burn rehabilitation

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Chapter 94Burn Rehabilitation

Lucretia Fitzpatrick Patrick Murphy Jill Androwick Deborah Goldblum Patricia Wardius John Wijtyk

There are approximately 1.25 million burn injuries in the United States yearly, accounting for 51,000 acute hospital admissions and 5500 deaths (1). The cause and the risks of burn injury and death are inuenced by age, economic circumstances, and occupation, with the greatest risk being economically disadvantaged. Seventy-ve percent of all burn-related deaths are due to house res, with young children and the elderly being most vulnerable. Flame burn is the predominant type of injury seen in patients admitted to burn centers, followed by scalding with hot liquids (2). The majority of burns can be treated on an outpatient basis. However, the extent of the burn, or a complicating factor such as an associated injury or extreme age or youth, may warrant hospital admission. Inhalation injury, concomitant trauma, and signicant preexisting medical conditions mandate burn center care for patients with burns of lesser extent (2). Major burns are best cared for in a burn treatment center where the specialized skills of a multidisciplinary staff and burn-specic equipment ensure optimal survival. Major burns are classied as follows: 1. Greater than 10% of total body surface area (TBSA) at an age younger than 10 years or older than 50 years Greater than 20% of TBSA in patients at an intervening age Signicant burns of the face, hands, feet, genitalia, perineum, or major joints

4. 5. 6.

Full-thickness burns greater than 5% of TBSA Signicant electrical injury Signicant chemical injury

2. 3.

Burns are coagulative lesions involving surface layers of the body. They are usually caused by thermal agents but can also result from chemical agents, radiation, and electrical injury when electrical energy is transferred to thermal energy. The skin is the largest organ of the human body and consists primarily of two layers, the epidermis and the dermis. The supercial cells of the epidermis are cells that arise from deeper germinal layers of keratinocytes. The underlying dermis consists of brous connective tissue, blood vessels, ataneous nerves, and the epithelial appendages (sweat glands and hair follicles). The epithelial cells that line these appendages can serve to repopulate lost epithelium when the entire epithelial layer is involved in a burn injury (3). Clinically, burns are classied based on depth and extent of tissue damage (4). Burn depth classications include supercial, partial thickness, and full thickness (Table 94-1). Supercial (or rst-degree) burns, such as a sunburn, are painful. This type of burn is limited to the epidermis and heals spontaneously without scarring. Partial-thickness burns include the entire epidermis and variable portions of the dermis. They can be supercial or deep. Supercial partial-thickness burns are usually more painful but can heal spontaneously from the epidermal


Table 94-1: Type of Burn WoundsDEGREE First Second TYPE Supercial Partial-thickness supercial Deep LAYER Epidermis Epidermis and upper layer of dermis Destroys epidermis and deeper dermal structuresOF INVOLVEMENT

APPEARANCE Red Blanches with pressure Sensitive to air, light, touch Red or pink skin color Blistered or mottled Blanches well Sensitive to touch Soft elastic texture Eschar Wavy white to red color Sensitive to pressure, not to pinprick Large thick blisters White, tan, black charred No blanching Dry texture Leathery, thrombosed blood vessels visible Wound is anestheticnerve endings destroyed Black Necrotic

HEALING Spontaneous 1 wk Spontaneous 521 days



Full thickness

Epidermis and entire dermis Subcutaneous tissue

Occurs from dermal appendages May require grafting: if wounds are not healed within 21 days potental for scarring Slowly from wound edges 1035 days Requires grafting



All epidermis All dermis Subcutaneous fat Bone

Requires grafting or amputation May need a muscle ap for coverage

Figure 94-1. Full-thickness burns sustained from a ame injury. Eschar is white/brown and leather-like in appearance.

appendages anchored deep in the dermis. With deep partial-thickness injury, spontaneous healing is slow, as fewer epidermal cells remain and more scarring may occur. A full-thickness burn destroys both the epidermis and dermis; therefore, healing can only occur from the wound edges (Fig. 94-1). Skin grafting is needed to close the wound (3). Surgical intervention may be required for either a deep partial-thickness wound or full-thickness wound.

