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Overview of the evaluation and management of surgical site infection

Overview of the evaluation and management of surgical site infection
Heather L Evans, MD, MS
Traci L Hedrick, MD, MS, FACS, FACRS
Section Editors:
Amalia Cochran, MD, FACS, FCCM
Daniel J Sexton, MD
Deputy Editor:
Kathryn A Collins, MD, PhD, FACS
Literature review current through: Dec 2022. | This topic last updated: Apr 01, 2022.

INTRODUCTION — Surgical site infection (SSI) is the most common health care–associated infection following surgery and is associated with significant morbidity and mortality, transfer to an intensive care unit setting, prolonged hospitalizations, and hospital readmission [1]. Among those who undergo surgical procedures annually in the United States, 2 to 4 percent will develop an SSI, representing a significant burden on the health care system as a whole [2]. In addition to the more quantifiable detrimental effects, the development of SSI has a significant impact on patient-reported outcomes and is a source of patient anxiety in the postoperative period, particularly after hospital discharge when patients are responsible for their own wound care and SSI triage [3,4].

The general approach to the evaluation and management of SSI is reviewed. Risk factors for SSI and measures to prevent SSI are reviewed separately. (See "Risk factors for impaired wound healing and wound complications" and "Overview of control measures for prevention of surgical site infection in adults" and "Antimicrobial prophylaxis for prevention of surgical site infection in adults".)

DEFINITION — The United States Centers for Disease Control and Prevention (CDC) definition of SSI is the most widely used. The CDC defines an SSI as an infection related to a surgical procedure that occurs near the surgical site within 30 days following surgery (or up to 90 days following surgery where an implant is involved) [5,6]. Incisional SSIs are further divided into those involving only skin and subcutaneous tissues (superficial incisional SSI) and those involving deeper softer tissues of the incision (deep incisional SSI) (figure 1 and table 1). Organ/space infections include abscess, anastomotic leak for intra-abdominal operations, and implant-associated infections.

Other tools have been used to describe SSIs using objective criteria. These include the ASEPSIS (Additional treatment, the presence of Serous discharge, Erythema, Purulent exudate, and Separation of the deep tissues, the Isolation of bacteria, and the duration of inpatient Stay) scoring system [7], which was created to assess sternal wounds, and a patient-centered wound questionnaire primarily intended for retrospective identification of SSI [8,9]. One review of SSI following colorectal surgery reported better inter-rater agreement between surgeons for ASEPSIS compared with the CDC definitions [10]. Patients or health care providers can use such tools in the hospital or at home following discharge to assess signs, symptoms, and wound care interventions. A key limitation to both these objective scoring systems is that they are cumbersome and may not be practical outside a research setting.

INCIDENCE AND RISK FACTORS — The most common reason for unplanned readmission after surgery is SSI [11]. The incidence of SSI varies widely, ranging from 5 to 30 percent depending upon the operative site and wound classification. It is estimated that SSI develops in 2 to 5 percent of patients undergoing inpatient surgical procedures each year in the United States [12]. SSIs are associated with increased morbidity and mortality [13-15]. The incidence of SSI has decreased over time due to widespread prevention efforts [16]. However, as the population in the United States ages, the number and complexity of patients undergoing surgery will continue to increase, leading to the development of more SSIs [17]. (See "Antimicrobial prophylaxis for prevention of surgical site infection in adults" and "Overview of control measures for prevention of surgical site infection in adults".).

Surgical site infection in middle- to low-income countries may be higher compared with high-income countries, possibly related to cumulative risk factors and resource limitations. In the FALCON study, the incidence of surgical site infection was 22 percent for clean-contaminated cases and 30 percent for contaminated/dirty cases in low- to middle-income countries [18]. Risk factors for SSI in the studied population included no antimicrobial prophylaxis, a high proportion of emergency cases, and current smoking.

SSI rates in ambulatory surgical settings are relatively low. One study reported overall rates at 14 and 30 days of 3.1 and 4.8 per 1000 procedures; however, the surveillance bias in this study was large [19].

Surgical volume may affect the risk of SSI. In a prospective study of surgical procedures performed at 18 community hospitals, hospitals were separated based on average surgical volume per year: small (<1500 procedures), medium (≥1500 and <4000 procedures), and large (≥4000 procedures) [20]. Prospective surveillance identified 1434 SSIs after 132,111 surgical procedures (prevalence rate = 1.09/100 procedures). After adjusting for differences between hospital category and important confounders, the risk of SSI at small hospitals was still 1.5 times higher than medium hospitals (adjusted prevalence rate ratio [PRR] 1.49, 95% CI 1.39-1.60), whereas the risk at large hospitals was substantially decreased compared with medium hospitals (adjusted PRR 1.29, 95% CI 1.22-1.36).

