Wound Healing & Care of Wounds PDF
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Dr. Felicianus A. Pereira
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Summary
These lecture notes cover wound healing and care. The document details the mechanisms of wound healing, including the inflammatory, proliferative, and remodeling phases. It also discusses factors influencing wound healing, including systemic factors and local factors. Different types of scars and their treatments are also examined.
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Wound healing & care of wounds Dr. Felicianus A. Pereira (PT) DPT, MSAPT – IPM&R, DUHS WOUND HEALING Wound healing is a mechanism whereby the body attempts to restore the integrity of the injured part. NORMAL WOUND HEALING A clean incised wound in a health...
Wound healing & care of wounds Dr. Felicianus A. Pereira (PT) DPT, MSAPT – IPM&R, DUHS WOUND HEALING Wound healing is a mechanism whereby the body attempts to restore the integrity of the injured part. NORMAL WOUND HEALING A clean incised wound in a healthy person, with no skin loss heals by undergoing: The inflammatory phase. The proliferative phase. The remodelling phase (maturing phase). INFLAMMATORY Begins immediately after wounding & PHASE lasts 2-3 days To limit Platelets stick to the BLEEDIN blood damaged endothelial G loss lining of vessels, releasing ADP causing VASOCONSTRICTION & THROMBUS thrombocytic FORMATION aggregates to fill the wound Vasoactive amines: Histamine, Serotonin, Prostaglandi ns Platelets release several cytokines from alpha granules which attract lymphocytes and macrophages PROLIFERATIVE PHASE Lasts from the 3rd day to the 3rd week. Fibroblast activity The wound formed in the early part of this phase is called granulation tissue. There is increase in type III collagen which is deposited randomly in the late part of the proliferative phase, increasing the wound in tensile strength REMODELLING PHASE The remodeling phase is characterized by: Maturation of collagen (type I being replaced by type III until a ratio of 4:1 is achieved). Realignment of collagen fibers along the lines of tension. Decreased wound vascularity. Wound contraction due to fibroblast and myofibroblast activity. FACTORS INFLUENCING WOUND HEALING Site of the wound Structures involved Mechanism of wounding: Incision, Crush, avulsion Contamination (foreign/bacteria) Loss of tissue Other local factors: Vascular insufficiency (arterial or venous), Previous radiation, Pressure Systemic factors Malnutrition or vitamin and mineral deficiencies Disease (e.g. diabetes mellitus) Medications (e.g steroids) Immune deficiencies(e.g. chemotherapy, acquired immunodeficiency syndrome) Smoking Classification of wound healing Primary intention Wound edges opposed & minimal surrounding tissue trauma Least inflammation, normal healing Minimal scar Secondary intention Wound left open Heals by granulation, contraction & epithelialization Increased inflammation and proliferation Poor scar Tertiary intention (delayed primary intention) Wound initially left open, necessary in contaminated or untidy wounds. Edges later opposed when healing conditions favorable. Less satisfactory scar. SCARS The immature scar is pink, hard, raised and often itchy. It becomes mature over a period lasting a year or more. As the collagen matures and becomes denser, the scar becomes acellular as the fibroblasts and blood vessels reduce The external appearance of the scar becomes paler, scar becomes softer, flattens and itchiness diminishes. Tensile strength continues to increase but would not be expected to exceed 60-80 % of the normal skin. Types of scars: Atrophic scars Hypertrophic scars Keloidal scars Atrophic scar It is pale, flat and stretched in appearance often appearing on the back and areas of tension. It is easily traumatized as the epidermis and dermis are thinned. Excision and resuturing may rarely improve such a scar. Atrophic scars form a depression or sunken area because of damage to the collagen, fat or other tissues below the skin. These scars are caused by: Acne, chickenpox, surgery and accidents. Hypertrophic scar Excessive scar tissue that does not extend beyond the boundary of the original incision or wound. It results from a prolonged inflammatory phase of wound healing and from unfavorable scar sitting (i.e., across the line of skin tension). Keloid scar Excessive scar tissue that extends beyond the boundaries of the original incision or wound. Etiology is unknown, but it is associated with elevated levels of growth factors, deeply pigmented skin, an inherited tendency and certain areas of the body (e.g. a triangle whose points are the xiphisternum and each shoulder tip). Histology of hypertrophic and keloid scars shows excess collagen with hypervascularity, more marked in keloids where there is more type III collagen. Treatment of hypertrophic and keloid scars Pressure – local molds or elasticated garments Silicone gel sheeting (mechanism unknown) Intralesional steroid injection Excision and steroid injection Excision and post-operative radiation (external beam or brachytherapy) Intralesional excision (keloids only). Laser – to reduce redness Vitamin E or palm oil massage Contractures When scar cross joints or flexion creases, a tight web may form restricting the range of movement at the joint called as a contracture. It can cause hyperextension or hyperflexion deformity. In the neck, it may interfere with head extension. Treatment: Multiple Z-plasties or more complex inset of grafts and flaps. Splintage and intensive physiotherapy are often required postoperatively. WOUND CARE – AVOIDABLE SCARRING A scar of