eMedicine Specialties > General Surgery > Wounds

Wound Infection

Hemant Singhal, MD, MBBS, FRCSE, FRCS(C), Senior Lecturer, Department of Surgery, Imperial College School of Medicine, UK; Consultant Surgeon, Northwick Park and St Marks Hospitals, UK
Kanchan Kaur, MBBS, MS, MRCS (Ed), Clinical Fellow, Department of Surgery, Northwick Park Hospital, UK; Charles Zammit, MD, Senior Specialist Registrar, Department of Surgery, Breast Unit Charing Cross Hospital of London, England

Updated: Sep 8, 2009

Introduction

Background

History

The ancient Egyptians were the first civilization to have trained clinicians to treat physical aliments. Medical papyri, such as the Edwin Smith papyrus (circa 1600 BC) and the Ebers papyrus (circa 1534 BC), provided detailed information of management of disease, including wound management with the application of various potions and grease to assist healing.^1,2 (See images below and Images 1-2.)

Wound infection due to disturbed coagulopathy. This patient has a pacemaker (visible below right clavicular space) and had previous cardiac surgery (median sternotomy wound visible) for a rheumatic mitral valve disorder, which was replaced. The patient was taking anticoagulants preoperatively. Despite converting to low-molecular weight subcutaneous heparin treatment and establishing normal coagulation studies, she developed a postoperative hematoma with subsequent wound infection. She had the hematoma evacuated and was administered antibiotic treatment as guided by microbiological results, and the wound was left to heal by secondary intention.

Abscess secondary to a subclavian line.

The scale of wound infections was most evident in times of war. During the American Civil War, erysipelas (necrotizing infection of soft tissue) and tetanus accounted for over 17,000 deaths, according to an anonymous source in 1883. Because compound fractures at the time almost invariably were associated with infection, amputation was the only option, despite a 25-90% risk of amputation stump infection.

Koch (Professor of Hygiene and Microbiology, Berlin, 1843-1910) first recognized the cause of infective foci as secondary to microbial growth in his 19th century postulates. Semmelweis (Austrian obstetrician, 1818-1865) demonstrated a 5-fold reduction in puerperal sepsis by hand washing between performing postmortem examinations and entering the delivery room. Joseph Lister (Professor of Surgery, London, 1827-1912) and Louis Pasteur (French bacteriologist, 1822-1895) revolutionized the entire concept of wound infection. Lister recognized that antisepsis could prevent infection.⁴ In 1867, Lister placed carbolic acid into open fractures to sterilize the wound and to prevent sepsis and hence the need for amputation. In 1871, Lister began to use carbolic spray in the operating room to reduce contamination. However, the concept of wound suppuration persevered even among eminent surgeons, such as John Hunter, 1728-1793.⁵

World War I (WWI) resulted in new types of wounds from high-velocity bullet and shrapnel injuries coupled with contamination by the mud from the trenches. Antoine Depage (Belgian military surgeon, 1862-1925) reintroduced wound debridement and delayed wound closure and relied on microbiological assessment of wound brushings as guidance for the timing of secondary wound closure.⁶ Alexander Fleming (microbiologist, London, 1881-1955) performed many of his bacteriological studies during WWI and is credited with the discovery of penicillin.

As late as the 19th century, aseptic surgery was not routine practice. Sterilization of instruments began in the 1880s as did the wearing of gowns, masks, and gloves. Halsted (Professor of Surgery, Johns Hopkins University, United States, 1852-1922) introduced rubber gloves to his scrub nurse (and future wife) because she was developing skin irritation from the chemicals used to disinfect instruments. The routine use of gloves was introduces by Halsted's student J. Bloodgood.

Penicillin first was used clinically in 1940 by Howard Florey. With the use of antibiotics, a new era in the management of wound infections commenced. Unfortunately, eradication of the infective plague affecting surgical wounds has not ended because of the insurgence of antibiotic-resistant bacterial strains and the nature of more adventurous surgical intervention in immunocompromised patients and in implant surgery.

