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Departments of Medicine and Preventive Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee
Due in large part to many landmark innovations in the care of the surgical patient, such as the use of anesthesia [1] and the development of the principles of antibiotic prophylaxis [2, 3], the number of surgical procedures performed annually has climbed steadily, with >24 million surgical procedures performed in 2001 in the United States alone [4]. Unfortunately, as surgical volume has increased and with the development of novel surgical procedures, the number of persons at risk of morbidity from surgical site infections (SSIs) has also increased. According to the most-recent estimates, 500,000 SSIs occur annually in the United States, leading to an estimated 3.7 million excess hospital days and >$1.6 billion in excess costs [5, 6]. A patient who develops an SSI while hospitalized has an 60% greater risk of being admitted to the intensive care unit, is >5 times more likely to be readmitted to the hospital within 30 days after discharge, and incurs an attributable extra hospital stay of 6.5 days, leading to a direct cost of an additional $3000/infection [7].
Attempts to reduce such morbidity have appropriately focused on the identification of specific risk factors for SSI. Such factors may be specific to single surgical types, such as the use of internal mammary arteries for coronary arterial bypass grafting [8, 9], but many are applicable to most surgical procedures. In general, these risk factors can be categorized into 2 groups: characteristics of the surgical patient and characteristics of the procedure itself (figure 1) [10, 11]. Some risk factorsin particular, patient characteristics such as altered immune responses and obesityare inherent at the time of surgery and are not amenable to any practical modification to reduce the conferred risk of SSI. However, others are modifiable in the short period preceding the surgical incision, thus leading to a reduction in risk of SSI for the individual surgical patient.
An added dimension in the prevention of SSIs is the rapid development of novel technological tools intended to help shorten operative duration, reduce the degree of tissue damage, and diminish the rate of SSI. Minimally invasive procedures using endoscopic techniques have increased in use [1215], with reductions in rates of SSI noted with laparoscopic procedures [16]. The advent of robotic surgery has promised to minimize the degree of tissue damage by increasing the precision of surgical incisions [1719]. Finally, the growing use of antimicrobial and antiseptic-impregnated operative materialssuch as sutures, mesh, and bandagesis hoped to provide long-term instillation of prophylactic antibiotics into the surgical field to reduce SSIs [2023].
The need to deftly and thoroughly examine the impact of these promising novel technologies on infectious outcomes seems readily apparent. New technology can be costly and difficult to implement, and the demonstration of improvement in all patient outcomes and, in particular, SSIs with any new procedure is imperative. What is less obvious but could be equally important, however, is the need for contemporary examination of classic risk factors for SSI. For instance, numerous studies have identified an increased risk of SSI in persons with diabetes mellitus [10, 2431]. The increased risk of infection due to diabetes has long been attributed to physiologic alterations precipitated by inadequate long-term glucose control [3234]. Thus, although the presence of diabetes could be used to stratify a patient's preoperative risk of SSI, conclusions about the degree to which such risk could be reduced in the perioperative period, especially after years of poor glycemic control, seemed pessimistic.
But, as the classic relationship between diabetes and SSI was reexamined, an interesting trend appeared. The risk of SSI in persons with diabetes was also significantly related to perioperative hyperglycemia [26, 30, 3537]. Equally striking was that this association also held for persons with impaired perioperative glycemic control but without previously diagnosed diabetes [30]. These novel examinations of a classic risk factor for SSI have led to the use of continuous insulin infusion in surgical patients and a subsequent reduction not only in SSI but also in overall mortality [3840]. Thus, an established risk factor for SSI that was an "unmodifiable" patient comorbidity became a modifiable target for intervention in contemporary surgical practice.
The latest example of a new examination of an "old" risk factor for SSI, with some revealing results, can be found in an impressive study investigating the relationship between age and risk of SSI in the current issue of the Journal of Infectious Diseases, conducted by Kaye et al. [41]. As summarized nicely in table 2 of their article [41], increasing age in adults has often been identified as a risk factor for SSI. However, controversy exists as to whether age serves simply as a marker for underlying illness or whether immunologic senescence associated with increased age leads to an increased risk of infection. Others have actually noted, albeit generally in single-site investigations with a relatively small sample size, that the risk of SSI decreases as patient age increases [42, 43].
