Eur J Cardio-thorac
Surg (1992) 6:455-457
0 Springer-Verlag 1992
Severe tricuspid regurgitation following blunt chest trauma: indication for emergency surgery M. Pasic I, L. von Segesser I, T. Carrel I, R. Jenni’, and M. Turina 1 1 Clinic for Cardiovascular Surgery, University Hospital Zurich, Switzerland ’ Department of Medicine, University Hospital Zurich, Switzerland
Abstract. A 24-year-old man with polytrauma and severe posttraumatic tricuspid regurgitation due to rupture of all three papillary muscles was subjected to emergency operation 3 days after a car accident. At operation, all Wee papillary muscles of the tricuspid valve were reinserted. Severe tricuspid regurgitation after blunt chest trauma is an indication for emergency surgical treatment, and can be performed with a low operative risk. [Eur J Cardio-thorac Surg (1992) 63455-4571 Key words: Traumatic tricuspid insufficiency - Posttraumatic
Symptomatic cardiac injury following blunt chest trauma is relatively rare, and valvular injury is even rarer. The valves most commonly affected are mitral and tricuspid [4]. Unlike the mitral valve, posttraumatic tricuspid insufficiency is usually well tolerated [l I]. Although severe tricuspid regurgitation can resolve spontaneously [4], we report a case of severe tricuspid regurgitation due to rupture of all three papillary muscles successfully treated by emergency surgery. Case report The patient, a 24-year-old man with a history of severe hashish abuse suffered blunt abdominal trauma with liver contusion, multiple rib fractures of the left side of the chest and left pulmonary contusion, trauma to the soft tissue of the left arm and the posterior side of the left thigh after a car accident. The patient had no previous symptoms nor signs of heart abnormality. On the day of admission, he underwent emergency operation because of the signs of abdominal hemorrhage. The bleeding from a small laceration of the liver was electrocoagulated. On the third day after admission, the patient developed clinical signs of right heart failure with distended neck veins, central venous pressure of 15 mmHg and large V waves of 40 mmHg and an enlarged liver with a positive hepatojugular reflux. An ECG showed sinus tachycardia and complete right bundle branch block. Serum creatine phosphokinase (CPK) was 1839 W/L, with an MB fraction of 80 IU/L. Echocardiographic examination revealed severe tricuspid regurgitation with rupture of all papillary muscles and prolapse into the right atrium during the systole (Fig. 1). A small patent foramen Received for publication: Accepted for publication:
January 2. 1992 March 11, 1992
tricuspid regurgitation
- Surgical repair
ovale with a right-to-left shunt was also noted. Cardiac catheterization was not performed. The patient was operated upon using cardiopulmonary bypass in normothermia and electrically induced fibrillation of the heart. Intraoperatively, moderate pericardial effusion and a dilated right atrium were found. All three papillary muscles of the tricuspid valve were ruptured and several chordae tendinae were torn (Fig. 2). All muscles were refixed by single stiches of 5-O Prolene with teflon-felt pledgets. The patent foramen ovale was also closed by direct suture. At the end of the procedure, testing the valve demonstrated it to be competent. Two days after operation, a large V wave reappeared. Repeat echocardiographic examination demonstrated recurrent tricuspid regurgitation with renewed detachment of the septal papillary muscle. The patient was reoperated upon and the septal papillary muscle was reinserted using several pledgetted 5-O Prolene sutures. Intraoperative transesophageal echocardiography showed a competent tricuspid valve. The postoperative course was complicated by sepsis, but there was no complication of the cardiac procedure. During the hospitalisation, the soft tissue lesions were treated appropriately. Over the next few weeks the patient continued to improve and was discharged 3 weeks after operation.
Discussion Acute tricuspid regurgitation is a rare complication of blunt chest trauma. Although injury of the tricuspid valve is rarer than injury of other heart valves, it is also less prone to become symptomatic and usually is better tolerated [2]. The onset of symptoms may be immediate or delayed several years after blunt trauma [l], and is related to the degree of regurgitation present. Symptoms are usually mild and consist of fatigue, dyspnea on exertion, and occasional orthopnea [8].