An inhalation injury is a chemical burn to the airways and can result in mucosal irritation, airway inammation, interstitial edema, or in most severe injuries, mucosal necrosis and sloughing. Increased secretions can lead to distal airway obstruction, atelectasis, and bronchopneumonia. Ciliary function is impaired and risk for infection, such as tracheobronchitis, is high. Bronchospasms and bronchial edema can lead to hypoventilation. Coughing, pulmonary toilet, secretion management, bronchodila-


Part V

Medical Rehabilitation for Diagnostic Groups

tor therapy, ventilator assistance, and infection surveillance are crucial during the initial postinjury phase. Risk for infection can last for several weeks (5).

WOUND CAREWounds can be treated with an open or closed technique. An open technique is sometimes used for a small supercial burn, where serum dries to form a scab and serves as an adherent protective dressing. This treatment can be uncomfortable and unsightly (5). Closed methods for wound care consist primarily of using 1) topical antimicrobial agents and dressings, 2) biologic dressings, and 3) synthetic dressings (Tables 94-2 and 94-3). Topical antimicrobial agents include silver nitrate, silver sulfadiazine, mafenide acetate (Sulfamylon), mupiricin (Bactroban), bacitracin, gentamicin sulfate (Garamycin) ointment, and Neosporin. One of the most common agents utilized is silver sulfadiazine (Silvadene), which provides broad antimicrobial coverage and assists in bringing eschar to the surface where it can be dbrided. Once the eschar is dbrided, the wound can then be covered with Xeroform, which assists in drying the tissue and promotes healing. The involved area can be wrapped in Kerlix or gauze dressing as needed. Fungal infections, which can occur, may respond to an equal-part mixture of nystatin, hydrocortisone, and mupiricin. With each dressing change, the old topical agent must be removed and the wound cleansed before reapplication. This method affords the opportunity for close surveillance of the wounds. The antimicrobial action lasts from 8 to 12 hours and the frequency of dressing changes will vary among institutions. Biologic dressings consist of viable or frozen skin allografts and xenograft (pigskin). These can be used as a

temporary skin covering until use of autografts is indicated. They are effective in promoting wound healing in all partial-thickness wounds. Biologic dressings may be used to test the readiness of a wound for autografting. Furthermore, these dressings reduce uid and electrolyte losses, promote healing under grafted areas, minimize pain, and maintain sterile conditions (6). Synthetic dressings include Opsite (semipermeable polyurethane lm), Duoderm, Comfeel (hydrocolloid dressing), Elasto-gel (hydrogel dressing), and Biobrane (7,8). Biobrane is composed of knitted elastic nylon bonded to a Silastic semipermeable membrane coated with collagen polypeptides (Fig. 94-2). It will adhere to a viable wound surface, reduce uid loss, and provide a wound vapor barrier. This minimizes uid accumulation under the dressing while preventing the passage of bacteria from the environment to the wound surface. In selected wounds, this treatment may have some advantage over traditional antimicrobial dressings. Biobrane is usually placed on a wound under sterile conditions while using an anesthetic. Wound infections can impede healing, delay wound closure, and cause skin graft loss. Pseudomonas species, Staphylococcus aureus, Escherichia species, Proteus mirabilis, and Streptococcus faecalis are the most common agents causing wound infections. Bacterial contamination leads to an increased inammatory response and local release of cytokines and proteases, and can lead to local tissue damage. Local infection alters systemic metabolic activity and nutritional intake and can alter healing (7). Both local and systemic defenses against infection are impaired after a major burn. Sepsis is a leading cause of morbidity and mortality during the postburn period, owing to the loss of the skin barrier to microbial invasion, the decreased immunosuppressive state, and the presence of invasive

Table 94-2: Antimicrobial AgentsDRESSING Silver nitrate (solution) Sliver sulfadiazine cream (Silvadene SSD) Mafenide acetate (Sulfamylon) Nitrofurazone Mupiricin (Bactroban) ADVANTAGES Excellent antibacterial spectrum No allergic reactions, no pain Broad antibacterial spectrum Minimal sensitivity, allergic reaction Eschar will dry after discontinuation Gram negative Penetrates eschar well Excellent gram-negative coverage Good antimicrobial action Dries wound well Good antibacterial spectrum Effective against gram-positive organisms, especially streptococcus and staphylococcus DISADVANTAGES Ineffective treating established infections Causes staining or bleaching of chloride ions Messy, poor penetration Delays spontaneous separation of eschar, thus delaying wound closing Reported transient leukopenia Ineffective against establishment of wound sepsis Does not penetrate eschar well May cause pain (stinging) 10% allergic rate Inhibits carbonic anhydrase results in metabolic acidosis May cause rash No effect o


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