Causes

A seroma is a collection of liquefied fat, serum, and lymphatic fluid under the incision. The fluid is usually clear, yellow, and somewhat viscous and is found in the subcutaneous layer of the skin. Seromas represent the most benign complication after an operative procedure and are particularly likely to occur when large skin flaps are developed in the course of the operation, as is often seen with mastectomy, axillary dissection, groin dissection, and large ventral hernias or when a prosthetic mesh (polytetrafluoroethylene) is used in the repair of a ventral hernia.

Presentation and Management

A seroma usually manifests as a localized and well-circumscribed swelling, pressure or discomfort, and occasional drainage of clear liquid from the immature surgical wound. Prevention of seroma formation may be achieved with placement of suction drains under the flaps. Their premature removal often results in large seromas that will require aspiration under sterile conditions, followed by placement of a pressure dressing. A seroma that reaccumulates after at least two aspirations is evacuated by opening the incision and packing the wound with saline-moistened gauze to allow healing by secondary intention. In the presence of synthetic mesh, open drainage is best performed in the operating room, the incision is best closed to avoid exposure and infection of the mesh, and suction drains are placed. An infected seroma is also treated with open drainage. The presence of synthetic mesh in these cases will prevent the wound from healing. Management of the mesh depends on the severity and extent of infection. In the absence of severe sepsis and spreading cellulitis and the presence of localized infection, the mesh can be left in situ and removed at a later date when the acute infectious process has resolved. Otherwise, the mesh must be removed and the wound managed with open wound care.

Causes

A hematoma is an abnormal collection of blood, usually in the subcutaneous layer of a recent incision or in a potential space in the abdominal cavity after extirpation of an organ (e.g., splenic fossa hematoma after splenectomy or pelvic hematoma after proctectomy). Hematomas are more worrisome than seromas because of the potential for secondary infection. Hematoma formation is related to inadequate hemostasis, depletion of clotting factors, or the presence of coagulopathy. A host of disease processes can contribute to coagulopathy, including myeloproliferative disorders, liver disease, renal failure, sepsis, clotting factor deficiencies, and medications. Medications most commonly associated with coagulopathy are antiplatelet drugs, such as acetylsalicylic acid (ASA, aspirin), clopidogrel, ticlopidine, eptifibatide, and abciximab, and anticoagulants, such as unfractionated heparin (UFH), low-molecular-weight heparin (LMWH [e.g., enoxaparin, dalteparin sodium, tinzaparin]), and vitamin K antagonist (VKA [e.g., warfarin sodium]).

Presentation and Management

The clinical manifestations of a hematoma may vary with its size, location, and presence of infection. A hematoma may manifest as an expanding, unsightly swelling and/or pain in the area of a surgical incision. In the neck, a large hematoma may cause compromise of the airway; in the retroperitoneum, it may cause a paralytic ileus, anemia, and ongoing bleeding caused by local consumptive coagulopathy; and, in the extremity and abdominal cavity, it may result in compartment syndrome. On physical examination, the hematoma appears as a localized soft swelling with purplish blue discoloration of the overlying skin. The swelling varies from small to large and may be tender to palpation or associated with drainage of dark red fluid out of the fresh wound.

Hematoma formation is prevented preoperatively by correcting any clotting abnormalities and discontinuing medications that alter coagulation. Antiplatelet medications and anticoagulants may be given to patients undergoing procedures for a variety of reasons. Clopidogrel is given after implantation of a coronary stent, ASA is given for the treatment of coronary artery disease (CAD) and stroke, and VKA is given after implantation of a mechanical mitral valve for atrial fibrillation, venous thromboembolism, and hypercoagulable states. These medications must be temporarily discontinued before surgery. There are no specific studies that have addressed the issue of timing of discontinuation of such medications.