,’ .‘.._.,
_:. ‘...
‘..___
:’ . .._
.._._
.”
Fig. 2. Artistic drawing of the intraoperative
finding showing all three papillary muscles of the tricuspid valve to be ruptured and prolapsed into the right atrium, and some chordae tendineae to be torn. There is a small patent foramen ovale
Fig. 1. Apical view of the right chambers showing ruptured papillary muscles in the right ventricle (RV) at the beginning of systole (A) and prolapse of the anterior (AM) and the septal papillary (SM) muscles into the right atrium (RA) in mid (B) and end systole (C)
Clinical signs and echocardiographic findings are sufficient to make the diagnosis [5]. In the acutely symptomatic patients, the signs of right heart failure with distended neck veins, a positive hepatojugular reflux, hepatomegaly occassionally associated with systolic pulsations, marked venous V waves, and increased central venous pressure are observed. Commonly, a holosystolic murmur is audible at the left parasternal area [5,6,8,11]. The murmur may be absent, or present only during inspiration. It can be best heard at the cardiac apex because of right heart dilation thereby simulating mitral insufficiency [5]. On chest X-ray, the heart is observed to be enlarged, and ECG usually shows heart block [7], often a right bundle branch block [5, 111. The ECG can also show ST-T wave abnormalities suggestive of pericarditis or myocardial injury [4, 81. In some patients, such as in our case, a patent foramen ovale may be found as the right atrium enlarges in response to the increased pressure secondary to the tricuspid regurgitation [lo]. The signs of a patent foramen ovale with right-to-left shunt from tricuspid regurgitation may be easily overlooked as cyanosis and systemic hypoxemia may be falsely attributed to associated lung trauma [7]. Echocardiography confirms the diagnosis, and cardiac catheterization is usually not necessary. Early diagnosis should be followed by early treatment. The optimal timing for surgical intervention, however, is still not clearly defined [8, 9, 111. Less symptomatic patients should be initially treated medically under close monitoring and later should be considered for an operative treatment to prevent late heart failure. Clinical signs of high venous pressure, hepatic congestion, ascites and oedema coupled with decreasing diuresis constitute the indication for early surgery in traumatic tricuspid insufticiency. The valve can be damaged by rupture of a papillary muscle and/or chordae tendineae which are the most
457
common modes [l 11,or by a torn annulus or cusps [3,8]. The operative treatment consists of reinsertion of the ruptured papillary muscles, as in our case, or of repair with resuture of the leaflet to the annulus and annuloplasty [l, 81. The Hannover group [12] reported an alternative approach to extensive rupture of the chorde tendineae and flail leaflets preserving as much of the free leaflet substance as possible: leaflet resection, suture of the cut edges of the anterior and posterior cusp, and additional annuloplasty restored proper valve function without stenosis. If the valve is not reparable, it should be replaced [6, 7, 111. Bioprostheses are preferable because of their lower thrombogenicity [5, 6, 91. The surgical treatment usually results in complete recovery [l, 5, 8, 111. Acknowledgement.
The authors
gratefully
thank
Mrs. Carol de
Simio for drawing.
