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 General Principles of Wound Healing 

Although there are many types of wounds, most undergo similar stages in healing that are mediated by cytokines and other chemotactic factors within the tissue. The duration of each state varies with the wound type, management, microbiologic, and other physiologic factors. There are 4 major stages of wound healing after a full-thickness skin wound.

Inflammation is the first stage of wound healing. It can be divided into 2 phases. During the initial phase, vasoconstriction occurs immediately to control haemorrhage, followed within minutes by vasodilation. During the second phase, cells adhere to the vascular endothelium. Within 30 min, leukocytes migrate through the vascular basement membrane into the newly created wound. Initially, neutrophils predominate (as in the peripheral blood); later, the neutrophils die off and monocytes become the predominant cell type in the wound.

Debridement is the second stage of wound healing. Although neutrophils phagocytose bacteria, monocytes, rather than neutrophils, are considered essential for wound healing. After migration out of the blood vessels, monocytes are considered macrophages, which then phagocytose necrotic debris. Macrophages also attract mesenchymal cells by an undefined mechanism. Finally, mononuclear cells coalesce to form multinucleated giant cells in chronic inflammation. Lymphocytes may also be present in the wound and contribute to the immunologic response to foreign debris.

Repair is the third stage of wound healing. It consists of fibroblast, capillary, and epithelial proliferation phases. During the repair stage, mesenchymal cells transform into fibroblasts, which lay fibrin strands to act as a framework for cellular migration. In a healthy wound, fibroblasts begin to appear ~3 days after the initial injury. These fibroblasts initially secrete ground substance and later collagen. The early collagen secretion results in an initial rapid increase in wound strength, which continues to increase more slowly as the collagen fibres reorganize according to the stress on the wound.

Migrating capillaries deliver a blood supply to the wound. The centre of the wound is an area of low oxygen tension that attracts capillaries following the oxygen gradient. Because of the need for oxygen, fibroblast activity depends on the rate of capillary development. As capillaries and fibroblasts proliferate, granulation tissue is produced. Because of the extensive capillary invasion, granulation tissue is both very friable and resistant to infection. 

Epithelial cell migration begins within hours of the initial wound. Basal epithelial cells flatten and migrate across the open wound. The epithelial cells may slide across the defect in small groups, or “leapfrog” across one another to cover the defect. Migrating epithelial cells secrete mediators, such as transforming growth factors a and ß, which enhance wound closure. Although epithelial cells migrate in random directions, migration stops when contact is made with other epithelial cells on all sides (ie, contact inhibition). Epithelial cells migrate across the open wound and can cover a properly closed surgical incision within 48 hr. In an open wound, epithelial cells must have a healthy bed of granulation tissue to cross. Epithelialization is retarded in a desiccated wound. 

Maturation is the final stage of wound healing. During this period, the newly laid collagen fibres and fibroblasts reorganize along lines of tension. Fibres in a non-functional orientation are replaced by functional fibres. This process allows wound strength to increase slowly over a long period (up to 2 yr). Most wounds remain 15-20% weaker than the original tissue. 


Uncomplicated simple lacerations are usually managed by complete closure if they are not grossly contaminated. The wound should be thoroughly lavaged and debrided as necessary before closure. If tension is present on the wound edges, it should be relieved by tension-relieving suture techniques, sliding tissue flaps, or grafts. Deep lacerations may be treated according to the same principles, depending on the extent of the injury. Damage to underlying structures (eg, muscles, tendons, and blood vessels) must be resolved before closure. If a laceration is grossly contaminated with debris, primary closure of the wound may not be indicated. Contaminated wounds may be closed with drains or treated as an open wound. 

 Bite Wounds: 

Bite wounds are a major cause of injuries, especially in free-ranging animals. Cat bites tend to be small, penetrating wounds that frequently become infected and must be treated as an abscess with culture, debridement, antibiotics, and drainage. Dog bites have a more varied presentation. Because of the slashing nature of dog bite injuries, the major tissue damage is usually found beneath the surface of the wound. While only small puncture marks or bruising may be evident on the surface, ribs may be broken or internal organs seriously damaged. The animal should be thoroughly examined and stabilized before definitive wound care is begun. The wound should be surgically extended as far as necessary to allow a thorough examination and determination of its extent before a decision on the repair can be made. After a proper assessment, debridement can be performed. Unless en bloc debridement is performed, complete wound closure is usually not recommended because the sites are usually contaminated. Closure can be accomplished with drains, as a delayed closure, or by second intention depending on the extent of the injury. 