Pathophysiology

Wound healing is a continuum of complex interrelated biological processes at the molecular level. Healing is divided into the following phases for descriptive purposes: inflammatory phase, proliferative phase, and maturation phase.

The inflammatory phase commences as soon as tissue integrity is disrupted by injury; this begins the coagulation cascade to limit bleeding. Platelets are the first of the cellular components that aggregate to the wound, and, as a result of their degranulation (platelet reaction), they release several cytokines (or paracrine growth factors). These cytokines include platelet derived growth factor (PDGF), insulinlike growth factor-1 (IGF-1), epidermal growth factor (EGF), and fibroblast growth factor (FGF). Serotonin is also released, which, together with histamine (released by mast cells), induces a reversible opening of the junctions between the endothelial cells, allowing the passage of neutrophils and monocytes (which become macrophages) to the site of injury.

This large cellular movement to the injury site is induced by cytokines secreted by the platelets (chemotaxis) and by further chemotactic cytokines secreted by the macrophages themselves once at the site of injury. These include transforming growth factor alpha (TGF-alpha) and transforming growth factor beta (TGF-beta). Consequently, an inflammatory exudate that contains red blood cells, neutrophils, macrophages, and plasma proteins, including coagulation cascade proteins and fibrin strands, fills the wound in a matter of hours. Macrophages not only scavenge but they also are central to the wound healing process because of their cytokine secretion.

The proliferative phase begins as the cells that migrate to the site of injury, such as fibroblasts, epithelial cells, and vascular endothelial cells, start to proliferate and the cellularity of the wound increases. The cytokines involved in this phase include FGFs, particularly FGF-2 (previously known as basic FGF), which stimulates angiogenesis and epithelial cell and fibroblast proliferation. The marginal basal cells at the edge of the wound migrate across the wound, and, within 48 hours, the entire wound is epithelialized. In the depth of the wound, the number of inflammatory cells decreases with the increase in stromal cells, such as fibroblasts and endothelial cells, which, in turn, continue to secrete cytokines. Cellular proliferation continues with the formation of extracellular matrix proteins, including collagen and new capillaries (angiogenesis). This process is variable in length and may last several weeks.

In the maturation phase, the dominant feature is collagen. The dense bundle of fibers, characteristic of collagen, is the predominant constituent of the scar. Wound contraction occurs to some degree in primary closed wounds but is a pronounced feature in wounds left to close by secondary intention. The cells responsible for wound contraction are called myofibroblasts, which resemble fibroblasts but have cytoplasmic actin filaments responsible for contraction.

The wound continuously undergoes remodeling to try to achieve a state similar to that prior to injury. The wound has 70-80% of its original tensile strength at 3-4 months postoperative.

Frequency

United States

Surgical site infections (SSIs) are not an extinct entity; they account for 14-16% of the estimated 2 million nosocomial infections affecting hospitalized patients in the United States.⁷

International

Internationally, the frequency of SSI is difficult to monitor because criteria for diagnosis might not be standardized. A survey sponsored by the World Health Organization demonstrated a prevalence of nosocomial infections varying from 3-21%, with wound infections accounting for 5-34% of the total.⁸ The 2002 survey report by the Nosocomial Infection National Surveillance Service (NINSS), which covers the period between October 1997 and September 2001, indicates that the incidence of hospital acquired infection related to surgical wounds in the United Kingdom is as high as 10% and costs the National Health Service in the United Kingdom approximately 1 billion pounds (1.8 billion dollars) annually.

Collated data on the incidence of wound infections probably underestimate true incidence because most wound infections occur when the patient is discharged, and these infections may be treated in the community without hospital notification.

Mortality/Morbidity

SSIs are associated not only with increased morbidity but also with mortality. Seventy-seven percent of the deaths of surgical patients were related to surgical wound infection.⁹ Kirkland et al calculated a relative risk of death of 2.2 attributable to SSIs, compared to matched surgical patients without infection.¹⁰

Clinical

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 and Image 3) 
  • 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.

