Burn Study Guide PDF

Incidence of Burn Injury The two most common burn etiologies are flame burns at 43% and scald at 34%. The home remains the most common place of occurrence, accounting for 73% of burn injuries cared for in burn centers. Scald injuries are the most preventable burn injury in children under 5 years of...

Incidence of Burn Injury The two most common burn etiologies are flame burns at 43% and scald at 34%. The home remains the most common place of occurrence, accounting for 73% of burn injuries cared for in burn centers. Scald injuries are the most preventable burn injury in children under 5 years of age (ABA, 2018; Carey et al., 2021). A burn can affect any person at any time, in any place. Burns involve people of all ages and socioeconomic groups. Each year, approximately 486,000 people with burn injuries receive medical treatment, and just over 3,000 deaths occur annually from fire and smoke inhalation. Residential fires account for 2,745 of these deaths, with the remaining 310 from motor vehicle crash fires. Approximately 68% of all burn victims are males. For children under the age 14, burns are the third leading cause of death and burns are included in the top 10 causes of death for all age groups. Those at either extreme (the young and the aged) are particularly vulnerable because the skin is naturally thinner, resulting in the person sustaining a deeper burn at any temperature (Carey et al., 2021; Myers et al., 2022). Although prognosis can be influenced by several factors, the most important variables include severity of the burn, the presence of inhalation injury, associated injuries, the patient's age, and comorbid conditions. People who are prone to burn injuries are older individuals; smokers; and people with disabilities, neurologic illness, substance use issues, and psychiatric illness. Gerontologic Considerations Representing an increasing population segment, older adults have an increased prevalence in the burned population; furthermore, mortality from burns increases with age (Herndon et al., 2018). Compared to their younger peers, older adults, aged 65 and above, experience more than twice as many deaths in housefires. Risk factors include reduced mobility, decreased sensory abilities, and potential cognitive decline which decreases reaction time, thereby increasing the risk for severe injury and death in a fire (Casteel et al., 2020). Thinning and loss of elasticity of the skin predispose them to deep injury from a thermal insult that might cause a less severe burn in a younger person. Furthermore, chronic illnesses decrease the older person's ability to withstand the multisystem stresses imposed by major burn injury. Mortality is nearly 90% in patients who are older than 60 years of age, have a burn that is greater than 40% of the total body surface area (TBSA), and have an inhalation injury (Sheridan, 2020). Successful prevention campaigns have been linked to smoke detectors, carbon monoxide detectors, fire extinguishers, escape plans, sprinkler systems, enforcement of fire codes, and fire-safe cigarettes. Scald injury prevention includes the use of an antiscald mixing valve for shower heads or tub faucets that stops or interrupts the flow of water when the temperature reaches a preset temperature (usually 110° to 114°F, but before it reaches 120°F) to reduce the frequency and severity of scald burns (Plummer, 2020). The nurse educates all patients about the importance of a working smoke alarm and, if possible, a working carbon monoxide detector. Classification of Burns Burn injuries are classified by the depth of the injury and the extent of the TBSA that is burned. Depth Burns are classified according to the depth of tissue destruction. Cell damage occurs at temperatures of at least 45°C (113°F). The depth depends on how much of the skin's dermis is affected. Burn depth determines whether spontaneous healing will occur and helps to determine the plan of care. FIGURE 52-1 Depth of burn injury. The following factors are considered in determining the depth of a burn: How the injury occurred Causative agent, such as flame, scald, chemical, or hot tar Temperature of the burning agent Duration of contact with the agent Thickness of the skin in the burned area Burns are described as superficial, superficial partial-thickness, deep partial-thickness, or full-thickness injuries (Fig. 52-1; Table 52-1). Formerly referred to as a first-degree burn, a superficial burn damages only the epidermis (outer layer of the skin). The area is red and dry, with slight swelling but no