One must balance the risk of significant bleeding caused by uncorrected medication-induced coagulopathy and the risk of thromboembolic events after discontinuation of therapy. The risk of bleeding varies with the type of surgery or procedure and adequacy of hemostasis; the risk of thromboembolism depends on the indication for antithrombotic therapy and presence of comorbid conditions.¹ In patients at high risk for thromboembolism (e.g., those with a mechanical mitral valve or older generation aortic valve prosthesis, venous thromboembolism within 3 months, severe thrombophilia, recent atrial fibrillation [within 6 months], stroke or transient ischemic attack who are scheduled to undergo an elective major surgical procedure involving a body cavity), the VKA must be discontinued 4 to 5 days before surgery to allow the international normalized ratio (INR) to be lower than 1.5. In patients whose INR is still elevated (>1.5), low-dose vitamin K (1 to 2 mg) is given orally. Patients are then given bridging anticoagulation—that is, a therapeutic dose of rapidly acting anticoagulant, intravenous (IV) UFH or to LMWH. Those receiving IV UFH (half-life, 45 minutes) can have the medication discontinued 4 hours before surgery and those receiving therapeutic dose LMWH SC (variable half-life) 16 to 24 hours before surgery. VKA is then resumed 12 to 24 hours after surgery (takes 2 to 3 days for anticoagulant effect to begin after start of VKA) and when there is adequate hemostasis. In patients at high risk of bleeding (major surgery or high bleeding risk surgery) for whom postoperative therapeutic LMWH or UFH is planned, initiation of therapy is delayed for 48 to 72 hours, low-dose LMWH or UFH is administered, or the therapy is completely avoided. Patients at low risk for thromboembolism do not require heparin therapy after discontinuation of the VKA. Patients on ASA or clopidogrel must have the medication withheld 6 to 7 days before surgery; otherwise, the surgery must be delayed until the patient has completed the course of treatment. Antiplatelet therapy is resumed approximately 24 hours after surgery. In patients with a bare metal coronary stent who require surgery within 6 weeks of stent placement, ASA and clopidogrel are continued in the perioperative period. In patients who are receiving VKAs and require urgent surgery, immediate reversal of anticoagulant effect requires transfusion with fresh-frozen plasma or other prothrombin concentrate and low-dose IV or oral vitamin K. During surgery, adequate hemostasis must be achieved with ligature, electrocautery, fibrin glue, or topical bovine thrombin before closure. Closed suction drainage systems are placed in large potential spaces and removed postoperatively when the output is not bloody and scant.

Evaluation of a patient with a hematoma, especially one that is large and expanding, includes assessment of preexisting risk factors and coagulation parameters (e.g., prothrombin time [PT], activated partial prothrombin time [aPTT], INR, platelet count, bleeding time) and appropriate treatment. A small hematoma does not require any intervention and will eventually resorb. Most retroperitoneal hematomas can be managed by expectant waiting after correction of associated coagulopathy (platelet transfusion if bleeding time is prolonged, desmopressin in patients who have renal failure, and fresh-frozen plasma in patients who have an increased INR). A large or expanding hematoma in the neck is managed in a similar fashion and best evacuated in the operating room urgently after securing the airway if there is any respiratory compromise. Similarly, hematomas detected soon after surgery, especially those developing under skin flaps, are best evacuated in the operating room.

Causes

Acute wound failure (wound dehiscence or a burst abdomen) refers to postoperative separation of the abdominal musculoaponeurotic layers. It is among the most dreaded complications faced by surgeons and is of great concern because of the risk of evisceration, the need for some form of intervention, and the possibility of repeat dehiscence, surgical wound infection, and incisional hernia formation.

Acute wound failure occurs in approximately 1% to 3% of patients who undergo an abdominal operation. Dehiscence most often develops 7 to 10 days postoperatively but may occur anytime after surgery, from 1 to more than 20 days. A multitude of factors may contribute to wound dehiscence (Box 13-1). Acute wound failure is often related to technical errors in placing sutures too close to the edge, too far apart, or under too much tension. Local wound complications such as hematoma and infection can also predispose to localized dehiscence. In fact, a deep wound infection is one of the most common causes of localized wound separation. Increased intra-abdominal pressure (IAP) is often blamed for wound disruption and factors that adversely affect wound healing are cited as contributing to the complication. In healthy patients, the rate of wound failure is similar whether closure is accomplished with a continuous or interrupted technique. In high-risk patients, however, continuous closure is worrisome because suture breakage in one place weakens the entire closure.

Presentation and Management

Acute wound failure may occur without warning and evisceration makes the diagnosis obvious. A sudden, dramatic drainage of a relatively large volume of a clear, salmon-colored fluid precedes dehiscence in 25% of patients. More often, patients report a ripping sensation. Probing the wound with a sterile, cotton-tipped applicator or gloved finger may detect a partial dehiscence.

Prevention of acute wound failure is largely a function of careful attention to technical detail during fascial closure, such as proper spacing of the suture, adequate depth of bite of the fascia, relaxation of the patient during closure, and achieving a tension-free closure. For very high-risk patients, interrupted closure is often the wisest choice. Alternative methods of closure must be selected when primary closure is not possible without undue tension. Although retention sutures were used extensively in the past, their use is less common today, with many surgeons opting to use a synthetic mesh or bioabsorbable tissue scaffold.