The risk of SSI for individual procedures varies widely. The highest rates occur after abdominal surgery, particularly colon surgery, for which the SSI rate is about 10 percent [21]. Other representative rates for various types of surgery are coronary bypass surgery (3.3 to 3.7 percent), vascular surgery (0.16 to 29 percent) [22], cesarean delivery (3.4 to 30 percent) [23], joint arthroplasty with a prosthesis (0.7 to 1.7 percent), and spinal fusion (1.3 to 3.1 percent). Eye surgery is associated with an extremely low rate of SSI (0.14 percent).

SSIs following surgeries that use implanted materials such as joint replacement, hernia repairs with mesh, and some cardiac surgeries are much less common but are associated with profound consequences. Although the use of implanted materials has revolutionized surgical practice, this technological advancement has come at a cost. Of the more than 2 million health care–associated infections diagnosed annually, as many as 50 percent are associated with an implant [24]. The evaluation and treatment of the implant-associated infection presents its own set of unique challenges. (See 'Deep infection associated with implanted materials' below.)

Risk assessment — Whether an SSI occurs depends upon a complex interaction between numerous factors, including the nature and number of organisms contaminating the surgical site, antimicrobial prophylaxis, the health of the patient, and the technique of the surgeon (table 2). Measures to prevent SSI are reviewed separately. (See "Overview of control measures for prevention of surgical site infection in adults".)

Many of the patient factors identified as risk factors for impaired wound healing (eg, cigarette smoking, older age, vascular disease, obesity, malnutrition, diabetes, immunosuppressive therapy) are also risk factors for SSI [25,26]. The presence of recent or remote infection at the surgical site, recent surgery, and hospitalization are also important. These risk factors are reviewed in more detail separately [27-30]. (See "Risk factors for impaired wound healing and wound complications".)

Other factors that may increase the risk for SSI include the following:

Transfusion – Allogeneic blood transfusion modulates the immune system; however, studies evaluating the association between transfusion and SSI may be confounded by other factors such as duration of surgery, preoperative anemia, and medical comorbidities [31,32]. In addition, many studies investigating this relationship were performed in an era of less restrictive indications for transfusion. Thus, transfusion of blood products should not be withheld from surgical patients when indicated solely as a means to prevent SSI [2].

Local wound factors – Local wound factors such as edema, proximity to other open or contaminated wound sites, and presence of remote infections may also influence the development of SSI [33]. (See "Overview of control measures for prevention of surgical site infection in adults", section on 'Timing of surgery'.)

Surgical wound classification — The degree of contamination of a surgical wound at the time of the operation is an important risk factor for infection and can be classified using the National Healthcare Safety Network (NHSN) wound class as clean, clean-contaminated, contaminated, or dirty/infected (table 3) [34], which is based upon an adaptation of the American College of Surgeons surgical wound classification [34-36]. Surgical site infection (SSI) occurs in approximately 4 percent of clean wounds and 35 percent of grossly contaminated wounds.

Procedure-specific risk factors identified in a logistic regression model using data from the NHSN generally outperform the traditional NHSN risk index based on wound classification [37]. The NHSN has made its risk adjustment models and methods available for participating hospitals via its web tool calculations of the Standardized Infection Ratio. Several of the procedure-specific risk adjustment models offer only raw or minimally adjusted risk calculations due to the lack of statistically significant predictor variables in the existing NHSN database. Other risk adjustment models have been published by the National Surgical Quality Improvement Program (NSQIP) [38] and the Society of Thoracic Surgeons [39].

Measures to reduce risk — Surgeons can reduce rates of SSI using preventive measures that include avoiding elective surgery in patients with active infection, timely administration of prophylactic antibiotics, proper skin preparation, and maintenance of sterile conditions [2,40]. These are discussed elsewhere; surgical techniques that may be helpful to reduce the risk for SSI are briefly reviewed below. (See "Overview of control measures for prevention of surgical site infection in adults".)

Good surgical technique can also help reduce the risk of SSI. Such practices include gentle traction, effective hemostasis, removal of devitalized tissues, obliteration of dead space, irrigation of tissues with saline to avoid excessive drying, wound closure without tension, and minimizing duration of closed-suction drainage [26,41]. The judicious use of electrosurgery can help reduce thermal damage to tissue. Excessive use can cause areas of tissue necrosis that can serve as a nidus for infection. (See "Overview of electrosurgery", section on 'Basic principles' and "Principles of abdominal wall closure".)

