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Ann Thorac Surg 1999;67:462-465
© 1999 The Society of Thoracic Surgeons


Original Articles

Is mediastinitis a preventable complication? A 10-year review

Roger J.F. Baskett, MDa, Carolyn E. MacDougall, RNa, David B. Ross, MDa

a Department of Cardiovascular Surgery, Dalhousie University and The Queen Elizabeth II Health Sciences Centre, Halifax, Nova Scotia, Canada

Accepted for publication July 9, 1998.

Address reprint requests to Dr Ross, IWK-Grace Health Centre, 5850 University Ave, Halifax, Nova Scotia, Canada B3J 3G9
e-mail: dross{at}iwkgrace.ns.ca


    Abstract
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Background. The incidence of mediastinitis after cardiac surgical intervention is reported to be between 0.15% and 5% and is a major cause of postoperative morbidity. A number of risk factors have been identified, most of which are not modifiable. It is our contention that this complication can be reduced to a minimum by the consistent application of good operative technique and postoperative management.

Methods. We reviewed the records of all 9,771 patients who underwent cardiac surgical procedures between 1987 and 1997. All operations were performed using a common skin preparation, draping, and antibiotic prophylaxis. Cases of mediastinitis were defined according to Centers for Disease Control and Prevention criteria and were identified from three sources: medical records database, hospital infection control, and the Society of Thoracic Surgeons database. Risk factors were assessed using {chi}2 and Fisher’s exact tests.

Results. Of 24 patients identified as having deep sternal wound infection (incidence, 0.25%), 2 died (mortality rate, 8.3%), 18 required reoperation (75%), and only 4 needed pectoral muscle flaps. Statistical analysis revealed only the presence of chronic obstructive pulmonary disease as a significant risk factor (p < 0.01). Other factors, including diabetes, renal failure, smoking, sex, age, reoperation, morbid obesity, and steroid use, were not significant. The use of internal mammary arteries (single or bilateral) was not associated with mediastinitis. Postoperative complications, including prolonged ventilation, inotropic support, and the need for blood products, were not significant risk factors. The patients who developed mediastinitis were more likely to be readmitted to the hospital (p < 0.005) and more likely to require reoperation (p < 0.005).

Conclusions. In a large patient series we found a low incidence of mediastinitis (0.25%) and an even lower incidence of required reoperation (0.19%). Except for the use of bone wax and the use of bilateral mammary arteries in diabetic patients, none of the previously identified risk factors are modifiable. We believe that with strict adherence to perioperative aseptic technique, attention to hemostasis, and precise sternal closure, a very low incidence of mediastinitis can be achieved.


    Introduction
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Deep sternal wound infection (DSWI), or mediastinitis, is a devastating complication of cardiac surgical procedures. The reported incidence ranges from 0.15% [1] to 8% [2] but is 1% to 2% in most series. The following possible causes and risk factors for DSWIs have been identified, but few of these risk factors are modifiable [36]:

Diabetes
Chronic obstructive pulmonary disease
Use of bilateral mammary grafts
Current smoker
Reoperation
Prolonged ventilation
Obesity
Age
Use of bone wax
Preoperative renal failure
Duration of operation
Use of electrocautery

It is our belief that this complication can be reduced to a minimum by the strict adherence to aseptic technique and proper sternal closure.

The purpose of the present study was to analyze the incidence of DSWI in a large series of patients undergoing cardiac surgical intervention at a tertiary care facility with a consistent perioperative protocol. Preoperative, operative, and postoperative risk factors were also assessed.


    Patients and methods
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
We retrospectively reviewed all cases of DSWI over 10 years treated by an adult cardiac surgical service. Cases were defined according to Centers for Disease Control and Prevention definitions for nosocomial infections [7] as infection of tissues or spaces deep to the subcutaneous tissue and one of the following:

  1. Evidence of mediastinitis seen at reoperation
  2. Positive culture of mediastinal tissue or fluid
  3. Sternal instability and positive blood culture
  4. Sternal instability and positive culture of mediastinal drainage
  5. Sternal instability and pus draining from mediastinum
  6. Chest pain and positive blood culture
  7. Chest pain and positive culture of mediastinal drainage
  8. Chest pain and pus draining from mediastinum
  9. Temperature higher than 38°C and positive blood culture
  10. Temperature higher than 38°C and positive culture of mediastinal drainage
  11. Temperature higher than 38°C and pus draining from mediastinum

Cases of DSWI were identified and cross-checked from three different sources: hospital medical records database, the cardiac surgical database of the Society of Thoracic Surgeons, and hospital infection control records. Our center is the only one in the region providing cardiac surgical services, and postoperative complications are referred back to our service.