Treatment of dehiscence depends on the extent of fascial separation and the presence of evisceration and/or significant intra-abdominal pathology (e.g., intestinal leak, peritonitis). A small dehiscence, especially in the proximal aspect of an upper midline incision 10 to 12 days postoperatively, can be managed conservatively with saline-moistened gauze packing of the wound and use of an abdominal binder. In the event of evisceration, the eviscerated intestines must be covered with a sterile, saline-moistened towel and preparations made to return to the operating room after a very short period of fluid resuscitation. Similarly, if probing of the wound reveals a large segment of the wound that is open to the omentum and intestines, or if there is peritonitis or suspicion of intestinal leak, plans to take the patient back to the operating room are made.

Once in the operating room, thorough exploration of the abdominal cavity is performed to rule out the presence of a septic focus or an anastomotic leak that may have predisposed to the dehiscence. Management of that infection is of critical importance before attempting to close. Management of the incision is a function of the condition of the fascia. When technical mistakes are made and the fascia is strong and intact, primary closure is warranted. If the fascia is infected or necrotic, débridement is performed. The incision can then be closed with retention sutures; however, to avoid tension, use of a prosthetic material may be preferred. Closure with an absorbable mesh (polyglactin or polyglycolic acid) may be preferable because the mesh is well tolerated in septic wounds and allows bridging the gap between the edges of the fascia without tension, prevents evisceration, and allows the underlying cause of the patient’s dehiscence to resolve. Once the wound has granulated, a skin graft is applied and wound closure is achieved by advancing local tissue. This approach uniformly results in the development of a hernia, the repair of which requires the subsequent removal of the skin graft and use of a permanent prosthesis. An alternative method of closure is dermabrasion of the skin graft followed by fascial closure using the component separation technique. Attempts to close the fascia under tension guarantee a repeat dehiscence and, in some cases, result in intra-abdominal hypertension (IAH). The incision is left open (laparotomy), closed with a temporary closure device (open abdomen technique), closed with synthetic mesh or biologic graft (acellular dermal matrix), or closed by using negative-pressure wound therapy.

The open abdomen technique avoids IAH, preserves the fascia, and facilitates reaccess of the abdominal cavity. With laparotomy, the wound is allowed to heal with secondary intention and/or subsequently closed with a skin graft or local or regional tissue. This approach is associated with prolonged healing time, fluid loss, and risk of complex enterocutaneous fistula formation as a result of bowel exposure, desiccation, and traumatic injury. Furthermore, definitive surgical repair to restore the integrity of the abdominal wall will eventually be required. A temporary closure device (vacuum pack closure) protects abdominal contents, keeps patients dry, can be quickly removed with increased IAP, and avoids secondary complications seen with laparotomy. A fenestrated, nonadherent, polyethylene sheet is applied on the bowel omentum, moist surgical towels or gauze with drains are placed on top, and an iodophore-impregnated adhesive dressing is placed. Continuous suction is then applied. If the fascia cannot be closed in 7 to 10 days, the wound is allowed to granulate and then covered with a skin graft.

Absorbable synthetic mesh provides wound stability and is resistant to infection. It is associated with fistula and hernia formation repair, which is difficult and may require reconstruction of the abdominal wall. Repair with nonabsorbable synthetic mesh such as polypropylene, polyester, or polytetrafluoroethylene (PTFE) is associated with complications that will require removal of the mesh (e.g., abscess formation, dehiscence, wound sepsis, mesh extrusion, bowel fistulization). Although PTFE is more desirable because it is nonadherent to underlying bowel, it is expensive, does not allow skin grafting, and is associated with chronic infections. An acellular dermal matrix (bioprosthesis) has the mechanical properties of a mesh for abdominal wall reconstruction and physiologic properties that make it resistant to contamination and/or infection. The bioprosthesis provides immediate coverage of the wound and serves as mechanical support in a single-stage reconstruction of compromised surgical wounds. It is bioactive because it functions as tissue replacement or scaffold for new tissue growth; it stimulates cellular attachment, migration, neovascularization, and repopulation of the implanted graft. A bioprosthesis also reduces long-term complications (e.g., erosion, infection, chronic pain). Available acellular materials are animal-derived (e.g., porcine intestinal submucosa, porcine dermis, cross-linked porcine dermal collagen) or human-derived (e.g., cadaveric human dermis). However, the rate of wound complications (e.g., superficial wound or graft infection, graft dehiscence, fistula formation, bleeding) and hernia formation or laxity of the abdominal wall is 25% to 50%.²

