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In the United States, there are over 450,000 burn injuries each year responsible for 40,000 hospitalizations and approximately 3400 deaths. The majority of burns are thermal injuries. Electrical burns usually cause tissue destruction by thermal and associated injuries. In chemical burns, the degree of injury depends on the particular chemical, its concentration, and duration of exposure. The majority of burn patients are men, with 70% occurring in a residential home.
The skin is the largest organ of the human body. It has three principal functions, all of which are disrupted by burn injury:
Sensory organ—Burn patients may have absent pain sensation particularly with deeper burns.
Thermoregulation—Burn patients have extensive evaporative heat and water loss, leading to hypothermia.
Infection—The skin serves as a barrier to protect the body against the entrance of microorganisms in the environment. Burn patients are at profound risk for infection and sepsis.
Superficial (first-degree)
Damage is limited to the epidermis. The burn site is red and painful but often resolves without sequelae. No surgical interventions are typically required.
Superficial partial thickness (superficial second-degree)
Papillary dermis is damaged. This is often severely painful and appears swollen with blistering. Such injuries generally require cleaning and sterile dressing for appropriate healing.
Deep partial thickness (deep second-degree)
Reticular dermis is damaged with decreased pain sensation to touch. This will require cleaning and sterile dressing, in addition to possible excision and skin grafting.
Full thickness (third-degree)
Damage extends into the epidermis, dermis, and subcutaneous tissue. Burn site appears white or charred. No pain sensation to superficial touch. Treatment is as previously discussed, with early skin grafting.
Fourth-degree
Damage includes deep tissues including bones, muscles, and tendons. This often requires surgical intervention for adequate healing.
Large burns cause massive tissue destruction and activation of a cytokine-mediated inflammatory response affecting virtually all organ systems. This includes the cardiovascular and respiratory systems; hepatic, renal, and endocrine system; the gastrointestinal tract; hematopoiesis; coagulation; and the immune system. The pathophysiology of major burn injuries has two characteristic phases: the early phase (< 48 hours after injury), followed by the hypermetabolic phase (> 48 hours after injury). A notable characteristic of the first phase is intravascular hypovolemia because of increased vascular permeability and that of the second phase is intravascular hypervolemia because of fluid reabsorption. Edema, particularly laryngeal edema, is a major concern in both phases.
The early phase (< 48 hours) of a burn injury is characterized by an increase in vascular permeability, resulting in “third spacing” of intravascular fluid, causing tissue edema and intravascular hypovolemia. This causes the cardiac output to decrease and the systemic vascular resistance (SVR) to increase. This is in contrast to the second phase of burn injury (i.e., hypermetabolic phase), which is characterized by an increase in oxygen consumption, CO 2 production, and cardiac output and a decrease in SVR. Fluid shifts during the second phase is opposite to that of the first phase, where fluid from the interstitial space reaccumulates into the intravascular space, causing problems, such as pulmonary edema. This is exacerbated by the fact that many patients received aggressive fluid resuscitation during the early phase. Complicating the second phase is the development of sepsis, which also increases cardiac output and decreases SVR.
Pulmonary complications of burn injuries and smoke inhalation can often go unrecognized. Chest x-rays are often normal, until multiple days after the initial insult. Smoke or carbonaceous material around the mouth or nose can clue providers to the presence of damage to the pulmonary system. Pulmonary complications can be divided into three distinct syndromes, based on clinical features and temporal relationship to the injury. Early complications, occurring the first 24 hours postburn, include carbon monoxide (CO), cyanide poisoning, and direct inhalation injury to the airway and lungs. This may lead to upper airway obstruction and pulmonary edema. Delayed injury, occurring 2 to 5 days after injury, includes adult respiratory distress syndrome (ARDS) and pneumonia. Damage to the mucociliary transport system increases the risk of developing pulmonary infections. Late pulmonary complications, which occurs days to weeks after injury include pneumonia, atelectasis, and pulmonary embolism (PE).
It is important to appreciate that patients with burn injuries often require aggressive volume resuscitation. Aggressive volume resuscitation during the initial, “early phase” of burn injury and/or fluid reabsorption during the latter phase of burn injury (i.e., hypermetabolism phase) can exacerbate these pulmonary complications: (1) pulmonary edema, and (2) upper airway obstruction because of edema.
Inhalation injury occurs when hot gases, toxic substances, and reactive smoke particles reach the tracheobronchial tree and damage tissues. These substances result in wheezing, bronchospasm, corrosion, and airway edema. Inhalation injury can cause damage to the upper airway (i.e., airway compromise, nasal obstruction, and acute laryngitis with varying degrees of laryngeal edema), damage to the conducting airway (i.e., tracheitis and bronchitis), and injury to the lower respiratory tract (i.e., pneumonitis, pulmonary edema, and ARDS). Bronchoscopy can be useful in the diagnosis of inhalation injury, as radiographic imaging often underestimates the extent of injury.
Management is generally supportive. Oxygen should be provided as necessary to ensure adequate oxygenation. Bronchospasm should be treated with beta-agonists. Pulmonary hygiene is important in these patients, as there can be excessive carbonaceous material in the lungs and some patients may require intubation because of laryngeal edema or respiratory failure.
Providers should have a low threshold to intubate patients with burns or injuries to the face and oropharynx. Patients with heat and smoke injury, plus extensive face and neck burns, usually all require intubation. Subsequent edema to the airway can rapidly develop, causing upper airway obstruction and potential loss of the airway. Careful examination of the airway during laryngoscopy should be performed, if possible, to examine the extent of injury to the airway. Patients with oral burns but no smoke injury should be considered for early intubation, as well because airway edema may ensue making intubation especially difficult.
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