Questions
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What is the epidemiology of burns in the United States?
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Which patients require care in specialized burn centers?
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What is cyanide poisoning, and how is it treated?
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A 52-year-old man was brought to the emergency department by ambulance after being injured in a house fire, and you were asked to assess him for inhalation injury and to assist with airway management. The patient’s injuries appeared to be partial-thickness burns to both upper arms, most of the anterior trunk, and right thigh. His vital signs were heart rate 108 beats per minute, respiratory rate 25 breaths per minute, blood pressure 158/92 mm Hg, and oxygen saturation 93% with supplemental oxygen by nasal cannula. When he complained of pain, his voice sounded hoarse, and you noticed carbonaceous sputum.
1
What is the epidemiology of burns in the United States?
Burns (thermal injuries) cause many complications and deaths. In the United States, >1.2 million people sustain thermal injuries every year. Most cases are minor, but approximately 50,000 burn cases are moderate to severe and require hospitalizations. Of these cases, 4000–5000 patients die from complications of thermal injury.
Deaths resulting from burns usually occur in a bimodal distribution—either immediately after injury or weeks later, from multiorgan failure. About one third of burn-related injuries and deaths occur in children. House fires account for 75% of all burn-related deaths.
Morbidity and mortality rates associated with thermal injury are decreasing; deaths and hospital admissions in the United States declined 50% over a 20-year period. This decline is attributed to prevention efforts resulting in a decreased number of patients with potentially fatal burns and improvements in the clinical care of patients with severe burns.
2
Describe how burns are classified, how the percentage of total body surface area burned is estimated, and the extent of injury that occurs with different burn depths.
Burns are classified according to the total body surface area (TBSA) involved, the depth of burn, and the presence or absence of inhalation injury. Additionally, burns are classified into five causal categories, as follows: injury from flame, hot liquids (scald), hot or cold, chemicals, and electricity.
The TBSA burned is calculated using the rule of nines ( Figure 76-1 ). In adults, each upper extremity and the head and neck are 9% each of the TBSA, the lower extremities and the anterior and posterior aspects of the trunk are 18% each of the TBSA, and the perineum and genitalia are 1% of the TBSA. Children have a larger proportion of body surface area contributed by the head and neck relative to the surface area of the lower extremities. The Lund-Browder chart can be used to estimate the TBSA in children ( Figure 76-2 ).
Burn depth is classified according to the degree of injury in the epidermis, dermis, subcutaneous fat, and underlying structures ( Table 76-1 ). First-degree burns are confined to the epidermis, are painful and erythematous, and do not result in scarring. Second-degree or partial-thickness burns are classified further as superficial and deep. Superficial second-degree burns are erythematous and painful, spontaneously heal in 7–14 days, and may result in skin discoloration. Deep second-degree burns appear pale and mottled but remain painful to pinprick, heal in 14–35 days by reepithelialization, and often result in severe scarring. Third-degree or full-thickness burns are characterized by eschar that is painless and black, white, or cherry red and result in scarring and some limitation of function. Fourth-degree burns involve organs beneath the skin, such as muscle and bone; require complete excision; and result in limited function.
| Classification | Depth of Injury | Appearance/Sensation | Outcome |
|---|---|---|---|
| First degree | Epidermis | Erythematous | No scarring |
| Painful | |||
| Second degree (partial thickness) | |||
| Superficial | Epidermis and superficial dermis | Erythematous Painful | Heals in 7–14 days Skin discoloration |
| Deep | Epidermis and into deep dermis | Pale, mottled Painful to pinprick | Heals in 14–35 days Severe scarring |
| Third degree (full thickness) | Epidermis, dermis, and into subcutaneous fat | Leathery eschar (black, white, or cherry red) Painless | Requires excision Scarring with some limitation of function |
| Fourth degree | Epidermis; dermis; subcutaneous fat; and into muscle, fascia, or bone | Brown, charred Painless | Requires excision Limitation of function |
Burn depth is most accurately assessed by the clinical judgment of experienced practitioners. It is important to determine burn depth accurately because of implications for management.
3
Which patients require care in specialized burn centers?
Specialized burn centers offer resources and experienced personnel that can optimize outcome after thermal injury. The American Burn Association established the following criteria to determine which burn patients should be acutely transferred to a burn center:
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Greater than 10% TBSA partial-thickness burns
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Full-thickness burns of any size
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Involvement of special areas of function or cosmesis (face, hands, feet, genitalia, perineum, or major joints)
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Smoke inhalation injury
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Serious chemical injury
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Electrical injury including lightning
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Trauma where burns are the major problem
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Pediatric patients if the referring hospital has no specific pediatric capabilities
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Smaller burns in patients with multiple comorbidities
The above-listed criteria also define the components of a major burn injury.
