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Types of Wounds 1.) Lacerations Injury where tissue is cut or torn.

. For treatment, tissue is first cleansed of any blood clots and foreign material, dbribed and irrigated. Local anesthetic is administered and atraumatic technique of wound closure is employed, where wound margins are realigned with careful regard to prevention of any further crush injury to tissues. Sterile dressings are applied and immobilization is recommended for complex extremity wounds. 2.) Abrasions Injury where a superficial layer of tissue is removed, as seen with 1st degree burns. The wound is cleansed of any foreign material, sometimes employing a scrub brush to prevent traumatic tattooing by dirt and gravel, and should be performed within the first day of injury. Local anesthetic can be used for pain, however treatment of the wound is non-surgical, using moist dressings and a topical antibiotic to protect the wound and aid healing. 3.) Contusions Injuries resulting from a forceful blow to the skin and soft tissue, however leaving the outer layer of skin intact. These injuries generally require minimal care as there is no open wound. However, contusions should be evaluated for possible hematoma deep to the surface or other tissue injuries that may indicate more severe morbidity. An expanding hematoma can damage overlying skin and demands evacuation. 4.) Avulsions Injuries where a section of tissue is torn off, either partially or in total. In partial avulsions, the tissue is elevated but remains attached to the body. A total avulsion means that the tissue is completely torn from the body with no point of attachment. In the case of a partial avulsion where the torn tissue is still well-vascularized and viable, the tissue is gently cleansed and irrigated and the flap is reattached to its anatomical position with a few sutures. If the torn tissue is non-viable, it is often excised and the wound closed using a skin graft or local flap. In the case of a total avulsion, the tissue is often very thick and demands debulking and defattening methods before it can be regrafted. Major avulsions describe amputation of extremities, fingers, ears, nose, scalp or eyelids and require treatment by a replant team. http://www.medstudentlc.com/page.php?id=65

A wound is a break in the continuity of a tissue of the body, either internal or external. Wounds are classified as open or closed. An open wound is a break in the skin or in a mucous membrane. A closed wound involves underlying tissues without a break in the skin or a mucous membrane. Causes Wounds usually result from external physical forces. The most common causes of wounds are motor vehicle accidents, falls and the mishandling of sharp objects, tools, machinery, and weapons. Effects

Any injury, unless it is very minor, may be harmful not only to the tissues directly involved but also to the functions of the entire body. Wounds that threaten life include those that produce cassation of breathing, severe bleeding shock, or damage to the brain, heart, or other vital organ. The local effects of an open or closed wound may include loss of blood, interference with blood supply, destruction of tissues, nerve injury, functional disturbances, and contamination with foreign material. These effects often involve nearby uninjured tissues. Even superficial wounds sometimes take a week or more to heal. The healing process includes absorption of blood and serum that have seeped into the area, repair of injured cells, replacement of dead cells with scar tissue, and recovery of the body from functional disturbances, if there were any. The two most serious first aid problems caused by open wounds are a large, rapid loss of blood, which may result in shock, and contamination and infection of exposed body tissue. TYPES AND CAUSES OF OPEN WOUNDS Open wounds range from those that bleed severely but are relatively free from the danger of infection to those that bleed little but have a greater potential for becoming infected. Often the victim has more than one type of wound. Abrasions An abrasions results from scraping (abrading) the skin and thereby damaging it. Bleeding in an abrasion is usually limited to oozing of blood from ruptured small veins and capillaries. However, there is a danger of contamination and infection, because of dirt and bacteria may have been ground into the broken tissues. Abrasions commonly result from falls or the handing of rough objects. Example are skinned knees, rope burns (which are actually abrasions, not burns), and shallow multiple scratches. Incisions Incised wounds, or cuts in-body tissues are commonly caused by knives, metal edges, broken glass, or other sharp objects commonly cause incised wounds, or cuts, in-body tissues. The degree of bleeding depends on the depth and extent of a cut. Deep cuts may involve blood vessels and may cause extensive bleeding. They may also damage muscle, tendons, and nerves. Lacerations Lacerations are jagged, irregular, or blunt breaks or tears in the soft tissues. Bleeding may be rapid and extensive. The destruction of tissue is greater in Lacerations than in

cuts. The deep contamination of wounds that result from accidents involving moving parts of machinery increases the chances of later infection. Punctures Puncture wounds are produced by bullets and pointed objects, such as pins, nails, and splinters. External bleeding is usually minor, but the puncturing object may penetrate deeply into the body and this damage organs and soft tissues and sever internal bleeding. Because puncture wounds generally are not flushed out by external bleeding, they are more likely than some other wounds to become infected. Tetanus organisms and other harmful bacteria that grow rapidly deep within body tissues by a penetrating object. Avulsions Avulsion wounds involve the forcible separation or tearing of tissue from the victims body. Avulsions are commonly caused by animal bites and accidents involving motor vehicle, heavy machinery, guns and explosives. They are usually followed immediately by a heavy bleeding, a detached finger, toe, nose tip, ear, or, in rare cases, whole limb may be successfully attached to a victims body by a surgeon if the severed part is sent with the victim to the hospital. http://nursingcrib.com/nursing-notes-reviewer/types-causes-of-open-wounds/

