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 BCE) and the Ebers papyrus (circa 1534 BCE), provided detailed information of management of disease, including wound management with the application of various potions and grease to assist healing.[1, 2]
See 5 Body Modifications and Piercing: Dermatologic Risks and Adverse Reactions, a Critical Images slideshow, to help recognize various body modifications and the related potential complications.
Hippocrates (Greek physician and surgeon, 460-377 BCE), known as the father of medicine, used vinegar to irrigate open wounds and wrapped dressings around wounds to prevent further injury. His teachings remained unchallenged for centuries.
Galen (Greek surgeon to Roman gladiators, 130-200 CE) was the first to recognize that pus from wounds inflicted by the gladiators heralded healing (pus bonum et laudabile ["good and commendable pus"]).
Unfortunately, Galen's observation was misinterpreted, and the concept of pus preempting wound healing persevered well into the 18th century. The link between pus formation and healing was emphasized so strongly that foreign material was introduced into wounds to promote pus formation-suppuration. The concept of wound healing remained a mystery, as highlighted by the famous saying by Ambroise Paré (French military surgeon, 1510-1590), "I dressed the wound. God healed it."[3]
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 fivefold 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, he 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.[5]
World War I 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 bacteriologic studies during World War I 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 introduced by Bloodgood, a student of Halsted.
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.
Wound healing is a continuum of complex interrelated biologic processes at the molecular level. For descriptive purposes, healing may be divided into the following three phases:
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-α) and transforming growth factor beta (TGF-β).
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 after operation.
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 (see the image below).
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 surgical-site infections (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).[7]
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.[8] (See Table 1 below.)
Table 1. Pathogens Commonly Associated with Wound Infections and Frequency of Occurrence [8] (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 |
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 group of bacteria most commonly responsible for SSIs are Staphylococcus aureus strains. 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.[9]
Of particular concern are the vancomycin intermediate S 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.
Decreased host resistance can be due to systemic factors affecting the patient's healing response, local wound characteristics, or operative characteristics, as follows:
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 below).[8, 10]
Table 2: Surgical Wound Classification and Subsequent Risk of Infection (If No Antibiotics Used) [8, 10] (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 |
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.[11]
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 (WHO) demonstrated a prevalence of nosocomial infections in the range of 3-21%, with wound infections accounting for 5-34% of the total.[12]
The 2002 survey report by the Nosocomial Infection National Surveillance Service (NINSS; now the Surgical Site Infection Surveillance Service [SSISS]),[13] which covered the period between October 1997 and September 2001, indicated that the incidence of hospital-acquired infection related to surgical wounds in the United Kingdom was as high as 10% and cost the country's National Health Service (NHS) approximately 1 billion pounds annually.
Collated data on the incidence of wound infections probably underestimate the true incidence because most wound infections occur when the patient is discharged, and these infections may be treated in the community without hospital notification.
SSIs are associated not only with increased morbidity but also with substantial mortality. In one study, 77% of the deaths of surgical patients were related to surgical wound infection.[14] Kirkland et al calculated a relative risk of death of 2.2 attributable to SSIs, in comparison with matched surgical patients without infection.[15]
Surgical-site infection (SSI) 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) has defined SSI to standardize data collection for the National Nosocomial Infections Surveillance (NNIS) program.[8, 16] SSIs are classified into incisional SSIs, which can be superficial or deep, and organ/space SSIs, which affect the rest of the body other than the body wall layers (see the image below). These classifications are defined as follows:
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, even when adjusted for other factors influencing length of stay.
A report by the NNIS program[17] cited particular clinical findings as characteristic of the different types of SSI.
Superficial incisional SSI is characterized by the following:
Deep incisional SSI is characterized by the following:
Organ/space SSI is characterized by the following:
Examples of wound infections are shown in the images below.
The simplest, and usually the quickest, staining method involves obtaining a Gram stain for infective organisms. Staining for fungal elements can be obtained at the same time.
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.
Other techniques include the following:
Ultrasonography (US) can be applied to the infected wound area to assess whether there is a collection for which drainage is required.
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.
Resultant increased hospital stay due to surgical-site infection (SSI) has been estimated at 7-10 days, increasing hospitalization costs by 20%.[18, 19, 20] Occasionally, further intervention in the form of wound debridement and subsequent packing and frequent dressing is necessary to allow healing by secondary intention.
Guidelines for the management of SSI were published in 2014 by the Infectious Diseases Society of America[21] (IDSA), in 2017 by the Centers for Disease Control and Prevention[22] (CDC), in 2018 by the World Health Organization[23] (WHO), and in 2019 by the Asia Pacific Society of Infection Control[24] (APSIC). (See Guidelines.)
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.[25, 26]
It is generally agreed that prophylactic antibiotics are indicated for clean-contaminated and contaminated wounds (see Table 2 in Overview). 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; infection in these cases would be disastrous for the patient. However, other clean procedures (eg, breast surgery) may be a matter of contention.[27, 28]
Criteria for the use of systemic preventive antibiotics in surgical procedures are as follows:
Qualities of prophylactic antibiotics include efficacy against predicted bacterial microorganisms most likely to cause infection (see Table 3 below), good tissue penetration to reach wound involved, cost effectiveness, and minimal disturbance to intrinsic body flora (eg, gut).[29]
Table 3. Recommendations for Prophylactic Antibiotics as Indicated by Probable Infective Microorganism Involved [8, 30] (Open Table in a new window)
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 |
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.[8] Antibiotics are administered intravenously, generally 30 minutes prior to incision[30] ; they 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.[18] High-risk cesarean surgical cases require antibiotic administration as soon as the clamping of the umbilical cord is completed.[8]
The current risk index used to predict the risk of developing a wound infection is the NNIS system of the CDC.[8] 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 (see Table 4 below) than the surgical wound classification is (see Table 2 in Overview).[31]
Table 4. Predictive Percentage of SSI Occurrence by Wound Type and Risk Index* [31] (Open Table in a new window)
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) |
The NNIS risk index integrates the three 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:
Table 5. American Society of Anesthesiologists (ASA) Classification of Physical Status [32] (Open Table in a new window)
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 |
Perioperative recommendations have been made for minimizing wound infection and SSI, supported by varying degrees of evidence (see Table 6 below).