blister, and painful, like a sunburn. These burns heal in about 7 days, usually with no scarring. In a superficial partial-thickness burn (one of two types of second-degree burns), the epidermis is destroyed and a small portion of the underlying dermis (deep, vascular inner portion of skin) is injured. The skin is blistered, the exposed dermis is red and moist, and hair follicles are intact. With appropriate wound care, these burns will heal in about 2 weeks without risk of scarring and therefore do not require surgical intervention; the chief symptom, which is pain, usually resolves within 72 hours (Brownson & Gibran, 2018; Myers et al., 2022). A deep partial-thickness burn (the second of the two types of second-degree burns) extends into the reticular layer of the dermis (dense connective tissue that gives the skin strength and elasticity and houses sweat glands, lymph vessels, and hair follicles) and is hard to distinguish from a full-thickness burn. It is red or white, mottled, and can be moist or fairly dry. The patient is in severe pain. Deep partial burns usually take longer than 3 weeks to heal (3 to 8 weeks) and can heal with permanent scarring (some of these burns tend to have a better appearance when grafted). If there has not been healing by 3 weeks, as a rule the burn should be excised and grafted (Brownson & Gibran, 2018). TABLE 52-1Characteristics of Burns According to Depth Depth of Burn Causes Skin Involvement Symptoms Wound Appearance Recuperative Course Superficial Thermal injury (heat/cold), electromagnetic energy, solar radiation, or topical caustic chemicals Involves only the epidermis Erythema and edema of skin Redness, swelling, does not blister, pain Three days or less Superficial partial-thickness (similar to first-degree) Sunburn Low-intensity flash Epidermis; possibly a portion of dermis Tingling Hyperesthesia (supersensitivity) Pain that is soothed by cooling Reddened, blanches with pressure, dry Minimal or no edema Possible blisters Complete recovery within 5--10 days; usually no scarring Peeling Deep partial-thickness (similar to second-degree) Scalds Flash flame Contact Epidermis, upper dermis, portion of deeper dermis Pain Hyperesthesia Sensitive to cold air Blistered, mottled red base; broken epidermis; weeping surface Edema Recovery in 3--8 weeks Some scarring and depigmentation contractures Infection may convert it to full thickness Full-thickness (similar to third-degree) Flame Prolonged exposure to hot liquids Electric current Chemical Contact Epidermis, entire dermis, and sometimes subcutaneous tissue; may involve connective tissue, muscle, and bone Pain free Shock Hematuria (blood in the urine) and possibly hemolysis (blood cell destruction) Possible entrance and exit wounds (electrical burn) Dry; pale white, leathery, or charred Broken skin with fat exposed Edema Eschar sloughs Grafting necessary Scarring and loss of contour and function; contractures Loss of digits or extremity possible A full-thickness burn (formerly called a third- or fourth-degree burn) involves total destruction of the dermis and extends into the subcutaneous fat. It can also involve muscle and bone. It heals by contraction or epithelial migration. Wound color ranges widely from mottled white to red, brown, or black. It may be charred and appear leathery. It will look and feel dry, firm, and depressed when compared to nonburned tissue and will seldom blanch with pressure. In some instances, the burn tissue may look translucent with clotted vessels visible. These wounds are insensate to touch and pinprick. Hair follicles and sweat glands are destroyed. Most full-thickness burns should undergo early excision and grafting. Burns that are deeper, extending beyond subcutaneous tissue into fascia, muscle, tendon, and bone (formerly referred to as fourth-degree burns) will require excision and grafting (Brownson & Gibran, 2018; Myers et al., 2022). Pearls for Practice It is important for the nurse to acknowledge that even when skin is no longer in contact with the burn source, skin damage can continue. In the case of scald burns, 1 second of contact with hot tap water at 69°C (156°F) may result in a burn that destroys both the epidermis and the dermis, causing a full-thickness injury. A deep partial-thickness burn can convert to a full-thickness burn within 24 hours of injury; thus, immediate assessment and management, which includes the application of cool tap water for a minimum of 5 minutes, is important to decrease the risk of thermal injury (first-aid-fact-sheet.pdf \[ameriburn.org\]). It is