The authors declare no conflicts of interest.
Clinical Practice Review
Severe burn injury, burn shock, and smoke inhalation injury in small animals. Part 1: Burn classification and pathophysiology
Version of Record online: 10 APR 2012
© Veterinary Emergency and Critical Care Society 2012
Journal of Veterinary Emergency and Critical Care
Volume 22, Issue 2, pages 179–186, April 2012
How to Cite
Vaughn, L. and Beckel, N. (2012), Severe burn injury, burn shock, and smoke inhalation injury in small animals. Part 1: Burn classification and pathophysiology. Journal of Veterinary Emergency and Critical Care, 22: 179–186. doi: 10.1111/j.1476-4431.2012.00727.x
- Issue online: 10 APR 2012
- Version of Record online: 10 APR 2012
- Manuscript Accepted: 7 FEB 2012
- Manuscript Received: 22 OCT 2010
- canine and feline;
- carbon monoxide;
- thermal injury
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.
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.
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.
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.