CASE REPORTS
Traumatic Mitral Valve Rupture in a Child David McCrory, FRCSI, Brian Craig, MRCP, and Hugh O’Kane, FRCS Department of Surgery, The Queen’s University of Belfast; Royal Belfast Hospital For Sick Children; and Cardiac Surgical Unit, Royal Victoria Hospital, Belfast, Northern Ireland
The case of a 6-year-old boy who ruptured his mitral valve after blunt chest trauma and who subsequently had successful mitral valve replacement with a size 25 St. Jude Medical prosthesis is reported. The diagnosis, investigation, and treatment of traumatic valvar rupture are discussed. (Ann Thorac Surg 1991;51:821-2)
A
6-year-old boy was struck by a car on the left side of his body on August 24, 1987. On admission to the local hospital he was noted to have sustained a fractured right radius and ulna, fractured left femur, and abrasions to the left side of his face and chest. His blood pressure was 90/50 mm Hg and his pulse rate was regular at 170 beats/min; two heart sounds were heard and no murmurs were detected. Respiratory examination was unremarkable. Chest roentgenography was normal and electrocardiography was not carried out. He was taken to the operating theater and the fractures were stabilized. Overnight his blood pressure remained around 90/50 mm Hg. His urinary output was only 30 mL over a 4-hour period. His intravenous fluids were then increased and in total he was given 540 mL of packed cells and 900 mL of a 4% dextrose/O.l8% saline mixture over a 12-hour period. Increasing respiratory difficulties developed despite treatment with diuretics and venesection of 200 mL of blood. His arterial oxygen tension was 4.8 kPa (normal range, 12.0 to 14.7 kPa) on room air and 5.8 kPa with 40% oxygen by face mask. An endotracheal tube was inserted and ventilation commenced. He was transferred to the Royal Belfast Hospital For Sick Children 24 hours after injury. On admission he was noted for the first time to have a harsh systolic murmur maximal at the apex. Chest roentgenography showed increased pulmonary vascularity and an enlarged left ventricle. ST depression in leads 2, V,, V,, and V, was noted on electrocardiography. Serum cardioselective enzyme levels (creatine kinase-MB) were elevated at 169 U/L (normal range, 0 to 35 U/L). Echocardiography confirmed the presence of marked mitral regurgitation with ruptured papillary muscle and good left ventricular function. He was treated conservatively with digoxin and diuretic therapy and was gradually weaned from assisted ventilation. His condition remained stable while he was immobilized and the fractures healed well. As he began mobiAccepted for publication Oct 18, 1990. Address reprint requests to Mr McCrory, Department of Surgery, Institute of Clinical Science, The Queen’s University of Belfast, Grosvenor Rd, Belfast BT12 6BJ Northern Ireland.
0 1991 by
The Society of Thoracic Surgeons
lization he was dyspneic even on mild exertion despite diuretic, digoxin, and vasodilator therapy. In light of this a cardiac operation was performed 12 weeks after injury. At operation the anterolateral papillary muscle was found to be ruptured but was obviously necrotic and beyond repair. The valve was excised and replaced with a size 25 St. Jude Medical prosthesis. He was discharged home 14 days after operation on a regimen of furosemide, spironolactone, digoxin, and warfarin. At his last review in March 1990 he was in excellent health. Diuretics were no longer required and he continues to receive digoxin and warfarin.