All elective patients were admitted on the day before operation and underwent standard preparation: two antiseptic baths with Bactistat (0.3% triclosan [Ecolab, St. Paul, MN]) the night before and the morning of operation. Hair was removed with clippers from the chest, both forearms, groin areas, and legs within 12 hours of operation.

In the operating room the chest and legs were prepared with 2% iodine, followed by 70% isopropyl alcohol. The patient was draped with towels, and the operative sites were covered with adhesive transparent drapes. The perineum was isolated with sterile towels and adhesive drapes. The skin was opened with a scalpel and the presternal layers with electrocautery. After sternotomy, hemostasis was achieved with electrocautery and bone wax. The thymus and pericardium were opened using electrocautery. After bypass, the pericardium was left open, and hemostasis was achieved. A mediastinal chest tube and pleural chest tube (if the pleural cavity was opened) were inserted. In addition, one to three temporary epicardial pacing wires were inserted. The sternum was closed using seven or eight stainless steel wires placed through the sternum and twisted together in pairs (Fig 1). The presternal layers were closed in two layers using 0 Dexon and the skin with staples or 4-0 subcuticular nylon.



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Fig 1. Postoperative lateral chest radiograph. Note the three superior pairs of wires; each individual wire passes through both sides of the sternum and is twisted to bring the sternal edges together. Then with the sternum reapproximated, the wires are twisted together in pairs.

 
Postoperatively the chest tubes were connected to 15 cm of water suction. Prophylactic antibiotics (cefazolin, 1 g intravenously) were given intraoperatively and continued every 8 hours until the chest tubes were removed 18 to 36 hours later. The wound dressing was removed on the second postoperative day and only redressed if there was drainage. Patients were allowed to shower after 48 hours. All incision sites were inspected daily.

Univariate risk factor analysis was carried out for the last 2,061 cases from The Society of Thoracic Surgeons database using {chi}2 and Fisher’s exact tests.


    Results
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
Between January 1987 and March 1997, 9,429 patients survived 4 or more days after cardiac surgical procedures through a median sternotomy (Table 1). Deep sternal wound infection was identified in 24 (0.25%) of 9,429 patients. All had evidence of infection deep to the subcutaneous tissue and met at least one of the Centers for Disease Control and Prevention criteria given previously. The mean time to diagnosis was 11.86 ± 14.68 days (range, 3 to 74 days), and 2 of these patients died (mortality rate, 8.3%). Eighteen (0.19%) of 24 patients required reoperation for debridement and sternal rewiring. Pectoral muscle flaps were required in 4 patients. Six patients did not require reoperation and were treated medically.


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Table 1. Clinical Characteristics of 9,771 Consecutive Patients (From January 1, 1987 to January 3, 1997)a

 
In all patients bacteria were identified either from mediastinal tissue or fluid, or from blood cultures. In 16 of 24 patients the only pathogen isolated was a coagulase-negative Staphylococcus species. In 1 patient the pathogen was Cornynebacterium and Enteroccocus faecalis in another. In the remaining patients two or more pathogens were identified (Table 2).


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Table 2. Bacterial Pathogens Isolated

 
Risk factor analysis was divided into preoperative, operative, and postoperative factors. In this series the only preoperative factor associated with DSWI was a history of chronic obstructive pulmonary disease (COPD), defined as the patient taking medications for COPD preoperatively. None of the intraoperative factors assessed were significantly associated with DSWIs. In the postoperative period no risk factors were identified, but patients with DSWIs were more likely to be readmitted to the hospital, require reoperation, and have a longer hospital course (Table 3).


