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(BQ) Part 2 book Emergency medicine procedure presents the following contents: Skin and soft tissue procedures, neurologic and neurosurgical procedures, anesthesia and analgesia, obstetrical and gynecologic procedures, genitourinary procedures, ophthalmologic procedures, otolaryngologic procedures, dental procedures, podiatric procedures, miscellaneous procedures.
SECTION Skin and Soft Tissue Procedures 92 General Principles of Wound Management Lisa Freeman Grossheim INTRODUCTION An acute wound can be defined as an unplanned disruption in the integrity of the skin, including the epidermis and dermis The goals of wound management are to restore tissue continuity and function, minimize infection, repair with minimal cosmetic deformity, and be able to distinguish wounds that require special care The principles of wound management should be emphasized over the repair technique Appropriate wound management prior to approximating the wound will allow it to heal with minimal complications This includes wound cleansing, debridement of the wound edges, wound approximation, and prevention of secondary injury HEALING OF WOUNDED TISSUE PHASES OF WOUND HEALING The response of tissue to an injury is described in three phases The first phase is coagulation and inflammation The second phase is the proliferative phase The final phase is the reepithelialization or remodeling phase Phase I consists of coagulation and inflammation It occurs in the first days This phase is also known as the vascular phase A fibrin clot forms a transitional matrix that allows for the migration of cells into the wound site over a period of 72 hours Inflammatory cells (i.e., neutrophils, monocytes, and macrophages) kill microbes, prevent microbial colonization, break down soluble wound debris, and secrete cytokines The cytokines signal synthetic cells, such as fibroblasts, to initiate phase II Most sutured wounds develop an epithelial covering that is impermeable to water within 24 to 28 hours Phase II is the proliferative phase It occurs during days to 14 after the injury Fibroblasts proliferate and synthesize a new connective tissue matrix that replaces the transitional fibrin matrix Granulation tissue consisting of fibroblasts, immature connective tissue, epidermal cells that have migrated, and abundant capillaries forms within the wound Fibroblasts release collagen, a protein substance that is the chief constituent of connective tissue At days, the tensile strength of the wound itself is 5% that of normal skin Collagen formation peaks at day Phase III is known as the remodeling, reepithelialization, or maturation phase It occurs from day 14 and lasts until there is complete healing of the wound The new granulation tissue is being converted into a scar The scar consists of a rich matrix with decreasing cell density, decreasing vascular density, and increasing thickness of collagen fiber bundles packed in parallel arrays.1 The wound will have 15% to 20% of its full strength at weeks and 60% of its full strength at months Tensile strength continues to increase up to year after wounding The skin will eventually regain only 70% to 90% of its original tensile strength FACTORS AFFECTING NORMAL REPAIR The most common causes of improper wound healing are tension on the wound edges, necrosis and/or ischemia of the tissues from local conditions (e.g., crush injuries and contusions decrease blood flow and lymphatic drainage, which alters local defense mechanisms), or shock Hypovolemia is the major deterrent to wound healing in patients with hemorrhage and shock, hemorrhage from inadequate hemostasis, infection, or retention of foreign bodies Systemic conditions such as malnutrition, immunosuppression, shock, diabetes secondary to microangiopathy, decreased oxygen and nutrient delivery to the wound, renal insufficiency, cytotoxic drugs, vitamin deficiency, trace metal deficiency, and collagen vascular disease can result in poor wound healing Polymorphonuclear leukocyte function is known to be impaired from hyperglycemia, jaundice, uremia, cancer, or chronic infections Drugs and medications can contribute to good wound healing or affect it adversely Malnutrition, lack of protein, and lack of vitamins (e.g., vitamins A and C) may inhibit or prolong healing Zinc deficiency, which is reversible, may play a role in retarding the healing process.3 Anti-inflammatory drugs (e.g., colchicine, aspirin, and glucocorticoids) disrupt macrophage function, collagen synthesis, and polymorphonuclear neutrophil concentrations Pretreatment or early introduction of glucocorticoids results in retarded wound repair by slowing cell proliferation.4 SCAR FORMATION Some to 12 months are required to form a mature scar This explains why scars should not be revised until 12 months have passed A wider scar, inadequate wound closure, or a wound dehiscence may occur in areas with increased skin tension or if the wound is in an area of excessive motion (e.g., over joints) Adequate immobilization of the approximated wound (but not necessarily the entire anatomic part) is mandatory after wound closure for efficient healing and minimal scar formation Contractures can develop when a scar crosses perpendicular to a joint crease These patients may require physical therapy to prevent the loss of range of motion secondary to contractures Hypertrophic scars result from full-thickness injuries Hypertrophic scars are characterized by a thick and raised scar that remains within the boundaries of the original injury They must often be corrected by surgical intervention.1 Keloids are hypertrophic scars (i.e., thick and raised) that exceed the boundaries of the initial injury They can develop from superficial injuries and appear to have a genetic basis Surgical intervention rarely resolves keloids They may be prevented or minimized by the local application of pressure dressings, Silastic dressings, glucocorticoids, and calcium channel blockers.1 The repair procedure may result in more scar tissue