Comment Rupture of the heart valves after blunt chest trauma is rare. Isolated valvar rupture most commonly affects the aortic valve, followed by the mitral valve and least commonly the tricuspid valve [l,21. Mitral valve rupture may affect various parts of the valvar mechanism. Rupture occurs when trauma takes place at the beginning of systole. This is when intracardiac pressures are at their highest and the added pressure of chest compression is enough to rupture the valvar apparatus. Papillary muscle rupture is the most usual injury, as was seen in this case (31. Less commonly the chordae tendineae rupture, and least common of all is laceration to the valve cusp [3]. Blunt trauma may result in instant papillary muscle rupture if compression forces are large enough. However, as each papillary muscle is supplied by a long central artery, ischemia may ensue with later infarction and rupture if this artery is damaged [4]. Mitral valve rupture should be suspected after trauma if a systolic murmur is heard in a patient with no previous cardiac history. The blood pressure is often low and the patient may become dyspneic and have pulmonary edema. Signs and symptoms may be misinterpreted. Low blood pressure may be attributed to hypovolemia secondary to other injuries. Dyspnea may be wrongly ascribed to lung contusion, aspiration pneumonia, fat embolism, adult respiratory distress syndrome, or over-hydration. The initial management in this case emphasizes these points. The low blood pressure was originally thought to be due to hypovolemia, and hence he was over-hydrated. This ultimately exacerbated any pulmonary symptoms that were going to develop because of his mitral regurgitation. The respiratory difficulties were then solely attributed to over-hydration and diuretics were given and venesection performed. Diagnosis is aided by chest roentgenography, which often shows pulmonary edema. The left atrium is small, which is typical of recent onset rather than long-standing 0003-4975/91/$3.50
822
Ann Thorac Surg
CASE REPORT McCRORY ET AL TRAUMATIC MITRAL VALVE RUPTURE
mitral regurgitation. A low oxygen tension is found on arterial blood gas analysis. An electrocardiogram should be carried out in all cases of chest trauma. It may show ischemic changes, as was the case with this patient after transfer to the children’s hospital. If an electrocardiogram had been carried out earlier it may have alerted the staff in the original hospital to the possibility of cardiac trauma, thereby preventing the initial mismanagement of this patient’s fluid balance. Even if the electrocardiogram is normal it will act as an accurate base line against which to judge any subsequent recording. Echocardiography is diagnostic in mitral valve rupture. It can identify rupture of the chordae or papillary muscles, valvar prolapse, or flail cusps [5, 61. It is reliable, easily performed, and a noninvasive diagnostic tool. In this case it was relied on completely and cardiac catheterization was not deemed necessary. With mitral valve rupture early diagnosis and treatment is essential as rapid deterioration may occur. There have been cases reported of papillary muscle fibrosis after injury thus allowing an adequate degree of mitral valve competence to remain [4]. It was decided for this reason to attempt to treat this child conservatively. Conservative management was possible while he was immobilized to allow his fractures to heal and he remained completely asymptomatic. This accounted for the bulk of the 12-week period before operation. Only when mobilization was commenced did he suffer persistent dyspnea, and mitral valve replacement was then performed. Mitral valve re-
1991;51:821-2
construction was not possible because of the marked necrosis in the papillary muscle. In children of this age we recommend that conservative management should be the first line of treatment, clinical status permitting. When operation is undertaken repair of the valvar apparatus should be attempted where possible and prosthetic replacement used only as a last resort. Successful repair avoids the obvious hazards of prosthetic replacement such as thrombosis, long-term anticoagulation, and endocarditis. Repair is particularly important in children as the valve ring may only allow the insertion of a small prosthesis, which may not be functionally large enough to cope with later growth.
References 1. Rumisek JD, Robinowitz M, Virmani R, Barry MJ, Steudel T. Bioprosthetic heart valve rupture associated with trauma. J Trauma 1986;26:276-9. 2. Flejou Y, Roland E, Ecoiffier J. The place of angiography in the evaluation of traumatic injuries to the heart and coronary arteries. Cardiovasc Radio1 1979;2:47-50. 3. Scorretti C. Traumatic rupture of the anterior papillary muscle. Z Rechtsmed 1983;91:153-7. 4. Devineni R, McKenzie FN. Acute mitral insufficiency resulting from blunt chest trauma. J Thorac Cardiovasc Surg 1983;85: 7974. 5. Miller SW, Deluca SA. Ruptured chordae tendineae. Am Fam Physician 1984;30:1256. 6. Mintz GS, Kotler MN, Segal BL, Parry WR. Two-dimensional echocardiographic recognition of ruptured chordae tendineae. Circulation 1978;5724450.
