1. What are the characteristics of primary wound healing?

a. Primary wound healing or healing by first intention occurs within hours of repairing a full­thickness surgical incision. . The edges of the wound are approximated and held together with sutures, tape or tissue adhesives. This surgical insult raesults in the mortality of a minimal number of cellular constituents. Wound closes with minimal intervention.

b. First intention wound healing is the most desirable. Most surgical wounds heal by first intention if the wound is not contaminated, dead spaces are closed, tissue is handled gently, hemostasis is achieved, and the tissues are approximated accurately.

2. What is meant by healing by secondary intention?

a. Wound closes by contraction and reepithelialization. [NB Remember the role of the myofibroblasts].

b. Wounds heal by secondary intention if there are post-operative complications such as: infection, wound dehiscence, excessive scar, or excessive drainage. If sutures were used prior to the development of the complication, they are removed and the wound is allowed to heal by forming granulation tissue from the bottom of the wound outward. If an infection is present when the surgical procedure takes place, the surgeon may not attempt any suturing of the wound, and allow the wound to head by secondary intention. This type of healing takes much longer than healing by first intention.

3. What is tertiary healing?

The last type of wound healing is by third intention. When granulation tissue has developed along the edges of a wound the surgeon may use large retention type sutures to assist in healing. Third intention healing is used when there is gross infection, or after tissue has been lost due to traumatic injury or surgical debridement. The use of skin grafts or free flaps may be necessary to effect healing.

4. Name the stages or phases of wound healing

a. The wound healing process has 3 phases. They are the inflammatory phase, the proliferative phase, and the maturational phase, also known as scar remodeling.

i. The inflammatory phase (days 1 to 10) is characterized by hemostasis and inflammation. Collagen exposed during wound formation activates the clotting cascade (both the intrinsic and extrinsic pathways), initiating the inflammatory phase. After injury to tissue occurs, the cell membranes, damaged from the wound formation, release thromboxane A2 and prostaglandin 2-alpha, potent vasoconstrictors. This initial response helps to limit hemorrhage. After a short period, capillary vasodilatation occurs secondary to local histamine release, and the cells of inflammation are able to migrate to the wound bed. The timeline for cell migration in a normal wound healing process is predictable. Cells involved in this phases are PMNs, macrophages; epithelialization 1-2 mm/day. Platelets, the first response cell, release multiple chemokines, including epidermal growth factor (EGF), fibronectin, fibrinogen, histamine, platelet-derived growth factor (PDGF), serotonin, and von Willebrand factor. These factors help stabilize the wound through clot formation. These mediators act to control bleeding and limit the extent of injury. Platelet degranulation also activates the complement cascade, specifically C5a, which is a potent chemoattractant for neutrophils. The inflammatory phase continues, and more immune response cells migrate to the wound. The second response cell to migrate to the wound, the neutrophil, is responsible for debris scavenging, complement-mediated opsonization of bacteria, and bacteria destruction via oxidative burst mechanisms (ie, superoxide and hydrogen peroxide formation). The neutrophils kill bacteria and decontaminate the wound from foreign debris. The next cells present in the wound are the leukocytes and the macrophages (monocytes). The macrophage, referred to as the orchestrator, is essential for wound healing. Numerous enzymes and cytokines are secreted by the macrophage. These include collagenases, which debride the wound; interleukins and tumor necrosis factor (TNF), which stimulate fibroblasts (produce collagen) and promote angiogenesis; and transforming growth factor (TGF), which stimulates keratinocytes. This step marks the transition into the process of tissue reconstruction, ie, the proliferative phase.