In the largest study of age and SSI to date, Kaye et al. used prospective surveillance data collected from selected adult surgical procedures performed in a network of 1 tertiary care institution and 10 community-based hospitals. SSIs were identified prospectively by use of standardized Centers for Disease Control and Prevention criteria, and various clinical datasuch as patient age, type of surgical procedure, American Society of Anesthesiologists (ASA) score, oprerative duration, and wound classwere collected at the time of surgery. To thoroughly assess the relationship between age and risk of SSI, patient age was examined as a dichotomous as well as a continuous variable.
In a derivation cohort of >72,000 patients and 873 SSIs (rate of SSI, 1.2%), patient age 65 years was significantly associated with an increased risk of SSI, compared with patient age <65 years. However, a more detailed analysis adjusted for hospital type, procedure type and duration, wound class, and ASA score, with age as a continuous variable, found that the rate of SSI peaked at age 65 years, with a subsequent decrease of 1.1%/year as patient age increased. These findings were confirmed in a validation cohort of similar size with a similar rate of SSI, in which the risk of SSI peaked at age 65 years, followed by a 1.3% decrease in incidence of SSI per year >65 years.
Before one infers from this well-designed study that increased age actually protects against development of SSIs, some limitations of the study must be acknowledged [41]. Differences in the surveillance methods existed at the individual study sites. The types of procedures differed by institution (only cardiothoracic, neurosurgical, and orthopedic procedures were examined at the tertiary hospital, whereas all types of surgical procedures were examined at the other 10 sites), by type of SSI included (superficial SSIs were assessed only at the community-based institutions, not at the tertiary center), and by the year of implementation of surveillance, which ranged from 1991 at one hospital, to 1994 at the tertiary hospital, to 1999 at the remaining 9 hospitals. In addition, nearly three-quarters of the procedures were performed at the community hospitals, which could indicate a patient population with a lesser severity of disease and, thus, a potentially lower inherent risk of SSI. Nonetheless, the association between increasing age and decreasing risk of SSI remained after adjustment for type of procedure and hospital. Furthermore, although the ASA score serves as a basic surrogate for the presence and severity of underlying illnesses in the study population, full details on comorbid patient conditions known to increase risk of SSIsuch as perioperative glucose control and tobacco usewere not included in the analysis, as acknowledged by the authors.
Despite these limitations, the study by Kaye et al. [41] has many strengths. Primarily, the sheer volume of patients and procedures studied affords substantial power to their findings, since >144,000 patients were included for analysis. This large sample size allowed for the study team not only to derive the relationship between age and risk of SSI but also to validate their findings in a similarly large sample of patients. The examination of age not only as a categorical variable but also as a continuous variable greatly enhanced their study. The use of different surgical types and multiple institutions reflects the generalizability of their results. In addition, the data were collected prospectively by use of standardized definitions of SSIs.
Finally, the thorough and thoughtful reexamination of the classic risk factor for SSI, age, by Kaye et al. also emphasizes the continued need for independent funding of investigations into the epidemiology and prevention of nosocomial infections. Traditionally, large-scale examinations of nosocomial infections, hospital epidemiological projects, and infection-control interventions have not been attractive to extramural funding sources. There is now a need for sophisticated investigations using large population-based data systems and detailed analyses to augment the time-honored standard of identification of risk factors through case-control investigations, programs that will obviously require an increase in dedicated resources. However, with the growing public and private interest in identifying measures to reduce the rates of nosocomial infections, especially SSIs [44, 45], the importance of designing and funding careful examinations of both the classic and novel aspects of surgical procedures and patients, to reduce SSI morbidity, cannot be overemphasized.