Negative-pressure wound therapy is based on the concept of wound suction. A vacuum-assisted closure device is most commonly used. The device consists of a vacuum pump, canister with connecting tubing, open-pore foam (e.g., polyurethane ether, polyvinyl alcohol foam) or gauze, and semiocclusive dressing. The device provides immediate coverage of the abdominal wound, acts as a temporary dressing, does not require suturing to the fascia, minimizes IAH, and prevents loss of domain. Applying suction of 125 mm Hg, the open-pore foam decreases in size and transmits the negative pressure to surrounding tissue, leading to contraction of the wound (macrodeformation) and removal of extracellular fluid (via decrease in bowel edema, evacuation of excess abdominal fluid, decrease in wound size), stabilization of the wound environment, and microdeformation of the foam-wound interface, which induces cellular proliferation and angiogenesis. The secondary effects of the vacuum-assisted closure device include acceleration of wound healing, reduction and changes in bacterial burden, changes in biochemistry and systemic responses, and improvement in wound bed preparation—increase in local blood perfusion and induction healing response through microchemical forces.³ This approach results in successful closure of the fascia in 85% of cases. However, the device is expensive and cumbersome to wear and may cause significant pain, cause bleeding (especially in patients on anticoagulant therapy), be associated with increased levels of certain bacteria, and be associated with evisceration and hernia formation. There is also an increased incidence of intestinal fistulization at enterotomy sites and enteric anastomoses, and in the absence of anastomoses.

Causes

Surgical site infections (SSIs) still continue to be a significant problem for surgeons. Despite major improvements in antibiotics, better anesthesia, superior instruments, earlier diagnosis of surgical problems, and improved techniques for postoperative vigilance, wound infections continue to occur. Although some may view the problem as merely cosmetic, that view represents a shallow understanding of this problem, which causes significant patient suffering, morbidity, and even mortality, and is a financial burden to the health care system. Furthermore, SSIs represent a risk factor for the development of incisional hernia, which requires surgical repair. Currently, in the United States, SSIs account for almost 40% of hospital-acquired infections among surgical patients.

The surgical wound encompasses the area of the body, internally and externally, that involves the entire operative site. Wounds are thus categorized into three general categories:

The Centers for Disease Control and Prevention has proposed specific criteria for the diagnosis of surgical site infections (Box 13-2).⁴

Surgical site infections develop as a result of contamination of the surgical site with microorganisms. The source of these microorganisms is mostly patients’ flora (endogenous source) when integrity of the skin and/or wall of a hollow viscus is violated. Occasionally, the source is exogenous when a break in the surgical sterile technique occurs, thus allowing contamination from the surgical team, equipment, implant or gloves, or surrounding environment. The pathogens associated with a surgical site infections reflect the area that provided the inoculum for the infection to develop. The microbiology, however, varies, depending on the types of procedures performed in individual practices. Gram-positive cocci account for half of the infections (Table 13-1)—Staphylococcus aureus (most common), coagulase-negative Staphylococcus, and Enterococcus spp. S. aureus infections normally occur in the nasal passages, mucous membranes, and skin of carriers. The organism that has acquired resistance to methicillin (methicillin-resistant S. aureus [MRSA]) consists of two subtypes, hospital- and community-acquired MRSA. Hospital-acquired MRSA is associated with nosocomial infections and affects immunocompromised individuals. It also occurs in patients with chronic wounds, those subjected to invasive procedures, and those with prior antibiotic treatment. Community-acquired MRSA is associated with a variety of skin and soft tissue infections in patients with and without risk factors for MRSA. Community-acquired MRSA (e.g., the USA300 clone) has also been noted to affect SSIs. Hospital-acquired MRSA isolates have a different antibiotic susceptibility profile—they are usually resistant to at least three β-lactam antibiotics and are usually susceptible to vancomycin, teicoplanin, and sulfamethoxazole. Community-acquired MRSA is usually susceptible to clindamycin, with variable susceptibility to erythromycin, vancomycin, and tetracycline. There is evidence to indicate that hospital-acquired MRSA is developing resistance to vancomycin (vancomycin intermediate-resistant S. aureus [VISA] and vancomycin-resistant S. aureus [VRSA]).⁵ Enterococcus spp. are commensals in the adult gastrointestinal (GI) tract, have intrinsic resistance to a variety of antibiotics (e.g., cephalosporins, clindamycin, aminoglycoside), and are the first to exhibit resistance to vancomycin.