ii. - The second stage of wound healing is the proliferative phase (5 days to 3 weeks). Epithelialization, angiogenesis, granulation tissue formation, and collagen deposition are the principal steps in this anabolic portion of wound healing. Epithelialization occurs early in wound repair. If the basement membrane remains intact, the epithelial cells migrate upwards in the normal pattem. This is equivalent to a first-degree skin bum. The epithelial progenitor cells remain intact below the wound, and the normal layers of epidermis are restored in 2-3 days. If the basement membrane has been destroyed, similar to a second­ or third-degree bum, then the wound is re-epithelialized from the normal cells in the periphery and from the skin appendages, if intact (eg, hair follicles, sweat glands). Angiogenesis, stimulated by TNF-alpha, is marked by endothelial cell migration and capillary formation. The new capillaries deliver nutrients to the wound and help maintain the granulation tissue bed. The migration of capillaries into the wound bed is critical for proper wound healing. The granulation phase and tissue deposition require nutrients supplied by the capillaries, and failure for this to occur results in a chronically unhealed wound. Mechanisms for modifying angiogenesis are under study and have significant potential to improve the healing process. The final part of the proliferative phase is granulation tissue formation. Fibroblasts differentiate and produce ground substance and then collagen. The ground substance is deposited into the wound bed; collagen is then deposited as the wound undergoes the final phase of repair. Many different cytokines are involved in the proliferative phase of wound repair. The steps and the exact mechanism of control have not been elucidated. Some of the cytokines include PDGF, insulin-like growth factor (IGF), and EGF. All are necessary for collagen formation.

iii. The final phase of wound healing is the maturational phase (3 weeks to 1 year). The wound undergoes contraction, ultimately resulting in a smaller amount of apparent scar tissue. The entire process is a dynamic continuum with an overlap of each phase and continued remodeling. The wound reaches maximal strength at one year, with a tensile strength that is 30% of normal skin. Collagen deposition continues for a prolonged period, but the net increase in collagen deposition plateaus after 21 days. Type three collagen replaced with type I; decreased vascularity. Collagen cross-linking occurs. Peripheral nerves regenerate at 1 mm/day.

5. Name local factors that influence wound healing?

a. Mechanical injury.

b. Infection.

c. Edema.

d. Ischemia/necrotic tissue.

e. Topical agents.

f. Ionizing radiation.

g. Low oxygen tension.

h. Foreign bodies.

6. Name some general principals in the management of clean wound?

a. Moist environment (avoid desiccation).

b. Oxygen delivery: optimal fluids, no smoking, pain control, arterial reconstruction,

c. supplemental oxygen.

d. Avoid edema: leg elevation, compression

e. Remove necrotic tissue,.

7. What are the general factors that influence wound healing:

a. Age.

b. Nutrition.

c. Metabolic diseases.

d. Trauma.

e. Immunosuppression. Steroid use is a well known inhibitor of wound healing. There is data that suggests the effects of steroids can be reversed by the application of Vitamin A.

f. Connective tissue disorders.

g. Smoking.

8. What is a contaminated wound:

a. Fresh, traumatic wound.

b. Gross spillage of gastrointestinal contents in the abdomen.

c. Mayor break in sterile technique.

d. Incision through an inflammed tissue.

It is generally not advisable to primarily close contaminated wounds. One option for their management is the delayed primary closure, in which the wound is dressed open with an occlusive dressing and then closed in 3-5 days if there is no sign of invasive infection. Otherwise tertiary closure, debride and irrigate wound and initiate dressing changes with antibacterial cream until bacterial count is less than 10⁵ / g tissue then proceed with closure. (ACS Surgery 2006)

9. How does one manage the contaminated chronic wounds:

The first principle in managing chronic wounds is to diagnose and treat any underlying circulatory disease. The second principle is never to allow open wounds to dry (ie, use moist dressings). Moist dressings may also relieve pain. A third principle is to control any infection with systemic antibiotics. Topical barriers to infection are useful but not always necessary. A fourth principle is to recognize that chronically scarred tissue is usually poorly perfused. Debridement of unhealthy tissue, often followed by skin grafting, may be required for healing. A fifth principle is to reduce autonomic vasoconstriction by means of warmth, moisture, pain relief, or pharmacologic vasodilation medications. The use of various wound preparations may be helpful in this situation

10. What are fibroblasts?

Fibroblasts are mesenchymal cells that secrete the collagen and proteoglycans of the connective tissue matrix that weld wound edges together. They assume high-molecular-weight polymeric forms and become the physical basis of wound strength.

11. Name some of the newer advances in wound dressings.

Some novel approaches to wound management have been developed since the latter part of the 1990s. One such approach involves the use of skin substitutes, such as Alloderm, Integra, and Apligraf. Alloderm and Integra contain only dermal elements, whereas Apligraf and others contain cellular components, including epithelium. The cellular elements most likely do not remain in the wound for long, but they are thought to provide cytokines that may stimulate the healing process in the short term. Hydrocolloids and negative pressure dressings, such as the wound VAC are other slick techniques that may improve wound healing.