References
1. Rutkow IM. History of surgery. In: Townsend CM, Beauchamp RD, Evers BM, Mattox KL, eds. Sabiston textbook of surgery. 17th ed. Philadelphia: Elsevier, 2004:320. First citation in article
2. Miles AA, Miles EM, Burke J. The value and duration of defence reactions of the skin to the primary lodgement of bacteria. Br J Exp Pathol 1957; 38:7996. First citation in article
3. Burke J. The effective period of preventive antibiotic action in experimental incisions and dermal lesions. Surgery 1961; 50:1618. First citation in article
4. Kozak LJ, Owings MF, Hall MJ. National hospital discharge survey: 2001 annual summary with detailed diagnosis and procedure data. Vital Health Stat 13 2004; 156:1198. First citation in article
5. Martone WJ, Nichols RL. Recognition, prevention, surveillance, and management of surgical site infections: introduction to the problem and symposium overview. Clin Infect Dis 2001; 33(Suppl 2):S678. First citation in article
6. Martone WJ, Jarvis WR, Edwards JR, Culver DH, Haley RW. Incidence and nature of endemic and epidemic nosocomial infections. In: Bennett JV, Brachman PS, eds. Hospital infections. Philadelphia: Lippencott-Raven, 1998:46176. First citation in article
7. Kirkland KB, Briggs JP, Trivette SL, Wilkinson WE, Sexton DJ. The impact of surgical-site infections in the 1990s: attributable mortality, excess length of hospitalization, and extra costs. Infect Control Hosp Epidemiol 1999; 20:72530. First citation in article
8. Gummert JF, Barten MJ, Hans C, et al. Mediastinitis and cardiac surgeryan updated risk factor analysis in 10,373 consecutive adult patients. Thorac Cardiovasc Surg 2002; 50:8791. First citation in article
9. Ridderstolpe L, Gill H, Granfeldt H, Ahlfeldt H, Rutberg H. Superficial and deep sternal wound complications: incidence, risk factors and mortality. Eur J Cardiothorac Surg 2001; 20:116875. First citation in article
10. Mangram AJ, Horan TC, Pearson ML, Silver LC, Jarvis WR. Guideline for prevention of surgical site infection, 1999. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol 1999; 20:25078. First citation in article
11. Talbot TR, Kaiser AB. Postoperative infections and antimicrobial prophylaxis. In: Mandell GL, Bennett JE, Dolen R, eds. Principles and practice of infectious diseases. 6th ed. New York: Churchill Livingstone, 2004. First citation in article
12. Fann JI, Stevens JH, Pompili MF, Burdon TA, Reitz BA. Minimally invasive coronary artery bypass grafting. Curr Opin Cardiol 1997; 12:4827. First citation in article
13. Fann JI, Pompili MF, Burdon TA, Stevens JH, St Goar FG, Reitz BA. Minimally invasive mitral valve surgery. Semin Thorac Cardiovasc Surg 1997; 9:32030. First citation in article
14. Burke RP. Minimally invasive pediatric cardiac surgery. Curr Opin Cardiol 1999; 14:6772. First citation in article
15. Bonde P, Graham AN, MacGowan SW. Endoscopic vein harvest: advantages and limitations. Ann Thorac Surg 2004; 77:207682. First citation in article
16. National Nosocomial Infections Surveillance (NNIS) System Report, data summary from January 1992 through June 2003, issued August 2003. Am J Infect Control 2003; 31:48198. First citation in article
17. Rayman R. Robot-assisted cardiac surgery. Semin Laparosc Surg 2004; 11:739. First citation in article
18. Hazey JW, Melvin WS. Robot-assisted general surgery. Semin Laparosc Surg 2004; 11:10712. First citation in article
19. Adili A. Robot-assisted orthopedic surgery. Semin Laparosc Surg 2004; 11:8998. First citation in article
20. Holder IA, Durkee P, Supp AP, Boyce ST. Assessment of a silver-coated barrier dressing for potential use with skin grafts on excised burns. Burns 2003; 29:4458. First citation in article
21. Barbolt TA. Chemistry and safety of triclosan, and its use as an antimicrobial coating on coated VICRYL* plus antibacterial suture (coated polyglactin 910 suture with triclosan). Surg Infect (Larchmt) 2002; 3(Suppl 1):S4553. First citation in article
22. Rothenburger S, Spangler D, Bhende S, Burkley D. In vitro antimicrobial evaluation of coated VICRYL* plus antibacterial suture (coated polyglactin 910 with triclosan) using zone of inhibition assays. Surg Infect (Larchmt) 2002; 3(Suppl 1):S7987. First citation in article
23. Choe JM, Ogan K, Bennett S. Antibacterial mesh sling: a prospective outcome analysis. Urology 2000; 55:51520. First citation in article
24. Vuorisalo S, Haukipuro K, Pokela R, Syrjala H. Risk features for surgical-site infections in coronary artery bypass surgery. Infect Control Hosp Epidemiol 1998; 19:2407. First citation in article