Various topical and local antibiotic delivery methods have been used to reduce the incidence of SSI, including antibiotic irrigation, topical antimicrobial agents, antibiotic sutures, and antimicrobial dressings. There is some low-quality evidence for some of these therapies for specific surgical populations and procedures [42-50]. Despite a wide array of delivery systems to deliver antibiotics near implants, few have found their way into routine clinical practice. (See "Overview of control measures for prevention of surgical site infection in adults", section on 'Topical and local antibiotic delivery'.)

A wide variety of surgical drains have also been used to prevent SSI, including closed suction drains within an anatomic space (eg, peritoneal cavity, joint space). In addition, open or closed system surgical drains have been used in the subcutaneous space to prevent SSI. While an exhaustive review of the literature specific to the various surgical subtypes is beyond the scope of this review, in general, there are insufficient data to support the routine use of drains for the prevention of SSI [51,52]. Furthermore, with the advent of Enhanced Recovery after Surgery protocols, the routine use of surgical drains has been discouraged given the negative impact of surgical drains/tubes on early mobilization after surgery [53].

Prophylactic negative pressure wound therapy (NPWT; ie, overlying a closed incision) has been described with the aim of preventing SSI [54,55]. While data are promising for certain high-risk surgeries and contaminated wounds, the evidence does not uniformly support its use. Outcomes likely vary due to the degree of contamination and features related to the incision site [56,57]. (See "Principles of abdominal wall closure", section on 'Negative pressure dressings' and "Negative pressure wound therapy", section on 'Prophylactic use'.)

Leaving the wound open at the primary operation for delayed primary closure is another strategy used to reduce the risk for SSI [58]. Although observational studies have supported this practice, a meta-analysis of randomized trials did not demonstrate a benefit to delayed primary closure [59]; even class III and IV contaminated wounds may be safe for primary closure [60]. Anticipatory management of wounds at high risk for postoperative seroma and SSI is possible with loosely stapled skin closure and daily probing between the staples with a cotton-tipped applicator until the wound is impenetrable [61]. Alternatively, a negative pressure wound dressing applied directly to the approximated wound can evacuate accumulated wound drainage and minimize seroma formation and is also thought to increase blood flow to the wound edges to promote healing. (See "Negative pressure wound therapy", section on 'Mechanism of action' and "Principles of abdominal wall closure", section on 'Negative pressure dressings'.)

There is no evidence to suggest that use of any particular wound dressing over a closed surgical wound has any effect on the rate of SSI [62]; however, wound protectors, which are designed to protect the wound edges from trauma and contamination, may be warranted for prevention of SSI in the setting of clean-contaminated, contaminated, and dirty abdominal procedures [63,64]. Wound protectors are available for laparotomy and laparoscopic incisions and orthopedic incisions [65-69]. (See "Overview of control measures for prevention of surgical site infection in adults", section on 'Intraoperative wound protectors'.)

CLINICAL FEATURES — When SSI is suspected, the wound should be examined directly to facilitate visual and tactile inspection (table 1). Depending upon severity of symptoms, the risk of other potential complications due to the nature of the index operation, and timing of development of symptoms, the patient may be evaluated while still hospitalized or requested to return to the clinic or emergency room if they have been discharged.

Superficial surgical site infection — Evaluation of the skin surrounding the wound includes documentation of the presence and extent of erythema and induration (edema). Symptoms of superficial SSI may include localized swelling, warmth, drainage with or without odor, wound breakdown and separation (ie, dehiscence), peri-incisional erythema, and pain at the incision site. Palpation of the wound area may demonstrate induration or tenderness. Some patients will have systemic evidence of their infection (eg, fever, leukocytosis).

Purulent wound drainage or separation of the wound edges are usually indicative of an infection, and a diagnosis of superficial SSI can usually be made without forced opening of the wound or supplemental imaging. However, superficial incisional dehiscence can occur in the absence of infection. As an example, if staples are removed too soon from a surgical incision in a patient with obesity or immunocompromised state, wound healing may not have progressed sufficiently to keep the edges of the wound together. The presence of purulence and/or surrounding erythema will typically distinguish an infected from uninfected dehiscence. In the absence of purulence or erythema, culturing the deep tissue may be helpful; however, care must be taken to avoid contaminating the culture with skin flora. If the wound is already open, or if underlying fluid or tissue necrosis is suspected, full evaluation of the wound includes examining the greatest depth of involvement and may require opening the skin overlying the area in question, which may need to be performed in an operating room setting.

The aggressiveness with which to further evaluate whether SSI extends to deeper tissues depends on the type of surgery and whether implanted material was used. (See 'Deep incisional surgical site infection' below.)

