Wound Infection Clinical Presentation
- Author: Hemant Singhal, MD, MBBS, FRCSE, FRCS(C); Chief Editor: John Geibel, MD, DSc, MA more...
History
Surgical site infection is a difficult term to define accurately because it has a wide spectrum of possible clinical features.
The Centers for Disease Control and Prevention (CDC) have defined SSI to standardize data collection for the National Nosocomial Infections Surveillance (NNIS) program.[11, 12] SSIs are classified into incisional SSIs, which can be superficial or deep, or organ/space SSIs, which affect the rest of the body other than the body wall layers.
- Definitions of surgical site infection (see image below)
Definitions of surgical site infection (SSI). - Superficial incisional SSI: Infection involves only skin and subcutaneous tissue of incision.
- Deep incisional SSI: Infection involves deep tissues, such as fascial and muscle layers. This also includes infection involving both superficial and deep incision sites and organ/space SSI draining through incision.
- Organ/space SSI: Infection involves any part of the anatomy in organs and spaces other than the incision, which was opened or manipulated during operation.
- Superficial incisional SSI is more common than deep incisional SSI and organ/space SSI. Superficial incisional SSI accounts for more than half of all SSIs for all categories of surgery. The postoperative length of stay is longer for patients with SSI, and when adjusted for other factors influencing length of stay.
Physical
According to a report by the NNIS program,[13] surgical site infections are defined as follows:
- Superficial incisional SSI
- Occurs within 30 days after the operation
- Involves only the skin or subcutaneous tissue
- At least 1 of the following:
- Purulent drainage is present (culture documentation not required).
- Organisms are isolated from fluid/tissue of the superficial incision.
- At least 1 sign of inflammation (eg, pain or tenderness, induration, erythema, local warmth of the wound) is present.
- The wound is deliberately opened by the surgeon.
- The surgeon or clinician declares the wound infected.
- Note: A wound is not considered a superficial incisional SSI if a stitch abscess is present; if the infection is at an episiotomy, a circumcision site, or a burn wound; or if the SSI extends into fascia or muscle.
- Deep incisional SSI
- Occurs within 30 days of the operation or within 1 year if an implant is present
- Involves deep soft tissues (eg, fascia and/or muscle) of the incision
- At least 1 of the following:
- Purulent drainage is present from the deep incision but without organ/space involvement.
- Fascial dehiscence or fascia is deliberately separated by the surgeon because of signs of inflammation.
- A deep abscess is identified by direct examination or during reoperation, by histopathology, or by radiologic examination.
- The surgeon or clinician declares that a deep incisional infection is present.
- Organ/space SSI
- Occurs within 30 days of the operation or within 1 year if an implant is present
- Involves anatomical structures not opened or manipulated during the operation
- At least 1 of the following:
- Purulent drainage is present from a drain placed by a stab wound into the organ/space.
- Organisms are isolated from the organ/space by aseptic culturing technique.
- An abscess in the organ/space is identified by direct examination, during reoperation, or by histopathologic or radiologic examination.
- A diagnosis of organ/space SSI is made by the surgeon or clinician.
Causes
All surgical wounds are contaminated by microbes, but in most cases, infection does not develop because innate host defenses are quite efficient in the elimination of contaminants. A complex interplay between host, microbial, and surgical factors ultimately determines the prevention or establishment of a wound infection. Factors that affect surgical wound healing are classified in the chart below.
Factors that affect surgical wound healing. - Microbiology: Microbial factors that influence the establishment of a wound infection are the bacterial inoculum, virulence, and the effect of the microenvironment. When these microbial factors are conducive, impaired host defenses set the stage for enacting the chain of events that produce wound infection.