Table 13-1 Pathogens Isolated from Postoperative Surgical Site Infections at a University Hospital

In approximately one third of SSI cases, gram-negative bacilli (Escherichia coli, Pseudomonas aeruginosa, and Enterobacter spp.) are isolated. However, at locations at which high volumes of GI operations are performed, the predominant bacterial species are the gram-negative bacilli. Infrequent pathogens are group A beta-hemolytic streptococci and Clostridium perfringens. In recent years, the involvement of resistant organisms in the genesis of SSIs has increased, most notable in MRSA.

A host of patient- and operative procedure–related factors may contribute to the development of SSIs (Box 13-3).⁶ The risk of infection is related to the specific surgical procedure performed and, hence, surgical wounds are classified according to the relative risk of surgical site infections occurring—clean, clean-contaminated, contaminated, and dirty (Table 13-2). In the National Nosocomial Infections Surveillance System, the risk of patients is stratified according to three important factors: (1) wound classification (contaminated or dirty); (2) longer duration operation, defined as one that exceeds the 75th percentile for a given procedure; and (3) medical characteristics of the patients as determined by the American Society of Anesthesiology score of III, IV, or V (presence of severe systemic disease that results in functional limitations, is life-threatening, or is expected to preclude survival from the operation) at the time of operation.⁷

Table 13-2 Classification of Surgical Wounds

Presentation

SSIs most commonly occur 5 to 6 days postoperatively but may develop sooner or later than that. Approximately 80% to 90% of all postoperative infections occur within 30 days after the operative procedure. With the increased use of outpatient surgery and decreased length of stay in hospitals, 30% to 40% of all wound infections have been shown to occur after hospital discharge. Nevertheless, although less than 10% of surgical patients are hospitalized for 6 days or less, 70% of postdischarge infections occur in that group.

Superficial and deep SSIs are accompanied by erythema, tenderness, edema, and occasionally drainage. The wound is often soft or fluctuant at the site of infection, which is a departure from the firmness of the healing ridge present elsewhere in the wound. The patient may have leukocytosis and a low-grade fever. According to the Joint Commission (TJC), a surgical wound is considered infected if (1) there is drainage of grossly purulent material drains from the wound, (2) the wound spontaneously opens and drains purulent fluid, (3) the wound drains fluid that is culture-positive or Gram stain–positive for bacteria, and (4) the surgeon notes erythema or drainage and opens the wound after determining it to be infected.

Treatment

Prevention of surgical site infections relies on changing or dealing with modifiable risk factors that predispose to surgical site infections. However, many of these factors cannot be changed, such as age, complexity of the surgical procedure, and morbid obesity. Patients who are heavy smokers are encouraged to stop smoking at least 30 days before surgery, glucose levels in diabetics must be treated appropriately, and severely malnourished patients should be given nutritional supplements for 7 to 14 days before surgery.⁸ Obese patients must be encouraged to lose weight if the procedure is elective and there is time to achieve significant weight loss. Similarly, patients who are taking high doses of corticosteroids will have lower infection rates if they are weaned off corticosteroids or are at least taking a lower dose. Patients undergoing major intra-abdominal surgery are administered a bowel preparation in the form of a lavage solution or strong cathartic, followed by oral nonabsorbable antibiotic(s), particularly for surgery of the colon and small bowel. Bowel preparation lowers the patient’s risk for infection from that of a contaminated case (25%) to a clean-contaminated case (5%). Hair is removed by clipping immediately before surgery and the skin is prepped at the time of operation with an antiseptic agent (e.g., alcohol, chlorhexidine, iodine).

