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Acute wounds are a significant source of morbidity and mortality in the United States and around the world. As the number of surgical procedures and traumatic injuries increase, the problem of acute wound complications will continue to confront surgeons. Unlike a chronic venous stasis ulcer or decubitus, an acute wound is expected to pass through a predictable sequence of biological pathways to result in sustained wound closure. Although most emphasis has been on chronic wounds and ways to improve impaired healing, the fact is that there are many more acute wounds occurring than there are chronic wounds.

Nearly 50 million surgical procedures are performed each year in the United States. Fifty million additional traumatic wounds add to the burden of acute wound morbidity. Complicated traumatic and surgical injury is not confined to the skin. There remains an unacceptably high incidence of laparotomy wound dehiscence, incisional hernia formation, gastrointestinal anastamotic leak, pancreatic fistulae, vascular pseudoaneurysms, and bony nonunion. Laparotomy incisions fail to heal 11% of the time and only 12-mm gaps in the laparotomy repair of the linea alba will progress to incisional hernias 94% of the time. Subsequent incisional hernia repairs fail to heal 24% to 58% of the time. This high rate of iatrogenic wound failure results in 200,000 reoperations each year in the United States at an estimated cost of $2.5 billion. With 4 million laparotomies performed each year in the United States, the true incidence of laparotomy wound failure and incisional hernia formation approaches 400,000 per year. The incidence of laparotomy wound failure and incisional hernia formation is increasing with the dramatic growth of bariatric surgery.

Burns and fires remain the leading cause of accidental death in the home for children 14 and younger and the third leading cause of accidental death for adults. Scalds are the leading cause of accidental death in the home for children from birth to age 4 and account for 40% of the burn injuries of children up to age 14. After the age of 60, the risk of burn injury is greater than at any time since childhood and the average size of the burn is larger than for any other age group.

Of 6 possible outcomes for an acute wound, 5 are less than desirable. These include wound dehiscence, herniation, wound infection, delayed healing, and excessive scar formation. The single desirable outcome—uncomplicated healing in a timely manner—is not always a given. Many factors contribute to the 5 undesirable outcomes or complications of healing of the acute wound. Minimizing or eliminating these factors, and thus optimizing healing, should result in improved outcomes.

The first documented evidence of a wound appeared in a man-ape ancestor, Australopithecus africanus, approximately 5 million years ago. Hippocrates wrote of his preference for healing by first intention in the 5th century BC. In his writings, he stressed suturing of wounds and the use of dry dressings. Later, Celsus described complications of wound healing due to infection, mechanical irritation, or inadequate circulation during the time of the Roman Empire. He also converted burns from a medical to a surgical disease and recommended an operative approach to the burn wound. Advances in the understanding of wounds, wound treatment, and wound complications flourished during the Renaissance. Ambrose Pare recommended early debridement and removing deterrents to healing. Great advances in the understanding of wound healing of the 20th century began in 1910 when Nobel Prize winner Alexis Carrel divided the stages of wound healing into 4 periods: quiescent, granulomatous retraction, epidermalization, and cicatricion, based on a series of animal experiments. The combination of preclinical and clinical experimentation led to the optimizing of acute wound healing and the minimizing of complications to tissue.

Based in large part on the work of Carrel, the phases of acute tissue repair are conceptually organized into a sequence of 4 time-dependent phases: hemostasis, inflammation (lag), proliferative, and remodeling. The “lag” phase of acute wound healing is a very metabolically active early period during which inflammatory and repair cells are recruited, but during which no meaningful tissue integrity or breaking strength is yet established. It is clinically relevant that this mechanically weakest point of acute tissue repair lasts several days. Within 24 hours of injury, circulating monocytes begin to enter the wound. The monocytes then terminally differentiate into tissue macrophages after exiting the vasculature and entering the wound site. Macrophages regulate many of the most important molecular signals for the propagation of the wound repair process through the generation of oxygen free radicals, inflammatory cytokines, and tissue growth factors. Tissue macrophages proliferate within the wound and, like polymorphonuclear leukocytes, clear the wound of contaminating microbes as well as nonviable tissue. It is predominantly macrophage synthesis and release of tissue growth factors that initiates the proliferative phase of the repair process.

Wound repair and normal healing depends on an adequate arterial circulation supplying the tissue with oxygen. All oxygen delivered to the wound must come by way of the arteries. Oxygen supports processes vital to the healing cascade including angiogenesis, cell motility, and extracellular matrix formation. Oxygen is necessary for collagen formation and proper collagen cross-linking. These processes are impaired when transcutaneous oxygen tension is less than 40 mm Hg. Wound healing is further impaired as the tissue oxygenation continues to drop. Breakdown of surgical incisions is more common in patients who have been hypotensive during their traumatic episode or operation. Dehiscence is more frequent in trauma patients or patients having repair of a ruptured abdominal aortic aneurysm if they have been hypotensive. Tissue oxygen tensions below 40 mm Hg inhibit fibroblast replication, collagen production, and epithelialization. Ischemic tissues are more likely to become infected. Revascularization is the mainstay of the treatment of ischemia.

Wound healing is impaired by infection. If the bacterial count is greater than 10⁵ bacteria per gram of tissue, healing is impaired. Streptococcus will inhibit healing, even when present in smaller numbers. Surgical debridement provides an opportunity to unroof and drain pus and to take a piece of tissue for culture from the deepest part of the wound. Necrotic tissue removed during debridement is the tissue with the highest bacterial counts. There is often no correlation between the bacteria responsible for cellulitis and what is cultured from a dry surface swab. Perhaps the most compelling proof of the benefit of debridement comes from the randomized blinded trial of platelet-derived growth factor (PDGF) (becaplermin) in the treatment of diabetic neurotrophic foot ulcers. In this study each patient underwent wide debridement before entry into the trial. There was a direct relationship between the incidence of debridement and the healing rate in both the PDGF-treated and the control groups. The more the wounds were debrided, the better they healed.

