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Subacute Tricuspid Regurgitation With Severe Hypoxemia Complicating Blunt Chest Trauma
7 8 9 10 ll
rial supply to the basal segments of the lung presenting with a murmur. Eur J Pediatr 1979; 131:125-31 Kirk DR, Kane PE, Free EA, et al. Systemic arterial supply to normal basilar segments of the left lower lobe. AJR 1976; 126:817-21 F ilsak MF: . Chanclrasekar AJ, Marsan RE. et al. Systemic arterialization of lung without sequestration. AJR 1982; 138:751-53 Campbell DC, Mumey JA, Dominy DE. Systemic arterial blood supply to a normal lung. JAMA 1962; 182:497-99 Painter RL, Billig DM, Epstein I. Anomalous systemic arterialization of the lung without sequestration. N Eng! J Med 1968; 279:866-67 Hessel EA, Boyden EA, Stamm SJ, et al. High systemic origin of the sole artery to the basal segments of the left lung: findings, surgical treatment, and embryologic interpretation. Surgery 1970; 67:624-32
Subacute Tricuspid Regurgitation With Severe Hypoxemia Complicating Blunt Chest Trauma* Flavio Ribichini, MD; Riccardo Conte, MD; Antonio Lioi, MD; Antonio Dellavalle, MD; and Giovanni Ugliengo, MD
A case is reported on subacute tricuspid regurgitation due to rupture of papillary muscles, with right-to-left shunting, in the absence of extracardiac lesions after blunt chest trauma. (CHEST 1996; 109:289-91)
TR=tricuspid regurgitation; R-L=right-to-left; PFO= patent foramen ovale
Key words: subacute papillary muscle rupture; traumatic heart injury; tricuspid regurgitation
C
ardiac injury after blunt chest trauma was well studied in the 1950s, and the diagnosis and treatment of rupture of the ventricular walls and interventricular septum have been d escribe d. 1 Severe hypoxemia is observed commonly after blunt chest trauma and usually is the result of lung damage and intrapulmonary shunting. 2 Traumatic tricuspid regurgitation (TR) with intracardiac right-to-left (R-L) shunting also has been reported as a rare finding-3·4 ; in all cases TR was accompanied by severe bony or visceral lesions, and R-L shunting was explained by e levated right atrial pressure s in the prese nce of a patent foramen ovale (PFO). A case ofTR with R-L shunt in the absence of extracardiac lesions and with no e levation of mean right atrial pressure is described. CASE REPORT
A 43-year-old man was admitted to th e hospital after a severe *From the Divisione di Cardiologia, Ospedale Santa Croce, Cuneo, Italy (Drs. Ribichini, Dellavalle, and Ugliengo); Divisione di Medicina, Ospedale di Fossano (Dr. Conte); DiVJsione di Cardiochirurgia, Ospedale San Martino, Genova, Italy (Dr. Lioi). Reprint requests: Dr. Ribichini, Laboratorio Emodinamica, Ospednle Santa Croce, via M. Coppino 26, 12100 Cuneo, Italy
FIGUHE l. Right ventriculogram in the posteroanterior projection. Prompt opacification of the feft atrium is observed. LA= left atrium; PA=pulmonary artery; RA=right atrium; RV=right ventricle.
vehicle accident in which he was squeezed against the steering wheel. He complained oflow-grade pain in the anterior area of the chest. He was in no distress, his arterial blood pressure was 110/60 mm Hg, with a pulse of 85 beats per minute and a respiratory rate of 20 breaths per minute. A grade 1/6 systolic murmur was audible at the apex. The rest of the physical examination disclosed no abnormalities. A chest x-ray film was normal. The ECG showed rotation of the electrical axis to the right, with poor R-wave progression in the precordial leads and ST-T segment changes of uncertain significance. No previous ECG was available for comparison. Two days later, neither physical examination findings nor the ECG showed changes. The patient felt very well and decided to leave the hospital against medical advice. He was admitted 10 days later due to increasingly severe shortness of breath and fatigue after a week of we ll-being. Examination revealed tachypnea, acrocyanosis, and a grade 2-3 systolic murmur at the apex. The ECG was unchanged, as was the chest x-ray film. Blood chemistry values were normal. Arterial blood gas value analysis revealed hypocapnic hypoxemia (PaOz, 48 mm Hg; PaC02, 16 mm Hg) with the patient breathing
Table l - Right and Left Heart Catheterization Data* Part of Heart
Pressure (mm Hg), Systolic/Diastolic, Mean
IVC
svc
High RA RA LowRA RV PA PCW Ao LV Body surface area Pulmonary flow Systemic flow R-L shunt Qp/Qs
6/5;
3
20/0; 5 19/5; 7 6/3; 3 125/95; 109 131/0-12 1.99 m2 2.9 Umin 6.8 Umin 3.9 Umin
Oxygen Saturation, %
63 56 60 63 65 56 53
80 81
1:2.34
*Abbreviations: Ao=aorta; IVC=inferior vena cava; LV=left ventricle; PA=pulmonary artery; PCW=pulmonary wedge pressure; RA=right atrium; RV=right ventricle; SVC=superior vena cava; Qp=pulmonary flow; Qs=systemic flow.
