Severe burn injury, burn shock, and smoke inhalation injury in small animals. Part 1: Burn classification and pathophysiology

Abstract Objective To review the literature related to severe burn injury ( SBI ), burn shock, and smoke inhalation injury in domestic animals. Current animal‐ and human‐based research and literature were evaluated to provide an overview of thermal burn classification and the pathophysiology of burn shock and smoke inhalation injury. Etiology Severe burn injury, burn shock, and smoke inhalation injury may be encountered as a result of thermal injury, radiation injury, chemical injury, or electrical injury. Diagnosis Burns can be subdivided based on the amount of total body surface area ( TBSA ) involved and the depth of the burn. Local burn injuries involve <20% of the TBSA whereas SBI involves >20–30% of the TBSA . The modern burn classification system classifies burns by increasing depth: superficial, superficial partial‐thickness, deep partial‐thickness, and full‐thickness. Summary Local burn injury rarely leads to systemic illness whereas SBI leads to significant metabolic derangements that require immediate and intensive management. SBI results in a unique derangement of cardiovascular dysfunction known as “burn shock.” The physiologic changes that occur with SBI can be divided into 2 distinct phases; the resuscitation phase and the hyperdynamic hypermetabolic phase. The resuscitation phase occurs immediately following SBI and lasts for approximately 24–72 hours. This period of hemodynamic instability is characterized by the release of inflammatory mediators, increased vascular permeability, reduced cardiac output, and edema formation. The hyperdynamic hypermetabolic phase begins approximately 3–5 days after injury. This phase is characterized by hyperdynamic circulation and an increased metabolic rate that can persist up to 24 months post burn injury in people.