References Branderburg RO. MC Goon DC. Campeau L, Gioliani ER (1966) Traumatic rupture of the chordae tendinae of the tricuspid valve. Successful repair twenty-four years later. Am J Cardiol 18:911-915 Bryant LR, Mobin-Uddin K, Dillon ML, Hinshaw MA, Utley JR (1973) Cardiac valve injury with major chest trauma. Arch Surg 107:279-283 Cuadros CL, Hutchinson JE, Mogtader AH (1984) Laceration of a mitral papillary muscle and the aortic root as a result of blunt trauma of the chest. J Thorac Cardiovasc Surg 88: 134140
4. Dodd DA, Johns JA, Graham TP Jr (1987) Transient severe mitral and tricuspid regurgitation following blunt chest trauma. Am Heart J 114:652-654 5. Gayet C, Pierre B, Delahaye JP, Champsaur G, Andre-Fouet X, Rueff P (1987) Traumatic tricuspid insufficiency: an underdiagnosed disease. Chest 921429-432 6. Glock Y, Massabuau P, Puel P (1989) Cardiac damage in nonpenetrating chest injuries: report of 5 cases. J Cardiovasc Surg 30127-33 7. Hilton T, Mezei L. Pearson AC (1990) Delayed rupture of tricuspid papillary muscle following blunt chest trauma. Am Heart J 119:1410-1412 8. Noera G, Sanguinetti M, Pensa P, Biagi B, Cremonesi A, Lodi R, Lessana A, Carbone C (1991) Tricuspid valve incompetence caused by nonpenetrating thoracic trauma. Ann Thorac Surg 51:320-322 9. Quatre JM, Ollivier JP, Aouate JM, Scheuble C, De Bourayne J, Gandjbakhch I, Brion R, Droniou J, Cabrol C (1988) L’insuftisance tricuspide traumatique: 5 observations. Arch Ma1 Coeur 81:325-330 10. Rao G. Garvey J, Gupta M (1977) Atria1 septal defect due to blunt thoracic trauma. J Trauma 17:405-406 11. Shahidnoorai S, Ameli M (1991) Post traumatic tricuspid insufficiency: when to intervene? J Cardiovasc Surg 32:585-588 12. Sutlic Z. Schmid C, Borst HG (1990) Repair of flail anterior leaflets of tricuspid and mitral valves by cusp remodelling. Ann Thorac Surg 50:927-930 Miralem Pasic, MD, ScD Klinik fur Herz- und GefaBchirurgie Universitltsspital Ramistrasse 100 CH-8091 Zurich Switzerland
Surg (1992) 6:455-457
0 Springer-Verlag 1992
Severe tricuspid regurgitation following blunt chest trauma: indication for emergency surgery M. Pasic I, L. von Segesser I, T. Carrel I, R. Jenni’, and M. Turina 1 1 Clinic for Cardiovascular Surgery, University Hospital Zurich, Switzerland ’ Department of Medicine, University Hospital Zurich, Switzerland
Abstract. A 24-year-old man with polytrauma and severe posttraumatic tricuspid regurgitation due to rupture of all three papillary muscles was subjected to emergency operation 3 days after a car accident. At operation, all Wee papillary muscles of the tricuspid valve were reinserted. Severe tricuspid regurgitation after blunt chest trauma is an indication for emergency surgical treatment, and can be performed with a low operative risk. [Eur J Cardio-thorac Surg (1992) 63455-4571 Key words: Traumatic tricuspid insufficiency - Posttraumatic
Symptomatic cardiac injury following blunt chest trauma is relatively rare, and valvular injury is even rarer. The valves most commonly affected are mitral and tricuspid [4]. Unlike the mitral valve, posttraumatic tricuspid insufficiency is usually well tolerated [l I]. Although severe tricuspid regurgitation can resolve spontaneously [4], we report a case of severe tricuspid regurgitation due to rupture of all three papillary muscles successfully treated by emergency surgery. Case report The patient, a 24-year-old man with a history of severe hashish abuse suffered blunt abdominal trauma with liver contusion, multiple rib fractures of the left side of the chest and left pulmonary contusion, trauma to the soft tissue of the left arm and the posterior side of the left thigh after a car accident. The patient had no previous symptoms nor signs of heart abnormality. On the day of admission, he underwent emergency operation because of the signs of abdominal hemorrhage. The bleeding from a small laceration of the liver was electrocoagulated. On the third day after