Table 6. Data Support Recommendations (Open Table in a new window)
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 |
Category IA recommendations for preoperative patient preparation include the following:
Category IB recommendations include the following:
The category II recommendation is as follows: Provided that preoperative patient preparation is adequate, minimize preoperative hospital stay.
No recommendations are made regarding the following:
Category IB recommendations regarding preoperative considerations for surgical team members are as follows:
Category II recommendations are as follows:
No recommendations are made regarding the following:
A category IA recommendation for preoperative and postoperative wound care is that asepsis is necessary in the insertion of indwelling catheters, such as intravascular, spinal, or epidural catheters, and subsequent infusion of drugs. (See the image below.)
Category IB recommendations include the following:
Category II recommendations include the following:
Category IB recommendations for the theater environment and the care of instrumentation include the following:
Category II recommendations include the following:
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 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 in the United States. Other combinations with neomycin include the use of metronidazole and tetracycline. Prophylactic parenteral antibiotics also are used with the above.
Intravascular device-related infections
Intravascular devices are of vital use in daily hospital practice. They are used 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 the use of these devices constitutes an invasive procedure, they are associated with infectious complications that could be of a local or systemic nature. Recommendations for prevention[33] and treatment[34] 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.[35] 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.
In this study, microbial skin colonization at the catheter insertion site and positive microbial cultures at the catheter tip were significantly reduced in the octenidine group.[35] No significant differences in catheter-associated bloodstream infections were found between the groups.
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.
Evidence shows that the close regulation of blood sugar may be a major determinant of wound morbidity.[36] 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. A prospective randomized study demonstrated that failure to maintain intraoperative core body temperature within 1-1.5°C of normal increases the SSI rate by a factor of 2.[37] It raises the scientific question of whether increasing core temperature during operations over normal temperature might in fact protect against infection.
A third issue is oxygenation.[38] 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.
A strategy that could bear fruit for preventing SSIs in the future is the establishment of dedicated infection surveillance units in hospitals with the aim of accomplishing the following:
A major concern is how to prevent or minimize the emergence of resistance. Although resistance is not a new phenomenon, the incidence has increased dramatically over the past two decades. The development of new drugs has slowed considerably and may be unable to keep pace with the continuing growth of pathogen resistance.
Accordingly, 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.
In 2019, the Asia Pacific Society of Infection Control (APSIC) issued the following guidelines for the prevention of surgical-site infection (SSI)[24] :
In 2018, the World Health Organization (WHO) published the second edition of its guidelines regarding SSI,[23] which included the following strong recommendations:
In 2017, the Centers for Disease Control and Prevention (CDC) published an updated guideline for the prevention of SSIs,[22] which included the following recommendations:
In 2014, the Infectious Diseases Society of America (IDSA) issued the following practice guidelines for the management of SSIs[21] :
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.
Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.
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.
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.
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.
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.
Overview
How were physical ailments and wound infections managed in antiquity?
At the start of the first millennium, what were the identifiable manifestations of wound infection?
What is the history of wound infection and management in the 19th century?
How were wound infections treated during the World War era?
What is the pathophysiology of wound healing?
What is the pathophysiology of the inflammatory phase of wound healing?
What is the pathophysiology of the proliferative phase of wound healing?
What is the pathophysiology of the maturation phase of wound healing?
What factors affect wound healing?
Which microbial factors influence the establishment of a wound infection?
What are the causes of surgical site infections (SSIs)?
What are the pathogens commonly associated with wound infections?
What is the role of MRSA in wound infections?
What factors decrease host resistance to wound infections?
What is the prevalence of surgical site infections (SSIs) in the US?
What is the global prevalence of surgical site infections (SSIs)?
What are the morbidity and mortality of surgical site infections (SSIs)?
Presentation
How does the CDC define and classify surgical site infections (SSIs)?
How are superficial surgical site infections (SSIs) characterized?
How are deep incisional surgical site infections (SSIs) characterized?
How are organ surgical site infections (SSIs) characterized?
What are examples of wound infections?
DDX
What are the differential diagnoses for Wound Infection?
Workup
What techniques may be used for identification of wound infections?
What is the role of ultrasonography in the identification of wound infections?
Treatment
How are wound infections managed?
When are prophylactic antibiotics indicated against wound infections?
What are recommended prophylactic antibiotics against wound infection?
How and when should antibiotic prophylaxis against wound infection be administered?
What is the current risk index for wound infection assessment?
What is the National Nosocomial Infections Surveillance (NNIS) risk index?
What are intravascular device-related infections and how are they managed?
How are surgical site infections (SSIs) treated?
What strategies can be employed to reduce pathogen resistance in wound infection?
Guidelines
What are the APSIC guidelines for the prevention of surgical-site infection?
What are the CDC guidelines for prevention of surgical site infection (SSI)?
What are the WHO guidelines for prevention of surgical site infection (SSI)?
What are the IDSA guidelines for prevention of surgical site infection (SSI)?
Medications
What is the basis for antibiotic selection for the treatment of wound infection?
Which medications in the drug class Antibiotics are used in the treatment of Wound Infection?