imperative that the nurse remove all jewelry, rings, watches, or belts, which are typically made of metal, since they can retain heat, cause thermal injury, and act as a tourniquet with tissue swelling. Burning clothing must be removed immediately, and the wound should be covered with a sterile dressing or clean cloth that is loosely wrapped. If clothing has adhered to the wound, it should notBurns are a dynamic injury set that result in a cascade of local tissue and systemic inflammatory effects depending on the percentage of TBSA involved. Local effects of burns include the denaturation of protein (which results in the disruption and potential destruction of cells), liberation of vasoactive substances, and the formation of edema. As a result of the cellular injury, the osmotic and hydrostatic pressure gradients are disrupted, and intravascular fluid leaks into interstitial spaces. This damage is distributed throughout the injury as some cells die instantly, some are irreversibly damaged, and some---if appropriate interventions occur---will survive. There are three distinct zones that appear in a bull's eye pattern. The zone of coagulation (in the center) is where the tissue is completely destroyed; the zone of stasis surrounds the nonviable tissue and is potentially viable; the zone of hyperemia has increased blood flow secondary to the natural inflammatory response (Fig. 52-3). BOX 52-1Classification of Extent of Burn Injury Minor Burn Injury Second-degree burn of less than 15% total body surface area (TBSA) in adults or less than 10% TBSA in children Third-degree burn of less than 2% TBSA not involving special care areas (eyes, ears, face, hands, feet, perineum, joints) Excludes all patients with electrical injury, inhalation injury, or concurrent trauma and all at-risk patients (e.g., extremes of age, intercurrent disease) Moderate, Uncomplicated Burn Injury Second-degree burns of 15--25% TBSA in adults or 10--20% in children Third-degree burns of less than 10% TBSA not involving special care areas Excludes all patients with electrical injury, inhalation injury, or concurrent trauma; all at-risk patients (e.g., extremes of age, intercurrent disease) Major Burn Injury Second-degree burns of at least 25% TBSA in adults or at least 20% in children All third-degree burns 10% or more TBSA All burns involving eyes, ears, face, hands, feet, perineum, joints All patients with inhalation injury, electrical injury, or concurrent trauma; all at-risk patients From Morton, P. G., & Fontaine, D. (2024). Critical care nursing: A holistic approach (12th ed.). Lippincott Williams & Wilkins. FIGURE 52-3 Zones of burn injury. Each burned area has three zones of injury. The inner zone (known as the area of coagulation, in which cellular death occurs) sustains the most damage. The middle area, or zone of stasis, has a compromised blood supply, inflammation, and tissue injury. The outer zone---the zone of hyperemia---sustains the least damage. Burns that exceed 20% TBSA may produce a local and a systemic response and are considered major burn injuries. The incidence and significance of pathophysiologic changes are proportional to the extent of burn injury. In addition, burns of 60% TBSA cause depressed myocardial contractility; this, in combination with the loss of circulating plasma volume, hemoconcentration, and massive edema formation (Myers et al., 2022), results in both distributive and hypovolemic shock (see Chapter 53). Severe burns are marked by large losses of intravascular fluid, protein and electrolytes; these are greatest during the first 8 to 12 hours. Loss of fluid occurs as a result of the altered capillary permeability, significant hypoproteinemia, and shifts of sodium into the interstitial space. These severe fluid shifts decrease substantially by 24 hours post burn (Nitzschke, 2020). These patients are best served when transferred to a verified burn center, as they are at risk for the occurrence of burn shock. Burn Shock: Cardiovascular Alterations Burn shock develops from several abnormalities of the circulation. It can occur when more than 20% TBSA is involved; however, it can occur when a lower percentage is seen if the patient is medically fragile (Clinical Overview, 2023). The initial systemic event is hemodynamic instability, which results from loss of capillary integrity and a subsequent shift of fluid, sodium, and protein from the intravascular space into the interstitial spaces, producing blisters and edema. This leaky capillary syndrome increases cell permeability at the burn site, as well as