CHEST I 109 I 1 I JANUARY, 1996
289
FIGURE 2. Cardiac surgical repair: the tom edge of the papillary muscle is visible (arrow).
room air. An echocardiogram showed minimal pericardia! effusion, a moderately enlarged right ventricle, and moderate TR. A thoracic CT scan was nonnal. Spirometry tests and a perfusion lung scan also showed no abnormalities. The patient was referred for cardiac catheterization, which showed (Table 1) normal right and left heart pressures with a R-L shunt of 3.9 Umin. Arterial oxygen saturation was 80%, with an PaOz of 46 mm Hg, rising to only 54 mm Hg after 10 min at Flo2 of 1. Hight ventriculography showed massive TR with rapid opacification of both atria (Fig 1). Transesophageal echocardiography confirmed the presence of severe TR due to papillary muscle rupture. Doppler color mapping also showed aberrant flow directed to the left atrium through a PFO. At surgery, the bases of two papillary muscles of the anterior leaflet were tom (Fig 2). The tricuspid valve was replaced with a Sorin 31 bioprosthesis, and the PFO was sutured. The patient was discharged on postoperative day 10, and returned to work after 1 month. Heremained asymptomatic at the time of follow-up 6 months after surgery. CONCLUSION
Injury of right heart structures is often well tolerated and the onset of distress may be delayed after chest trauma. 5 In our patient, mild TR probably was already present at first admission after the trauma and was worsened by complete rupture of the papillary muscles when this young man resumed his work as a mason with intense isometric efforts. R-L shunting through the PFO may have appeared at this time. The Doppler color study suggests that it was the result of opening of the foramen by the stream of the regurgitant jet, which entered almost selectively the left atrium by this route. This is consistent with the finding of normal right atrial pressures; low pulmonary pressures were explained in this 290
case by reduction of pulmonary flow due to R-L shunting. In fact, R-L shunting may be observed in patients with congenital atrial septal defect and TR even without reversal of the normal pressure gradient between the left and right atrium.6 This same mechanism also has been described in subsets of patients with PFO and TR from other causes 7 and may occur during normal respiration or during the Valsalva maneuver in about 18% of healthy individuals. 8 Subacute TR due to delayed rupture of papillary muscles with severe R-L shunting and no elevation of right atrial pressure, in the absence of extracardiac lesions after blunt chest trauma, is an unusual presentation. To our knowledge, it has not been reported thus far. REFEHENCES
1 Mattox KL, Feliciano DV, Burch J, et al. Five thousand seven hundred sixty cardiovascular injuries in 4,459 patients: epidemiologic evolution 1958 to 1987. Ann Surg 1989; 209:698-705 2 Ashbaugh D. Chest trauma: analysis of 685 patients. Arch Surg 1973; 65:165-70 3 Bardy GH, Talano JV, Meyers S, et al. Acquired cyanotic heart disease secondary to traumatic tricuspid regurgitation: case report and review of the literature. Am J Cardiol1979; 44:1401-06 4 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 5 Hilton T, Mezei L, Pearson AC. Delayed rupture of tricuspid papillary muscle following blunt chest trauma. Am Heart J 1990; 119:1410-12 6 Kai H, Koyanagi S, Hirooka Y, et al. Right-to-left shunt across atrial septal defect related to tricuspid regurgitation: assessment Selected Reports
by transesophageal Doppler echocardiography. Am Heart J 1994; 127:578-84 7 Langholz D, Louie EK, Konstadt SN, et a!. Transesophageal echocardiographic demonstration of distinct mechanism for right-to-left shunting across a patent foramen ovale in the absence
of pulmonary hypertension. JAm Coll Cardiol1991; 18:1112-17 8 Lynch JJ, Schuchard GH, Gross CM, eta!. Prevalence of rightto-left atrial shunting in a healthy population: detection by Valsalva maneuver contrast echocardiography. Am J Cardiol 1984; 53: 1478-80
CHEST I 109 I 1 I JANUARY, 1996
291