Wound infection can be viewed as a failure of wound healing caused by an imbalance of bacteria. Each of the processes involved in the wound healing scheme is specifically modulated by the presence of bacteria in tissue. A major advance in the prevention and treatment of various types of wound infection has been the understanding that the mere presence of organisms in a wound is less important than the level of invasive bacterial growth. A wealth of clinical and experimental data has shown that a level of bacterial growth of greater than 10⁵ organisms per gram of tissue is necessary to cause impaired wound healing for most species of bacteria. Only the β-hemolytic streptococci appear capable of routinely causing infection at levels of less than 10⁵ or 100,000 organisms per gram of tissue.

The increased clinical use of anticoagulants and antiplatelet agents has increased the incidence and relevance of hematoma formation following operations. The problem is exacerbated by quality measures that now recommend routine prophylaxis for deep venous thrombosis in most surgical patients. Large hematomas cause ischemia of adjacent tissue due to the pressure effect and increase the risk of infection. These should be immediately evacuated when safe. Natural liquefaction of smaller hematomas is an option, with the opportunity for percutaneous aspiration.

The high prevalence of nonhealing wounds has stimulated the development of novel adjuvants designed to improve wound healing outcomes. Negative pressure wound therapy (NPWT) systems can improve closure rates. The most common designs provide maintenance of a moist wound environment and the drainage of wound exudates while applying continuous negative pressure to the open wound surface. This arrangement may accelerate the appearance of repair fibroblasts in the wound and improve wound perfusion. Importantly, NPWT reduces the frequency of dressing changes and mechanically stabilizes against repeated trauma and loads. Together, this should reduce wound trauma.

Wounds and malignancies are related in several ways. The treatment of malignancies can lead to impaired acute wound healing and the development of a chronic wound. Malnutrition, cachexia, anemia, uremia, and other manifestations of malignancy have been shown or suggested to impede acute wound healing. Wounds may be directly associated with malignancy. Pyoderma gangrenosum and vasculitis leading to cutaneous ulcers have both been associated with malignancy. Any nonhealing wound with no explanation for the delay should be considered at risk for malignant transformation.

The skin serves a vital function as an immune barrier. There are multiple cells in the skin that are involved in host defense. Keratinocytes produce interleukin-1 (IL-1), a proinflammatory cytokine. Langerhans cells are derived from the bone marrow and are part of the monocyte-macrophage group of cells. Steroids interrupt the normal inflammatory phase and thus delay healing by impairing macrophage function, angiogenesis, fibrogenesis, and subsequently normal wound contraction. Patients with human immunodeficiency virus (HIV) have a significant impairment in wound healing. It has been recognized, for example, that HIV-positive (HIV+) patients have a greater incidence of wound complication and breakdown after abdominal operations than patients without HIV infection.

Management of the burned patient is essentially the management of the burn wound. After resuscitation, care of the burn patient prioritizes the prevention of infection while simultaneously preparing for wound closure. The goal of nonoperative treatment of shallow partial-thickness burns is epithelialization. This is achieved by temporarily closing the burn wound with a biologic or biosynthetic dressing, or bioengineered skin, which will lift off as epithelialization progresses. Alternatively, the shallow burn wound can be treated with an antibacterial cream. This is usually unnecessary for shallow burn wounds unless they cover a large extent of the total body surface area (TBSA) because burn wound sepsis is not a great risk. Treatment of the deep burn wound is operative and similar to management of any acute traumatic wound (ie, debridement of all necrotic or nonviable tissue and wound closure).

Acute wound failure may be defined as an interruption in the timely and predictable recovery of mechanical integrity in the injured tissue. The restoration of mechanical structure should ideally reestablish normal function. Tissue repair is an anabolic process that requires both energy and molecular substrates. Patients who are malnourished or actively catabolic such as in the systemic inflammatory response syndrome demonstrate impaired healing. Inadequate nutrition also retards the immune response, limiting opsonization of bacterial and sterilization of wounds. Many drugs are known to impair wound healing. Clinically, this can introduce a conflict between the primary therapeutic modality and its deleterious effect on wound healing. Underlying disease in the injured host is another common cause for impaired wound healing. Delayed tissue repair is a widely recognized complication in patients with diabetes mellitus, for example. Tissue inflammation is abnormal and fibroblast and endothelial cell proliferation are impaired.

Hyperproliferative scar formation can result in any wound and in every organ system. This presents a clinical problem not only with integumentary wounds, but also in pathologic conditions such as intestinal or tendon adhesions, bile duct strictures, cirrhosis of the liver, and glomerulonephritis. The processes of wound healing are the same in wounds that develop excessive or proliferative scarring as in those that do not, but the degree or genetic penetration of the individual processes may differ from that of normal healing. Epidermal regeneration or epithelialization does not appear to play a major role in scar overproduction. The overproduction seems to be controlled at the mesenchymal level. Various operative techniques can be used to prevent or minimize excessive scar formation. A classic example of this is early excision and closure of the burn wound. This technique decreases the time and intensity of the inflammatory phase of healing. Mechanical measures have also been used, such as the application of pressure. Intralesional corticosteroids are also used to treat excessive scarring. The most promising treatment for excessive or proliferative scarring appears to be the molecular approach. Emerging data implicate the fibrogenic isoforms of transforming growth factor (TGF)-β (TGF-β1 and TGF-β2) in the pathogenesis of proliferative scarring. Inhibitors of fibroproliferative growth factors might abrogate the hyperproliferative response seen during pathological scarring.