How to avert postoperative wound complication—and treat it when it occurs
Avoid wound infection and dehiscence with the help of thorough preoperative assessment, careful technique, tried-and-true strategies, and a few novel products
IN THIS ARTICLE
The authors report no financial relationships relevant to this article.
Despite advances in medicine and surgery over the past century, postoperative wound complication remains a serious challenge. When a complication occurs, it translates into prolonged hospitalization, lost time from work, and greater cost to the patient and the health-care system.
Prevention of wound complication begins well before surgery. Requirements include:
- understanding of wound healing (see below) and the classification of wounds (TABLE 1)
- thorough assessment of the patient for risk factors for impaired wound healing, such as diabetes or use of corticosteroid medication (TABLE 2)
- antibiotic prophylaxis, if indicated (TABLE 3)
- good surgical technique, gentle tissue handling, and meticulous hemostasis
- placement of a drain, when appropriate
- awareness of technology that can enhance healing
- close monitoring in the postoperative period
- intervention at the first hint of abnormality.
In this article, we describe predisposing factors and preventive techniques and measures, and outline the most common wound complications, from seroma to dehiscence, including effective management strategies.
Biologic phases of wound healing—overlapping and interdependent
It was pioneering Scottish surgeon John Hunter who noted that “injury alone has in all cases the tendency to produce the disposition and means of a cure.”15
Unlike the tissue regeneration that occurs primarily in lower animals, human wound healing is mediated by collagen deposition, or scarring, which provides structural support to the wound. This scarring process may itself cause a variety of clinical problems.
Wound healing is characterized by overlapping, largely interdependent phases, with no clear demarcation between them. Failure in one phase may have a negative impact on the overall outcome.
In general, wound healing involves two phases: inflammation and proliferation. Within these phases, the following processes occur: scar maturation, wound contraction, and epithelialization. These repair mechanisms are activated in response to tissue injury even when it is surgically induced.
The initial response to tissue injury is inflammation, which is mediated by various amines, enzymes, and other substances. This inflammation can be further broken down into vascular and cellular responses.
Inflammation triggers increased blood flow and migration of neutrophils, monocytes, macrophages, and other cells into the wound.
The first burst of blood acts to cleanse the wound of foreign debris. It is followed by vasoconstriction, which is mediated by thromboxane 2, to decrease blood loss. Vasodilation then occurs once histamine and serotonin are released, permitting increased blood flow to the wound. The surge in blood flow accounts for the increased warmth and redness of the wound. Vasodilation also increases capillary permeability, allowing the migration of red blood cells, platelets, leukocytes, plasma, and other tissue fluids into the interstitium of the wound. This migration accounts for wound edema.
In the cellular response, which is facilitated by increased blood flow, cell migration occurs as part of an immune response. Neutrophils, the first cells to enter the wound, engage in phagocytosis of bacteria and debris. Subsequently, there is migration of monocytes, macrophages, and other cells. This nonspecific immune response is sustained by prostaglandins, aided by complement factors and cytokines. A specific immune response follows, aimed at destroying specific antigens, and involves both B- and T-lymphocytes.
Proliferation is characterized by the infiltration of endothelial cells and fibroblasts and subsequent collagen deposition along a previously formed fibrin network. This new, highly vascularized tissue assumes a granular appearance—hence, the term “granulation tissue.”
Collagen that is deposited in the wound undergoes maturation and remodeling, increasing the tensile strength of the wound. The process continues for months after the initial insult.
All wounds undergo some degree of contraction, but the process is more relevant in wounds that remain open or involve significant tissue loss.
Last, the external covering of the wound is restored by epithelialization.
Classification of surgical wounds
CLASS I – Clean wounds (infection rate <5%)
CLASS II – Clean–contaminated wounds (infection rate 2–10%)
CLASS III – Contaminated wounds (infection rate 15–20%)
CLASS IV – Dirty or infected wounds (infection rate >30%)
SOURCE: Centers for Disease Control and Prevention and the American College of Surgeons
Risk factors for poor wound healing and dehiscence
Poor wound healing
Abdominal wound dehiscence
Conditions and drugs that impair healing
Preexisting medical conditions may limit healing, especially conditions associated with diminished delivery of oxygen and nutrients to healing tissues.
Diabetes can damage the vasculature and may impair healing if the blood glucose level is markedly elevated in the perioperative period. Such an elevation impedes transport of vitamin C, a key component of collagen synthesis.
Malignancy and immunosuppressive disorders may prevent optimal healing by compromising the immune response.
Bacterial vaginosis, a common polymicrobial infection involving aerobic and anaerobic bacteria, appears to be associated with postoperative febrile morbidity and surgical-site infection, particularly after hysterectomy.1 Current guidelines recommend that medical therapy for bacterial vaginosis be instituted at least 4 days before surgery and continued postoperatively.