throughout the body. In the major burn, this syndrome far exceeds the useful effect of the inflammatory response. Progressive edema develops in unburned tissue and organs, causing hypoperfusion and hypovolemic shock. As fluid loss continues from the burn wound(s) and the diffuse capillary leakage (from the intravascular space to the interstitial space), the blood volume decreases, the blood pressure (BP) falls, the cardiac output (CO) decreases, and urine output declines (Haglund & Phillips, 2023). This is the onset of burn shock. Burn shock is unique as it is a combination of hypovolemic and distributive shock indicated by intravascular volume depletion, increased pulmonary vascular resistance (PVR), elevated systemic vascular resistance, and depressed cardiac output (Myers et al., 2022). The systemic response is caused by the release of cytokines and other mediators into the systemic circulation. The outcome is a dramatic outpouring of fluids, electrolytes, and proteins into the interstitium; thus, burn shock is characterized by capillary leak, "third spacing" of fluid, severe hypovolemia, hemoconcentration, and decreased CO. If the burn patient is not resuscitated adequately, circulatory collapse ensues. Pearls for Practice: Why Distributive Shock in Burns? Distributive shock occurs when the blood volume is abnormally displaced within the body (e.g., when blood pools in peripheral blood vessels), causing a relative hypovolemia because not enough blood returns to the heart, which leads to inadequate tissue perfusion. It occurs primarily in conditions that cause vasodilation as in septic shock, neurogenic shock, or anaphylaxis. But in burn injury, there is systemic and pulmonary vasoconstriction (related to catecholaminergic release), so why distributive shock? It occurs due to the capillary leakage that causes the loss of fluid, electrolytes, and albumin from the blood into the interstitium. Thus, when the fluid is still retained in the body, just not where it is supposed to be, this is distributive shock. That is why you will see burn injury described as an actual fluid loss (hypovolemia) and fluid loss within the body (distributive). FIGURE 52-4 Measuring intra-bladder pressure. To assess for the development of abdominal compartment syndrome, the intra-bladder pressure may be monitored. Fluid and Electrolyte Alterations Prompt fluid resuscitation maintains the BP in the low-normal range and improves CO. IV fluid resuscitation is based on the extent of burn injury and the patient's weight in kilograms (discussed shortly). In general, the greatest volume of fluid leak occurs in the first 24 to 36 hours after the burn. As the capillaries begin to regain their integrity, burn shock resolves and fluid returns to the vascular compartment. As fluid is reabsorbed from the interstitial tissue into the vascular compartment, blood volume increases. If kidney and cardiac function is adequate, urinary output increases. Lactated Ringer (LR) solution is the preferred IV fluid for burn resuscitation because of its physiologic similarity to the composition of extracellular fluid; for example, in LR sodium is 130 mEq/L and potassium (K+) is 4 mEq/L, and normal intravascular levels are a sodium level of 135 to 145 mEq/L and K+ of 3.5 to 5 mEq/L. LR also contains lactate (28 mEq/L), which can be converted by the liver to bicarbonate (the blood buffer) to aid in correcting the metabolic acidosis frequently seen in burn shock. Patients with large burn wounds are at risk for abdominal compartment syndrome (ACS). This is one of the more life-threatening complications, with a mortality rate of 75% (Wurzer et al., 2018). With large burns, fluid shifts into the abdominal cavity, causing increased abdominal distention that interferes with pulmonary ventilation. The volume loss into the peritoneal space results in decreased CO, hypotension, and decreased urine output. When the intra-abdominal pressure exceeds 25 mm Hg or 34 cm H2O (normally the intra-abdominal pressure ranges from 0 to 7 mm Hg, measured at end-expiration), the inferior vena cava is compressed, which restricts blood flow and perfusion to abdominal organs, further compromising renal, hepatic, and visceral organ function; the nurse observes for a tense abdomen, increased abdominal girth, oliguria (\65 mm Hg is required for organ perfusion (normal range is 70 to 110 mm Hg). If the MAP drops below this point for an extended period, end-organ ischemia and infarction can occur. For example, a MAP \>60 mm Hg is needed to perfuse the coronary arteries. If the MAP drops \