- Most SSIs are contaminated by the patient's own endogenous flora, which are present on the skin, mucous membranes, or hollow viscera. The traditional microbial concentration quoted as being highly associated with SSIs is that of bacterial counts higher than 10,000 organisms per gram of tissue (or in the case of burned sites, organisms per cm2 of wound).[14]
- The usual pathogens on skin and mucosal surfaces are gram-positive cocci (notably staphylococci); however, gram-negative aerobes and anaerobic bacteria contaminate skin in the groin/perineal areas. The contaminating pathogens in gastrointestinal surgery are the multitude of intrinsic bowel flora, which include gram-negative bacilli (eg, Escherichia coli) and gram-positive microbes, including enterococci and anaerobic organisms. See Table 1 for pathogens and their frequencies. Gram-positive organisms, particularly staphylococci and streptococci, account for most exogenous flora involved in SSIs. Sources of such pathogens include surgical/hospital personnel and intraoperative circumstances, including surgical instruments, articles brought into the operative field, and the operating room air.
- The most common group of bacteria responsible for SSIs are Staphylococcus aureus. The emergence of resistant strains has considerably increased the burden of morbidity and mortality associated with wound infections.
- Methicillin resistant Staphylococcus aureus (MRSA) is proving to be the scourge of modern day surgery. Like other strains of S aureus, MRSA can colonize the skin and body of an individual without causing sickness, and, in this way, it can be passed on to other individuals unknowingly. Problems arise in the treatment of overt infections with MRSA because antibiotic choice is very limited. MRSA infections appear to be increasing in frequency and are displaying resistance to a wider range of antibiotics.[15]
- Of particular concern are the vancomycin intermediate Staphylococcus aureus (VISA) strains of MRSA. These strains are beginning to develop resistance to vancomycin, which is currently the most effective antibiotic against MRSA. This new resistance has arisen because another species of bacteria, called enterococci, relatively commonly express vancomycin resistance.
Table 1. Pathogens Commonly Associated with Wound Infections and Frequency of Occurrence[11] (Open Table in a new window)
| Pathogen | Frequency (%) |
| Staphylococcus aureus | 20 |
| Coagulase-negative staphylococci | 14 |
| Enterococci | 12 |
| Escherichia coli | 8 |
| Pseudomonas aeruginosa | 8 |
| Enterobacter species | 7 |
| Proteus mirabilis | 3 |
| Klebsiella pneumoniae | 3 |
| Other streptococci | 3 |
| Candida albicans | 3 |
| Group D streptococci | 2 |
| Other gram-positive aerobes | 2 |
| Bacteroides fragilis | 2 |
- Risk factors (other than microbiology)
- Decreased host resistance can be due to systemic factors affecting the patient's healing response, local wound characteristics, or operative characteristics.
- Systemic factors include age, malnutrition, hypovolemia, poor tissue perfusion, obesity, diabetes, steroids, and other immunosuppressants.
- Wound characteristics include nonviable tissue in wound; hematoma; foreign material, including drains and sutures; dead space; poor skin preparation, including shaving; and preexistent sepsis (local or distant).
- Operative characteristics include poor surgical technique; lengthy operation (>2 h); intraoperative contamination, including infected theater staff and instruments and inadequate theater ventilation; prolonged preoperative stay in the hospital; and hypothermia.
- The type of procedure is a risk factor. Certain procedures are associated with a higher risk of wound contamination than others. Surgical wounds have been classified as clean, clean-contaminated, contaminated, and dirty-infected (see Table 2).
- Decreased host resistance can be due to systemic factors affecting the patient's healing response, local wound characteristics, or operative characteristics.
Table 2: Surgical Wound Classification and Subsequent Risk of Infection (If No Antibiotics Used)[11, 16] (Open Table in a new window)
| Classification | Description | Infective Risk (%) |
| Clean (Class I) | Uninfected operative wound No acute inflammation Closed primarily Respiratory, gastrointestinal, biliary, and urinary tracts not entered No break in aseptic technique Closed drainage used if necessary | < 2 |
| Clean-contaminated (Class II) | Elective entry into respiratory, biliary, gastrointestinal, urinary tracts and with minimal spillage No evidence of infection or major break in aseptic technique Example: appendectomy | < 10 |
| Contaminated (Class III) | Nonpurulent inflammation present Gross spillage from gastrointestinal tract Penetrating traumatic wounds < 4 hours Major break in aseptic technique | About 20 |
| Dirty-infected (Class IV) | Purulent inflammation present Preoperative perforation of viscera Penetrating traumatic wounds >4 hours | About 40 |
Breasted D. The Edwin Smith Surgical Papyrus. University of Chicago: University of Chicago Press; 1930.
