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A wound may be described in numerous ways; by its aetiology, physiological place, by whether it is acute or chronic1, by the method of closure, by its presenting signs or indeed by the appearance of the primary tissue enters the wound bed. All meanings serve a vital purpose in the assessment and suitable management of the wound through to sign resolution or, if viable, healing. A wound by true definition is a breakdown in the protective function of the skin; the loss of connection of epithelium, with or without loss of underlying connective tissue (i.
e. muscle, bone, nerves) following injury to the skin or underlying tissues/ organs triggered by surgical treatment, a blow, a cut, chemicals, heat/ cold, friction/ shear force, pressure or as an outcome of disease, such as leg ulcers or carcinomas. Injuries heal by main intent or secondary objective relying on whether the wound might be closed with sutures or left to repair, where harmed tissue is brought back by the development of connective tissue and re-growth of epithelium.
Wounds may be categorized by numerous techniques; their aetiology, area, kind of injury or providing signs, wound depth and tissue loss or scientific look of the injury. Separate grading tools exist for Pressure Ulcers (EPUAP), Burns (Guideline of Nines), Diabetic Foot Ulcers (Wagner/ San Antonio) and General Wounds. General injuries are categorized as being:
The most typical approach for classification of a wound is identification of the primary tissue types present at the wound bed; i.
e. black– lethal and the respective quantity of each revealed as a portion. This category approach is really visual, supports good evaluation and planning and assists with continuous reassessment.
The phases of wound healing are:
The inflammatory phase is the body’s natural response to injury. After initial wounding, the blood vessels in the wound bed contract and a clot is formed. Once haemostasis has been achieved, blood vessels then dilate to allow essential cells; antibodies, white blood cells, growth factors, enzymes and nutrients to reach the wounded area. This leads to a rise in exudate levels so the surrounding skin needs to be monitored for signs of maceration. It is at this stage that the characteristic signs of inflammation can be seen; erythema, heat, oedema, pain and functional disturbance. The predominant cells at work here are the phagocytic cells; ‘neutrophils and macrophages’; mounting a host response and autolysingany devitalised ‘necrotic / sloughy’ tissue. During proliferation, the wound is ‘rebuilt’ with new granulation tissue which is comprised of collagenand extracellular matrix and into which a new network of blood vessels develop, a process known as ‘angiogenesis’.
Healthy granulation tissue is dependent upon the fibroblast receiving sufficient levels of oxygen and nutrients supplied by the blood vessels. Healthy granulation tissue is granular and uneven in texture; it does not bleed easily and is pink / red in colour. The colour and condition of the granulation tissue is often an indicator of how the wound is healing. Dark granulation tissue can be indicative of poor perfusion, ischaemia and / or infection. Epithelial cells finally resurface the wound, a process known as ‘epithelialisation’. Maturation is the final phase and occurs once the wound has closed. This phase involves remodelling of collagen from type III to type I. Cellular activity reduces and the number of blood vessels in the wounded area regress and decrease.
This type of healing occurs when there is essentially no contamination of the wound and the edges of the wound are approximated thus closing the wound. The best example of this situation is the surgical incision where contamination of the wound is minimized and the wound is closed by suturing. Once the wound is sutured, the incision space fills with blood, which contains fibrin and blood cells and which subsequently clots. The surface of this clot becomes dehydrated and forms a scab. Within 24 hours, neutrophils appear at the edges of the incision and the epithelium at the edges of the incision begins to proliferate. It migrates under the scab and forms a thin continuous epithelial layer. By 72 hours, macrophages are usually the most numerous inflammatory cells and granulation tissue starts to develop. Collagen fibres are present but do not bridge the incision site.
The epithelial cells continue to proliferate under the scab and the epidermal covering over the incision becomes thicker. By day 5, the incision space is filled with granulation tissue and collagen fibres begin to bridge the incision. The epidermis returns to its normal thickness and keratinized architecture. During the second week, there is continued accumulation of collagen fibres and proliferation of fibroblasts. Inflammatory cells and oedema disappear and the process of blanching begins. Blanching refers to the process whereby collagen fibres accumulate and excessive vascular channels regress causing the area to become lighter in colour. By the end of one month, there is a connective tissue scar that is devoid of inflammatory cells and is covered by an intact epidermis. The damaged adnexal structures are permanently lost and the tensile strength is still well below its maximum.
Describes a wound left open and allowed to close by epithelialization and contraction. Commonly used in the management of contaminated or infected wounds. Wound is left open to heal without surgical intervention. Indicated in infected or severely contaminated wounds. Unlike primary wounds, approximation of wound margins occurs via reepithelialization and wound contraction by myofibroblasts. Presence of granulation tissue.
