Thermal Injuries

Cutaneous Injury

The classical three zones of burn injury to the skin include the central zone of coagulation or irreversible necrosis, the intermediate and potentially reversible zone of stasis or ischemia, and the peripheral reversible zone of hyperemia or inflammation.

The exact cellular-level of pathophysiology in the different zones is not entirely known, however it involves mechanisms of necrosis or necroptosis that result in significant inflammatory responses as well as autophagy—which, may have a protective effect—and either early or delayed apoptosis, that results in cellular loss, but with less inflammatory response. ^{, ,} All of these mechanisms result in immediate loss of skin tissue and play a role in burn injury progression if not managed both in the ED and throughout the three phases of wound healing: the inflammatory phase , the proliferative phase , and the remodeling phase .

Thermal injury not only sets into motion a cascade of local events, but also results in systemic responses, especially in larger burns. Local processes include inflammation, activation, and aggregation of immune cells. Additionally, this causes microthrombosis with ischemia as a result of endothelial damage, vasoconstriction, dilation, edema, and reperfusion with production of reactive oxygen species and toxic cytokines. Systemic processes not only include inflammatory, cytokine, and immunologic responses, but also metabolic and endocrine responses.

Burn shock is characterized by macro- and microcirculatory impairment and cellular damage, both at the site of injury and throughout the body. The initial resuscitation phase (hypodynamic or ebb phase) occurs within the first 24 to 72 hours and involves cytokine and inflammatory pathway activation as well as systemic circulation of reactive oxygen species, leading to diffuse alterations of transmembrane potentials, plasma extravasation, and edema. This process has either a biphasic pattern—most severe in the first hour and then again at 12 to 24 hours post-burn—or single peak with the most significant manifestations in the first eight hours followed by a slow but steady reduction over the following 16 hours. Subsequently, there is increased vascular resistance, reduced cardiac output, and diffuse end-organ damage. ^{, , ,} Given the resulting hypoproteinemia and capillary leak, an imbalance between oncotic and hydrostatic forces develop, making resuscitation essential at this stage. The second phase is the hyperdynamic or hypermetabolic flow phase that begins 24 to 72 hours post-injury. As vascular permeability and systemic vascular resistance drop, heart rate and cardiac output increase and metabolic rates can rise two- to three-fold. ^, Additional systemic effects include impaired immunity, insulin resistance, renal and hepatic dysfunction, increased serum triglycerides and free fatty acids, muscle wasting, bowel mucosa degradation with reduced absorptive capacity, and hormonal changes, including reductions in growth hormone, TSH, T3, T4, and testosterone. ^{, ,}

Inhalation Injury

The incidence of inhalation injury with thermal burns is approximately 6%, however incidences range from 2% in smaller burn injuries to nearly 60% in larger burn injuries and burns to the face. ^, It can occur with or without cutaneous burns, and, after age and TBSA, it is the most important predictive factor of mortality and is associated with a nearly threefold increase in mortality and a decrease in the LD-50 by 25% in certain population groups. ^,

Inhalational injury is caused by thermal injury to the upper airway and chemical injury to the lower airway. Additionally, systemic toxicity occurs from inhalation of substances such as carbon monoxide and cyanide. Heat can stimulate the glottic closure reflex resulting in rapid asphyxiation and death. At the cellular level, the effect of thermal injury on the upper airway is similar to the pathophysiologic cutaneous response with inflammation, including activation and aggregation of immune cells as well as ischemia, followed by edema and reperfusion injury. Progressive airway edema after significant thermal injury is predictable and may threaten airway patency within hours of initial presentation. Additional complications can occur in the first 24 to 48 hours such as bronchoconstriction, ulceration and hemorrhage, pseudomembrane formation, loss of surfactant, and impaired ciliary transport. These can lead to ventilation/perfusion (V/Q) mismatch, decreased lung compliance, obstruction, barotrauma, increased dead space ventilation, and infection.