocardiographic demonstration of an echo-free space between echoes from the posterior left ventricular wall and the pericardium. No evidence of tamponade was found. The electrocardiogram revealed right bundle branch block, QRS duration of 0.14 second, and left axis deviation with a QRS axis of -40”. During the 4th week of hospitalization, a diagnostic pericardiocentesis was performed because of the fever. Serosanguineous sterile fluid was obtained using a subxyphoid approach. After the procedure, a paradoxical pulse of 20 mm Hg was observed, and the patient was closely monitored during the next 3 days with no further complications. By the 6th week of hospitalization, the pericardial rub resolved, and the cardiac silhouette returned to normal. The right bundle branch block resolved leaving a QRS axis of -35’ and a QRS duration of 0.10 second. The QRS duration subsequently shortened to 0.08 to 0.09 second. Physical examination: At this time, vital signs were within normal limits, and there was no paradoxical pulse noted. Jugular venous and carotid arterial pulsations were normal. The lungs were clear. Cardiac examination revealed a normal left ventricular impulse in the fifth intercostal space within the midclavicular line. The sternal and left parasternal area was abnormally dynamic with apparent systolic outward motion; but this finding was diffi-

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FIGURE 1. Echocardiogram showing enlarged right ventricular cavity (30 mm) and abnormal, type A, anterior systolic septal motion. MV = anterior mitral valve leaflet echo; RV = right ventricular enddiastolic dimension; 3 = intraventricular septum.

cult to interpret because of the sternal fracture. The first heart sound was normal; the second was physiologically split. A third heart sound was heard better along the left sternal border than at the apex and increased in intensity with inspiration, suggesting it was of right ventricular origin; no fourth heart sound was heard. A grade 216 highpitched systolic ejection murmur was noted in the third and fourth intercostal spaces left of the sternum. The murmur increased slightly in intensity and duration during inspiration, especially when the patient was standing. At no time was this murmur holosystolic. Echocardiography: Because of the murmur, (the “right-sided” third heart sound and the suggestion of right ventricular enlargement in the echocardiogram obtained for the diagnosis of pericardial effusion, repeat echocardiographic evaluation was performed with the patient in the supine position using a 0.5 cm diameter, 2.25 megahertz, 10 cm focused transducer (Echoline 20, Smith Klein Instruments, Palo Alto, Calif.) (Fig. 1). This revealed an enlarged right ventricular end-diastolic dimension of 30 mm or 17 mm/m2 (normal 7 to 23 mm or 5 to 12 mm/m2).4 The right ventricular end-diastolic dimension was measured immediately before the electrocardiographic Q wave as the vertical distance between the echoes from the anterior right ventricular wall and those from the anterior surface of the intraventricular septum. The latter are clearly shown in Figure 1. The anterior right ventricular wall was defined in accord with the standards suggested by Feigenbaum,” that is, the first moving echo posterior to the nonmoving chest wall echoes or a distance of 0.5 cm posterior to the chest wall. Both criteria were met by our measurement. Moreover, selective obliteration of this echo by increase in damping on other recordings confirmed its identity. Both the anterior and posterior intraventricular septal echoes demonstrated a sustained anterior motion during

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systole. This finding has been defined as abnormal type A septal motion in contrast to abnormal type B septal motion wherein the posterior septal echo remains essentially fixed and the anterior intraventricular septal echo moves anteriorly due to septal thickening during systole. Both A and B types of abnormal septal motion are indicative of volume overload of the right ventricle and are in contradistinction to the normal posterior motion of the intraventricular septum during systole.6 The echocardiogram presented and others in this patient were performed with the ultrasonic beam directed sufficiently toward the apex to avoid confusion with the systolic anterior septal motion that normally occurs nearer the aortic root. 7,8 No abnormality of the tricuspid or mitral valve was demonstrated in spite of adequate visualization of the anterior leaflet of the mitral and tricuspid valves and partial visualization of the posterior leaflet of the mitral valve. Cardiac catheterization and angiography: The clinical course compatible with traumatic tricuspid insufficiency and supported by the echocardiographic findings of right ventricular volume overload led to the patient’s referral to Walter Reed Army Medical Center, Washington, D.C., for cardiac catheterization. Right heart catheterization performed on January 24, 1974, revealed the following pressures (mm Hg): Right atria1 mean 3 (a wave 4, v wave 4); right ventricular 30/O-5; pulmonary arterial 30/8, mean 16; pulmonary wedge mean 10 (a wave 10, u wave 12). A hydrogen curve with sensing in the pulmonary artery was normal (7 seconds). Ascorbate curves revealed immediate appearance in the right atrium after right ventricular injection but not in the superior vena cava after pulmonary arterial injection. Cineangiography with 25 cc of contrast medium injected in 1 second into the right ventricle revealed contrast regurgitation from the right ventricle to the right atrium both before and after the angiographic catheter was removed from the right ventricular cavity (Fig. 2). Firm angiographic evidence of tricuspid insufficiency is difficult to

FIGURE 2. Right ventricular angiogram. Systolic frame after withdrawal of angiographic catheter and clearing of contrast dye from right atrium during the preceding diastole. Contrast dye again regurgitates from the right ventricle with opacification of the right atrium, superior and inferior venae cavae.