Healing by third intention (tertiary wound healing or delayed primary closure) Useful for managing wounds that are too heavily contaminated for primary closure but appear clean and well vascularized after 4-5 days of open observation. Over this time, the inflammatory process has reduced the bacterial concentration of the wound to allow safe closure. Subsequent repair of a wound initially left open or not previously treated. Indicated for infected or unhealthy wounds with high bacterial content, wounds with a long time lapse since injury, or wounds with a severe crush component with significant tissue devitalization. Often used for infected wounds where bacterial count contraindicates primary closure and the inflammatory process can be left to débribe the wound. Wound edges are approximated within 3-4 days and tensile strength develops as with primary closure.
Tissue repair may be altered by a variety of influences, frequently reducing the quality or adequacy of the reparative process. Variables that modify healing may be extrinsic (e.g., infection) or intrinsic to the injured tissue. Particularly important are infections and diabetes. Infection is clinically the most important cause of delay in healing; it prolongs inflammation and potentially increases the local tissue injury. Nutrition has profound effects on repair; protein deficiency, for example, and especially vitamin C deficiency inhibit collagen synthesis and retard healing. Glucocorticoids (steroids) have well-documented anti-inflammatory effects, and their administration may result in weakness of the scar because of inhibition of TGF-β production and diminished fibrosis. In some instances, however, the anti-inflammatory effects of glucocorticoids are desirable. For example, in corneal infections, glucocorticoids are sometimes prescribed (along with antibiotics) to reduce the likelihood of opacity that may result from collagen deposition. Mechanical variables such as increased local pressure or torsion may cause wounds to pull apart, or dehisce. Poor perfusion, due either to arteriosclerosis and diabetes or to obstructed venous drainage (e.g., in varicose veins), also impairs healing.
Foreign bodies such as fragments of steel, glass, or even bone impede healing. The type and extent of tissue injury affects the subsequent repair. Complete restoration can occur only in tissues composed of stable and labile cells; injury to tissues composed of permanent cells must inevitably result in scarring, as in healing of a myocardial infarct. The location of the injury and the character of the tissue in which the injury occurs are also important. For example, inflammation arising in tissue spaces (e.g., pleural, peritoneal, or synovial cavities) develops extensive exudates. Subsequent repair may occur by digestion of the exudate, initiated by the proteolytic enzymes of leukocytes and resorption of the liquefied exudate. This is called resolution, and generally, in the absence of cellular necrosis, normal tissue architecture is restored. In the setting of larger accumulations, however, the exudate undergoes organization: Granulation tissue grows into the exudate, and a fibrous scar ultimately forms. Aberrations (a departure from what is normal) of cell growth and ECM production may occur even in what begins as normal wound healing.
For example, the accumulation of exuberant amounts of collagen can give rise to prominent, raised scars known as keloids. There appears to be a heritable predisposition to keloid formation, and the condition is more common in African-Americans. Healing wounds may also generate exuberant granulation tissue that protrudes above the level of the surrounding skin and hinders re-epithelialization. Such tissue is called “proud flesh” in old medical parlance, and restoration of epithelial continuity requires cautery or surgical resection of the granulation tissue.
Pus is a protein-rich fluid called liquor puris, usually whitish-yellow, yellow, or yellow brown in color. Pus consists of a buildup of dead leukocytes (white blood cells) from the body’s immune system in response to infection. It accumulates at the site of inflammation. When the buildup is on or very near the surface of the skin it is called a pustule or pimple. An accumulation of pus in an enclosed tissue space is called an abscess. Pus is a fluid that had filtered from the circulatory system into an area of inflammation caused by an infection; an exudate. What causes the accumulation of pus? The presence of pus is the result of our body’s natural immune system responding to an infection, usually caused by bacteria or fungi. When the body detects an infection, our immune system immediately reacts to get rid of it and limit the damage.
Leukocytes (white blood cells), which are produced in the marrow of bones, attack the organism that are causing the infection. Neutrophils, a type of leukocyte, have the specific task of attacking harmful fungi or bacteria. Another type of leukocyte, called macrophages, detect the foreign bodies and release an alarm system in the form of small cell-signaling protein molecules called cytokines. Cytokines alert the neutrophils, which filter from the bloodstream into the affected area. Experts say that the neutrophils are within the affected area about an hour after an infection starts. The rapid accumulation of neutrophils eventually leads to the presence of pus – a large quantity of dead neutrophils.