Deep incisional surgical site infection — Involvement of the fascia and/or muscle with infection is the hallmark of a deep incisional SSI. As with superficial SSI, symptoms of a deep SSI may include localized swelling, warmth, drainage with or without odor, wound breakdown and separation (ie, dehiscence), peri-incisional erythema, and pain at the incision site. Palpation of the wound area may demonstrate tenderness or a fluctuant mass. Deep SSIs are more often accompanied by fever and local tenderness. Systemic signs of infection may include fever, leukocytosis, or elevation of other markers of acute inflammation, such as C-reactive protein or procalcitonin.

A high degree of suspicion is warranted, as it can be difficult to diagnose a deep SSI clinically, particularly in a patient with obesity. Imaging (eg, ultrasound, computed tomography) is helpful to estimate the depth and extent of infection to guide appropriate source control. Confirmation of fascial or muscular involvement requires opening of the wound, which facilitates optimal debridement. (See 'Wound exploration and debridement' below and 'Imaging' below.)

Exploration and inspection of the wound with suspected deep SSI is often performed in the operating room to facilitate inspection and the debridement. When examining an infected wound for deep SSI, it is important to open it wide enough to evaluate the underlying tissue. This is of particular importance for certain types of incisions (eg, spine, sternotomy), or when implanted material was used during the surgery (eg, hernia mesh, breast implant, vascular graft, orthopedic implant). (See 'Deep infection associated with implanted materials' below.)

Organ/space surgical site infection — Patients with organ/space infection typically present with malaise, fever, and pain/tenderness in the body region where their operation was performed, often without overlying skin changes. Organ/space SSI can also occur as a complication of progressive deep incisional SSI. (See 'Deep incisional surgical site infection' above.)

The identification of organ/space SSI is typically made after an imaging study demonstrates an abscess in the cavity or organs involved in the prior operation and Gram stain and culture analysis of the drainage (percutaneous, surgical) confirms the infection. (See 'Diagnosis' below.)

Common examples of organ/space SSI are right lower quadrant abscess after laparoscopic appendectomy for acute perforated appendicitis or empyema after video-assisted thoracoscopic surgery. Intra-abdominal abscess is not always associated with anastomotic leak or unrecognized intestinal injury, but these should be considered as a potential cause if there was no infection present at the index operation. (See "Overview of gastrointestinal tract perforation" and "Management of anastomotic complications of colorectal surgery".)

Recognizing necrotizing infection — Necrotizing soft tissue infection can be lethal and is a surgical emergency. Necrotizing infections often manifest rapidly after surgery (as early as 24 hours for group A Streptococcus and clostridia) and often present with sepsis. Peri-incisional pain is often severe and out of proportion to the expected degree of postoperative pain. Depending upon the causative organism and the depth of involvement, it may be characterized by skin discoloration, blistering and devitalization; a copious, dishwater-like drainage; dusky and friable subcutaneous tissue; and/or pale, devitalized fascia. Patients may display extremes of leukopenia or leukocytosis and other laboratory abnormalities, such as hyponatremia or evidence of end-organ failure. The extent of infection may not be apparent on visual inspection, as well-perfused overlying skin often belies the underlying necrosis; infection may spread through any tissue, including myositis and fasciitis. Obtaining imaging studies should not delay operative wound exploration and definitive debridement due to the risk of rapid dissemination of infection. (See "Necrotizing soft tissue infections" and "Surgical management of necrotizing soft tissue infections".)

DIAGNOSIS — Superficial SSI can be fully evaluated through direct observation of the wound. Serial patient-generated wound images and symptom reports transmitted via telemedicine may document the emergence of infection. If there is concern for involvement of underlying tissues or the organ space, imaging can provide valuable diagnostic information.

Imaging — In the presence of signs or symptoms concerning for a systemic infection, clinicians should have a low threshold for obtaining cross-sectional imaging to evaluate for an undrained abscess requiring source control.

Ultrasound is a widely available imaging technique and can identify the presence of fluid in the subcutaneous tissues. However, in the setting of deep or organ space SSIs, computed tomography or magnetic resonance imaging provide a more detailed evaluation of the underlying soft tissue and organ space. In the setting of prior gastrointestinal resection with the possibility of an underlying anastomotic leak or intra-abdominal infection, oral contrast aids in diagnosis. The presence of extraluminal contrast and/or air on imaging is concerning for an underlying perforation requiring surgical intervention. (See "Management of anastomotic complications of colorectal surgery", section on 'Anastomotic complications' and "Overview of gastrointestinal tract perforation", section on 'Imaging signs of perforation'.)