Traumatic Mitral Valve Rupture in a Child David McCrory, FRCSI, Brian Craig, MRCP, and Hugh O’Kane, FRCS Department of Surgery, The Queen’s University of Belfast; Royal Belfast Hospital For Sick Children; and Cardiac Surgical Unit, Royal Victoria Hospital, Belfast, Northern Ireland
The case of a 6-year-old boy who ruptured his mitral valve after blunt chest trauma and who subsequently had successful mitral valve replacement with a size 25 St. Jude Medical prosthesis is reported. The diagnosis, investigation, and treatment of traumatic valvar rupture are discussed. (Ann Thorac Surg 1991;51:821-2)
A
6-year-old boy was struck by a car on the left side of his body on August 24, 1987. On admission to the local hospital he was noted to have sustained a fractured right radius and ulna, fractured left femur, and abrasions to the left side of his face and chest. His blood pressure was 90/50 mm Hg and his pulse rate was regular at 170 beats/min; two heart sounds were heard and no murmurs were detected. Respiratory examination was unremarkable. Chest roentgenography was normal and electrocardiography was not carried out. He was taken to the operating theater and the fractures were stabilized. Overnight his blood pressure remained around 90/50 mm Hg. His urinary output was only 30 mL over a 4-hour period. His intravenous fluids were then increased and in total he was given 540 mL of packed cells and 900 mL of a 4% dextrose/O.l8% saline mixture over a 12-hour period. Increasing respiratory difficulties developed despite treatment with diuretics and venesection of 200 mL of blood. His arterial oxygen tension was 4.8 kPa (normal range, 12.0 to 14.7 kPa) on room air and 5.8 kPa with 40% oxygen by face mask. An endotracheal tube was inserted and ventilation commenced. He was transferred to the Royal Belfast Hospital For Sick Children 24 hours after injury. On admission he was noted for the first time to have a harsh systolic murmur maximal at the apex. Chest roentgenography showed increased pulmonary vascularity and an enlarged left ventricle. ST depression in leads 2, V,, V,, and V, was noted on electrocardiography. Serum cardioselective enzyme levels (creatine kinase-MB) were elevated at 169 U/L (normal range, 0 to 35 U/L). Echocardiography confirmed the presence of marked mitral regurgitation with ruptured papillary muscle and good left ventricular function. He was treated conservatively with digoxin and diuretic therapy and was gradually weaned from assisted ventilation. His condition remained stable while he was immobilized and the fractures healed well. As he began mobiAccepted for publication Oct 18, 1990. Address reprint requests to Mr McCrory, Department of Surgery, Institute of Clinical Science, The Queen’s University of Belfast, Grosvenor Rd, Belfast BT12 6BJ Northern Ireland.
0 1991 by
The Society of Thoracic Surgeons
lization he was dyspneic even on mild exertion despite diuretic, digoxin, and vasodilator therapy. In light of this a cardiac operation was performed 12 weeks after injury. At operation the anterolateral papillary muscle was found to be ruptured but was obviously necrotic and beyond repair. The valve was excised and replaced with a size 25 St. Jude Medical prosthesis. He was discharged home 14 days after operation on a regimen of furosemide, spironolactone, digoxin, and warfarin. At his last review in March 1990 he was in excellent health. Diuretics were no longer required and he continues to receive digoxin and warfarin.