4
What is the pathophysiology of burn injury, what are the local and systemic effects, and how do burns affect different organ systems?
Burns cause coagulative necrosis of the epidermis and underlying tissues with the depth of injury determined by the temperature and duration of exposure. After the initial focus of injury is removed, the response of local tissues can lead to injury in deeper layers. The area of injury is divided into three zones, as follows:
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Coagulation contains irreversibly damaged necrotic tissue.
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Stasis surrounds the necrotic zone and has a moderate degree of damage with decreased tissue perfusion. Depending on the wound environment, the zone of stasis can either survive or progress to coagulative necrosis.
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Hyperemia is characterized by vasodilation from inflammation surrounding the burn wound and contains viable tissue from which the healing process begins.
Mediators released from the burn wound contribute to local inflammation and wound edema. Oxygen-free radicals, histamine, bradykinin, vasoactive amines, and interleukins have been implicated. In major burns, local injury triggers the release of inflammatory mediators into the circulation, resulting in a systemic response characterized by immune suppression, hypermetabolism, and protein catabolism. Systemic inflammation may progress to sepsis and multiorgan failure.
The cardiovascular system is affected by fluid shifts associated with major burn injury and effect of circulating mediators on contractility and systemic vascular resistance. Hypovolemic shock, described as burn shock, can occur immediately after a burn and primarily results from altered microvascular permeability of both burned and nonburned tissue in response to the above-described mediators. This altered microvascular permeability results in protein loss from the intravascular compartment to the interstitial compartment. There is also a marked transient decrease in interstitial pressure caused by the release of osmotically active particles, causing a vacuum effect whereby fluid is pulled in from the intravascular space. The rapid influx of fluid into the interstitium neutralizes the vacuum effect but does not prevent further edema formation. Finally, an increase in interstitial space compliance adds to changes in oncotic and hydrostatic pressures, exacerbating tissue edema formation further.
Initially, cardiac output is decreased independent of intravascular volume status. Cardiac contractility is reduced because of circulating mediators, decreased responsiveness to catecholamines, and decreased coronary blood flow. Systemic vascular resistance is increased. After successful resuscitation and the first 24–48 hours after burn injury, the cardiovascular response evolves into systemic inflammatory response syndrome, manifested by increased cardiac output and reduced systemic vascular resistance.
Burn injury affects the lungs directly and indirectly. Direct effects include upper airway obstruction and smoke inhalation injury (discussed in further detail subsequently). Indirect injury occurs as a result of the effects of circulating inflammatory mediators, complications of burn therapy, and infection. Pulmonary edema and pulmonary hypertension can also occur.
The kidneys are affected by diminished plasma volume and cardiac output. Increased levels of catecholamines, angiotensin, aldosterone, and vasopressin cause systemic vasoconstriction and contribute to renal dysfunction. Decreased renal blood flow and glomerular filtration rate result in oliguria, which, if left untreated, progresses to acute tubular necrosis and renal failure. Early resuscitation decreases the incidence of renal failure.
Mucosal atrophy, changes in digestive absorption, and increased intestinal permeability are gastrointestinal responses to a burn. The extent of atrophy of the small bowel mucosa is proportional to the burn size. There is reduced uptake of glucose and amino acids and decreased absorption of fatty acids. Gut permeability is increased further when burn wounds become infected. Gastric mucosal stress ulceration occurs with major burns but may be minimized by enteral feeding.
Hypermetabolism develops after major burns and resuscitation. It is characterized by tachycardia, increased cardiac output, elevated energy expenditure, increased oxygen consumption, increased carbon dioxide production, and catabolism. These changes in metabolism are due partly to release of catabolic hormones, which include catecholamines, glucocorticoids, and glucagon. The ambient temperature when below thermoneutral (28°–32° C) further increases metabolic rate in burn patients, and this should be avoided.
Burns cause global depression in immune function, which places burn patients at risk for infectious complications, including bacterial wound infection, pneumonia, sepsis, and multiorgan failure. Immune system impairment results from depressed cellular function in all parts of the immune system, including decreased activation and activity of neutrophils, macrophages, and T and B lymphocytes. When >20% of the TBSA is affected by burns, impairment of immune function becomes proportional to burn size.
The hematologic and coagulation systems are affected by burns based on the magnitude of injury and time from injury. In the immediate injury, hematocrit increases as noncellular fluid moves to the interstitial space. Despite fluid resuscitation, hematocrit tends to remain elevated during the first 48 hours. Anemia then develops secondary to erythrocyte loss from wounds, bleeding during operations, and shortened erythrocyte half-life. Platelet counts are decreased secondary to dilution and formation of microaggregates. Both thrombotic and fibrinolytic mechanisms are activated after major burns. Table 76-2 summarizes the pathophysiologic effects of burns on different organ systems.
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