admission, the patient developed clinical signs of right heart failure with distended neck veins, central venous pressure of 15 mmHg and large V waves of 40 mmHg and an enlarged liver with a positive hepatojugular reflux. An ECG showed sinus tachycardia and complete right bundle branch block. Serum creatine phosphokinase (CPK) was 1839 W/L, with an MB fraction of 80 IU/L. Echocardiographic examination revealed severe tricuspid regurgitation with rupture of all papillary muscles and prolapse into the right atrium during the systole (Fig. 1). A small patent foramen Received for publication: Accepted for publication:
January 2. 1992 March 11, 1992
tricuspid regurgitation
- Surgical repair
ovale with a right-to-left shunt was also noted. Cardiac catheterization was not performed. The patient was operated upon using cardiopulmonary bypass in normothermia and electrically induced fibrillation of the heart. Intraoperatively, moderate pericardial effusion and a dilated right atrium were found. All three papillary muscles of the tricuspid valve were ruptured and several chordae tendinae were torn (Fig. 2). All muscles were refixed by single stiches of 5-O Prolene with teflon-felt pledgets. The patent foramen ovale was also closed by direct suture. At the end of the procedure, testing the valve demonstrated it to be competent. Two days after operation, a large V wave reappeared. Repeat echocardiographic examination demonstrated recurrent tricuspid regurgitation with renewed detachment of the septal papillary muscle. The patient was reoperated upon and the septal papillary muscle was reinserted using several pledgetted 5-O Prolene sutures. Intraoperative transesophageal echocardiography showed a competent tricuspid valve. The postoperative course was complicated by sepsis, but there was no complication of the cardiac procedure. During the hospitalisation, the soft tissue lesions were treated appropriately. Over the next few weeks the patient continued to improve and was discharged 3 weeks after operation.
Discussion Acute tricuspid regurgitation is a rare complication of blunt chest trauma. Although injury of the tricuspid valve is rarer than injury of other heart valves, it is also less prone to become symptomatic and usually is better tolerated [2]. The onset of symptoms may be immediate or delayed several years after blunt trauma [l], and is related to the degree of regurgitation present. Symptoms are usually mild and consist of fatigue, dyspnea on exertion, and occasional orthopnea [8].
,’ .‘.._.,
_:. ‘...
‘..___
:’ . .._
.._._
.”
Fig. 2. Artistic drawing of the intraoperative
finding showing all three papillary muscles of the tricuspid valve to be ruptured and prolapsed into the right atrium, and some chordae tendineae to be torn. There is a small patent foramen ovale
Fig. 1. Apical view of the right chambers showing ruptured papillary muscles in the right ventricle (RV) at the beginning of systole (A) and prolapse of the anterior (AM) and the septal papillary (SM) muscles into the right atrium (RA) in mid (B) and end systole (C)
Clinical signs and echocardiographic findings are sufficient to make the diagnosis [5]. In the acutely symptomatic patients, the signs of right heart failure with distended neck veins, a positive hepatojugular reflux, hepatomegaly occassionally associated with systolic pulsations, marked venous V waves, and increased central venous pressure are observed. Commonly, a holosystolic murmur is audible at the left parasternal area [5,6,8,11]. The murmur may be absent, or present only during inspiration. It can be best heard at the cardiac apex because of right heart dilation thereby simulating mitral insufficiency [5]. On chest X-ray, the heart is observed to be enlarged, and ECG usually shows heart block [7], often a right bundle branch block [5, 111. The ECG can also show ST-T wave abnormalities suggestive of pericarditis or myocardial injury [4, 81. In some patients, such