rial supply to the basal segments of the lung presenting with a murmur. Eur J Pediatr 1979; 131:125-31 Kirk DR, Kane PE, Free EA, et al. Systemic arterial supply to normal basilar segments of the left lower lobe. AJR 1976; 126:817-21 F ilsak MF: . Chanclrasekar AJ, Marsan RE. et al. Systemic arterialization of lung without sequestration. AJR 1982; 138:751-53 Campbell DC, Mumey JA, Dominy DE. Systemic arterial blood supply to a normal lung. JAMA 1962; 182:497-99 Painter RL, Billig DM, Epstein I. Anomalous systemic arterialization of the lung without sequestration. N Eng! J Med 1968; 279:866-67 Hessel EA, Boyden EA, Stamm SJ, et al. High systemic origin of the sole artery to the basal segments of the left lung: findings, surgical treatment, and embryologic interpretation. Surgery 1970; 67:624-32
Subacute Tricuspid Regurgitation With Severe Hypoxemia Complicating Blunt Chest Trauma* Flavio Ribichini, MD; Riccardo Conte, MD; Antonio Lioi, MD; Antonio Dellavalle, MD; and Giovanni Ugliengo, MD
A case is reported on subacute tricuspid regurgitation due to rupture of papillary muscles, with right-to-left shunting, in the absence of extracardiac lesions after blunt chest trauma. (CHEST 1996; 109:289-91)
TR=tricuspid regurgitation; R-L=right-to-left; PFO= patent foramen ovale
Key words: subacute papillary muscle rupture; traumatic heart injury; tricuspid regurgitation
C
ardiac injury after blunt chest trauma was well studied in the 1950s, and the diagnosis and treatment of rupture of the ventricular walls and interventricular septum have been d escribe d. 1 Severe hypoxemia is observed commonly after blunt chest trauma and usually is the result of lung damage and intrapulmonary shunting. 2 Traumatic tricuspid regurgitation (TR) with intracardiac right-to-left (R-L) shunting also has been reported as a rare finding-3·4 ; in all cases TR was accompanied by severe bony or visceral lesions, and R-L shunting was explained by e levated right atrial pressure s in the prese nce of a patent foramen ovale (PFO). A case ofTR with R-L shunt in the absence of extracardiac lesions and with no e levation of mean right atrial pressure is described. CASE REPORT
A 43-year-old man was admitted to th e hospital after a severe *From the Divisione di Cardiologia, Ospedale Santa Croce, Cuneo, Italy (Drs. Ribichini, Dellavalle, and Ugliengo); Divisione di Medicina, Ospedale di Fossano (Dr. Conte); DiVJsione di Cardiochirurgia, Ospedale San Martino, Genova, Italy (Dr. Lioi). Reprint requests: Dr. Ribichini, Laboratorio Emodinamica, Ospednle Santa Croce, via M. Coppino 26, 12100 Cuneo, Italy
FIGUHE l. Right ventriculogram in the posteroanterior projection. Prompt opacification of the feft atrium is observed. LA= left atrium; PA=pulmonary artery; RA=right atrium; RV=right ventricle.
vehicle accident in which he was squeezed against the steering wheel. He complained oflow-grade pain in the anterior area of the chest. He was in no distress, his arterial blood pressure was 110/60 mm Hg, with a pulse of 85 beats per minute and a respiratory rate of 20 breaths per minute. A grade 1/6 systolic murmur was audible at the apex. The rest of the physical examination disclosed no abnormalities. A chest x-ray film was normal. The ECG showed rotation of the electrical axis to the right, with poor R-wave progression in the precordial leads and ST-T segment changes of uncertain significance. No previous ECG was available for comparison. Two days later, neither physical examination findings nor the ECG showed changes. The patient felt very well and decided to leave the hospital against medical advice. He was admitted 10 days later due to increasingly severe shortness of breath and fatigue after a week of we ll-being. Examination revealed tachypnea, acrocyanosis, and a grade 2-3 systolic murmur at the apex. The ECG was unchanged, as was the chest x-ray film. Blood chemistry values were normal. Arterial blood gas value analysis revealed hypocapnic hypoxemia (PaOz, 48 mm Hg; PaC02, 16 mm Hg) with the patient breathing
Table l - Right and Left Heart Catheterization Data* Part of Heart
Pressure (mm Hg), Systolic/Diastolic, Mean
IVC
svc
High RA RA LowRA RV PA PCW Ao LV Body surface area Pulmonary flow Systemic flow R-L shunt Qp/Qs
6/5;
3
20/0; 5 19/5; 7 6/3; 3 125/95; 109 131/0-12 1.99 m2 2.9 Umin 6.8 Umin 3.9 Umin
Oxygen Saturation, %
63 56 60 63 65 56 53
80 81
1:2.34
*Abbreviations: Ao=aorta; IVC=inferior vena cava; LV=left ventricle; PA=pulmonary artery; PCW=pulmonary wedge pressure; RA=right atrium; RV=right ventricle; SVC=superior vena cava; Qp=pulmonary flow; Qs=systemic flow.
