Ann Thorac Surg 2006;82:1111-1113
© 2006 The Society of Thoracic Surgeons
Case report
Deep Sternal Wire Infection Resulting in Severe Pulmonary Valve Endocarditis
Sekar S. Bhavani, MS, FRCS,
Worawong Slisatkorn, MD,
Susan J. Rehm, MD,
Gosta B. Pettersson, MD, PhD*
Department of Thoracic and Cardiovascular Surgery, and Infectious Disease, The Cleveland Clinic Foundation, Cleveland, Ohio
Accepted for publication January 11, 2006.
* Address correspondence to Dr Pettersson, Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation/F24, 9500 Euclid Avenue, Cleveland, OH 44195 (Email: petterg{at}ccf.org).
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Abstract
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Right-sided infective endocarditis is uncommon, comprising less than 5% of all cases of endocarditis. This is primarily seen in patients with drug abuse, long-term intravenous catheters, and congenital malformations, or a combination of these. Isolated pulmonary valve endocarditis is difficult to recognize due to its rarity, minimal cardiac manifestations, and predominance of pulmonary infections secondary to embolization of the vegetations. We describe an unusual case of chronic sternal wound infection and migration of an infected braided sternal wire causing right ventricular outflow tract and pulmonary valve endocarditis, which necessitated a complicated reoperation including pulmonary valve replacement with a homograft.
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Introduction
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Deep sternal wound infection after open heart surgery occurs in a small percentage of all cases. Sternal infection associated with erosion of sternal wires into the heart is very uncommon, as is pulmonary valve endocarditis. It is unheard of to have one cause the other.
In 2001, a 73-year-old man underwent coronary artery bypass surgery. His postoperative course was complicated by sternal wound infection and dehiscence. The sternum was rewired and the wound healed after a period of open dressings.
During the fall of 2005 he presented with a 1-year history of increasing shortness of breath and recurrent episodes of fever, leading to treatment for pneumonia on several occasions. However, 2 months prior to his presentation he had an echocardiogram that revealed the presence of vegetations in the right ventricular outflow tract (RVOT) and on the pulmonary valve. Blood cultures were positive for Staphylococcus epidermidis and he was treated with vancomycin for 6 weeks. Transesophageal echocardiogram confirmed large vegetations in the RVOT and on the pulmonary valve with moderately severe pulmonary regurgitation. A chest roentgenogram, computed tomographic scan, and heart catheterization demonstrated the presence of a sternal wire in the right ventricular outflow tract (Fig 1). The sternum itself showed multiple defects consistent with chronic osteitis. The lungs had multiple inflammatory infiltrates and emphysematous changes. The cardiac catheterization revealed a patent left internal mammary artery to the mid anterior descending artery and a sequential saphenous vein graft to first diagonal and first obtuse marginal arteries. The left internal mammary artery crossed the midline and was in proximity to the chest wall. Left ventricular ejection fraction was 60%.
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Fig 1. Computed tomographic scan cut at the level of the pulmonary valve showing the wire inside the lumen and vegetations. The patent internal thoracic artery (ITA) is seen lateral to the pulmonary artery.
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Careful review of the computed tomographic scan of the chest and the catheterization suggested that the chest could be opened in a standard fashion. The braided sternal wire making a loop through the RVOT was divided and pulled out after the sternum was opened. The sternum was found to be infected and was debrided. The right atrium and the aorta were exposed and saphenous vein was harvested. The patient was heparinized and cannulated and total cardiopulmonary bypass was initiated. The left internal thoracic artery was engulfed in an inflammatory mass involving the right ventricular outflow tract and the infected wire and its tract. The inflammatory process was pealed off the chest wall. The left internal thoracic artery was electively divided, the aorta was clamped, and the heart was arrested with antegrade and retrograde cardioplegia. The RVOT was then opened along the wire track and the right ventricular outflow tract, and the destroyed pulmonary valve was debrided (Fig 2). A 30-mm pulmonary homograft was used to reconstruct the RVOT, and proximal to the valve the right ventriculotomy was closed with direct suture. The left anterior descending artery, obtuse marginal 1, were re-grafted using saphenous vein grafts. The patient was weaned off bypass with minimal support. The postoperative course was uneventful. The Gram stain and culture from sternal pus, wire, and vegetations all demonstrated coagulase negative staphylococcus species. The patient was discharged on postoperative day 8, and he was treated with vancomycin for a total of 8 weeks. He was free of infection and doing well 2 months after completion of antibiotic therapy.
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Fig 2. Operative photograph showing the wire traversing the lumen of the right ventricular outflow tract and vegetations in the right ventricular outflow tract and on the pulmonary valve.
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Comment
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In the absence of intravenous drug abuse or a long-term indwelling intravascular catheter, pulmonary valve endocarditis is very rare [1–3]. The clinical manifestations of this disease are often nonspecific, and often patients present with symptoms related to embolization of the vegetations to the lungs. This was true in our patient who was treated for recurrent pneumonias for almost a year.
Pulmonary regurgitation is well tolerated in the absence of pulmonary hypertension and this contributes to a delay in the diagnosis of pulmonary valve endocarditis. Severe pulmonary valve regurgitation although tolerated for a long time is not always benign [4] and late deterioration in right heart hemodynamics after pulmonary valvotomy for infective endocarditis without replacement of the valve has been reported [5].
Indications for surgical management in right-sided endocarditis include failure to cure the infection with antibiotics alone, persistent fever and recurrent pulmonary emboli, or uncontrollable right heart failure. Pulmonary allograft is most commonly used to reconstruct the RVOT and is currently the preferred conduit on the right side of the heart [6, 7].
Disruption of the anterior right ventricular wall early after open heart surgery due to mediastinitis has been described [8], but the erosion or migration of a pliable braided sternal wire into the right ventricular outflow tract leading to severe bacterial endocarditis has never been reported in the literature. The presence of inflammation and adhesions prevented catastrophic bleeding and development of a true pseudoaneurysm in spite of the fact that the wire traversed the lumen of the RVOT in our patient. The migration of the wire could be explained on the basis of the pliability and inherent tendency of the braided wire to assume a spherical shape when it cuts through. Braided wires should probably not be used for sternal closure.
The operation was technically not different from a regular reoperation. We studied the computed tomographic scan and the catheterization carefully and decided that although the RVOT and the internal mammary artery were both close to the chest wall, they were to the left of the sternum making peripheral cannulation unnecessary. It is of course critically important to make these considerations beforehand and have ready plans of action for different scenarios. Radical debridement of all infected tissue including the sternum allowed primary healing of the heart and the sternum.
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References
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Abstract
Introduction