Bryan PW. The Papyrus Ebers. London/Washington DC: Government Printing Office; 1883.
Cohen IK. A Brief History of Wound Healing. Yardley, Pa: Oxford Clinical Communications Inc; 1998.
Lister J. On a new method of treating compound fractures. Lancet. 1867;1:326-329,387-389,507-509.
Qvist G. Hunterian Oration, 1979. Some controversial aspects of John Hunter's life and work. Ann R Coll Surg Engl. Jul 1979;61(4):309-11. [Medline].
Helling TS, Daon E. In Flanders fields: the Great War, Antoine Depage, and the resurgence of débridement. Ann Surg. Aug 1998;228(2):173-81. [Medline].
Emori TG, Gaynes RP. An overview of nosocomial infections, including the role of the microbiology laboratory. Clin Microbiol Rev. Oct 1993;6(4):428-42. [Medline].
Mayon-White RT, Ducel G, Kereselidze T, et al. An international survey of the prevalence of hospital-acquired infection. J Hosp Infect. Feb 1988;11 Suppl A:43-8. [Medline].
Mangram AJ, Horan TC, Pearson ML, et al. Guideline for prevention of surgical site infection, 1999. Hospital Infection Control Practices Advisory Committee. Infect Control Hosp Epidemiol. Apr 1999;20(4):250-78; quiz 279-80. [Medline].
Kirkland KB, Briggs JP, Trivette SL, et al. The impact of surgical-site infections in the 1990s: attributable mortality, excess length of hospitalization, and extra costs. Infect Control Hosp Epidemiol. Nov 1999;20(11):725-30. [Medline].
National Nosocomial Infections Surveillance (NNIS) System. NNIS report, data summary from October 1986-April 1996, issued May 1996. A report from the NNIS System. Am J Infect Control. Oct 1996;24(5):380-8. [Medline].
Di Leo A, Piffer S, Ricci F, et al. Surgical site infections in an Italian surgical ward: a prospective study. Surg Infect (Larchmt). Aug 18 2009;[Medline].
National Nosocomial Infections Surveillance (NNIS) System. NNIS report, data summary from January 1992 to June 2002, issued August 2002. Am J Infect Control. Dec 2002;30(8):458-75. [Medline].
Krizek TJ, Robson MC. Evolution of quantitative bacteriology in wound management. Am J Surg. Nov 1975;130(5):579-84. [Medline].
Hsiao CH, Chuang CC, Tan HY, Ma DH, Lin KK, Chang CJ, et al. Methicillin-Resistant Staphylococcus aureus Ocular Infection: A 10-Year Hospital-Based Study. Ophthalmology. Dec 14 2011;[Medline].
Cruse PJ, Foord R. The epidemiology of wound infection. A 10-year prospective study of 62,939 wounds. Surg Clin North Am. Feb 1980;60(1):27-40. [Medline].
Burke JF. The effective period of preventive antibiotic action in experimental incisions and dermal lesions. Surgery. Jul 1961;50:161-8. [Medline].
Barchitta M, Matranga D, Quattrocchi A, Bellocchi P, Ruffino M, Basile G, et al. Prevalence of surgical site infections before and after the implementation of a multimodal infection control programme. J Antimicrob Chemother. Nov 29 2011;[Medline].
Gupta R, Sinnett D, Carpenter R, et al. Antibiotic prophylaxis for post-operative wound infection in clean elective breast surgery. Eur J Surg Oncol. Jun 2000;26(4):363-6. [Medline].
Platt R, Zucker JR, Zaleznik DF, et al. Perioperative antibiotic prophylaxis and wound infection following breast surgery. J Antimicrob Chemother. Feb 1993;31 Suppl B:43-8. [Medline].
Woodfield JC, Beshay N, van Rij AM. A meta-analysis of randomized, controlled trials assessing the prophylactic use of ceftriaxone. A study of wound, chest, and urinary infections. World J Surg. Aug 2 2009;[Medline].
Woods RK, Dellinger EP. Current guidelines for antibiotic prophylaxis of surgical wounds. Am Fam Physician. Jun 1998;57(11):2731-40. [Medline].