Definitions of surgical site infection (SSI).

• 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 and in Image 4.

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.
  • 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.

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).

Table 2: Surgical Wound Classification and Subsequent Risk of Infection (If No Antibiotics Used)^11,15

Differential Diagnoses

Abdominal Abscess

Workup

Laboratory Studies

• Staining methods: The simplest, and usually the quickest, method involves obtaining a Gram stain for infective organisms. Staining for fungal elements can be obtained at the same time.
• Culture techniques: Most laboratories routinely will culture for both aerobic and anaerobic organisms. Fungal cultures can be requested. Isolation of single colonies allows further growth and identification of the specific organism. Sensitivity testing then follows mainly for aerobic organisms.
• Newer techniques
  • Tests for antigens from the organism through enzyme-linked immunoassay (ELISA) or radioimmunoassay
  • Detection of antibody response to the organism in the host sera
  • Detection of RNA or DNA sequences or protein from the infective organism by Northern, Southern, or Western blotting, respectively
  • Polymerase chain reaction (PCR) is a sensitive assay to detect small amounts of microbe DNA.

Imaging Studies

• Ultrasonography can be applied to the infected wound area to assess whether any collection needs drainage.

Treatment

Medical Care

The use of antibiotics was a milestone in the effort to prevent wound infection. The concept of prophylactic antibiotics was established in the 1960s when experimental data established that antibiotics had to be in the circulatory system at a high enough dose at the time of incision to be effective.¹⁶

General agreement exists that prophylactic antibiotics are indicated for clean-contaminated and contaminated wounds (see Table 2). Antibiotics for dirty wounds are part of the treatment because infection is established already. Clean procedures might be an issue of debate. No doubt exists regarding the use of prophylactic antibiotics in clean procedures in which prosthetic devices are inserted because infection in these cases would be disastrous for the patient. However, other clean procedures (eg, breast surgery) may be a matter of contention.^17,18

Criteria for the use of systemic preventive antibiotics in surgical procedures are as follows:

• Systemic preventive antibiotics should be used in the following cases:
  • A high risk of infection is associated with the procedure (eg, colon resection).
  • Consequences of infection are unusually severe (eg, total joint replacement).
  • The patient has a high NNIS risk index.
• The antibiotic should be administered preoperatively but as close to the time of the incision as is clinically practical. Antibiotics should be administered before induction of anesthesia in most situations.
• The antibiotic selected should have activity against the pathogens likely to be encountered in the procedure.
• Postoperative administration of preventive systemic antibiotics beyond 24 hours has not been demonstrated to reduce the risk of SSIs.

Qualities of prophylactic antibiotics include efficacy against predicted bacterial microorganisms most likely to cause infection, good tissue penetration to reach wound involved, cost effectiveness, and minimal disturbance to intrinsic body flora (eg, gut).¹⁹

The timing of administration is critically important because the concentration of the antibiotic should be at therapeutic levels at the time of incision, during the surgical procedure, and, ideally, for a few hours postoperatively.¹¹ Administration of the antibiotic is by IV; 30 minutes prior to incision is the recommended time.²⁰ Antibiotics should not be administered more than 2 hours prior to surgery. Colorectal surgical prophylaxis additionally requires bowel clearance with enemas and oral nonabsorbable antimicrobial agents 1 hour before surgery.²¹ High-risk cesarean surgical cases require antibiotic administration as soon as the clamping of the umbilical cord is completed.¹¹ See Table 3 for specific antibiotics recommended.

The current risk index used to predict the risk of developing a wound infection is the NNIS system of the CDC.¹¹ The risk index category is established by the added total of the risk factors present at the time of surgery. For each risk factor present, a point is allocated; risk index values range from 0-3. This risk index is a better predictor for SSIs than the surgical wound classification (see Table 2 and Table 5).²²

The NNIS risk index integrates the 3 main determinants of infection, namely, bacteria, local environment, and systemic host defenses (patient health status). The risk index does not include other risk variables, like smoking, tissue oxygen tension, glucose control, shock, and maintenance of normothermia. All these factors are relevant for clinicians but difficult to monitor and fit into a manageable risk assessment.