Cultures — If there is a wound opening present upon initial evaluation, or if the wound has been opened for initial diagnosis and management of a suspected SSI, a Gram stain and culture should be obtained to document the causative organisms. It is best to obtain swab cultures directly from the specific site of infection in the open wound. Sampling the surrounding skin often reveals polymicrobial growth, making it difficult to distinguish colonization from true infection. During surgical debridement, a sample of synthetic material (eg, surgical mesh, implant) or necrotic material may also be sent for culture. Treatment of SSI can be initiated based on Gram stain results, which provide the earliest information to guide empiric therapy. However, specific therapy is based on subsequent culture results. Culture of purulent drainage obtained from an indwelling or radiographically placed drain can be also used to tailor antibiotic therapy.

Negative cultures in an obviously infected wound can be a sign of an underlying atypical infection (eg, acid-fast bacillus [AFB]) or fungal infection. In the setting of immunosuppressive therapies (eg, chemotherapy, post-transplant antirejection therapies), consideration should be given to obtaining AFB and fungal cultures.

If systemic signs of infection are present, concomitant blood cultures should be obtained. Resulting culture specificities and sensitivities may be used to narrow empiric antibiotics. (See 'Antimicrobial therapy' below.)

DIFFERENTIAL DIAGNOSIS — Important causes of skin erythema following surgery include reactions to suture material, hypersensitivity to dressings or skin preparation materials (picture 1), and subcutaneous hematoma or seroma. Eliciting a thorough history of prior skin reactions as well as review of operative notes for documented areas of prior skin redness near the surgical site may be helpful in determining the etiology of erythema.

A "stitch abscess" is a typically small sinus tract that develops at the site of a subcuticular or deep tissue knot. In the absence of purulence, these should not be considered infections and typically do not warrant treatment beyond local wound care. Braided polyester and silk sutures are more likely to cause a reaction compared with other suture materials. Removing the suture and future avoidance of the material causing the reaction is recommended, if possible.

Hematoma or seroma may be difficult to distinguish from infection. With a significant hematoma that develops suddenly or acute drainage of blood through an incision, there may be a concomitant drop in the hemoglobin, which is not likely to be seen with SSI. In the case of a seroma, palpation of the wound typically yields a soft fluid wave with absence of significant pain; erythema may or may not be present. Ultrasound or computed tomography may facilitate identification of hematoma/seroma and can be helpful in distinguishing blood from serous fluid or purulent fluid.

Long-term resorption of hematoma/seroma is possible with conservative management. Because percutaneous aspiration is commonly associated with recurrent seroma, asymptomatic postoperative seromas should be observed initially. Clinicians should resist the temptation to aspirate a hematoma/seroma because an uninfected hematoma/seroma can easily become contaminated through percutaneous manipulation. If a seroma persists, it should only be aspirated under sterile conditions. Recurrent seromas following aspiration should be treated with surgical drainage and excision of the seroma lining, if possible [70].


Wound exploration and debridement — Treatment of suspected/confirmed superficial/deep incisional SSI involves opening the wound; drainage of infected fluid, which should be cultured; and debridement of necrotic and devitalized tissue, which are imperative for adequate treatment. In the setting of an undrained fluid collection in communication with an abdominal fascial closure, or in cases when the risk of SSI is high, opening the wound is favored over percutaneous drainage. Antibiotics are required in the setting of surrounding skin erythema, evidence of deeper soft tissue infection, or in the presence of systemic signs and symptoms of infection. (See 'Antimicrobial therapy' below.)

Deep tissue should also be sent for culture and sensitivities to guide specific antimicrobial therapy. In the presence of underlying bone, metal hardware, mesh, or other implanted material, there may be concern about opening the surgical wound. This issue is discussed below. (See 'Deep infection associated with implanted materials' below.)

Most superficial wound exploration can be performed in the clinic, emergency room, or bedside, with attention to reducing patient discomfort and using meticulously clean technique to prevent superinfection of the wound. In addition to removing surgical skin staples, sutures, or glue, it may be necessary to forcibly separate the wound edges to sufficiently evacuate any accumulated fluid or pus and to fully evaluate the integrity of the underlying fascial closure, if present. Sufficient wound opening also facilitates serial dressing changes. After opening of the wound, a saline-filled syringe can be used to irrigate the wound to remove loose devitalized tissue, exudate, and clots. Saline is isotonic and does not interfere with healing; however, tap water has also been used for wound care in the home or ambulatory setting with good results [71]. (See "Basic principles of wound management", section on 'Irrigation'.)

Mechanical debridement is performed with forceps and scalpel or scissors. Ideally, all foreign bodies are excised as well because they can delay healing and promote infection. However, for SSI of laparotomy wounds, any benefit of removal of exposed fascial sutures is typically outweighed by the risk of evisceration. Enzymatic agents are an option when manual debridement is not possible [72]. Serial debridement is continued until no necrotic tissue remains and granulation tissue is present. (See "Basic principles of wound management", section on 'Wound debridement'.)