Absorbable suture materials contribute to the formation of suture marks because of their increased reactivity, whereas nonabsorbable materials 609 610 SECTION 7: Skin and Soft Tissue Procedures not Wounds that are approximated too tightly can result in tissue ischemia and more scar tissue formation WOUND CLOSURE TECHNIQUES clean the wound Scrub the wound base and edges with salinemoistened gauze and irrigate the wound to remove any dirt, debris, and granulation tissue Suture the wound to approximate and evert the wound edges The postprocedural wound care is the same as if the wound was closed primarily PRIMARY INTENTION Primary intention involves surgically approximating the wound edges shortly after the time of injury The skin’s greatest strength is in the dermal layer The best repair results when the entire depth of the dermis is accurately approximated to the entire depth of the opposite dermis Accurate approximation of the epidermis gives a cosmetically appealing effect to the repair but does not contribute to its strength Wound eversion and the use of buried sutures can greatly improve healing by primary intention SECONDARY INTENTION Secondary intention involves allowing the wound to heal without any surgical intervention The wound is left open and allowed to heal from the inner layer to the outer surface It is a more complicated and prolonged healing process than primary intention Infection, excessive trauma, tissue loss, or imprecise approximation of tissue can result due to healing by secondary intention Wound contraction by granulation tissue containing myofibroblasts is the major influence on this type of healing Wound contraction becomes more significant when the dermis is lost Concave skin wounds heal with the best results These areas often heal better by secondary intention than by primary intention Such concave areas include the inner ear, the nasal alar crease, the nasolabial fold, the temple, and the concave areas of the pinna Flat surfaces can also heal well by secondary intention, although surgical intervention may be best Some examples include the forehead, the side of the nose, and periorbital areas Wounds on convex surfaces are not optimal for healing by secondary intention Convex surfaces include the malar cheek, the tip of the nose, and the vermilion border of the lip.2 TERTIARY INTENTION Tertiary intention, or delayed primary closure, can often decrease infection rates Wound closure by tertiary intention is accomplished to days following the initial injury It is a combination of allowing the wound to heal secondarily for to days and then primarily closing the wound It is the safest method of repair for wounds that are contaminated, dirty, infected, traumatic, associated with extensive tissue loss, at high risk for infection, and for wounds that are “too old” to close The ultimate cosmetic result is the same as that of primary wound closure This method may not be suitable for young children, having to return a second time for an uncomfortable procedure During the interim period, instruct the patient to apply wetto-dry dressing changes twice a day Upon the patients return, assess the wound for any signs of infection Anesthetize and WOUND INFECTION Wound infections occur as a result of the patient’s resident flora and the environment It is related to wound age, the amount of devitalized tissue, and the tissue concentration of pyogenic bacteria A wound infection exists when there are bacterial densities of more than 10,000 organisms per gram of tissue.5 Bacteria slow wound healing by secreting proteases that directly injure the tissue in the wound.2 They also secrete other factors that lead to excess inflammatory cells in the wound, which also injures the tissue.2 PATIENT EVALUATION AND ASSESSMENT HOST HISTORY A thorough and accurate history and physical examination are essential for optimum wound management Documentation of the patient’s age, prior tetanus immunization history, systemic illnesses, medications, allergies (such as to latex or local anesthetics), and the circumstances of the injury are essential to good wound management These principles are emphasized because the presence of disease processes (such as diabetes mellitus, chronic malnutrition, alcoholism, hepatic or renal insufficiency, asplenism, malignancies, and extremes of age) may impair host defenses or complicate wound healing.6,7 Second, the wound itself is often less important than an associated injury to an adjacent structure or cavity Associated injuries can easily be missed without a specific directed search for their presence TETANUS PROPHYLAXIS A thorough history must be obtained concerning the patient’s tetanus immunization status Important factors to consider in assessing the risk of developing tetanus include prior immunization history, the type of wound, the degree of wound contamination, the time from injury to treatment, and the presence of underlying medical disease Wounds may or may not be prone to tetanus (Table 92-1) The administration of tetanus prophylaxis is based upon the patient’s immunization history and the risk of developing tetanus (Table 92-2) Current guidelines state that tetanus toxoid (Td) may be deferred in patients with “clean, minor” wounds who have completed a primary series or received a booster dose (Td 0.5 mL IM) within 10 years Consider tetanus immune globulin (TIG 250 to 500 U IM) in addition to Td for patients at risk of developing tetanus Elderly patients without documentation of a primary series, patients from nonindustrialized nations, and those from rural or TABLE 92-1 Characteristics of Tetanus-Prone and Non-Tetanus-Prone Wounds Clinical feature Tetanus-prone wounds Contaminants (feces, foreign body saliva, and soil) Present Devitalized tissue Present Infection Present Ischemic or denervated tissue Present Mechanism of injury Burn, crush, bullet Wound age >6 h Wound depth >1 cm Wound type Abrasion, avulsion, crush, irregular, stellate Non-tetanus-prone wounds Absent Absent Absent Absent Sharp and smooth (knife or glass)