Chapter 81: Burns Flashcards
What are the 4 etiological classifications of burns?
- Thermal
- Chemical
- Electrical
- Radiation
What are the 5 degrees of thermal burns?
1st degree: Superficial, only epidermis effected. No blistering, wounds or scarring
2nd degree: Full thickness epidermal necrosis extending into underlying dermis. Results in blistering (rare in dogs/cats)
3rd degree: Extends through dermis to underlying SQ
4th degree: Extend to underlying muscle or fascia
5th degree: Extends to bone
What occurs when the skin temperature reaches 40-44C?
60C? and 70C?
40-44C: Failure of cell membrane Na pump
60C: Epidermal necrosis within 1 second
70C: Full-thickness burns in less than 1 second
What is the rule of 9s?
A method of estimating the % surface area effected by a burn
- Head and neck 9%
- Each thoracic limb 9%
- Each pelvic limb 18%
- Dorsal and ventral trunk 18% each
What are the three zones of tissue injury secondary to thermal burns?
Moving outward from point of greatest energy:
- Zone of coagulation: no viable tissue remains
- Zone of stasis: reduced perfusion due to damage to RBC membrane proteins causing reduction in deformability and reduced luminal diameter due to increased interstitial pressure from increased capillary permeability. **Tissues in this zone may be saved or may deteriorate (vulnerable)
- Zone of hyperemia - Primary zone of the inflammatory response
What causes vasodilation as an acute response to a burn injury?
- Postganglionic autonomic stimulation
- Upregulation of nitrous oxide synthesis within the burned area and surrounding skin
Why do burns heal slower that usual?
- Only 5% of normal levels of fibroblast growth factor -2 (FGF-2)
- None of the capillary endothelial chemotactic and proliferative activity seen in normal surgical wounds
List the main toxins associated with smoke inhalation:
- Carbon monoxide (preferentially binds Hgb)
- Hydrogen cyanide (binds mitochondrial cytochrome oxidase, disrupting electron transport and preventing cellular respiration)
- Inorganic acids (intensely irritating causing bronchospasm and laryngospasm)
What pathophysiological changes occur in the lungs in response to smoke inhalation?
- Increased pulmonary vasculature permeability
- Venoconstriction
- Rapid accumulation of fluid, mucus and neutrophils within the alveoli and airways
Pulmonary edema
What are the main sources of the cytokines causing the changes resulting in ARDS?
- Smoke damaged lungs
- Burn-injured tissues
- GIT
What is the pathophysiology of systemic vascular permeability in response to a major burn injury?
Within 10 minutes (burns over 25%), systemic vascular permeability to fluid and albumin increases because of myosin-mediated contraction of vascular endothelial cells and direct damage to endothelial cells
Mediated by complement, histamine and oxygen free radicals from the burn site
When does generalized edema and hypovolemia peak after burn injury?
Within the first 12 hours
What are the main sources of fluid loss in burn patients?
- Extravasation
- Evaporative (3-20 times greater)
What are the main causes of myocardial effects of burn patients?
- Decreased left ventricular contractility (increase of myocyte intracytoplasmic Ca)
- Myocardial damage and decreased cardiac output secondary to carbon monoxide (decreased ATP production and necrosis)
How is the GIT effected by burns?
- Barrier is compromised leading to translocation of bacteria and endotoxins as well as cytokines leading to septic shock
- Increases apoptotic rate of gut mucosa
- Impaired motility (increased expression of inducible nitrous oxide from myenteric plexus)