The role of preoperative decolonization in carriers of S. aureus undergoing general surgery is questionable, and the routine use of prophylactic vancomycin or teicoplanin (effective against MRSA) is not recommended. Although perioperative antibiotics are widely used, prophylaxis is generally recommended for clean-contaminated or contaminated procedures in which the risk of SSIs is high or in procedures in which vascular or orthopedics prostheses are used because the development of SSIs will have grave consequences (Table 13-3). For dirty or contaminated wounds, the use of antibiotics is for therapeutic purposes rather than for prophylaxis. For clean cases, prophylaxis is controversial. For some surgical procedures, a first- or second-generation cephalosporin is the accepted agent of choice. A small but significant benefit may be achieved with the prophylactic administration of a first-generation cephalosporin for certain types of clean surgery (e.g., mastectomy, herniorrhaphy). For clean-contaminated procedures, administration of preoperative antibiotics is indicated. The appropriate preoperative antibiotic is a function of the most likely inoculum based on the area being operated. For example, when a prosthesis may be placed in a clean wound, preoperative antibiotics would include something to protect against S. aureus and streptococcal species. A first-generation cephalosporin, such as cefazolin, would be appropriate in this setting. For patients undergoing upper GI tract surgery, complex biliary tract operations, or elective colonic resection, administration of a second-generation cephalosporin such as cefoxitin or a penicillin derivative with a β-lactamase inhibitor is more suitable. Alternatively, ertapenem can be used for operations involving the lower GI tract. The surgeon will give a preoperative dose, intraoperative doses approximately 4 hours apart, and two postoperative doses appropriately spaced. The timing of administration of prophylactic antibiotics is critical. To be most effective, the antibiotic is administered IV within 30 minutes before the incision so that therapeutic tissue levels have developed when the wound is created and exposed to bacterial contamination. Usually, a period of anesthesia induction, preparation, and draping takes place that is adequate to allow tissue levels to build up to therapeutic levels before the incision is made. Of equal importance is making certain that the prophylactic antibiotic is not administered for extended periods postoperatively. To do so in the prophylactic setting is to invite the development of drug-resistant organisms, as well as serious complications, such as Clostridium difficile–associated colitis.

Table 13-3 Prophylactic Antimicrobial Agent for Selected Surgical Procedures

At the time of surgery, the operating surgeon plays a major role in reducing or minimizing the presence of postoperative wound infections. The surgeon must be attentive to personal hygiene (hand scrubbing) and that of the entire team. In addition, the surgeon must make certain that the patient undergoes a thorough skin preparation with appropriate antiseptic solutions and is draped in a sterile, careful fashion. During the operation, steps that have a positive impact on outcome are followed:

The use of drains remains somewhat controversial in preventing postoperative wound infections. In general, there is almost no indication for drains in this setting. However, placing closed suction drains in very deep, large wounds and wounds with large wound flaps to prevent the development of a seroma or hematoma is a worthwhile practice.

Treatment of SSIs depends on the depth of the infection. For both superficial and deep SSIs, skin staples are removed over the area of the infection and a cotton-tipped applicator may be easily passed into the wound, with efflux of purulent material and pus. The wound is gently explored with the cotton-tipped applicator or a finger to determine whether the fascia or muscle tissue is involved. If the fascia is intact, débridement of any nonviable tissue is performed; the wound is irrigated with normal saline solution and packed to its base with saline-moistened gauze to allow healing of the wound from the base anteriorly, thus preventing premature skin closure. If widespread cellulitis or significant signs of infection (e.g., fever, tachycardia), are noted, administration of IV antibiotics must be considered. Empirical therapy is started and tailored according to culture and sensitivity data. The choice of empirical antibiotics is based on the most likely culprit, including the possibility of MRSA. MRSA is treated with vancomycin, linezolid, or clindamycin. Cultures are not routinely performed, except for patients who will be treated with antibiotics so that resistant organisms can be treated adequately. However, if the fascia has separated or purulent material appears to be coming from deep to the fascia, there is obvious concern about dehiscence or an intra-abdominal abscess that may require drainage or possibly a reoperation.

Wound cultures are controversial. If the wound is small, superficial, and not associated with cellulitis or tissue necrosis, cultures may not be necessary. However, if fascial dehiscence and a more complex infection are present, a culture is sent. A deep SSI associated with grayish, dishwater-colored fluid, as well as frank necrosis of the fascial layer, raises suspicion for the presence of a necrotizing type of infection. The presence of crepitus in any surgical wound or gram-positive rods (or both) suggests the possibility of infection with C. perfringens. Rapid and expeditious surgical débridement is indicated in these settings.

Most postoperative infections are treated with healing by secondary intention, allowing the wound to heal from the base anteriorly, with epithelialization being the final event. In some cases, when there is a question about the amount of contamination, delayed primary closure may be considered. In this setting, close observation of the wound for 5 days may be followed by closure of the skin or negative-pressure wound therapy if the wound looks clean and the patient is otherwise doing well.