PEDRETTI BURN Flashcards
Skin Anatomy
The skin is the largest organ of the body. It varies greatly in thickness, flexibility, presence and amount of hair, degree of pigmentation, vascularity, nerve supply and sensitivity, amount of keratin, and types of glands present in different locations. Keratin is the tough protein substance present in skin and also forms the primary elements of hair, nails, and callused areas of the skin on the hands and feet. Most of the body is covered with thin, hairy skin. However, thicker, tougher, hairless skin, known as glabrous skin, covers the soles of the feet and the palmar surfaces of the hand and fingers.
Anatomically, the skin consists primarily of two layers: the dermis and the epidermis (Figure 42-1). The dermis, or corium, is composed of fibrous connective tissue made of collagen and elastin and contains numerous capillaries, lym- phatics, and nerve endings. In it are the hair follicles and their smooth muscle fibers, sebaceous glands, and sweat glands and their ducts.89
The epidermis is the outermost layer of epithelium, and it also lines the nail beds and the skin appendages, which are pockets of epithelium that extend down into the dermis and contain the hair follicles, sweat glands, and sebaceous glands. The epidermis consists of four or five layers, depend- ing on the location and type of skin. The innermost layer of the epidermis is the stratum germinativum, where the keratinocytes that synthesize keratin are formed. Above this layer lies the stratum spinosum, in which the progressive stages of keratinization occur. The keratinocytes in this layer have a well-developed capacity for phagocytosis, which helps control infection by ingesting and breaking down bacteria and particulate debris. Melanin granules, which give the skin and hair their color, are present in the cyto- plasm of certain cells in the stratum spinosum. In the next layer, the stratum granulosum, the cells making their way
Epidermis
Dermis (corium)
Subcutaneous fatty tissue
toward the surface become flattened and accumulate many large keratin granules, termed keratohyalin. In this layer, cells lose their nucleus, change from viable to nonviable, and become a cornified layer composed chiefly of keratin filaments. Above this layer is the stratum lucidum, seen best in glabrous skin, which is thicker. The outermost layer, the stratum corneum, is composed of tightly packed dead kera- tinocytes known as squames that become the cornified, flattened skin cells that eventually separate from one another and detach from the surface of the epidermis. The time taken by a newly formed keratinocyte to pass from the deepest layer to the surface to be shed is estimated to be 45 to 75 days. This is the natural manner in which the epider- mis continually renews itself.89
Skin Function
The skin serves as an environmental barrier that protects against ultraviolet rays, chemical contamination, and bacte- rial invasion. It also serves as a moisture barrier to prevent excessive absorption of moisture or evaporative loss. Tem- perature regulation is also a function of the skin, with hair to insulate and perspiration to cool the body. The skin perceives injury or infection through tactile sensory recep- tors located in the dermis layer of the skin. These receptors heighten environmental awareness through perceived touch, pressure, pain, and temperature. When the skin is damaged, various systemic, physiologic, and functional problems can occur. A burn injury causes destruction of the protective environmental barrier, which results in exposed nerve endings, loss of body heat, seepage of body fluids, and exposure to bacterial invasion.
The skin also influences the development of an indi- vidual’s body image and personal identity and enhances nonverbal social interaction. Along with age, gender, body type, and voice, the skin’s scent, texture, and coloration and the appearance of facial features contribute strongly to a person’s external context (physical) and self-concept–related internal contexts (e.g., body image, self-regard, sense of social and cultural acceptance). Because of all these factors a large burn injury is considered to be one of the most physically and psychologically painful forms of trauma.
After a burn injury, many factors are taken into consid- eration in determining the severity of injury, potential for functional recovery, and treatment needs. Primary consid- erations in evaluating burn wounds are the mechanism of injury, the depth and extent of the burn, specific body areas burned, and associated or concurrent injuries such as inha- lation injury and fractures. The individual’s age, medical history, preinjury health, and previous life context are of equal importance in determining the impact of a serious burn injury on future occupational performance.
