wound healing

General principles of wound healing can be divided into 3 distinct but overlapping phases: 1- haemostasis and inflammation; 2- proliferation; and 3- maturation or remodelling. The 3 basic responses following injury are: resolution, regeneration, and repair. Neutrophils normally begin arriving at the wound site within minutes of injury to clearing the initial rush of contaminating bacteria, also as a source of pro-inflammatory cytokines. Adequate oxygen delivery is a prerequisite to the hydroxylation of lysine and proline during collagen synthesis. Hypovolaemia decreases tissue oxygen tension.

Sutures need to be placed at an appropriate distance from the margin and surgical knots must be tied securely without strangulating the intervening tissue. Two layers anastomosis increase the inflammatory response in the early stages of healing owing to extra suture material and the ischaemia to the inverted tissue. Because of the diameter of each staple is less than that of a suture, staples are at greater risk of pulling through the tissue edges in the presence of tension. There is increased risk of bleeding from the anastomotic line secondary to the B-shaped staples, which are designed to permit blood flow through to the tissue edges. The ideal suture should be strong enough to provide the necessary mechanical support for the anastomosis but fine enough to minimise trauma as it passes through the tissue. Suture tensile strength is required for a short period only.

Granulocytes are responsible for a significant degree of collagenolytic activity, and their presence is increased by contamination, faecal soiling, and tissue necrosis. Sepsis increases collagenolysis. NSAIDs decrease collagenolysis in the first 3 days.

GH enhances amino acid transport in the jejunum and ileum, in particular glutamine, which is the principle fuel of the small intestine. Both prolonged and short-term types of malnutrition diminish anastomotic healing. Ketone bodies inhibit the intestinal mucosal atrophy associated with glucose-based parenteral nutrition.

Wound disruption may occur without warning. The recommended daily requirement for protein during burns or severe sepsis is 1.5-2 g/kg/day. The most common cause of acute wound failure is suture tearing out of the tissue. The patient with risk factors is at a higher risk than a patient with none.

Adhesion formation begins with a fibrin matrix that typically occurs during coagulation. Zinc is lost in excessive amounts after operation because of stress, sepsis, diarrhoea, or fistulas, plays an important role in cell mitosis and proliferation during the fibroblastic phase of wound healing. Epithelialization requires oxygen. When >100,000 bacteria are present, normal wound healing will not occur. The golden period of closure of an open wound appears to be the length of time it takes an inoculation to reach the critical level of 100,000 bacteria/gm of tissue (5.17 hrs).

Suture materials acting as corpus alienum, cause an immunological and inflammatory reaction at the site of the healing wound. Surgical wound infections are common and expensive perioperative complications. Oxidative killing is a function of tissue oxygen. For healing to occur in a wound, fibrin must be removed from the inflamed tissue. Metalloproteinases enhance fibrin clot and eschar dissolution. The presence of bacteria does not imply invasion of tissues, therefore, presence of microorganisms is only indicative, not diagnostic of infection.

Adhesive interactions between leukocytes and the vascular endothelium are mediated by lymphocyte-function-associated antigen (LFA-1) and ICAM, respectively. These interactions help determine the rate of inflammation and granulation tissue formation. Excessive wound drainage is poorly managed by hydrocolloid dressings, creating a problem of leakage for outpatients. Calcium alginate dressings are transformed into a biodegradable, non-toxic hydrophilic gel at the wound surface by way of an ion exchange reaction between the calcium in the alginate and sodium in the wound exudate.

WOUND HEALING

Since 2000

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