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Ann Thorac Surg 2001;72:723-724
© 2001 The Society of Thoracic Surgeons
a Department of Thoracic and Cardiovascular Surgery, The Cleveland Clinic Foundation, 9500 Euclid Ave, Desk F25, Cleveland, OH 44195, USA
e-mail: smedirn{at}ccf.org
Sternal wound infections following cardiac surgery have been well defined. Subscribing to the CDC definition of surgical wound infection (SWI) a "deep" infection is characterized by a subfascial location or involving the bone or retrosternal space (mediastinitis). The incidence is generally well below 1% for valve procedures and increases to 1% to 2% for coronary artery bypass grafting. Risk factors are consistent across series and include older age, diabetes, obesity, chronic obstructive pulmonary disease, current smoking, use of bilateral internal thoracic arteries and surgical techniques that traumatize the tissue or interfere with wound healing. Mortality is significant at 10% to 20%.
Heart transplantation SWI rate should be similar to that of a valve procedure. In fact, one could expect an even lower incidence because many of the risk factors for SWI are contraindications to transplantation and the sternum is not acutely devascularized. So on initial reading, the 3.9% superficial SWI and 4.9% deep infection rates reported by Carrier and colleagues appear quite high. However as they point out there is very little information published to compare these rates with. A quick (unconfirmed) review of our transplant database (excluding left ventricular assist device [LVAD] patients) found a 5% SWI rate and a separate database managed by the Infectious Disease Department found a 2% incidence of superficial SWI and a 3.3% deep SWI rate. Not that much different than Carrier’s incidence.
Could it be that different risk factors play a role in SWI after heart transplantation? Malnutrition, cardiac cachexia, chronic low cardiac output state, anemia, prolonged hospitalization on inotropic support through central lines, and infections or colonization with nosocomial flora followed immediately by intense immunosuppression may put these patients at increased infection risk. Unfortunately, very few variables were investigated in this series. Inexplicably, 80% of the SWI occurred in what would appear to be a low risk population of United Network for Organ Sharing status II patients waiting on average only 4 months for transplantation, and, unlike SWI in nontransplant patients, mortality was not significantly increased (although a trend was suggested). This undoubtedly reflects the small numbers affected.
Their management paradigm supports an aggressive diagnostic and therapeutic approach, which I support. Prevention is the best. All nonpermanent central venous lines are replaced at the time of transplant and in LVAD patients the pump pocket and mediastinum are debrided of all necrotic material and copiously irrigated before implanting the heart. If a deep SWI occurs, especially in the patient who has had multiple previous operations and a fixed mediastinum, obliteration of the infected dead space with vascularized tissue is probably the safest approach. Managing the immunosuppression regimen becomes a very delicate balance. Rejection risk is assessed by flow cytometry HLA antibody crossmatch and frequent endomyocardial biopsies. Tacrolimus and mycophenolate mofetil are avoided, as we believe these drugs are more potent immunosuppressives. Steroids are reduced and often eliminated. Mediastinal imaging is used to detect mycotic infection.
Doctor Carrier’s report should encourage us to further define the risk factors, incidence and outcomes of deep SWI after heart transplantation. It may not be as infrequent and inconsequential as we think.
Related Article
Ann. Thorac. Surg. 2001 72: 719-723.
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