Deep SSI (involving tissue below the subcutaneous fat) in abdominal wounds is a major risk factor for fascial dehiscence and may require emergency exploration of the wound in the operating room to safely debride deeper tissue given the risk of evisceration, and to facilitate abdominal exploration if sub-fascial infection is present. In the case when fascial debridement is necessary, it may be necessary to augment fascial closure with biologic or absorbable synthetic mesh to contain the viscera. If the deepest level of infection extends into the abdominal cavity (organ/space SSI), particularly if dense intra-loop adhesions are present, abdominal exploration combined with percutaneous drainage of abscesses inaccessible during laparotomy may be necessary to obtain source control prior to definitive fascial closure. (See "Complications of abdominal surgical incisions", section on 'Fascial dehiscence' and "Management of the open abdomen in adults".)

Organ/space SSI is somewhat different from superficial or deep SSI, and morbidity and mortality from this class of SSI tend to be higher. Computed tomography or ultrasound are used to guide placement of closed suction percutaneous drains into abscess collections, when possible. For abdominal organ/space SSI, it can be challenging in some cases to differentiate an abscess from anastomotic leak. The National Healthcare Safety Network (NHSN) definitions include anastomotic leak as an organ/space SSI, but not all post-enterectomy or colectomy abscesses are due to anastomotic leak. However, if the abscess is associated with a recently performed bowel anastomosis, anastomotic leak should be strongly suspected. On imaging studies, extraluminal air or contrast within the abscess cavity are indicative of an anastomotic leak or underlying perforation. The distinction is critical, as achieving source control may require additional percutaneous drains, reducing afferent gastrointestinal flow through complete bowel rest and/or proximal stoma diversion, and/or intra-abdominal re-exploration and washout.

Antimicrobial therapy — The need for antimicrobial therapy is determined by the extent of the infection, presence of systemic manifestations, and patient comorbidities (eg, chronic glucocorticoids, diabetes). Antibiotics are required in the setting of surrounding cellulitis or in the presence of systemic signs and symptoms of infection. While antibiotics are not always necessary to treat superficial SSI, antibiotics are nearly always required to treat deep and organ/space SSI.

Antibiotics are initiated under the following clinical circumstances [73,74]:

Surrounding cellulitis.

Cellulitis associated with intact but indurated surgical incision (even in the absence of wound drainage or subcutaneous fluid collection).

Persistent cellulitis in the surrounding skin after wound opening.

Subcutaneous or deeper tissue has persistent inflammation after debridement or drainage (ie, source control not achieved).

Implanted material (eg, mesh, vascular grafts, orthopedic hardware) is present within the infected area.

Systemic signs of infection are present (eg, temperature ≥38°C, white blood cell count ≥12).

Septic shock is persistent despite source control.

The most common pathogens isolated from infected surgical wounds are Staphylococcus aureus, coagulase-negative staphylococci, Streptococcus spp, and Enterococcus spp [75]. Empiric selection of antibiotics depends upon the initial Gram stain, wound class, site of the wound, prior exposure to antibiotics, a history of colonization with antibiotic-resistant organisms (eg, methicillin-resistant S. aureus [MRSA]), and local antimicrobial resistance patterns. Empiric gram-negative therapy is often not necessary (eg, Gram stain shows only gram-positive organisms in clusters). But, if the wound was known to be grossly contaminated in the case of traumatic injury or gastrointestinal tract perforation, adequate coverage includes antibiotics directed against gram-negative coliforms and anaerobic organisms, as well as typical gram-positive skin organisms.

Definitive antimicrobial treatment is guided by the clinical response of the patient and, when available, results of wound culture and sensitivities.

In the absence of retained foreign material, antibiotics should be stopped with resolution of cellulitis and/or normalization of physiologic parameters such as leukocytosis. Guidelines suggest a short course of antibiotics (24 to 48 hours) for cellulitis that has not improved with opening the wound [76,77]. In the case of intra-abdominal organ/space infection, antimicrobial treatment may be discontinued four days after source control has been achieved [78].

For complicated SSI, there is no formal evidence to guide the appropriate duration of antimicrobial therapy. If worsening of infection occurs within 24 hours of initiation of treatment, broadening antimicrobial treatment and wound exploration and debridement should be strongly considered because necrotizing soft tissue infection can develop, particularly if Streptococcus or clostridial spp are the causative agents. (See 'Recognizing necrotizing infection' above.)

In general, deep or organ/space SSI involving implanted material that cannot safely be explanted will require substantially longer-duration intravenous antimicrobial treatment and, in some cases, lifelong suppressive antimicrobial therapy. (See 'Deep infection associated with implanted materials' below.)

Wound management — The basic principles of wound management following the opening of a wound for superficial or deep SSI follow those of wound management, in general. (See "Basic principles of wound management".)