The elements constituting this index are as follows:

• Preoperative patient physical status assessed by the anesthesiologist and classified by the American Society of Anesthesiologists (see Table 4) as greater than 3
• Operation status as either contaminated or dirty-infected (see Table 2)
• Operation lasting longer than T hours, where T is the 75th percentile of the specific operation performed

*Hospital Infection Control Practices Advisory Committee (HICPAC) recommendations (partial) for the prevention of SSIs, April 1999 (non–drug based)

*Previous nomenclature of 1992 CDC guidelines

• Category IA criteria
  • Identify and treat all infections remote from the surgical site. Delay operation in elective cases until infection is treated.
  • Do not remove hair unless it infringes on the surgical field. If hair removal is required, it should be removed immediately before operation and preferably with electric clippers.
• Category IB criteria
  • Patients should cease tobacco consumption in any form for at least 1 month preoperatively.
  • Optimize blood glucose level and avoid hyperglycemia.
  • Patients are to shower/bathe with antiseptic on at least the night before surgery.
  • Necessary blood products may be administered.
• Category II criteria: Provided preoperative patient preparation is adequate, minimize preoperative hospital stay.
• No recommendation
  • Gradual reduction/discontinuation steroid use before elective surgery
  • Enhanced nutritional intake solely to prevent SSI
  • Preoperative topical antibiotic use in nares to prevent SSI
  • Measures to enhance wound space oxygenation

Surgical team members

• Category IB
  • Keep fingernails short; do not wear artificial nails.
  • Scrub hands and forearms as high as the elbows for at least 2-5 minutes with appropriate antiseptic.
  • After scrub, keep hands up with elbows flexed and away from the body; use a sterile towel to dry the hands and put on a sterile gown and gloves.
  • Masks should be worn in the operating suite if sterile instruments are exposed and throughout the surgical procedure. Masks should cover the mouth and nose.
  • The hair on the head and face is to be covered with a hood or cap.
  • Liquid-resistant sterile surgical gowns and sterile gloves are to be worn by scrubbed surgical team members.
  • Visibly soiled gowns are to be changed.
  • Shoe covers are not necessary.
  • Routine exclusion of personnel colonized by organisms, such as S aureus or group A streptococci, is not necessary unless they are specifically linked to dissemination of such organisms.
  • Personnel with skin lesions that are draining are to be excluded from duty until treated and the infection has resolved.
  • Educate and encourage surgical personnel regarding reporting illness of transmissible nature to supervisory and occupational health personnel.
  • Policies should be established concerning patient care responsibilities for personnel with potentially transmissible infective illnesses. This should include aspects of work restrictions, personnel responsibility in utilizing health services, and declaring illness. Policies also should direct the responsible person to remove personnel from duty, and policy should be established for clearance to resume work.
• Category II
  • Clean the under fingernails prior to the first scrub of the day.
  • Do not wear arm/hand jewelry.
• No recommendation
  • Nail polish
  • Restriction of scrub suits to the operating theater
  • Covering the scrub suits when outside the theater
  • How or where to launder theater suites

Preoperative and postoperative wound care

• Category IA: Asepsis is necessary in the insertion of indwelling catheters, such as intravascular, spinal, or epidural catheters, and subsequent infusion of drugs. (See image below and Image 2.)

Abscess secondary to a subclavian line.

• Category IB
  • Handle tissues gently with good hemostasis, minimize foreign bodies, and minimize devitalized tissue and dead space.
  • For Class III and IV wounds, use delayed closure or leave the wound incision open to heal by secondary intention.
  • If draining of a wound is necessary, the drain exit should be via separate incision distant from the wound. Remove the drain as soon as possible.
  • Primary closed incisions should be protected with a sterile dressing for 24-48 hours.
  • Hands are to be washed before and after wound dressing changes/or contact.
• Category II
  • Use sterile technique for wound dressing change.
  • Educate the patient and relatives regarding wound care symptoms of SSIs and the need to report such problems.

