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Eur J Cardiothorac Surg 2002;21:825-830
© 2002 Elsevier Science NL
a Department of Infectious Diseases, Karolinska Hospital, Stockholm, Sweden
b Department of Thoracic Surgery, Karolinska Hospital, Stockholm, Sweden
Received 24 August 2001; received in revised form 27 January 2002; accepted 31 January 2002.
* Corresponding author. Tel.: +46-8-5177-0000; fax: +46-8-5177-1885
e-mail: bengt.gardlund{at}ks.se
| Abstract |
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Key Words: Cardiac surgery Mediastinitis Postoperative complications Surgical wound infection Staphylococcus
| 1. Introduction |
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| 2. Materials and methods |
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Patients who developed postoperative mediastinitis were identified in a prospective surveillance program. The final diagnosis of mediastinitis was based on positive bacterial cultures from the mediastinal space and/or obvious clinical signs of mediastinitis on reexploration, and/or positive cultures from pericardial effusions according to the Centers for Disease Control and Prevention (CDC) definitions of surgical site infections [9]. In addition, one patient who presented with mediastinitis 38 days after operation was included although the CDC definition limits the time from operation to first signs of infection to 30 days. The clinical data were retrospectively collected from the hospital records.
2.1. Statistical analysis
Data were analyzed using Statistica for Windows from StatSoft Inc. Statistical analyses of categorical data were done using Pearson Chi-square test. For continuous variables, significance testing was done using the MannWhitney U-test unless the variable was normally distributed when the t-test for independent samples was used. For correlation analyses, the Spearman Rank Order Correlation was used. Two-sided analyses were done throughout. P-values are given as exact values except for values <0.001 and >0.20.
| 3. Results |
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Length of operation, time on cardiopulmonary bypass, age, diabetes, type of operation or the time span from operation until signs of infection was not associated with a special bacterial etiology. In contrast, high body mass index was associated with coagulase negative staphylococci (mean body mass index 30.1 in coagulase negative staphylococcal etiology vs. 26.7 for other bacteria, P<0.001) and with sternal dehiscence (mean body mass index 29.2 in patients with sternal dehiscence vs. 26.9 in patients with stable sternum, P=0.008). Chronic obstructive pulmonary disease was also associated with sternal dehiscence (29% of patients with sternal dehiscence had chronic obstructive pulmonary disease vs. 3% of patients with stable sternum, P<0.001) and with coagulase negative staphylococci (19/54, 30% of patients with coagulase negative staphylococcal etiology had chronic obstructive pulmonary disease vs. 9/64, 14% in patients with other bacterial etiology, P=0.04). Body mass index was lower with higher age (R=-0.34, P<0.001). Patients who had been reoperated before onset of mediastinitis tended to have an increased risk for a gram-negative etiology (32 vs. 15% in patients not reoperated, P=0.06). Coagulase negative staphylococcal mediastinitis was more often associated with little or no clinical signs of mediastinitis before reoperation (20/54, 37%) than mediastinitis caused by other bacteria (6/64, 9%, P<0.001). Despite less clinical symptoms, the time from operation until signs of infection appeared was not significantly longer in patients with mediastinitis caused by coagulase negative staphylococci than in mediastinitis of other etiology (Table 2). Bacteriemia with coagulase negative staphylococci was unusual (7%), despite aggressive invasive tissue infection. In contrast, about two-thirds of the patients with S. aureus and about half of those with gram-negative mediastinitis had bacteriemia.
3.5. Mortality
The 90-day all cause mortality in patients with mediastinitis was 19%. No specific bacterial etiology was associated with increased mortality (Table 2) nor was presence of bacteriemia. Mortality was associated with higher age (median age 72.8 years vs. 66.5 years in survivors, P=0.008), need for reoperation before mediastinitis (39% mortality in reoperated patient vs. 15% in non-reoperated, p=0.007), and a long-lasting primary operation (254 vs. 210 min in survivors, P=0.01).
| 4. Discussion |
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Reoperation, mainly as acute reoperations due to bleeding, has been recognized as a risk factor for mediastinitis in some studies [2,4,6,7,15], but not in others [8,1618]. We observed that reoperations were preceded by unusually long and complicated primary operations. The observed increase in mortality in these patients is most likely associated with the surgical problems encountered. No specific bacterial etiology of mediastinitis carried a higher mortality risk, which may appear surprising considering the aggressive and septic nature of many S. aureus and gram negative infections as compared to infections caused by coagulase negatives. In our study, factors related to the surgical procedure and patient-related factors like age were more critical for survival than the bacterial etiology.
In the present investigation, coagulase negative staphylococcus was the most common pathogen, accounting for almost half of the cases of postoperative mediastinitis. Coagulase negative staphylococci have previously been regarded as fairly benign bacteria, rarely causing serious infections except for in connection with implanted prostheses and other foreign material. However, in cardiac surgery, this bacterium has emerged as a major pathogen carrying a substantial mortality, not different from the mortality of mediastinitis caused by other more virulent pathogens. The clinical presentation of mediastinitis caused by coagulase negative staphylococci was far less fulminant than other pathogens with little or no signs of systemic infection in many of the patients. These observations confirm the results from other studies [19,20].