Mechanism of Injury and Burn Depth
Burns can be thermal, chemical, or electrical in nature and can be caused by flame, steam, hot liquids, hot surfaces, and radiation. The severity of the injury depends on the area of the body exposed and the duration and intensity of thermal exposure. Burn wounds are classified by depth, which is determined by clinical assessment of the appearance, sensi- tivity, and pliability of the wound.93 Burn injuries were traditionally classified as first, second, third, and fourth degree. They are now classified as superficial, superficial
partial thickness, deep partial thickness, full thickness, and subdermal.41 The depth of injury is established by clinical determination of which anatomic layers of the skin are involved.86
A superficial burn, sometimes referred to as a first-degree burn, involves only the upper layers of the epidermis. Damage through the epidermis and upper third of the dermis is referred to as a superficial partial-thickness burn. The term deep partial-thickness burn describes damage to the epidermis and upper two thirds of the dermis, and a full-thickness burn describes an injury that extends down through the entire dermis. A subdermal burn involves the fatty layer, fascia, muscle, tendon, bone, or other subdermal tissues (e.g., those seen in electrical injuries; Table 42-1).
Superficial burns are usually caused by sun exposure or brief contact with rapidly cooling, nonviscous hot fluids or surfaces (e.g., spilled coffee and a hot pan). Superficial partial-thickness burns are typically caused by prolonged sun exposure, contact with flames, or brief contact with hot viscous liquids (Figure 42-2, A). Deep partial-thickness burns are caused by longer exposure to intense heat, such as immersion in hot water or contact of the skin with flaming material. Full-thickness burns usually result from prolonged immersion scalding, contact with flaming or high-temperature viscous material such as hot grease or
melted tar, extended exposure to chemical agents, and contact with electrical current (Figure 42-2, B).
Superficial partial-thickness and deep partial-thickness burns generally heal without surgical intervention. However, once healed, they tend to be excessively dry, itchy, and subsequently susceptible to excoriation (i.e., abrasion or tearing of the skin surface) secondary to shear forces caused by rubbing, scratching, and other trauma. These shear forces can give rise to blisters and compromise long-term skin integrity as a result of repetitious reopening of the wound. Partial-thickness and full-thickness burns usually lead to uneven pigmentation of the healed scar. Deep partial- and full-thickness burns have a greater potential for thick, hypertrophic scar and contracture formation because of the prolonged healing period. This is especially true if a burn converts from partial thickness to full thickness because of infection or repeated trauma. Most full-thickness wounds require surgical intervention or skin grafting for wound closure. Skin graft donor sites generally heal in the same manner that superficial partial-thickness burns do, with less scarring but uneven pigmentation. In all three of the case studies, the majority of the patients’ burns were deep partial-thickness injuries but with serious scar develop- ment after healing.
Percent Total Body Surface Area Involved
The extent of a burn is classified as a percentage of the total body surface area (%TBSA) burned. The two most common methods for estimating %TBSA are the “rule of nines” and the Lund and Browder chart.32,54,84 The rule of nines divides the body surface into areas consisting of 9%, or multiples of 9%, with the perineum making up the final 1%. The head and neck area is 9%, each upper extremity (UE) is 9%, each lower extremity (LE) is 18%, and the front and back of the trunk are each 18%. Body proportions vary in children, depending on their age, especially in the head and legs (Figure 42-3). The Lund and Browder chart50 provides a more accurate estimate of TBSA64 and is used in most burn centers. This chart assigns a percentage of surface area to body segments (Figure 42-4), with the calculations adjusted for different age groups. For smaller %TBSA inju- ries, the therapist can obtain a quick, rough estimate by using the size of the patient’s palm (the hand excluding the fingers) to equal approximately 1% of the individual’s TBSA. Steven’s burns included his right arm and hand (8%), upper part of his chest and back (13%), anterior aspect of his neck (1%), and face (3%), for a total of 25% TBSA. Kenjii’s burns included circumferential burns on his arms and the dorsal surfaces of his hands (9% each) and burns on his face and neck (5%), for a total of 23% TBSA. Neither Steven’s nor Kenjii’s TBSA estimates included their skin graft donor sites, which added to their total injured body surface area.