HEALING BY FIRST INTENTION:

fibrosis

Paper cuts Well-approximated surgical incisions Replaced periodontal flaps http://dr-adel.com/pdf/Healing%20and%20Repair-1.pdf

Primary wound healing or healing by first intention occurs within hours of repairing a full-thickness surgical incision. This surgical insult results in the mortality of a minimal number of cellular constituents. http://emedicine.medscape.com/article/1298129-overview#aw2aab6b4

PHASES OF WOUND HEALING

Sequence of Events in Wound Healing Following tissue injury via an incision, the initial response is usually bleeding. The cascade of vasoconstriction and coagulation commences with clotted blood immediately impregnating the wound, leading to hemostasis, and with dehydration, a scab forms. An influx of inflammatory cells follows, with the release of cellular substances and mediators. Angiogenesis and re-epithelization occur and the deposition of new cellular and extracellular components ensues.

Initial phase - Hemostasis Following vasoconstriction, platelets adhere to damaged endothelium and discharge adenosine diphosphate (ADP), promoting thrombocyte clumping, which dams the wound. The inflammatory phase is initiated by the release of numerous cytokines by platelets. Alpha granules liberate platelet-derived growth factor (PDGF), platelet factor IV, and transforming growth factor beta (TGF-b), while vasoactive amines such as histamine and serotonin are released from dense bodies found in thrombocytes. PDGF is chemotactic for fibroblasts and, along with TGF-b, is a potent modulator of fibroblastic mitosis, leading to prolific collagen fibril construction in later phases. Fibrinogen is cleaved into fibrin and the framework for completion of the coagulation process is formed. Fibrin provides the structural support for cellular constituents of inflammation. This process starts immediately after the insult and may continue for a few days. Second phase - Inflammation Within the first 6-8 hours, the next phase of the healing process is underway, with polymorphonuclear leukocytes (PMNs) engorging the wound. TGF-b facilitates PMN migration from surrounding blood vessels where they extrude themselves from these vessels. These cells "cleanse" the wound, clearing it of debris. The PMNs attain their maximal numbers in 24-48 hours and commence their departure by hour 72. Other chemotactic agents are released, including fibroblastic growth factor (FGF), transforming growth factors (TGF-b and TGF-a), PDGF, and plasma-activated complements C3a and C5a (anaphylactic toxins). They are sequestered by macrophages or interred within the scab or eschar.[5]

As the process continues, monocytes also exude from the vessels. These are termed macrophages. The macrophages continue the cleansing process and manufacture various growth factors during days 3-4. The macrophages orchestrate the multiplication of endothelial cells with the sprouting of new blood vessels, the duplication of smooth muscle cells, and the creation of the milieu created by the fibroblast. Many factors influencing the wound healing process are secreted by macrophages. These include TGFs, cytokines and interleukin-1 (IL-1), tumor necrosis factor (TNF), and PDGF. Third phase - Granulation This phase consists of different subphases. These subphases do not happen in discrete time frames but constitute an overall and ongoing process. The subphases are "fibroplasia, matrix deposition, angiogenesis and re-epithelialization".[4] In days 5-7, fibroblasts have migrated into the wound, laying down new collagen of the subtypes I and III. Early in normal wound healing, type III collagen predominates but is later replaced by type I collagen. Tropocollagen is the precursor of all collagen types and is transformed within the cell's rough endoplasmic reticulum, where proline and lysine are hydroxylated. Disulfide bonds are established, allowing 3 tropocollagen strands to form a triple left-handed triple helix, termed procollagen. As the procollagen is secreted into the extracellular space, peptidases in the cell wall cleave terminal peptide chains, creating true collagen fibrils. The wound is suffused with GAGs and fibronectin produced by fibroblasts. These GAGs include heparan sulfate, hyaluronic acid, chondroitin sulfate, and keratan sulfate. Proteoglycans are GAGs that are bonded covalently to a protein core and contribute to matrix deposition. Angiogenesis is the product of parent vessel offshoots. The formation of new vasculature requires extracellular matrix and basement membrane degradation followed by migration, mitosis, and maturation of endothelial cells. Basic FGF and vascular endothelial growth factor are believed to modulate angiogenesis. Re-epithelization occurs with the migration of cells from the periphery of the wound and adnexal structures. This process commences with the spreading of cells within 24 hours. Division of peripheral cells occurs in hours 48-72, resulting in a thin epithelial cell layer, which bridges the wound. Epidermal growth factors are believed to play a key role in this aspect of wound healing. This succession of subphases can last up to 4 weeks in the clean and uncontaminated wound. Fourth phase - Remodeling After the third week, the wound undergoes constant alterations, known as remodeling, which can last for years after the initial injury occurred. Collagen is degraded and deposited in an equilibrium-producing fashion, resulting in no change in the amount of collagen present in the wound. The collagen deposition in normal wound healing