Open wound care — The mainstay of treatment for the wound that has been opened due to SSI is healing by secondary intention with serial dressing changes that consist of frequent wound packing and removal, which aims to decrease microbial wound burden by removing wound slough and accumulated drainage. The disadvantages of healing by secondary intention with open wound care include prolonged time to wound healing, as well as painful and cumbersome wound care for the patient.

Wound packing — Dressings that maintain moisture and warmth facilitate healing [79]. Retention of moisture is important because wound fluids contain tissue growth factors that facilitate re-epithelialization and promote autolytic debridement.

Gauze is moistened with normal saline and placed into the wound and covered with dry layers of gauze [79]. When the gauze is removed (preferably before it dries out), necrotic tissue is removed with it, which provides a form of debridement. However, once debridement is no longer necessary, the packing material should be changed from gauze to one that is less traumatic to the developing granulation tissue and new epithelial cells. Dressing changes may initially be required up to three times daily and are continued until the wound surface is mostly covered by granulation tissue. Dressings can then be changed once a day or every other day to avoid disturbing the healing process. (See "Basic principles of wound management", section on 'Wound packing'.)

Many dressing choices are available for wounds healing by secondary intention without good data to recommend one over another (table 4) [80]. The ideal dressing should absorb exudate without leakage, be impermeable to water and bacteria, lack particulate contaminants that could be left in the wound upon removal, and not cause trauma to granulation tissue [81]. Topical agents (eg, povidone-iodine, sodium hypochlorite, hydrogen peroxide) are often used in heavily infected wounds. However, the utility of these solutions in wound healing is unknown, as they may be toxic to fibroblasts and, as a result, impede wound healing. (See "Basic principles of wound management", section on 'Wound dressings'.)

Negative pressure wound therapy — Negative pressure wound therapy (NPWT; also called vacuum-assisted wound closure) provides an alternative to wound healing by secondary intention with wound packing. Therapeutic NPWT can be applied to open wounds that have a clean, granulating base reducing excess fluid accumulation and, with time, the size of the wound. NPWT also helps protect the patient's skin from frequent dressing changes. NPWT is associated with the need for fewer dressing changes since it is only changed once every three to five days and as such may facilitate earlier progression from hospital care to outpatient management for larger wounds. Techniques for placement and care of wounds with these devices are discussed elsewhere. (See "Negative pressure wound therapy".)

Whether NPWT can been used earlier in the treatment of SSI is controversial. Too early placement of NPWT may fail to adequately debride the wound, and the wound may not be adequately monitored, thereby allowing SSI to progress. However, NPWT devices are available that can instill saline irrigation with or without antibiotics for the treatment of severely contaminated wounds (eg, those associated with enterocutaneous fistula), but their effectiveness is uncertain. Contaminated wounds sustained in combat-related soft tissue injuries have been successfully managed with NPWT and subsequent delayed primary closure [82].

NPWT is relatively contraindicated under certain conditions, such as exposure of underlying organs including blood vessels or intestine. In these settings, modifications to standard NPWT include application of non-adherent sponges with layered non-adherent barrier dressings, as well as use of reduced negative pressure settings to prevent fistula formation. (See "Negative pressure wound therapy", section on 'Contraindications'.)

Delayed primary closure and reconstruction — Wounds that are opened due to SSI are often left to heal by secondary intention (see 'Open wound care' above); however, delayed primary closure may be an option. Whether this approach is used generally depends on the location of the incision, severity of infection, extent of required debridement, and the handling of any implanted materials.

Delayed skin closure has the benefit of more rapid wound healing but must be weighed against the risk of recurrent infection. In a study of postoperative obstetric and gynecologic patients with laparotomy wounds opened due to either seroma, hematoma, or superficial SSI, delayed primary closure of the skin was safe and effective with a 5 percent incidence of re-exploration for reinfection [83]. Closure significantly shortened the overall wound healing time.

For wounds with skin contracture or tissue loss from debridement, delayed primary closure may require skin grafting or flap reconstruction to provide adequate coverage of the wound. Careful planning at the time of the initial debridement may lead to improved options for wound closure. Nutritional support and meticulous wound care are critical to preparing the wound bed. The presence of tissue granulation in the wound bed signals that blood supply and nutritional factors are adequate to support wound healing and to suppress pathological bacterial growth. Nevertheless, granulation tissue may be debrided prior to wound coverage. (See "Skin autografting" and "Overview of flaps for soft tissue reconstruction", section on 'Principles of reconstruction'.)