Severity of Injury
The %TBSA and depth of burn are primary indicators of the severity of injury. A burned surface area of 20% or greater was once the determining criterion for admission to a burn intensive care unit. However, depending on the burn’s location, patient’s age, and preinjury health, partial- or full-thickness burn wounds of less than 10% TBSA can be considered serious enough to warrant admission.
A review of national data from 1999 to 2008 found that 67% of reported burn sizes on admission were less than 10% TBSA and only 4.8% were 40% TBSA or greater.5 This reflects both a decrease in the number of large burn injuries and increased recognition of the importance of specialized burn care experience and facilities for treating significant burn injuries, regardless of size.
Deep partial- and full-thickness burns of greater than 30% TBSA usually require a prolonged period to achieve wound closure and intensive rehabilitation for functional recovery. Because of the complexity of medical treatment and rehabilitation, the severity of an injury is greater if inhalation injury occurs or if deep partial- or full-thickness burns involve the hands, face, or perineum.
Phases of Wound Healing
Inflammatory Phase
Proliferation Phase
Maturation Phase
Scar Formation
Inflammatory Phase
The inflammatory phase usually lasts 3 to 10 days after onset. This phase is characterized by a vascular and cellular response, with neutrophils and monocytes migrating to the wound to attack bacteria, débride the wound, and initiate the healing process. The wound is typically painful, warm, and erythematous (red), and edema develops.
Proliferation Phase
The proliferation phase begins by the third day after the injury and lasts until the wound heals. It is during this phase that revascularization, re-epithelialization, and contraction of the burn wound take place. Endothelial cells bud at the end of capillaries, and they grow and create a vascular bed for new skin growth. Epithelial cells migrate over the vas- cular bed to form a new skin layer. Fibroblasts deposit col- lagen fibers, which contract to reduce wound size. During this phase the wound remains erythremic, and raised, rigid scars may develop. The tensile strength of the newly healed scars is poor and they are easily excoriated or injured.
Maturation Phase
The maturation phase generally begins by the third week after initial healing and may last 2 or more years after the initial burn injury or the date of the last reconstructive surgical procedure performed. During this phase, the fibroblasts leave and collagen remodeling takes place. The erythema fades, and the scar softens and flattens. The tensile strength of the scars increases but never recovers to more than 80% of the original tensile strength of the unburned skin.
Scar Formation
After initial healing, most burn wounds have an erythema- tous, flat appearance. As the healing process continues, the wound’s appearance may change as a result of scar hyper- trophy and contraction. The long-term quality of a mature burn scar can be affected by numerous factors, some of which occur during the early phases of burn care.37 The amount of time needed to achieve wound closure is a strong determinant. Age, race, and burn depth are other variables.32 Bacterial infections in the wound increase the inflammatory response, which can delay wound healing and contribute to scar formation. However, any factor that delays healing will increase the potential for scarring.
Hypertrophic scars are thick, rigid, erythematous scars that become apparent 6 to 8 weeks after wound closure.1 Histologically, these immature scars have increased vascular- ity, fibroblasts, myofibroblasts, mast cells, and collagen fibers arranged in whorls or nodules that make the scar appear raised and rigid.10,63 Biochemical investigations have discovered increased synthesis of collagen fibers and con- nective tissue in hypertrophic scars. As a hypertrophic scar matures, capillaries, fibroblasts, and myofibroblasts decrease significantly, collagen fibers relax into parallel bands, and the scar becomes flatter and more pliable. The time needed for scars to mature differs markedly among individuals and depends on genetics (as with Kenjii, who has a genetic predisposition to hypertrophic scarring), the age of the patient, the location and depth of the original burn wound, the presence of chronic inflammation, wound contamina- tion, and other factors that have been reported to influence hypertrophic scarring.24,85 Superficial burns that heal in less than 2 weeks will not generally form a hypertrophic scar. Deeper burns that take longer than 2 weeks to heal have a greater potential to form hypertrophic scars. Although most
hypertrophic scars mature in 12 to 24 months,22 excessive scar formation, including keloid scars, may take up to 3 years to mature (Figure 42-5). All three subjects in the case studies were of different age groups and ethnic/genetic background and had different occupational therapy (OT) interventions. Nevertheless, they all experienced serious scarring as a result of their burns.