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Table 3. Univariate Risk Factor Analysis

 

    Comment
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 
It was not our intent to establish risk factors for DSWI; these have been well established by others [36, 812, 13]. It is our contention that a low incidence of DSWI can be achieved in a tertiary care center for all patients. The incidence reported here is at least half that reported in any series of comparable size [5, 6, 8, 1012]. Lower rates have been reported only in small selected series [1, 14].

Chronic obstructive pulmonary disease was the only factor in the present series found to be statistically significantly associated with DSWI. This association has been demonstrated in other series, although the mechanism is unclear [10]. It is hypothesized that patients with COPD have greater colonization and thus are more likely to become infected or are more likely to require prolonged ventilation; however, this was not a factor in our series (Table 3). Associated pneumonia was found in only 5 patients, 3 of whom had COPD. In no patient was the pneumonia and DSWI caused by the same pathogen. Perhaps COPD is merely a marker for general debility.

Because of the very low incidence of DSWI in the present series it is not surprising that only one variable was found to be a significant risk factor. We did not consider that multivariate analysis would further enhance the analysis.

The bacterial pathogens found in the present series are similar to those reported by others. In most series Staphylococcus aureus and S. epidermidis account for one-half to three-quarters of all bacterial isolates [8, 9, 11, 15, 16]. This finding reinforces the notion of skin flora being introduced into the surgical wound at the time of operation [4, 17]. Perhaps the leg incision is a source of pathogens in those undergoing saphenous vein harvest [18] and may account for the gastrointestinal flora found in some cases (Table 2) [19]. Postoperative contamination is also a possible source of these pathogens [20, 21]. In the present series the low incidence of infections by typical intensive care unit pathogens (Pseudomonas, Klebsiella, Enterobacter, Escherichia coli) lends strength to the belief that most of our infections were intraoperative in origin. The most frequent pathogen, coagulase-negative Staphylococcus, is known to be a frequent contaminant of operating room personnel and equipment [17].

The 6 patients not requiring reoperation did not differ from those requiring reoperation in any risk factor. None of the 6 patients had sternal dehiscence, whereas 15 of 18 patients requiring reoperation had sternal dehiscence or instability. Those patients not requiring reoperation had a milder clinical course and no dehiscence and were therefore treated conservatively. The 3 patients requiring reoperation who did not have evidence of sternal dehiscence were treated with superficial debridement and, in 1 patient, sternal debridement and rewiring.

As with any retrospective study the present series is susceptible to selection bias. Prospective studies tend to have higher incidence rates [3, 4, 9, 10]. Some series have insufficient follow-up data, and a significant number of cases are identified after hospital discharge. Wouters and colleagues [13] found that 11 of 23 cases of mediastinitis were diagnosed after discharge. Three of our cases were found after discharge, and several were identified beyond 8 days postoperatively. There is no other hospital in our region providing cardiac surgical services, and patients with DSWI must therefore return to our center. Thus, we are confident that all significant postoperative complications were captured in the present series.

In conclusion, DSWI is a devastating complication of cardiac surgical intervention. Numerous risk factors have been identified by various centers, few of which are modifiable. On the basis of this review of our experience over the past 10 years, we conclude that it is possible to achieve a very low incidence of DSWI in all patients. Most of these patients will require reoperation; however, if prompt treatment and early debridement are used, only a few will need pectoral muscle flaps. Most infections appear to be introduced in the operating theater. Strict adherence to a consistent protocol of perioperative aseptic technique is crucial. Careful attention to hemostasis and meticulous surgical technique remain the mainstays of prevention and must include precise sternal alignment and stable closure (Fig 1). We believe that our low incidence of DSWI in a large group of patients undergoing cardiac surgical procedures is the result of our adherence to our simple protocol and our method of sternal closure.