DEEP INFECTION ASSOCIATED WITH IMPLANTED MATERIALS — The basic principles of managing SSI discussed above can generally be applied to most surgical sites. For sites associated with implanted material, the risk of incomplete treatment of SSI must be weighed against the risks associated with removal of the implanted materials. "Treating through" an infection with intravenous antibiotics without removal of implanted materials may allow disease progression and further deterioration of the surgical site.

The selection of treatment should be guided by signs of local wound and systemic inflammation, response to initial therapy, and patient comorbidities.

Specific deep incisional SSIs are discussed in separate topic reviews.

Hernia mesh – Management of mesh infection following abdominal wall reconstruction is reviewed separately. (See "Wound infection following repair of abdominal wall hernia", section on 'Treatment'.)

Vascular grafts – Management of vascular graft infection requires removal of the infected segment of graft typically in conjunction with revascularization. If a new bypass graft is used, it is tunneled through a noninfected area. (See "Arteriovenous graft creation for hemodialysis and its complications", section on 'Graft infection'.)

Orthopedic procedures – The management of infected orthopedic hardware may involve wound irrigation and debridement, placement of intrawound antibiotic-impregnated beads, or hardware removal and bone debridement, with immediate or delayed reconstruction. (See "Nonvertebral osteomyelitis in adults: Treatment", section on 'Retained hardware' and "Prosthetic joint infection: Treatment".)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Prevention of surgical site infections in adults" and "Society guideline links: Abdominal incisions and closure".)


Definition – A surgical site infection (SSI) is an infection related to a surgical procedure that occurs near the surgical site within 30 days of surgery (or up to 90 days if an implant was involved). SSIs are described as incisional SSIs (superficial, deep) and organ/space SSIs (figure 1 and table 1). Anastomotic leak is included in the definition of organ/space SSI, but not all abscesses that occur following bowel resection are due to anastomotic leak. (See 'Definition' above.)

Risk factors – Risk factors for SSI are similar with those associated with impaired wound healing and include cigarette smoking, older age, vascular disease, obesity, malnutrition, diabetes, and immunosuppressive therapy. Other risk factors for SSI include higher wound classification, proximity to other wounds, and possibly transfusion. (See 'Risk assessment' above.)

Preventive measures – Surgeons can reduce rates of SSI using control measures and good surgical techniques. Leaving the wound open at the primary operation for delayed primary closure is a strategy that is often used but is unproven to reduce the risk for SSI. Alternatively, negative pressure wound therapy (NPWT) dressings applied directly to a closed surgical wound (ie, prophylactic NPWT) and use of wound protectors have reduced the incidence of SSI for some types of surgical incisions. (See 'Measures to reduce risk' above and "Overview of control measures for prevention of surgical site infection in adults".)

Diagnosis and treatment – The diagnosis of SSI is predominantly clinical. Full evaluation of the wound includes examination of the skin surrounding the surgical site with documentation of the presence and extent of erythema, edema or induration, and any drainage. (See 'General management' above and 'Wound exploration and debridement' above and 'Wound management' above.)

Superficial SSI – For patients with clinical signs of superficial SSI (eg, localized swelling, warmth, drainage) and active drainage or surgical wound separation, additional imaging is generally unnecessary. Treatment of superficial SSI involves wound exploration and debridement. Antibiotics are administered only if there is associated cellulitis.

Deep incisional SSI – For patients with clinical signs of deep SSI, which are like those of superficial SSI, imaging (eg, ultrasound, computed tomography) may be helpful to estimate the depth and extent of infection to guide the approach to source control. Treatment of deep SSI requires antibiotic administration and wound exploration/debridement.

Organ/space SSI – For patients with clinical signs of organ/space infection (eg, malaise, fever, and pain/tenderness), imaging is necessary to identify any fluid collections or abscess in operated region. The diagnosis is confirmed through positive cultures of fluid obtained during a drainage procedure (percutaneous, surgical), which guides antimicrobial therapy.

Empiric therapy – Empiric antimicrobial therapy is directed at the most likely organisms for a given wound site, Gram stain, wound class, prior antibiotics, and antibiotic resistance patterns. Definitive antimicrobial treatment is guided by results of wound culture, and sensitivity. The duration of treatment is guided by the clinical response. (See 'Antimicrobial therapy' above.)

Wound care and closure – Wounds that have been opened due to SSI are managed with serial debridement and dressing changes and often left to heal by secondary intention; however, delayed primary closure may be an option. The approach used generally depends on location of the surgical incision, severity of infection, extent of required debridement and amount of tissue loss, and the handling of any implanted materials. NPWT with or without instillation can be used as an adjunctive technique to facilitate closure. For surgical wounds with significant tissue loss from debridement or loss of domain from skin contraction, skin grafting or flap reconstruction will be necessary. (See 'Wound management' above and 'Deep infection associated with implanted materials' above.)

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