All scars initially have increased vascularity and a red appearance. Scars that remain erythematous for longer than 2 months are more likely to develop into hypertrophic scars. They become progressively firmer and thicker and rise above the original surface level of the skin. There is a marked increase in the production of fibroblasts, myofibroblasts, collagen, and interstitial material, all with contractile proper- ties that help draw together the borders of a wound but can also result in scar tightness. Pain and skin tightness cause most patients to become less active. These patients prefer to rest in a flexed, adducted position for comfort. This allows the new collagen fibers in the wound to link and fuse together in the contracted position. The fibers become progressively more compact and coil up into the whorls and nodules that give the scar surface the textured appearance that often leads to disfigurement. If the scar extends over one or more joints, the progressive tightness leads to a scar contracture and loss of motion. Fortunately, collagen linkage is less stable in new scars, and restructuring of an immature hypertrophic scar contracture can be influenced by sustained mechanical forces such as proper positioning, exercise, splinting, and compres- sion. Scar hypertrophy and contracture are most active for the initial 4 to 6 months after healing.22
Initial Medical Management
Fluid Resuscitation and Edema
Respiratory Management
Wound Care and Infection Control
Fluid Resuscitation and Edema
Immediately after a burn injury, during the inflammatory phase, the permeability of blood vessels increases. This causes rapid leakage of protein-rich intravascular fluid into the surrounding extravascular tissues.57 In larger burns, extensive loss of intravascular fluid can result in hypovole- mia or burn shock because of decreased plasma and blood volumes and reduced cardiac output.34 Fluid resuscitation with an intravenous fluid such as lactated Ringer solution is essential for promptly replacing venous fluid and electro- lytes. The fluid volume required is determined by various formulas, such as the Parkland and modified Brook formu- las,8 and is based on the extent of the burn and weight of the patient. The rate of fluid infusion is determined by monitoring the pulse rate, central venous pressure, hemato- crit, and urinary output.
The lymphatic system, which normally carries excess tissue fluid away, often becomes overloaded, and subcutane- ous edema develops. With circumferential full-thickness burns, loss of elasticity of the burned skin combined with increased edema can cause compartment syndrome, a con- dition in which interstitial pressure becomes severe enough to compress blood vessels, tendons, or nerves, which could result in secondary tissue damage. When blood vessels are compressed, ischemia, or restriction of circulation, could lead to tissue death in the areas of compromised circulation or even the entire distal end of the extremity. Tight burned tissue can also restrict chest expansion during respiration. Escharotomy, or incision through the necrotic burned
tissue, is performed to release the binding effect of the tight eschar (adherent dead tissue that forms on skin with deep partial- or full-thickness burns), relieve the interstitial pres- sure, and restore the distal circulation (Figure 42-6, A). In deeper wounds, an incision down to and through the muscle fascia, or fasciotomy, may be required to achieve adequate relief of pressure
Respiratory Management
A smoke inhalation injury is a common secondary diagnosis with thermal injury and can significantly increase mortality. When the face is burned, when the burn was caused by a fire in an enclosed space, or when other objective evidence of a possible inhalation injury is present, bronchoscopy, arterial blood gas readings, and chest x-ray examinations are used to confirm the diagnosis. Intubation and mechanical ventilatory support may be required in addition to vigorous respiratory therapy. A tracheostomy is performed if the airway is difficult to maintain or if ventilatory support is prolonged.94 This procedure, which involves surgical inci- sion through the trachea and relocation of the ventilation tube to the neck, is more comfortable for the patient, allows oral care, and helps prevent permanent damage to the larynx or vocal cords, which may occur with extended oral intubation.