 Degloving Injuries:

Degloving injuries result in an extensive loss of skin and a varied amount of deeper tissues. These injuries are a result of a shear force on the skin. Sources include fan belt injuries and loss of tissue during a collision with a motor vehicle. With a physiologic degloving injury, the skin is still present but completely freed from the underlying fascia. If the injury results in a loss of blood supply to the skin, necrosis may develop later. In an anatomic degloving injury, the skin is torn off the body. Anatomic degloving injuries frequently require marked and repeated debridement. Differentiating viable and nonviable tissue may be a problem in the early wound debridement process. An attempt should be made to salvage tissue in which viability is questionable. Subsequent debridement can be used to remove any necrotic tissue. In orthopaedic injuries that typically accompany degloving injuries, final stabilization may be delayed until local infection is under control. 

 Gunshot Injuries: 

In gunshot injuries, most of the damage is not visible. As the projectile penetrates, it drags skin, hair, and dirt through the wound. If the projectile exits the body, the exit wound is larger than the entrance wound. The amount of damage caused by the projectile is a function of its shape, aerodynamic stability, mass, and velocity. High-velocity projectiles tend to produce more damage as a result of impact-induced shock waves that move through the tissue. The shock waves create blunt force trauma resulting in tissue and vascular damage.

Gunshot wounds are always considered to be contaminated, and primary closure is generally not recommended. These wounds should be managed as open wounds or by delayed primary closure. After initial assessment and stabilization of the animal, the wound may be explored to evaluate the extent of damage and to determine a plan for repair. If the projectile caused a fracture, the method of repair depends on the location and type of fracture. External fixation or bone plates are common choices for rigid stabilization of the fracture so that the soft tissues may be appropriately managed. Gunshot wounds to the abdomen are an indication for an exploratory celiotomy. Gunshot wounds to the thorax may require a thoracotomy if haemorrhage or pneumothorax cannot be conservatively managed. 

 Pressure Wounds: 

Pressure wounds or decubital ulcers develop as a result of pressure-induced necrosis. Pressure wounds can be extremely difficult to treat and are best prevented. Preventive measures include changing the position of the animal frequently, maintaining adequate nutrition and cleanliness, and providing a sufficiently padded bed. Factors that predispose to pressure wounds include paraplegia, tetraplegia, improper coaptation, and immobility. Mild ulcers may be managed with debridement and bandaging to prevent further trauma to the affected site. More severe wounds require extensive surgical management. After debridement and development of a granulation bed, an advancement flap or pedicle graft may be required for closure. 

 Factors that Interfere with Wound Healing 

Factors that interfere with wound healing may be divided by source into physical, endogenous, and exogenous categories. Physical factors are environmental issues. Temperature affects the tensile strength of wounds. Ideal conditions allow wound healing to occur at 30°C. Decreasing the temperature to 12°C results in a 20% loss of tensile wound strength. Adequate oxygen levels are also required for appropriate wound healing. Because of vessel disruption, wounds contain lower oxygen levels than surrounding healthy tissue. Low levels of oxygen interfere with protein synthesis and fibroblast activity, causing a delay in wound healing. Oxygen levels may be compromised for many reasons, including hypovolemia, the presence of devitalised tissue, and excessively tight bandages. 

Endogenous factors (previously known as systemic factors) typically reflect the overall condition of the animal. Anaemia may interfere with wound healing by creating low tissue oxygen levels. Hypoproteinemia delays wound healing only when the total serum protein content is <2.0 g/dL. Because wound healing is a function of protein synthesis, malnutrition may alter the healing process. The addition of dl-methionine or cysteine (an important amino acid in wound repair) prevents delayed wound healing. Uraemia can interfere with wound healing by slowing granulation tissue formation and inducing the synthesis of poor quality collagen. Although diabetes is a known problem with wound healing in humans, it has not been demonstrated to cause a problem in animals. Obesity contributes to poor wound healing primarily as a consequence of poor suture holding in the subcutaneous fat layers.

Exogenous factors include any external chemical that alters wound healing. Cortisone is commonly implicated in wound complications. Corticosteroids markedly inhibit capillary budding, fibroblast proliferation, and the rate of epithelialization. Similar to cortisone, vitamin E adversely affects wound healing by slowing collagen production. This effect may be reversed with vitamin A. Additional vitamin A will not improve wound healing in the absence of vitamin E or cortisone. Vitamin C is required for the hydroxylation of proline and lysine. Zinc is required for epithelial and fibroblastic proliferation; however, excessive zinc delays wound healing by inhibiting macrophage function. Radiation is detrimental to wound healing. Given 7 days prior to wound creation, healing is impaired. Administered 7 days following wound creation, it has no effect on wound strength. Cytotoxic drugs may also delay wound healing. Alkylating agents (eg, cyclophosphamide, melphalan) slow wound healing by blocking DNA synthesis. 

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