CHEST I 109 I 1 I JANUARY, 1996
289
FIGURE 2. Cardiac surgical repair: the tom edge of the papillary muscle is visible (arrow).
room air. An echocardiogram showed minimal pericardia! effusion, a moderately enlarged right ventricle, and moderate TR. A thoracic CT scan was nonnal. Spirometry tests and a perfusion lung scan also showed no abnormalities. The patient was referred for cardiac catheterization, which showed (Table 1) normal right and left heart pressures with a R-L shunt of 3.9 Umin. Arterial oxygen saturation was 80%, with an PaOz of 46 mm Hg, rising to only 54 mm Hg after 10 min at Flo2 of 1. Hight ventriculography showed massive TR with rapid opacification of both atria (Fig 1). Transesophageal echocardiography confirmed the presence of severe TR due to papillary muscle rupture. Doppler color mapping also showed aberrant flow directed to the left atrium through a PFO. At surgery, the bases of two papillary muscles of the anterior leaflet were tom (Fig 2). The tricuspid valve was replaced with a Sorin 31 bioprosthesis, and the PFO was sutured. The patient was discharged on postoperative day 10, and returned to work after 1 month. Heremained asymptomatic at the time of follow-up 6 months after surgery. CONCLUSION
Injury of right heart structures is often well tolerated and the onset of distress may be delayed after chest trauma. 5 In our patient, mild TR probably was already present at first admission after the trauma and was worsened by complete rupture of the papillary muscles when this young man resumed his work as a mason with intense isometric efforts. R-L shunting through the PFO may have appeared at this time. The Doppler color study suggests that it was the result of opening of the foramen by the stream of the regurgitant jet, which entered almost selectively the left atrium by this route. This is consistent with the finding of normal right atrial pressures; low pulmonary pressures were explained in this 290
case by reduction of pulmonary flow due to R-L shunting. In fact, R-L shunting may be observed in patients with congenital atrial septal defect and TR even without reversal of the normal pressure gradient between the left and right atrium.6 This same mechanism also has been described in subsets of patients with PFO and TR from other causes 7 and may occur during normal respiration or during the Valsalva maneuver in about 18% of healthy individuals. 8 Subacute TR due to delayed rupture of papillary muscles with severe R-L shunting and no elevation of right atrial pressure, in the absence of extracardiac lesions after blunt chest trauma, is an unusual presentation. To our knowledge, it has not been reported thus far. REFEHENCES
1 Mattox KL, Feliciano DV, Burch J, et al. Five thousand seven hundred sixty cardiovascular injuries in 4,459 patients: epidemiologic evolution 1958 to 1987. Ann Surg 1989; 209:698-705 2 Ashbaugh D. Chest trauma: analysis of 685 patients. Arch Surg 1973; 65:165-70 3 Bardy GH, Talano JV, Meyers S, et al. Acquired cyanotic heart disease secondary to traumatic tricuspid regurgitation: case report and review of the literature. Am J Cardiol1979; 44:1401-06 4 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 5 Hilton T, Mezei L, Pearson AC. Delayed rupture of tricuspid papillary muscle following blunt chest trauma. Am Heart J 1990; 119:1410-12 6 Kai H, Koyanagi S, Hirooka Y, et al. Right-to-left shunt across atrial septal defect related to tricuspid regurgitation: assessment Selected Reports
by transesophageal Doppler echocardiography. Am Heart J 1994; 127:578-84 7 Langholz D, Louie EK, Konstadt SN, et a!. Transesophageal echocardiographic demonstration of distinct mechanism for right-to-left shunting across a patent foramen ovale in the absence
of pulmonary hypertension. JAm Coll Cardiol1991; 18:1112-17 8 Lynch JJ, Schuchard GH, Gross CM, eta!. Prevalence of rightto-left atrial shunting in a healthy population: detection by Valsalva maneuver contrast echocardiography. Am J Cardiol 1984; 53: 1478-80
CHEST I 109 I 1 I JANUARY, 1996
291