Mediastinitis caused by coagulase negative staphylococci was more often associated with sternal instability than other bacterial etiology. Sternal instability itself is strongly associated with mediastinitis [2,7,8,19,21,22] and it is likely that mediastinitis often develop from a minor skin or subcutaneous infection in the sternal wound and that the infection may spread inwards to the mediastinal space if sternal dehiscence breaks the mechanical barrier between the presternal tissue and the mediastinum. A presternal wound infection with coagulase negative staphylococci would otherwise be expected to be benign and self-contained and not to pose a clinical problem.
S. aureus is another major pathogen in mediastinitis [2,5,7,2022] which unlike coagulase negative staphylococci is not associated with sternal dehiscence or obesity. Obesity has otherwise consistently been identified as a major risk factor for mediastinitis, except for a few studies in which S. aureus was the predominant pathogen [1,17]. S. aureus mediastinitis has particularly been associated with carriage of S. aureus in the nose of the patient [17,23] or with the presence of a specific surgeon who is a carrier and disseminator of S. aureus in the operating theater [1]. The accumulated data suggest that S. aureus mediastinitis is due to peroperative contamination and that postoperative infection may occur regardless of sternal instability.
The third major group of bacteria identified in postoperative mediastinitis are aerobic gram negative rods. The typical pathogenic mechanisms could be entirely different from that of the staphylococci. Peroperative contamination of the sternal wound with gram-negatives appears unlikely considering the known bacterial flora in the chest region and that the isolation of gram-negative bacteria from air in the operating theater or from the wound after a long operation is rare [24]. The use of a vein graft harvested from a contaminated donor site in the groin or leg in coronary by-pass surgery could be a way of introducing gram-negative bacteria in the sternal wound. However, coronary artery bypass grafting did not carry an increased risk for gram-negative mediastinitis either in this or in previously published studies [19,22], or in bypass surgery with vein grafts compared to other bypass conduits [25]. Instead, gram-negative mediastinitis has been shown to be associated with concomitant infections, mainly pneumonia, with gram-negative bacteria in the immediate postoperative period and is typically associated with a more complicated postoperative course with prolonged mechanical ventilation, which increases the risk for nosocomial infections with gram-negatives [1,21,22,25]. Furthermore, outbreaks or accumulation of mediastinitis caused by specific gram-negatives like Pseudomonas or Serratia may suggest that nosocomial spread of gram-negative infections in the postoperative period is important for the development of gram-negative mediastinitis [7,12,15].
In conclusion, we propose that three basically different types of postoperative mediastinitis can be distinguished: (1) mediastinitis associated with obesity and sternal dehiscence, sometimes also with chronic obstructive pulmonary disease, and often caused by coagulase negative staphylococci; (2) mediastinitis following peroperative contamination of the mediastinal space often caused by S. aureus, and (3) mediastinitis caused by spread from concomitant infections in other sites than the mediastinum in the postoperative period, often caused by gram negative rods. This classification is of course not strict, but may be helpful in understanding the discrepancies and sometimes contradictory results from studies on risk factors in postoperative mediastinitis.
The classification of postoperative mediastinitis into the three major groups with partly different pathogenic mechanisms may also be useful in designing infection control programs. If gram-negative mediastinitis is a major problem in the institution, strict enforcing of hygienic barrier routines to reduce the spread of nosocomial infections in the postoperative ward seems most important. If S. aureus mediastinitis were a major problem, investigations aimed at identifying and eradicating sources of bacteria in individuals in the operating theater and to make sure the antibiotic prophylaxis is administered in a timely fashion would seem more appropriate. In addition, routines for hair removal, skin preparation and also the hygienic and ventilation standard of the operating rooms should be scrutinized. In mediastinitis caused by coagulase negative staphylococci, appropriate preventive measures are not as evident. Careful median sternotomy is vital to reduce the risk for subsequent sternal dehiscence [26]. Use of bilateral internal mammary arteries in coronary surgery may cause sternal ischemia and subsequent delayed sternal healing, especially in diabetics [4,8,16,25] who already suffer from impaired wound and bone healing. In such patients, the number of wires should be increased or alternative, stronger techniques of fixation should be considered. In addition, coughing and symptoms of chronic obstructive pulmonary disease in the postoperative period should be aggressively alleviated to relieve the sternal fixation from excessive strain.
| Acknowledgments |
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| Footnotes |
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| References |
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rdlund B. Fewer reoperations and shorter stay in the cardiac surgical ward when stabilising the sternum with the Ley prosthesis in postoperative mediastinitis. Eur J Cardiothorac Surg 2001;20:133-139.
rdlund B. Mediastinitis after cardiovascular operations: a case-control study of risk factors. Ann Thorac Surg 1998;65:36-40.
hle E., Tammelin A., Bergström R., Hambreus A., Nyström S.O., Hansson H.E. Sternal wound complications incidence, microbiology and risk factors. Eur J Cardio-thorac Surg 1997;11:1146-1153.[Abstract]
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