reaches a peak by the third week after the wound is created. Contraction of the wound is an ongoing process resulting in part from the proliferation of the specialized fibroblasts termed myofibroblasts, which resemble contractile smooth muscle cells. Wound contraction occurs to a greater extent with secondary healing than with primary healing. Maximal tensile strength of the wound is achieved by the 12th week, and the ultimate resultant scar has only 80% of the tensile strength of the original skin that it has replaced. http://emedicine.medscape.com/article/1298129-overview#aw2aab6b6

Factors Affecting Wound Healing A delicate physiological balance must be maintained during the healing process to ensure timely repair or regeneration of damaged tissue. Wounds may fail to heal or have a greatly increased healing time when unfavorable conditions are allowed to persist. An optimal environment must be provided to support the essential biochemical and cellular activities required for efficient wound healing and to remove or protect the wound from factors that impede the healing process. Factors affecting wound healing may be considered in one of two categories depending on their source. Extrinsic factors impinge on the patient from the external environment, whereas intrinsic factors directly affect the performance of bodily functions through the patients own physiology or condition. Extrinsic Factors. Extrinsic factors affecting wound healing include: Mechanical stress Debris Temperature Desiccation and maceration Infection

Chemical stress Medications Other factors such as alcohol abuse, smoking, and radiation therapy

Mechanical Stress. Mechanical stress factors include pressure, shear, and friction. Pressure can result from immobility, such as experienced by a bed- or chair-bound patient, or local pressures generated by a cast or poorly fitting shoe on a diabetic foot.

When pressure is applied to an area for sufficient time and duration, blood flow to the area is compromised and healing cannot take place. Shear forces may occlude blood vessels, and disrupt or damage granulation tissue. Friction wears away newly formed epithelium or granulation tissue and may return the wound to the inflammatory phase. Debris. Debris, such as necrotic tissue or foreign material, must be removed from the wound site in order to allow the wound to progress from the inflammatory stage to the proliferative stage of healing. Necrotic debris includes eschar and slough. The removal of necrotic tissue is called debridement and may be accomplished by mechanical, chemical, autolytic, or surgical means. Foreign material includes sutures; dressing residues; fibers shed by dressings; and foreign material introduced during the wounding process, such as dirt or glass. Temperature. Temperature controls the rate of chemical and enzymatic processes occurring within the wound and the metabolism of cells and tissue engaged in the repair process. Frequent dressing changes or wound cleansing with room temperature solutions may reduce wound temperature, often requiring several hours for recovery to physiological levels. Thus, wound dressings that promote a cooling effect may not support wound repair. Desiccation and Maceration. Desiccation of the wound surface removes the physiological fluids that support wound healing activity. Dry wounds are more painful, itchy, and produce scab material in an attempt to reduce fluid loss. Cell proliferation, leukocyte activity, wound contraction, and revascularization are all reduced in a dry environment. Epithelialization is drastically slowed in the presence of scab tissue that forces epithelial cells to burrow rather than freely migrate over granulation tissue. Advanced wound dressings provide protection against desiccation. Maceration resulting from prolonged exposure to moisture may occur from incontinence, sweat accumulation, or excess exudates. Maceration can lead to enlargement of the wound, increased susceptibility to mechanical forces, and infection. Advanced wound products seek to remove sources of moisture, manage wound exudates, and protect skin around the wound from exposure to exudates, incontinence, or perspiration. Infection. Infection at the wound site will ensure that the healing process remains in the inflammatory phase. Pathogenic microbes in the wound compete with macrophages and fibroblasts for limited resources and may cause further necrosis in the wound bed.