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obtain since the angiographic catheter may induce tricuspid insufficiency while across the tricuspid valve and, less often, after removal. This possibility was certainly considered but, in view of the contrast regurgitation even into the inferior vena cava after catheter withdrawal and the other supportive data, a final diagnosis of mild hemodynamically insignificant tricuspid regurgitation was made. Because the patient was essentially asymptomatic, prophylaxis for sub-

acute bacterial endocarditis and yearly medical follow-up were deemed the only necessary treatment. Discussion

Tricuspid insufficiency is a rare complication of either penetrating1 or nonpenetrating2s3 chest trauma. Ours represents the 28th reported case of tricuspid regurgitation secondary to nonpenetrating trauma since the description by Williams9 in 1829. Features in common with previous reports, as reviewed by Marvin et a1.,3 include the patient’s male sex, his receipt of major chest trauma in an automobile accident, the nonholosystolic murmur at the left sternal border and electrocardiographic findings of (transient) right bundle branch block as well as persistent left axis deviation. Several other features were either atypical or deserve specific comment. First, the physical findings were initially obscured by the trauma itself, the instability of the sternum due to fracture and the loud pericardial friction rub. Only by careful follow-up examinations was the murmur at the left sternal border heard. Furthermore, its interpretation was moot. Inspiratory accentuation was inconsistent in the supine position but could at times be appreciated with the patient standing. Cobbs’O has stressed the importance of examining any patient with suspected tricuspid insufficiency in the standing position. Nevertheless, most observers were willing to ascribe the murmur to a physiologic pulmonary outflow murmur. With the aid of echocardiography, abnormal type A septal motion and an enlarged right ventricular end-diastolic dimension were noted (Fig. 1). Although no specific abnormality of tricuspid valve motion was noted, this indirect evidence of right ventricular volume overload”-l3 was the key feature that encouraged cardiac catheterization for definitive diagnosis.

To our knowledge, this is the first case in which echocardiography was an essential diagnostic procedure in the diagnosis of traumatic tricuspid insufficiency due to nonpenetrating trauma. Similar echocardiographic findings were reported in one case of traumatic tricuspid insufficiency after penetrating trauma, but the diagnosis of cardiac abnormality was clinically obvious in that case from the outset1 The tricuspid valve is more difficult to study by echocardiography than the mitral valve because of both the location and the plane of the tricuspid valve leaflets. Visualization of the anterior tricuspid leaflet alone is most frequent and is often incomplete; rarely, the posterior leaflet is visualized in part or in full. Absence or incomplete recording of valve echoes cannot be used to denote abnormality since such incomplete echoes are most frequently technical. Thus, inability to demonstrate specific abnormality of the tricuspid valve leaflet echoes in our case is not surprising. Indeed, mitral valve echocardiography in which full visualization of posterior as well as anterior leaflet echoes throughout the cardiac cycle can be more readily accomplished shows no diagnostic abnormality in most cases of mitral regurgitation of rheumatic origin and is diagnostic only in limited forms of mitral regurgitaion such as the mitral valve prolapse syndrome or flail mitral valve.i4 In contrast, the sensitivity of the echocardiogram in detecting a right ventricular volume overload pattern in our case was impressive. Finally, chamber pressures found at cardiac catheterization were atypical in that the only abnormality was equalization of the right atria1 a and v waves at 4 mm Hg. In each of the 24 previous cases studied at cardiac catheterization, there was a dominant right atria1 u wave of more than 8 mm Hg.” Other causes of right ventricular volume overload such as left to right

shunts were ruled out during catheterization. These findings, together with the absence of murmur or cardiac history before the chest trauma and the typical and changing electrocardiographic abnormalities caused by the trauma, all dictate that the findings of tricuspid insufficiency were secondary to the nonpenetrating chest trauma the patient sustained.

References 1. Mary DA, Day JB, Pakrashi BC, et al: Tricuspid insufficiency after penetrating trauma. Am J Cardiol 31:792-795, 1973 2. Liedtke AJ, DeMuth WE Jr: Nonpenetrating cardiac injuries: a collective review. Am Heart J 86:687-697, 1973 3. Marvin RF, Schrank JP, Nolan SP: Traumatic tricuspid insufficiency. Am J Cardiol 32:723-726, 1973 4. Feigenbaum H: Echocardiography. Philadelphia, Lea & Febiger, 1972, p 216 5. Idem, p 131, 142 6. Idem, p 129-143 7. Idem, p 139 8. Hagan AD, Francis GS, Sahn DJ, et al: Ultrasound evaluation of systolic anterior septal motion in patients with and without right ventricular volume overload. Circulation 50:248-254, 1974

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9. Williams A: Laceration of the tricusoid valve. Lond Med Gaz 4: 78-79, 1829 10. Cobbs BW Jr: Clinical recognition and medical management of rheumatic heart disease and other acquired valvular disease, chap 45. In, The Heart, third edition (Hurst JW, Logue RB, Schlant RC, et al., ed). New York, McGraw-Hill, 1974, p 949 11. Diamond MA, Dellon JC, Haine CL, et al: Echocardiographic features of atrial septal defect. Circulation 43:129-135, 1971 12. Popp RL, Wolfe SB, Hirata T, et al: Estimation of right and left ventricular size by ultrasound. A study of the echoes from the interventricular septum. Am J Cardiol 24:523-530, 1969 in 13. McCann WD, Harbold NB, Fuiliani ER: The echocardiogram right ventricular overload. JAMA 221: 1243-1245, 1972 14. In Ref. 4, p 57-63

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Tricuspid insufficiency due to nonpenetrating trauma.

This case of tricuspid insufficiency due to nonpenetrating trauma involved a male patient who had received major chest trauma in an automobile acciden...
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