Mahmoud NN, Turpin RS, Yang G, et al. Impact of surgical site infections on length of stay and costs in selected colorectal procedures. Surg Infect (Larchmt). Aug 26 2009;[Medline].
Culver DH, Horan TC, Gaynes RP, et al. Surgical wound infection rates by wound class, operative procedure, and patient risk index. National Nosocomial Infections Surveillance System. Am J Med. Sep 16 1991;91(3B):152S-157S. [Medline].
Anesthesiology. New classification of physical status. Anesthesiology. 1963;24:111.
Pearson ML. Guideline for prevention of intravascular device-related infections. Part I. Intravascular device-related infections: an overview. The Hospital Infection Control Practices Advisory Committee. Am J Infect Control. Aug 1996;24(4):262-77. [Medline].
Mermel LA, Farr BM, Sherertz RJ, et al. Guidelines for the management of intravascular catheter-related infections. Clin Infect Dis. May 1 2001;32(9):1249-72. [Medline].
Dettenkofer M, Wilson C, Gratwohl A, et al. Skin disinfection with octenidine dihydrochloride for central venous catheter site care: a double-blind, randomized, controlled trial. Clin Microbiol Infect. Aug 17 2009;[Medline].
Haley RW, Schaberg DR, Crossley KB, et al. Extra charges and prolongation of stay attributable to nosocomial infections: a prospective interhospital comparison. Am J Med. Jan 1981;70(1):51-8. [Medline].
Eagye KJ, Kim A, Laohavaleeson S, et al. Surgical site infections: does inadequate antibiotic therapy affect patient outcomes?. Surg Infect (Larchmt). Aug 2009;10(4):323-31. [Medline].
Baquero F. Gram-positive resistance: challenge for the development of new antibiotics. J Antimicrob Chemother. May 1997;39 Suppl A:1-6. [Medline].
Belda FJ, Aguilera L, Garcia de la Asuncion J, et al. Supplemental perioperative oxygen and the risk of surgical wound infection: a randomized controlled trial. JAMA. Oct 26 2005;294(16):2035-42. [Medline].
Bratzler DW, Houck PM. Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Clin Infect Dis. Jun 15 2004;38(12):1706-15. [Medline].
Buggy D. Can anaesthetic management influence surgical-wound healing?. Lancet. Jul 29 2000;356(9227):355-7. [Medline].
Centers for Disease Control and Prevention. Prevent antimicrobial resistance in health care settings. Available at http://www.cdc.gov/drugresistance/healthcare/problem.htm.
Coello R, Charlett A, Wilson J, et al. Adverse impact of surgical site infections in English hospitals. J Hosp Infect. Jun 2005;60(2):93-103. [Medline].
Gaynes RP. Surgical-site infections (SSI) and the NNIS Basic SSI Risk Index, part II: room for improvement. Infect Control Hosp Epidemiol. May 2001;22(5):266-7. [Medline].
Heinzelmann M, Scott M, Lam T. Factors predisposing to bacterial invasion and infection. Am J Surg. Feb 2002;183(2):179-90. [Medline].
Kurz A, Sessler DI, Lenhardt R. Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group. N Engl J Med. May 9 1996;334(19):1209-15. [Medline].
Latham R, Lancaster AD, Covington JF, et al. The association of diabetes and glucose control with surgical-site infections among cardiothoracic surgery patients. Infect Control Hosp Epidemiol. Oct 2001;22(10):607-12. [Medline].
Nathens AB, Dellinger EP. Surgical site infections. Curr Treatment Options Infect Dis. 2000;2:347-348.
Nosocomial Infection National Surveillance Service (NINSS). Surgical site infection in English hospitals: a national surveillance and quality improvement program. Public Health Laboratory Service. 2002.