Because steroids, NSAIDs, and chemotherapy agents impede wound healing, and anticoagulants may interfere with granulation, it is crucial to review the patient’s medications well in advance of surgery.
Nutrition plays a critical role
The importance of nutrition cannot be overstated. A significant percentage of patients are thought to have some degree of nutritional deficiency preoperatively. This deficiency may alter the inflammatory response, impair collagen synthesis, and reduce the tensile strength of the wound.
Because healing requires energy, deficits in carbohydrates may limit protein utilization, and deficiencies of vitamins and micronutrients can also interfere with healing.2
Obesity, too, increases the risk of postoperative wound complication. Markedly obese patients have a thick, avascular, subcutaneous layer of fat that compromises healing.3
Meticulous technique required
Good surgical technique and appropriate use of antibiotics are critical components of successful wound healing.
When placing the incision, avoid the moist, bacteria-laden subpannicular crease in the markedly obese.
During a procedure, handle tissue gently, keep it moist, and make minimal use of electrocautery to reduce tissue injury and promote healing. Keep operating time and blood loss to a minimum, and debride the wound of any foreign material and devitalized tissue.
Multiple studies have demonstrated that judicious use of prophylactic antibiotics significantly decreases the incidence of wound infection, particularly in relation to hysterectomy and vaginal procedures and when entry into bowel is anticipated.4,5 A number of prophylactic regimens are given in TABLE 3.
Meticulous hemostasis at the time of closure is imperative. When complete hemostasis cannot be confirmed, place a small drain in the subcutaneous space (or subfascial space, if there is oozing on the muscle bed) and apply a pressure dressing to help prevent hematoma. Although a drain is not a substitute for precise hemostasis or careful surgical technique, it may be helpful when there is concern about oozing or a “wet” surface, or when the patient is markedly obese.
Some practitioners have expressed concern over the risk of bacterial migration and infection with placement of a drain, but others, including us, advocate use of a drain in the subcutaneous space to help remove residual blood, fluid, and other debris to prevent the formation of dead space and infection and promote wound closure and healing. In a small study, Gallup and associates demonstrated a decreased incidence of wound breakdown when a drain was placed.6
A closed-suction drain, such as a Jackson-Pratt or Hemovac model, helps minimize wound complication when it is placed in the subcutaneous layer. (Avoid a rubber Penrose drain because it may allow bacteria to enter the wound.) It is imperative that the drain exit the body via a separate site and not through the incision itself. We advocate removal when less than 30 mL of fluid accumulates in the reservoir over 24 hours.
3 prophylactic antibiotic regimens
Single intravenous dose
Hysterectomy and urogynecologic procedures, including those that involve mesh
1 g or 2 g
Clindamycin plus gentamicin, a quinolone, or aztreonam
600 mg plus 1.5 mg/kg, 400 mg, or 1 g, respectively
Metronidazole plus gentamicin or a quinolone
500 mg plus 1.5 mg/kg or 400 mg, respectively
SOURCE: American College of Obstetricians and Gynecologists5
Fluid within the wound does not always indicate infection
Wound collections are not necessarily indicative of infection; collections of fluid within the wound may represent a serous transudate, blood, pus, or a combination of these. If the fluid is not addressed, however, fulminant infection may be the result.
Seroma is usually painless
A seroma is a collection of wound exudates within the dead space. Seroma typically involves thin, pink, watery discharge and minimal edge separation. In some cases, there may be surrounding edema but generally little to no tenderness.
When a seroma is detected, remove the staples or stitches in the area of concern and explore the wound. It is essential to ensure fascial integrity, as serous wound drainage may be a sign of impending evisceration. After these measures are taken, cleanse and lightly pack the wound to permit drainage.
Hematoma requires identification of the source of bleeding
Hematoma represents blood or a blood clot within the tissues beneath the skin. It may be caused by persistent bleeding of a vessel, although the pressure within the wound and the pressure produced by the dressing often provide tamponade on the bleeding source, in which case the hematoma forms with no active bleeding.
Hematoma is usually caused by small bleeding vessels that were not apparent at the time of surgery or were not cauterized or ligated at the time of closure. For this reason, it is important to achieve good hemostasis and a “dry” wound before closing the skin.
When hematoma is suspected, open the wound enough to permit adequate exposure and identify the source of bleeding. Evacuate as much blood and clot as possible because blood is an ideal medium for bacterial growth. If active bleeding is found, use a silver nitrate applicator or handheld cautery pen to accomplish hemostasis at bedside. If bleeding is more severe, or the source cannot be visualized, consider returning to the operating room for more extensive exploration.
Once hemostasis is achieved, irrigate the wound copiously and institute local wound care.
How common is infection?
Before it is possible to address this question, it is necessary to clarify the terminology of infection. Contamination and colonization are different entities. The first refers to the presence of bacteria without multiplication. The latter describes the multiplication of bacteria in the absence of a host response. When infection is present, bacterial proliferation produces clinical signs and symptoms.