Wound Care and Infection Control
Topical Antibiotics Biologic Dressings Biosynthetic Products Hydrotherapy Sepsis Surgical Intervention Vacuum-Assisted Closure Nutrition
Wound Care and Infection Control
After a patent airway and fluid resuscitation have been established, attention is directed to wound care. A burn wound is dynamic, and improper treatment (e.g., lack of proper wound care, edema formation, lack of resuscitation) may actually increase the size and depth of the wound.
Wound treatment may involve a combination of surgical and nonsurgical therapy.42 Nonsurgical treatment involves the use of products to promote healing in a partial-thickness wound. These products are usually in the form of topical antibiotics, biologic dressings, and nonbiologic skin substi- tute dressings.
Topical Antibiotics
Topical antimicrobial agents have been shown to decrease wound-related infections and morbidity in burn wounds when used appropriately. The goal of topical antimicrobial therapy is to control microbial colonization, thereby pre- venting the development of invasive infections.
An ever-increasing variety of topical antimicrobials are used for burn wound care.92 Neomycin/polymyxin B/ bacitracin antibiotic ointments are often used for facial and superficial burns. The ointment is applied, and the burn wound is left open. Silver sulfadiazine (Silvadene cream, Keltman Pharmaceuticals, Inc.) is a commonly used anti- bacterial cream applied heavily over larger burns and held in place with layers of gauze dressings. Mafenide acetate (Sulfamylon, UDL laboratories, Inc.) and papain/urea (Accuzyme, DPT Laboratories, Ltd.) topical solution and creams are used to loosen eschar and facilitate débridement through enzymatic digestion.61 Mafenide hydrochloride cream is hyperosmolar and can be painful when applied to larger areas. However, it is often used on the ears, where it can penetrate eschar to prevent chondritis, or inflammation of the ear cartilage. Mupirocin (Bactroban, GlaxoSmith- Kline Beecham) is an agent used to treat wounds infected with methicillin-resistant Staphylococcus aureus and Staphy- lococcus pyogenes.87 A modified Dakin solution is a highly diluted, neutral antiseptic solution consisting of 0.025% sodium hypochlorite (household bleach [NaOCl]) and boric acid to neutralize the alkalinity. Its solvent action on dead cells hastens the separation of eschar from living tissue. Nystatin (Nilstat, Lederle Laboratories) may be used in combination with other topical agents for fungal infections caused by secondary immunosuppression. These fungal infections are often caused by long-term antibacterial use, usually originate in the gastrointestinal tract, and can be life-threatening if they infect burns covering a large surface area or invade the bloodstream.
With the improved resuscitation measures developed for burns in the 1960s, infection became the predominant cause of morbidity and mortality. Silver salts and other chemically active silver compounds have been used in various forms because of their potent antimicrobial proper- ties and ability to reduce burn wound infection. These substances have included silver colloidal solution, which
was later replaced by silver nitrate solution, and silver sul- fadiazine. Silver sulfadiazine is a water-soluble cream that is usually applied twice a day to the wound surface, as opposed to the continuous soaking required with silver nitrate. Over the past 40 years, silver sulfadiazine has become the preferred option for antimicrobial silver therapy for burns.23
Recent major technological advances have resulted in the ability to crystallize silver in a nanocrystal form, which can release pure silver onto a wound surface in large quantities. This silver nanocrystalline delivery system is a three-ply dressing that may consist of an inner rayon/polyester core between two layers of silver-coated mesh.13,97 The ionic silver and silver radicals are released in high concentration when exposed to water. A layer between the wound and silver membrane maintains moisture for healing and decreases the formation of exudate.23 The dressings, applied directly to the wound surface, promote healing by stimulat- ing cellular dedifferentiation, followed by cellular prolifera- tion. The dressings also have antibacterial, antifungal, and analgesic properties. These dressings have been found to be highly microbicidal against aerobic and anaerobic bacteria (including antibiotic-resistant strains), yeasts, and filamen- tous fungi13 and can remain active and in place for up to 7 days instead of having to be changed every 12 to 24 hours.