25. Spelman DW, Russo P, Harrington G, et al. Risk factors for surgical wound infection and bacteraemia following coronary artery bypass surgery. Aust NZ J Surg 2000; 70:4751. First citation in article
26. Trick WE, Scheckler WE, Tokars JI, et al. Modifiable risk factors associated with deep sternal site infection after coronary artery bypass grafting. J Thorac Cardiovasc Surg 2000; 119:10814. First citation in article
27. Olsen MA, Lock-Buckley P, Hopkins D, Polish LB, Sundt TM, Fraser VJ. The risk factors for deep and superficial chest surgical-site infections after coronary artery bypass graft surgery are different. J Thorac Cardiovasc Surg 2002; 124:13645. First citation in article
28. Russo PL, Spelman DW. A new surgical-site infection risk index using risk factors identified by multivariate analysis for patients undergoing coronary artery bypass graft surgery. Infect Control Hosp Epidemiol 2002; 23:3726. First citation in article
29. Talbot TR, D'Agata EM, Brinsko V, Lee B, Speroff T, Schaffner W. Perioperative blood transfusion is predictive of poststernotomy surgical site infection: marker for morbidity or true immunosuppressant Clin Infect Dis 2004; 38:137882. First citation in article
30. Latham R, Lancaster AD, Covington JF, Pirolo JS, Thomas CS. The association of diabetes and glucose control with surgical-site infections among cardiothoracic surgery patients. Infect Control Hosp Epidemiol 2001; 22:60712. First citation in article
31. Malone DL, Genuit T, Tracy JK, Gannon C, Napolitano LM. Surgical site infections: reanalysis of risk factors. J Surg Res 2002; 103:8995. First citation in article
32. Bagdade JD, Stewart M, Walters E. Impaired granulocyte adherence: a reversible defect in host defense in patients with poorly controlled diabetes. Diabetes 1978; 27:67781. First citation in article
33. Delamaire M, Maugendre D, Moreno M, Le Goff MC, Allannic H, Genetet B. Impaired leucocyte functions in diabetic patients. Diabet Med 1997; 14:2934. First citation in article
34. Pozzilli P, Leslie RD. Infections and diabetes: mechanisms and prospects for prevention. Diabet Med 1994; 11:93541. First citation in article
35. Golden SH, Peart-Vigilance C, Kao WH, Brancati FL. Perioperative glycemic control and the risk of infectious complications in a cohort of adults with diabetes. Diabetes Care 1999; 22:140814. First citation in article
36. Zerr KJ, Furnary AP, Grunkemeier GL, Bookin S, Kanhere V, Starr A. Glucose control lowers the risk of wound infection in diabetics after open heart operations. Ann Thorac Surg 1997; 63:35661. First citation in article
37. Furnary AP, Wu Y, Bookin SO. Effect of hyperglycemia and continuous intravenous insulin infusions on outcomes of cardiac surgical procedures: the Portland Diabetic Project. Endocr Pract 2004; 10(Suppl 2):2133. First citation in article
38. Furnary AP, Zerr KJ, Grunkemeier GL, Starr A. Continuous intravenous insulin infusion reduces the incidence of deep sternal wound infection in diabetic patients after cardiac surgical procedures. Ann Thorac Surg 1999; 67:35260; discussion 3602. First citation in article
39. Furnary AP, Gao G, Grunkemeier GL, et al. Continuous insulin infusion reduces mortality in patients with diabetes undergoing coronary artery bypass grafting. J Thorac Cardiovasc Surg 2003; 125:100721. First citation in article
40. van den Berghe G, Wouters P, Weekers F, et al. Intensive insulin therapy in the critically ill patients. N Engl J Med 2001; 345:135967. First citation in article
41. Kaye KS, Schmit K, Pieper C, et al. The effect of increasing age on the risk for surgical site infection. J Infect Dis 2005;191:105662 (in this issue). First citation in article
42. Delgado-Rodriguez M, Gomez-Ortega A, Sillero-Arenas M, Llorca J. Epidemiology of surgical-site infections diagnosed after hospital discharge: a prospective cohort study. Infect Control Hosp Epidemiol 2001; 22:2430. First citation in article
43. Byrne DJ, Lynch W, Napier A, Davey P, Malek M, Cuschieri A. Wound infection rates: the importance of definition and post-discharge wound surveillance. J Hosp Infect 1994; 26:3743. First citation in article
44. The National Quality Forum. Safe practices for better healthcare: a consensus report. Washington, DC: The National Quality Forum, 2003. First citation in article
45. Consumers Union. Stop hospital infections. Available at: http://www.StopHospitalInfections.org. Accessed 7 December 2004. First citation in article