Theater environment and care of instrumentation

• Category IB
  • Maintain positive pressure ventilation of the operating suite relative to corridors and surrounding areas.
  • Maintain a minimum of 15 air changes per hour, with a minimum of 3 being fresh air.
  • Appropriate filters (as recommended by the American Institute of Architects) should be used for filtration of all air whether recirculated or fresh.
  • Air should enter through the ceiling and exit near the floor.
  • Keep operating room doors closed except for necessary entry.
  • The use of ultraviolet lamps in the theater is not necessary as a deterrent of SSI.
  • Prior to subsequent procedures, visibly soiled surfaces should be cleaned with Environmental Protection Agency (EPA)–approved disinfectants.
  • Following a contaminated or dirty procedure, special cleaning or closure of the operating suite is not necessary.
  • Use of tacky mats prior to entry in the operating suite is not necessary.
  • Sterile surgical instruments and solutes should be assembled just prior to use.
  • All surgical instruments should be sterilized according to guidelines. Flush sterilization should only be used for instruments that are required for immediate patient use.
• Category II
  • Limit the number of personnel entering the operating suite.
  • Orthopedic implant surgery should be performed in an ultra clean air environment.
  • Wet vacuum the floor of the operating theater at the end of day/night using an EPA-approved disinfectant.

Special situations

• Elective colon surgery: Bowel surgery results in the breakdown of the protective intestinal mucous membrane, with release of the facultative and anaerobic bacteria that heavily colonize the distal small bowel and colon. Eradication of aerobes and anaerobes is necessary to reduce infective complications following intestinal procedures. Mechanical cleansing and antibiotics could achieve this. Mechanical cleansing for colonic surgery can take the form of dietary restrictions; whole gut lavage with one of several preparations, such as 10% mannitol solution, Fleet's phospho-soda, or polyethylene glycol, usually is performed on the day of surgical intervention. Enteral antibiotic regimes to eradicate intrinsic bowel flora vary, with oral neomycin and erythromycin being the most popular combination used in the United States. Other combinations with neomycin include the use of metronidazole and tetracycline. Prophylactic parenteral antibiotics also are used with the above as recommended in Table 3.
• Intravascular device-related infections: Intravascular devices are of vital use in daily hospital practice. Their use is for the parenteral administration of fluids, blood products, nutritional fluids, and medication and for access in hemodialysis; equally important is their use in the monitoring of critically ill patients. Unfortunately, because their use constitutes an invasive procedure, they are associated with infectious complications that could be of a local or systemic nature. Recommendations for prevention²⁴ and treatment²⁵ are available to limit their associated morbidity and mortality (which could be as high as 20% in patients with catheter-related bloodstream infections).
  
  In a double-blind, randomized, controlled study of 400 patients with nontunnelled central venous catheters, Dettenkofer et al investigated the effectiveness of the antiseptic octenidine dihydrochloride, used in combination with alcohol-based antiseptic, against infection at central venous catheter insertion sites.²⁶ One group of patients received skin disinfection with 0.1% octenidine with 30% 1-propanol and 45% 2-propanol, while a control group was disinfected with 74% ethanol with 10% 2-propanol.
  
  The investigators found that microbial skin colonization at the catheter insertion site and positive microbial cultures at the catheter tip were significantly reduced in the octenidine group. No significant differences in catheter-associated bloodstream infections were found between the octenidine and control groups.

Surgical Care

Although the goal of every surgeon is to prevent wound infections, they will arise. Treatment is individualized to the patient, the wound, and the nature of the infection. The operating surgeon should be made aware of the possibility of infection in the wound and determine the treatment for the wound.