as in our case, a patent foramen ovale may be found as the right atrium enlarges in response to the increased pressure secondary to the tricuspid regurgitation [lo]. The signs of a patent foramen ovale with right-to-left shunt from tricuspid regurgitation may be easily overlooked as cyanosis and systemic hypoxemia may be falsely attributed to associated lung trauma [7]. Echocardiography confirms the diagnosis, and cardiac catheterization is usually not necessary. Early diagnosis should be followed by early treatment. The optimal timing for surgical intervention, however, is still not clearly defined [8, 9, 111. Less symptomatic patients should be initially treated medically under close monitoring and later should be considered for an operative treatment to prevent late heart failure. Clinical signs of high venous pressure, hepatic congestion, ascites and oedema coupled with decreasing diuresis constitute the indication for early surgery in traumatic tricuspid insufticiency. The valve can be damaged by rupture of a papillary muscle and/or chordae tendineae which are the most
457
common modes [l 11,or by a torn annulus or cusps [3,8]. The operative treatment consists of reinsertion of the ruptured papillary muscles, as in our case, or of repair with resuture of the leaflet to the annulus and annuloplasty [l, 81. The Hannover group [12] reported an alternative approach to extensive rupture of the chorde tendineae and flail leaflets preserving as much of the free leaflet substance as possible: leaflet resection, suture of the cut edges of the anterior and posterior cusp, and additional annuloplasty restored proper valve function without stenosis. If the valve is not reparable, it should be replaced [6, 7, 111. Bioprostheses are preferable because of their lower thrombogenicity [5, 6, 91. The surgical treatment usually results in complete recovery [l, 5, 8, 111. Acknowledgement.
The authors
gratefully
thank
Mrs. Carol de
Simio for drawing.
References Branderburg RO. MC Goon DC. Campeau L, Gioliani ER (1966) Traumatic rupture of the chordae tendinae of the tricuspid valve. Successful repair twenty-four years later. Am J Cardiol 18:911-915 Bryant LR, Mobin-Uddin K, Dillon ML, Hinshaw MA, Utley JR (1973) Cardiac valve injury with major chest trauma. Arch Surg 107:279-283 Cuadros CL, Hutchinson JE, Mogtader AH (1984) Laceration of a mitral papillary muscle and the aortic root as a result of blunt trauma of the chest. J Thorac Cardiovasc Surg 88: 134140
4. Dodd DA, Johns JA, Graham TP Jr (1987) Transient severe mitral and tricuspid regurgitation following blunt chest trauma. Am Heart J 114:652-654 5. Gayet C, Pierre B, Delahaye JP, Champsaur G, Andre-Fouet X, Rueff P (1987) Traumatic tricuspid insufficiency: an underdiagnosed disease. Chest 921429-432 6. Glock Y, Massabuau P, Puel P (1989) Cardiac damage in nonpenetrating chest injuries: report of 5 cases. J Cardiovasc Surg 30127-33 7. Hilton T, Mezei L. Pearson AC (1990) Delayed rupture of tricuspid papillary muscle following blunt chest trauma. Am Heart J 119:1410-1412 8. Noera G, Sanguinetti M, Pensa P, Biagi B, Cremonesi A, Lodi R, Lessana A, Carbone C (1991) Tricuspid valve incompetence caused by nonpenetrating thoracic trauma. Ann Thorac Surg 51:320-322 9. Quatre JM, Ollivier JP, Aouate JM, Scheuble C, De Bourayne J, Gandjbakhch I, Brion R, Droniou J, Cabrol C (1988) L’insuftisance tricuspide traumatique: 5 observations. Arch Ma1 Coeur 81:325-330 10. Rao G. Garvey J, Gupta M (1977) Atria1 septal defect due to blunt thoracic trauma. J Trauma 17:405-406 11. Shahidnoorai S, Ameli M (1991) Post traumatic tricuspid insufficiency: when to intervene? J Cardiovasc Surg 32:585-588 12. Sutlic Z. Schmid C, Borst HG (1990) Repair of flail anterior leaflets of tricuspid and mitral valves by cusp remodelling. Ann Thorac Surg 50:927-930 Miralem Pasic, MD, ScD Klinik fur Herz- und GefaBchirurgie Universitltsspital Ramistrasse 100 CH-8091 Zurich Switzerland