Comment Rupture of the heart valves after blunt chest trauma is rare. Isolated valvar rupture most commonly affects the aortic valve, followed by the mitral valve and least commonly the tricuspid valve [l,21. Mitral valve rupture may affect various parts of the valvar mechanism. Rupture occurs when trauma takes place at the beginning of systole. This is when intracardiac pressures are at their highest and the added pressure of chest compression is enough to rupture the valvar apparatus. Papillary muscle rupture is the most usual injury, as was seen in this case (31. Less commonly the chordae tendineae rupture, and least common of all is laceration to the valve cusp [3]. Blunt trauma may result in instant papillary muscle rupture if compression forces are large enough. However, as each papillary muscle is supplied by a long central artery, ischemia may ensue with later infarction and rupture if this artery is damaged [4]. Mitral valve rupture should be suspected after trauma if a systolic murmur is heard in a patient with no previous cardiac history. The blood pressure is often low and the patient may become dyspneic and have pulmonary edema. Signs and symptoms may be misinterpreted. Low blood pressure may be attributed to hypovolemia secondary to other injuries. Dyspnea may be wrongly ascribed to lung contusion, aspiration pneumonia, fat embolism, adult respiratory distress syndrome, or over-hydration. The initial management in this case emphasizes these points. The low blood pressure was originally thought to be due to hypovolemia, and hence he was over-hydrated. This ultimately exacerbated any pulmonary symptoms that were going to develop because of his mitral regurgitation. The respiratory difficulties were then solely attributed to over-hydration and diuretics were given and venesection performed. Diagnosis is aided by chest roentgenography, which often shows pulmonary edema. The left atrium is small, which is typical of recent onset rather than long-standing 0003-4975/91/$3.50
822
Ann Thorac Surg
CASE REPORT McCRORY ET AL TRAUMATIC MITRAL VALVE RUPTURE
mitral regurgitation. A low oxygen tension is found on arterial blood gas analysis. An electrocardiogram should be carried out in all cases of chest trauma. It may show ischemic changes, as was the case with this patient after transfer to the children’s hospital. If an electrocardiogram had been carried out earlier it may have alerted the staff in the original hospital to the possibility of cardiac trauma, thereby preventing the initial mismanagement of this patient’s fluid balance. Even if the electrocardiogram is normal it will act as an accurate base line against which to judge any subsequent recording. Echocardiography is diagnostic in mitral valve rupture. It can identify rupture of the chordae or papillary muscles, valvar prolapse, or flail cusps [5, 61. It is reliable, easily performed, and a noninvasive diagnostic tool. In this case it was relied on completely and cardiac catheterization was not deemed necessary. With mitral valve rupture early diagnosis and treatment is essential as rapid deterioration may occur. There have been cases reported of papillary muscle fibrosis after injury thus allowing an adequate degree of mitral valve competence to remain [4]. It was decided for this reason to attempt to treat this child conservatively. Conservative management was possible while he was immobilized to allow his fractures to heal and he remained completely asymptomatic. This accounted for the bulk of the 12-week period before operation. Only when mobilization was commenced did he suffer persistent dyspnea, and mitral valve replacement was then performed. Mitral valve re-
1991;51:821-2
construction was not possible because of the marked necrosis in the papillary muscle. In children of this age we recommend that conservative management should be the first line of treatment, clinical status permitting. When operation is undertaken repair of the valvar apparatus should be attempted where possible and prosthetic replacement used only as a last resort. Successful repair avoids the obvious hazards of prosthetic replacement such as thrombosis, long-term anticoagulation, and endocarditis. Repair is particularly important in children as the valve ring may only allow the insertion of a small prosthesis, which may not be functionally large enough to cope with later growth.
References 1. Rumisek JD, Robinowitz M, Virmani R, Barry MJ, Steudel T. Bioprosthetic heart valve rupture associated with trauma. J Trauma 1986;26:276-9. 2. Flejou Y, Roland E, Ecoiffier J. The place of angiography in the evaluation of traumatic injuries to the heart and coronary arteries. Cardiovasc Radio1 1979;2:47-50. 3. Scorretti C. Traumatic rupture of the anterior papillary muscle. Z Rechtsmed 1983;91:153-7. 4. Devineni R, McKenzie FN. Acute mitral insufficiency resulting from blunt chest trauma. J Thorac Cardiovasc Surg 1983;85: 7974. 5. Miller SW, Deluca SA. Ruptured chordae tendineae. Am Fam Physician 1984;30:1256. 6. Mintz GS, Kotler MN, Segal BL, Parry WR. Two-dimensional echocardiographic recognition of ruptured chordae tendineae. Circulation 1978;5724450.