Ideally, surgical care should start with meticulous detail to strategies that prevent the development of SSIs in the first place. Preoperatively, attention should be paid to factors like optimization of patient status, proper asepsis, and surgical site preparation. Intraoperatively, adherence to good basic surgical principles of minimal and fine tissue dissection, proper selection of suture materials, and proper wound closure is important.

If a SSI sets in, the treatment often involves opening the wound, evacuating pus, and cleansing the wound. The deeper tissues are inspected for integrity and for a deep space infection or source. Dressing changes allow the tissues to granulate, and the wound heals by secondary intention over several weeks. Early/delayed closure of infected wounds is often associated with relapse of infection and wound dehiscence.

• Newer concepts in the prevention of SSIs
  • Evidence shows that the close regulation of blood sugar may be a major determinant of wound morbidity. Although investigators have vigorously pursued for decades the identification of a specific innate or acquired immune deficiency among patients with diabetes, it may be the blood sugar that is the determinant of infection for these patients.
  • A second issue of considerable interest is body temperature. There is now a prospective randomized study that demonstrates that failure to maintain intraoperative core body temperature within 1-1.5°C of normal increases the SSI rate by a factor of 2. It begs the scientific question whether increasing core temperature during operations over normal temperature might in fact protect against infection.
  • The third issue is oxygenation. The fresh, hemostatic surgical incision is a hypoxic, ischemic environment. Maintaining or increasing oxygen delivery to the wound by increasing the inspired oxygen concentration administered to the patient perioperatively has also been shown to reduce the incidence of SSIs. It is presumed that increased oxygen availability is a positive host factor, perhaps via enhanced production of oxidant products that facilitate phagocytic eradication of microbes.
• Future strategies
  • The establishment of dedicated infection surveillance units in hospitals that aim to accomplish the following:
    • Identify epidemics by common or uncommon organisms.
    • Establish the correct use of prophylaxis (ie, timing, dose, duration, choice).
    • Document costs, risk factors, and readmission rates.
    • Monitor postdischarge infections and secondary consequences.
    • Ensure patient safety.
  • Preventing the emergence of resistance: Although resistance is not a new phenomenon, the incidence has increased dramatically over the past 2 decades. The development of new drugs has slowed considerably and may be unable to keep pace with the continuing growth of pathogen resistance. Therefore, effective strategies are needed to prevent the continuing emergence of antimicrobial resistance. These strategies include avoiding unnecessary antibiotic administration and increasing the effectiveness of prescribed antibiotics, as well as implementing improvements in infection control and optimizing medical practice.
• Although an SSI rate of zero may not be achievable, continued progress in understanding the biology of infection at the surgical site and consistent applications of proven methods of prevention will further reduce the frequency, cost, and morbidity associated with SSIs.

Medication

The choice of antibiotic depends on 2 factors—the patient and the known or probable infecting microorganism. Patient factors include allergies, hepatic and renal function, severity of disease process, interaction with other medication(s), and age. In women, pregnancy and breastfeeding must be considered.

Antibiotics

Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.

Cefazolin (Ancef, Kefzol, Zolicef)

First-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Primarily active against skin flora, including Staphylococcus aureus. Typically used alone for skin and skin-structure coverage. IV and IM dosing regimens are similar.

Dosing

Adult

250 mg to 2 g IV/IM q6-12h depending on severity of infection; not to exceed 12 g/d

Pediatric

25-100 mg/kg/d IV/IM divided q6-8h depending on severity of infection; not to exceed 6 g/d

Interactions

Probenecid prolongs effect; coadministration with aminoglycosides may increase renal toxicity; may yield false-positive urine-dip test for glucose

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Adjust dose in renal impairment; superinfections and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy

Erythromycin (EES, E-Mycin, Eryc)

Inhibits bacterial growth possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections.
In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.