Biologic Dressings
Biologic dressings serve as temporary coverings to close a wound, prevent contamination, reduce fluid loss, and alleviate pain.52 Theoretically, biologic products may deliver growth factors to a wound as well. Traditional biologic dressings, such as xenografts (porcine skin) and allografts (human cadaver skin), are still widely used in burn care. Xenografts may adhere to the superficial surface film of partial-thickness burns and facilitate débridement of eschar. Human amnion has also been used as a biologic burn dress- ing, especially in developing countries.82
Biosynthetic Products
Biosynthetic products have been used widely for burn care. Closure of wounds with these dressings may lead to less pain, faster skin regrowth, and therefore less scarring. They are used until the wound is healed over, typically in 10 to 14 days, and then the dressing peels off.
Biobrane, a biosynthetic skin substitute wound-dressing sheet (Bertek Pharmaceuticals), has been used extensively. It is constructed of an outer silicone film (the epidermal analogue) with a nylon fabric partially embedded into the film collagen. The nylon components bind to the wound surface fibrin and collagen, which results in initial adher- ence (dermal analogue). Small pores are present in the struc- ture to allow drainage of exudate and increase the permeability to topical antibiotics. However, if used improp- erly, the dressing can enclose dead tissue in the wound and provide a medium for bacterial overgrowth and invasive wound infection.82
Hydrotherapy
Once the patient’s condition is sufficiently stable, hydro- therapy is usually performed at least once a day to remove loose debris and “stale” topical antibiotics. It provides thor- ough cleansing of both the wound and the uninvolved areas. Hydrotherapy is generally accomplished by placing the patient on a “shower trolley” covered with a sterile plastic sheet and washing and showering the wounds for 20 to 30 minutes. This nonsubmersive showering method of hydro- therapy has become the preferred method of cleansing burn wounds to prevent cross-contamination of wounds between patients and has replaced the traditional whirlpool form of hydrotherapy.2,27 Fresh topical agents are then reapplied to delay colonization of organisms and reduce bacterial counts in the burn wounds. During hydrotherapy the patient has usually received some form of analgesics and is unencum- bered by dressings. Therefore, hydrotherapy provides an excellent opportunity for the therapist to perform assess- ments and range-of-motion (ROM) exercises.
Sepsis
Burn wound colonization begins at the moment of injury, with gram-negative organisms replacing normal bacterial flora. Wound cultures and biopsies are performed to monitor such growth when signs of possible serious infection are present.35 A severe infection can result in sepsis, in which the infection spreads from the original site through the bloodstream, a condition known as septicemia. Septicemia initiates a systemic response that affects the flow of blood to vital organs. Bacterial infections are the most common source of sepsis, but it can also result from fungal, parasitic, and mycobacterial infections, especially if the patient is immunocompromised. Broad-spectrum antibiotic therapy is typically initiated. However, if host defenses continue to be overwhelmed, the bacterial by-products or endotoxins accumulate in the bloodstream, a condition known as toxemia, which eventually leads to septic shock, a cardio- vascular response that impedes blood flow to the organ systems, and to generalized circulatory collapse. Septic shock may be characterized by ischemia, diminished urine output, tachycardia, hypotension, tachypnea, hypothermia, disorientation, and coma. Septicemia and septic shock often require multisystem supportive measures for recovery, such as the use of cardiovascular medications, hemodialysis, and mechanical ventilation.