some description will form after wounding. A dirt ingrained (tattooed) scar is usually preventable by proper initial scrubbing and cleansing of the wound. Late treatment may require excision of the scar or pigment destruction by laser. Suture marks may be minimized by using monofilament sutures that are removed early (3-5 days). Wounds can be strengthened post-suture removal by the use of sticky strips. Fine sutures placed close to the wound margins tend to leave less scarring. SURGICAL DRESSINGS DEBRIDING AGENTS Used only in necrotic sloughing skin ulcers. Provide acidic environment. Claimed to enhance healing with debriding action. ENZYMATIC AGENTS Activates fibrinolysis and liquefy pus on chronic skin ulcers. BEAD DRESSINGS Remove bacteria and excess moisture by capillary action in deep granulating wounds POLYMERIC FILMS Primary adhesive transparent dressing for sutured wounds or donor sites FOAMS Elastomeric dressing can be shaped to fit deep cavities and granulating wounds. Absorbent and non-adherent. HYDROGELS Maintain moist environment , polymers can absorb exudate or antiseptics. Semi permeable, allow gas exchange. HYDROCOLLOIDS Complete occlusion. Promote epithelialisation and granulation tissue. Maintain moisture without gaseous exchange across them. FIBROUS POLYMERS Absorptive alginate dressings. Derived from natural (seaweed) source. Like polymeric hydrocolloids and hydrogels, they can be used to pack deep wounds. BIOLOGICAL MEMBRANES Used for superficial chronic skin ulcers. No proven advantage. SIMPLE MISCELLANEOUS Simple absorptive dressings only used as secondary dressings to absorb exudate. Added antimicrobials probably confer no benefit. Added charcoal absorbents may reduce swelling. Relatively cheap but of questionable effectiveness. BANDAGES & DRESSINGS Superficial partial-thickness wounds and mixed-depth wounds The simplest method of treating a superficial wound is by exposure. The initial exudate needs to be managed by frequent changes of clean linen around the patient but, after a few days, a dry eschar forms, which then separates as the wound epithelializes. This is often used in hot climates and for small burns on the face. Covering the wound with a permeable wound dressing avoids the wounds adhering to the sheets and clothes. A similar method of managing these types of burns is to place a Vaseline covered gauze over the wound. An alternative is a fenestrated silicone sheet backed with swabs to absorb the exudate More interactive dressings include hydrocolloids and biological dressings. Hydrocolloid dressings need to be changed every 3-5 days. They are particularly useful in mixed depth burns as the high protease levels under the occlusive dressings aid in the debridement of the deeper areas of burn. They also provide a moist environment, which is good for epithelialization. Biological, synthetic and natural e.g. dressings also provide good healing environments and do not need to be changed. They are ideal for one stop management of superficial burns, being easy to apply and comfortable. They are not useful in mixed-depth wounds as they will become detached when as the eschar needs to separate. It is prudent to clean heavily contaminated wounds, resulting from accidents, formally under a general anesthetic. With more chronic contamination, silver sulphadiazine cream dressing for 2 or 3 days is very effective and can be changed to a dressing that is more efficient at promoting healing after this period. Early debridement and grafting is the key to effectively treating deep partial and full thickness burns in a majority of cases. Dressing for full thickness and contaminated wounds DRESSINGS WITH NANOCRYSTALLINE SILVER Silver sulphadiazine cream (1%) This gives broad spectrum prophylaxis against bacterial colonization and is particularly effective against psuedomonas and also methicillin resistant staphylococcus. Silver nitrate solution (0.5%) It is highly effective as a prophylaxis against pseudomonas aeruginosa colonization. Disadvantage: It is not as active as silver sulphadiazine cream against some of the gram negative aerobes. It needs to be changed or the wounds resoaked every 2-4 hours. It also produces black staining of all the furniture surrounding the patient. Silver sulphadiazine and cerium nitrate: Useful dressing for full thickness burns. Induces hard effect on burned skin (Cerium nitrate forms a sterile eschar and is specially useful in treating burns). It has been shown in certain instances, especially in elderly patients, to reduce some of the cell mediated immunosuppression that occurs in the burn thus boosts the cell mediated immunity. BURN WOUND CARE INITIAL CLEANING OF BURN WOUND Washing the burn wound with chlorhexidine solution TOPICAL AGENTS: For initial management of minor burns that are superficial or partial thickness, dressings with a non-adherent material, such as vaseline-covered gauze is often sufficient. These dressings are left in place for 5 days and should heal after 7-10 days. Silver sulphadiazine (1%) is the most commonly used topical agent for treatment with minor burns. Dressing the minor burn wound The aims of dressing are to decrease wound pain and to protect and isolate the burn wound. Synthetic burn wound dressings are popular as they: Decrease pain associated with dressings Improve healing times Decrease outpatient appointments Lower overall costs Healing of burn wound Burns that are being managed conservatively should be healed within 3 weeks. If there are no signs of re-epithelialisation in this time, the wound requires debridement and grafting. References Bailey And Love's Short Practice of Surgery. 25th Edition. Chaper 3.