Dosing

Adult

250 mg erythromycin (stearate, base) or 400 mg ethylsuccinate q6h PO 1 h ac or 500 mg q12h; alternatively, 333 mg q8h; increase to 4 g/d depending on severity of infection

Pediatric

30-50 mg/kg/d (15-25 mg/lb/d) PO divided q6-8h; double dose for severe infection

Interactions

Coadministration may increase toxicity of theophylline, digoxin, carbamazepine, and cyclosporine; may potentiate anticoagulant effects of warfarin; coadministration with lovastatin and simvastatin increases risk of rhabdomyolysis

Contraindications

Documented hypersensitivity; hepatic impairment

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Caution in liver disease; estolate formulation may cause cholestatic jaundice; GI adverse effects are common (administer ac); discontinue use if nausea, vomiting, malaise, abdominal colic, or fever occur

Cefoxitin (Mefoxin)

Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin.

Dosing

Adult

1-2 g IV q6-8h

Pediatric

Infants and children: 80-160 mg/kg/d IV divided q4-6h; higher doses for severe or serious infections; not to exceed 12 g/d

Interactions

Probenecid may increase effects of cefoxitin; coadministration with aminoglycosides or furosemide may increase nephrotoxicity (closely monitor renal function)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged use or repeated treatment; caution in patients with previously diagnosed colitis

Cefotetan (Cefotan)

Second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods.
Dose and route of administration depend on condition of patient, severity of infection, and susceptibility of causative organism.

Dosing

Adult

1-2 g IV/IM q12h for 5-10 d

Pediatric

20-40 mg/kg/dose IV/IM q12h for 5-10 d

Interactions

Consumption of alcohol within 72 h of cefotetan may produce disulfiramlike reactions; cefotetan may increase hypoprothrombinemic effects of anticoagulants; coadministration with potent diuretics (eg, loop diuretics) or aminoglycosides may increase nephrotoxicity

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Reduce dose by one half if CrCl <10-30 mL/min and by one fourth if CrCl <10 mL/min; bacterial or fungal overgrowth of nonsusceptible organisms may occur with prolonged or repeated therapy

Follow-up

Further Inpatient Care

• Resultant increased hospital stay due to SSI has been estimated at 7-10 days, increasing hospitalization costs by 20%.^21,27,28
• Occasionally, further intervention in the form of wound debridement and subsequent packing and frequent dressing is necessary to allow healing by secondary intention.

Further Outpatient Care

• Most patients with wound infections are managed in the community. Management usually takes the form of dressing changes to optimize healing, which usually is by secondary intention.

Miscellaneous

Medicolegal Pitfalls

• Always inquire about whether the patient has any medication allergies before prescribing antibiotics.
• Failure to prescribe prophylactic antibiotics for a procedure as recommended above may result in the surgeon being held accountable if the patient has increased morbidity or mortality from the surgical procedure.
• A medicolegal issue may arise for failure to recognize an infected prosthesis and institute prompt action.

Multimedia

Media file 1: Wound infection due to disturbed coagulopathy. This patient has a pacemaker (visible below right clavicular space) and had previous cardiac surgery (median sternotomy wound visible) for a rheumatic mitral valve disorder, which was replaced. The patient was taking anticoagulants preoperatively. Despite converting to low-molecular weight subcutaneous heparin treatment and establishing normal coagulation studies, she developed a postoperative hematoma with subsequent wound infection. She had the hematoma evacuated and was administered antibiotic treatment as guided by microbiological results, and the wound was left to heal by secondary intention.

Media file 2: Abscess secondary to a subclavian line.

Media file 3: Definitions of surgical site infection (SSI).

Media file 4: Factors that affect surgical wound healing.

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Keywords

wound infection, MRSA infection, nosocomial infection, hospital infection, methicillin-resistant Staphylococcus aureus, surgical infection, surgical infections, MRSA vancomycin, surgical site infection, surgical wound infection, surgical wound healing

Contributor Information and Disclosures

Author

Hemant Singhal, MD, MBBS, FRCSE, FRCS(C), Senior Lecturer, Department of Surgery, Imperial College School of Medicine, UK; Consultant Surgeon, Northwick Park and St Marks Hospitals, UK
Hemant Singhal, MD, MBBS, FRCSE, FRCS(C) is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada and Royal College of Surgeons of Edinburgh
Disclosure: Nothing to disclose.