- Table 1. Pathogens Commonly Associated with Wound Infections and Frequency of Occurrence[11]
- Table 2: Surgical Wound Classification and Subsequent Risk of Infection (If No Antibiotics Used)[11, 16]
- Table 3. Recommendations for Prophylactic Antibiotics as Indicated by Probable Infective Microorganism Involved[11, 22]
- Table 4. American Society of Anesthesiologists (ASA) Classification of Physical Status[25]
- Table 5. Predictive Percentage of SSI Occurrence by Wound Type and Risk Index*[24]
- Table 6. Data Support Recommendations
| Pathogen | Frequency (%) |
| Staphylococcus aureus | 20 |
| Coagulase-negative staphylococci | 14 |
| Enterococci | 12 |
| Escherichia coli | 8 |
| Pseudomonas aeruginosa | 8 |
| Enterobacter species | 7 |
| Proteus mirabilis | 3 |
| Klebsiella pneumoniae | 3 |
| Other streptococci | 3 |
| Candida albicans | 3 |
| Group D streptococci | 2 |
| Other gram-positive aerobes | 2 |
| Bacteroides fragilis | 2 |
| Classification | Description | Infective Risk (%) |
| Clean (Class I) | Uninfected operative wound No acute inflammation Closed primarily Respiratory, gastrointestinal, biliary, and urinary tracts not entered No break in aseptic technique Closed drainage used if necessary | < 2 |
| Clean-contaminated (Class II) | Elective entry into respiratory, biliary, gastrointestinal, urinary tracts and with minimal spillage No evidence of infection or major break in aseptic technique Example: appendectomy | < 10 |
| Contaminated (Class III) | Nonpurulent inflammation present Gross spillage from gastrointestinal tract Penetrating traumatic wounds < 4 hours Major break in aseptic technique | About 20 |
| Dirty-infected (Class IV) | Purulent inflammation present Preoperative perforation of viscera Penetrating traumatic wounds >4 hours | About 40 |
| Operation | Expected Pathogens | Recommended Antibiotic |
| Orthopedic surgery (including prosthesis insertion), cardiac surgery, neurosurgery, breast surgery, noncardiac thoracic procedures | S aureus, coagulase-negative staphylococci | Cefazolin 1-2 g |
| Appendectomy, biliary procedures | Gram-negative bacilli and anaerobes | Cefazolin 1-2 g |
| Colorectal surgery | Gram-negative bacilli and anaerobes | Cefotetan 1-2 g or cefoxitin 1-2 g plus oral neomycin 1 g and oral erythromycin 1 g (start 19 h preoperatively for 3 doses) |
| Gastroduodenal surgery | Gram-negative bacilli and streptococci | Cefazolin 1-2 g |
| Vascular surgery | S aureus, Staphylococcusepidermidis, gram-negative bacilli | Cefazolin 1-2 g |
| Head and neck surgery | S aureus, streptococci, anaerobes and streptococci present in an oropharyngeal approach | Cefazolin 1-2 g |
| Obstetric and gynecological procedures | Gram-negative bacilli, enterococci, anaerobes, group B streptococci | Cefazolin 1-2 g |
| Urology procedures | Gram-negative bacilli | Cefazolin 1-2 g |
| ASA Score | Characteristics |
| 1 | Normal healthy patient |
| 2 | Patient with mild systemic disease |
| 3 | Patient with a severe systemic disease that limits activity but is not incapacitating |
| 4 | Patient with an incapacitating systemic disease that is a constant threat to life |
| 5 | Moribund patient not expected to survive 24 hours with or without operation |
| At Risk Index | Predictive Percentage of SSI |
| 0 | 1.5 |
| 1 | 2.9 |
| 2 | 6.8 |
| 3 | 13.0 |
| *Hospital Infection Control Practices Advisory Committee (HICPAC) recommendations (partial) for the prevention of SSIs, April 1999 (non–drug based) | |
| Category | Description |
| Category IA | Well designed, experimental, strong; recommended (Category I*) clinical or epidemiological best practice; should be studies; adapted by all practices |
| Category IB | Some experimental, fairly strong; recommended (Category II*) clinical or epidemiological best practice; should be studies and theoretical grounds; adapted by all practices |
| Category II | Fewer scientific supporting data; limited to specific nosocomial (Category III*) problems |
| No recommendation | Insufficient scientific personnel judgment for use (Category III*) supporting data |
| *Previous nomenclature of 1992 CDC guidelines | |