Serious wound infection can lead to sepsis and death. While all ulcers are considered contaminated, the diagnosis of infection is made when the wound culture demonstrates bacterial counts in excess of 105 microorganisms per gram of tissue. The clinical signs of wound infection are erythema, heat, local swelling, and pain. Chemical Stress. Chemical stress is often applied to the wound through the use of antiseptics and cleansing agents. Routine, prolonged use of iodine, peroxide, chlorhexidine, alcohol, and acetic acid has been shown to damage cells and tissue involved in wound repair. Their use is now mainly limited to those wounds and circumstances when infection risk is high, and they are rapidly discontinued in favor of less cytotoxic agents, such as saline and non-ionic surfactants. Medication. Medication may have significant effects on the phases of wound healing. Anti-inflammatory drugs such as steroids and non-steroidal anti-inflammatory drugs may reduce the inflammatory response necessary to prepare the wound bed for granulation. Chemotherapeutic agents affect the function of normal cells as well as their target tumor tissue; their effects include reduction in the inflammatory response, suppression of protein synthesis, and inhibition of cell reproduction. Immunosuppressive drugs reduce WBC counts, reducing inflammatory activities and increasing the risk of wound infection. Other Extrinsic Factors. Other extrinsic factors that may affect wound healing include alcohol abuse, smoking, and radiation therapy. Alcohol abuse and smoking interfere with bodys defense system, and side effects from radiation treatments include specific disruptions to the immune system, including suppression of leukocyte production that increases the risk of infection in ulcers. Radiation for treatment of cancer causes secondary complications to the skin and underlying tissue. Early signs of radiation side effects include acute inflammation, exudation, and scabbing. Later signs, four to six months after radiation, include woody, fibrous, and edematous skin. Advanced radiated skin appearances can include avascular tissue and ulcerations in the circumscribed area of the original radiation. The radiated wound may not manifest until 10-20 years after the termination of therapy. Intrinsic Factors. Intrinsic factors that directly affect the performance of healing are: Health status Age factors

Nutritional status

Body

build

Health Status. Chronic diseases, such as circulatory conditions, anemias and autoimmune diseases influence the healing process as a result of their influence on a number of bodily functions. Illnesses that cause the most significant problems include diabetes, chronic obstructive pulmonary disease (COPD), arteriosclerosis, peripheral vascular disease (PVD), heart disease, and any conditions leading to hypotension, hypovolemia, edema, and anemia. While chronic diseases are more frequent in the elderly, wound healing will be delayed in any patient with underlying illness. Chronic circulatory diseases reducing blood flow, such as arterial or venous insufficiency, lower the amount of oxygen available for normal tissue activity and replacement. Anemias such as sickle-cell anemia result in reduced delivery of oxygen to tissues and decreased ability to support wound healing. Normal immune function is required during the inflammatory phase by providing the WBCs (white blood cells) that orchestrate or coordinate the normal sequence of events in wound healing. Autoimmune diseases such as lupus and rheumatoid arthritis interfere with normal collagen deposition, and impair granulation. Diabetes is associated with delayed cellular response to injury, compromised cellular function at the site of injury, defects in collagen synthesis, and reduced wound tensile strength after healing. Diabetes-related peripheral neuropathy, reducing the ability to feel pressure or pain, contributes to a tendency to ignore pressure points and avoid pressure relief strategies. Age Factors. Observable changes in wound healing in the elderly include increased time to heal and the fragile structure of healed wounds. Delays are speculated to be the result of a general slowing of metabolism and structural changes in the skin of elderly people. Structural changes include a flattening of the dermal-epidermal junction that often leads to skin tears, reduced quality and quantity of collagen, reduced padding over bony prominences, and reduction in the intensity of the immune response. Body Build. Body build can affect the delivery and availability of oxygen and nutrients at the wound site. Underweight individuals may lack the necessary energy and protein

reserves to provide sufficient raw materials for proliferative wound healing. Bony prominences lack padding and become readily susceptible to pressure due to the reduced blood supply of wounds associated with bony prominences. Poor nutritional habits and reduced mobility of overweight individuals lead to increased risk of wound dehiscence, hernia formation, and infection. Nutritional Status. Healing wounds, especially full-thickness wounds, require an adequate supply of nutrients. Wounds require calories, fats, proteins, vitamins and minerals, and adequate fluid intake. Calories provide energy for all cellular activity, and when in short supply in the diet, the body will utilize stored fat and protein. The metabolism of these stored substances causes a reduction in weight and changes in pressure distribution through reduction of adipose and muscle padding. Sufficient dietary calories maintain padding and ensure that dietary protein and fats are available for use in wound healing. In addition, adequate levels of protein are necessary for repair and replacement of tissue. Increased protein intake is particularly important for wounds where there is significant tissue loss requiring the production of large amounts of connective tissue. Protein deficiencies have been associated with poor revascularization, decreased fibroblast proliferation, reduced collagen formation, and immune system deficiencies. Reduced availability of vitamins, minerals, and trace elements will affect wound healing. Vitamin C is required for collagen synthesis, fibroblast functions, and the immune response. Vitamin A aids macrophage mobility and epithelialization. Vitamin B complex is necessary for the formation of antibodies and WBCs, and Vitamin B or thiamine maintains metabolic pathways that generate energy required for cell reproduction and migration during granulation and epithelialization. Iron is required for the synthesis of hemoglobin, which carries oxygen to the tissues, and copper and zinc play a role in collagen synthesis and epithelialization. http://mediligence.com/blog/2010/05/26/factors-affecting-wound-healing/