Coauthor(s)

Kanchan Kaur, MBBS, MS, MRCS (Ed), Clinical Fellow, Department of Surgery, Northwick Park Hospital, UK
Disclosure: Nothing to disclose.

Charles Zammit, MD, Senior Specialist Registrar, Department of Surgery, Breast Unit Charing Cross Hospital of London, England
Disclosure: Nothing to disclose.

Medical Editor

Brian James Daley, MD, MBA, FACS, Associate Program Director, Professor, Department of Surgery, Division of Trauma and Critical Care, University of Tennessee School of Medicine
Brian James Daley, MD, MBA, FACS is a member of the following medical societies: American Association for the Surgery of Trauma, American College of Chest Physicians, American College of Surgeons, American Medical Association, Association for Academic Surgery, Association for Surgical Education, Eastern Association for the Surgery of Trauma, Shock Society, Society of Critical Care Medicine, Southeastern Surgical Congress, and Tennessee Medical Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Amy L Friedman, MD, Professor of Surgery, Director of Transplantation, State University of New York Upstate Medical University College of Medicine, Syracuse
Amy L Friedman, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Medical Women's Association, American Society for Artificial Internal Organs, American Society of Transplant Surgeons, American Society of Transplantation, Association for Academic Surgery, Association of Women Surgeons, International College of Surgeons, International Liver Transplantation Society, New York Academy of Sciences, Pennsylvania Medical Society, Philadelphia County Medical Society, Society of Critical Care Medicine, and Transplantation Society
Disclosure: Nothing to disclose.

CME Editor

Michael E Zevitz, MD, Assistant Professor of Medicine, Finch University of the Health Sciences, The Chicago Medical School; Consulting Staff, Private Practice
Michael E Zevitz, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Chief Editor

John Geibel, MD, DSc, MA, Vice Chairman, Professor, Department of Surgery, Section of Gastrointestinal Medicine and Department of Cellular and Molecular Physiology, Yale University School of Medicine; Director of Surgical Research, Department of Surgery, Yale-New Haven Hospital
John Geibel, MD, DSc, MA is a member of the following medical societies: American Gastroenterological Association, American Physiological Society, American Society of Nephrology, Association for Academic Surgery, International Society of Nephrology, New York Academy of Sciences, and Society for Surgery of the Alimentary Tract
Disclosure: AMGEN Royalty Other

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Clinical guidelines:
Best practice policy statement on urological surgery antimicrobial prophylaxis. American Urological Association Education and Research, Inc. - Medical Specialty Society.  2007 Jan.  46 pages.  NGC:006297

Prevention of surgical site infections. In: Prevention and control of healthcare-associated infections in Massachusetts. Betsy Lehman Center for Patient Safety and Medical Error Reduction - State/Local Government Agency [U.S.]
Massachusetts Department of Public Health - State/Local Government Agency [U.S.].  2008 Jan 31.  8 pages.  NGC:006635

Strategies to prevent catheter-associated urinary tract infections in acute care hospitals. Infectious Diseases Society of America - Medical Specialty Society
Society for Healthcare Epidemiology of America - Professional Association.  2008 Oct.  10 pages.  NGC:006805

Strategies to prevent surgical site infections in acute care hospitals. Infectious Diseases Society of America - Medical Specialty Society
Society for Healthcare Epidemiology of America - Professional Association.  2008 Oct.  11 pages.  NGC:006810

Surgical site infection: prevention and treatment of surgical site infection. National Collaborating Centre for Women's and Children's Health - National Government Agency [Non-U.S.].  2008 Oct.  142 pages.  NGC:006827

Clinical trials:
Prevention of Surgical Site Infections

Supplemental Oxygen and the Risk of Surgical Site Infection (PORSSI)

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