If the patient has a weakened immune system, which may occur if they are being administered chemotherapy, are organ transplant recipients and taking immunosuppressant medications, are HIV positive, or have poorly controlled diabetes, the immune system may not have responded properly and there may be an infection with no pus. People who have undergone surgery and detect the discharge of pus should tell their doctor immediately. The doctor will likely prescribe an antibiotic, ointments and recommend a special incision care program. Antibiotics help the white blood cells attack the infection, speed up the healing process, and prevent an infection complication. Patients who have undergone surgery and are discharging pus should not slather the incision with antibiotic cream, use alcohol or peroxide. They should see their doctor or surgeon.
Assess the following:
Adequate nutrition is an often-overlooked requirement for normal wound healing. Vitamin and mineral deficiencies also require correction.
Vitamin A deficiency reduces fibronectin on the wound surface, reducing cell chemotaxis, adhesion, and tissue repair. Vitamin C is required for the hydroxylation of proline and subsequent collagen synthesis. Vitamin E, a fat-soluble antioxidant, accumulates in cell membranes, where it protects polyunsaturated fatty acids from oxidation by free radicals, stabilizes lysosomes, and inhibits collagen synthesis. Vitamin E inhibits prostaglandin synthesis by interfering with phospholipase-A2 activity and is therefore anti-inflammatory. Vitamin E supplementation may decrease scar formation. Zinc is a component of enzymes in the human body, including DNA polymerase, which is required for cell proliferation, and superoxide dismutase, which scavenges superoxide radicals produced by leukocytes during debridement.
A positive wound culture does not confirm a wound infection. Opportunistic microorganisms may colonize any wound. Wound exudate, which is naturally bactericidal, inhibits the spread of surface contamination from becoming a deep wound infection. However, when wound is ischemic or systemic immune is compromised, pathogenic microorganisms propagate until an excessive concentration of bacteria in the wound precludes healing. This heralds a true wound infection. Multidrug resistant organisms are becoming increasingly common. Common systemic manifestations of wound infection:
Wound infection requires surgical debridement (removal of unhealthy tissue from a wound to promote healing done surgically, can also be done by chemical, mechanical, or autolytic) and appropriate systemic antibiotic therapy. Subsequent debridement in an outpatient setting can be performed by using topical lidocaine gel or spray anesthesia and by gentle excision using iris scissors and forceps or by scraping using a curette. Topical antiseptics are usually avoided because they interfere with wound healing because of cytotoxicity to healing cells. Dressing changes require clean but not necessarily sterile technique.
For exudative wounds, absorptive dressings, such as calcium alginates (eg, Kaltostat [Calgon Vestal], Curasorb [Kendall]) and hydrofiber dressings (eg, Aquacel and Aquacel-AG [Convatec]), are highly absorptive and are appropriate for exudative wounds. Alginates are available in rope form, which is useful for packing deep wounds. For very exudative wounds, impregnated gauze dressings, such as Mesalt (Scott), are useful. Twice-daily dressing changes may be needed. For infected wounds, use silver sulfadiazine (Silvadene) if the patient is not allergic to sulfa drugs. If the patient is allergic to sulfa, bacitracin-zinc ointment is a good alternative. An ionic-silver hydrofiber dressing (Aquacel-AG) is also a good choice. Bandaging a challenging anatomic area (eg, around a heel ulcer) requires a highly conformable dressing, such as an extra-thin hydrocolloid. Securing a dressing in a highly moist challenging site (eg, around a sacrococcygeal ulcer) requires a conformable and highly adherent dressing, such as a wafer hydrocolloid. Hydrogel sheets and nonadhesive forms are useful for securing a wound dressing when the surrounding skin is fragile. Consider other topical agents
Topically applied platelet-derived growth factors have a modestly beneficial effect in promoting wound healing. Other topical agents that have been used for wound treatment are sugar, antacids, and vitamin A&D ointment.
The choice of antibiotic depends on 2 factors—the patient and the known or probable infecting microorganism. Patient factors include allergies, hepatic and renal function, severity of disease process, interaction with other medication(s), and age. In women, pregnancy and breastfeeding must be considered.
First-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Primarily active against skin flora, includingStaphylococcus aureus. Typically used alone for skin and skin-structure coverage. IV and IM dosing regimens are similar.
Inhibits bacterial growth possibly by blocking dissociation of peptidyl tRNA from ribosomes, causing RNA-dependent protein synthesis to arrest. For treatment of staphylococcal and streptococcal infections. In children, age, weight, and severity of infection determine proper dosage. When bid dosing is desired, half-total daily dose may be taken q12h. For more severe infections, double the dose.
Second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin.
Second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. Dose and route of administration depend on condition of patient, severity of infection, and susceptibility of causative organism.
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