    References
 Top
 Abstract
 Introduction
 Patients and methods
 Results
 Comment
 References
 

  1. Blanchard A., Hurni M., Ruchat P., Stumpe F., Fischer A., Sadeghi H. Incidence of deep and superficial sternal infection after open heart surgery: a ten year retrospective study 1981 to 1991. Eur J Cardiothorac Surg 1995;9:153-157.[Abstract]
  2. Culliford A.T., Cunningham J.N., Zeff R.H., et al. Sternal and costochondral infections following open-heart surgery: a review of 2,594 cases. J Thorac Cardiovasc Surg 1976;72:714-726.[Abstract]
  3. Kouchoukos N.T., Wareing T.H., Murphy S.F., Pelate C., Marshall W.G. Risks of bilateral internal mammary artery bypass grafting. Ann Thorac Surg 1990;49:210-219.[Abstract]
  4. The Parisian Mediastinitis Study Group. Risk factors for deep sternal wound infection after sternotomy: a prospective, multicentre study. J Thorac Cardiovasc Surg 1996;111:1200-1207.[Abstract/Free Full Text]
  5. Semper O., Leclerc Y., Carrier M. Mediastinité post-sternotomie: strategie de traitement. Ann Chir 1991;45,9:770-773.[Medline]
  6. He G.W., Ryan W.H., Acuff T.E., et al. Risk factors for operative mortality and sternal wound infection in bilateral internal mammary artery grafting. J Thorac Cardiovasc Surg 1994;107:196-202.[Abstract/Free Full Text]
  7. Garner J.S., Jarvis W.R., Emori T.G., Horan T.C., Hughes J.M. CDC definitions for nosocomial infections, 1988. Am J Infect Control 1988;16:128-140.[Medline]
  8. Grossi E.A., Culliford A.T., Krieger K.H., et al. A survey of 77 major infectious complications of median sternotomy: a review of 7,949 consecutive operative procedures. Ann Thorac Surg 1985;40:214-223.[Abstract]
  9. Nagachinta T., Stephens M., Reitz B., Polk B.F. Risk factors for surgical wound infection following cardiac surgery. J Infect Dis 1987;156:967-973.[Medline]
  10. Newman L.S., Szczukowski L.C., Bain R.P., Perlino C.A. Suppurative mediastinitis after open heart surgery: a case control study of risk factors. Chest 1988;94:546-553.[Abstract/Free Full Text]
  11. Loop F.D., Lytle B.W., Cosgrove D.M., et al. Sternal wound complications after isolated coronary artery bypass grafting: early and late mortality, morbidity, and cost of care. Ann Thorac Surg 1990;49:179-187.[Abstract]
  12. Milano C.A., Kesler K., Archibald N., Sexton D.J., Jones R.H. Mediastinitis after coronary artery bypass graft surgery. Circulation 1995;92:2245-2251.[Abstract/Free Full Text]
  13. Wouters R., Wellens F., Vanermen H., De Geest R., Degrieck I., De Meerleer F. Sternitis and mediastinitis after coronary artery bypass grafting. Texas Heart Inst J 1994;21:183-188.[Medline]
  14. Ferrazzi P., Allen R., Crupi G., et al. Reduction of infection after cardiac surgery: a clinical trial. Ann Thorac Surg 1986;42:321-325.[Abstract]
  15. Demmy T.L., Park S.B., Liebler G.A., et al. Recent experience with major sternal wound complications. Ann Thorac Surg 1990;49:458-462.[Abstract]
  16. Kohman L.J., Coleman M.J., Parker F.B. Bacteremia and sternal infection after coronary artery bypass grafting. Ann Thorac Surg 1990;49:454-457.[Abstract]
  17. Sarr M.G., Gott V.I., Townsend T.R. Mediastinal infection after cardiac surgery. Ann Thorac Surg 1984;38:415-423.[Abstract]
  18. Wells F.C., Newson S.W.B., Rowlands C. Wound infection in cardiothoracic surgery. Lancet 1983;321:1209-1210.
  19. Farrington M., Webster M., Fenn A., Phillips I. Study of cardiothoracic wound infection at St. Thomas Hospital. Br J Surg 1985;72:759-762.[Medline]
  20. Ehrenkranz N.J., Pfaff S.J. Mediastinitis complicating cardiac operations: evidence of postoperative causation. Rev Infect Dis 1991;13:803-814.[Medline]
  21. Ottino G., De Paulis R., Pansini S., et al. Major sternal wound infection after open heart surgery: a multivariate analysis of risk factors in 2,579 consecutive operative procedures. Ann Thorac Surg 1987;44:173-179.[Abstract]



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