Ch 81 - Burns Flashcards
What are the 4 aetiological classifications of burns?
- Thermal
- Chemical
- Electrical
- Radiation
What are the 5 degrees of thermal burns?
- Frist degree - Superficial, only epidermis effected (erytema). No blistering, wounds or scarring
- Second degree - Full-thickness epidermal necrosis extending into underlying dermis. Results in blistering (rare in dogs/cats)
- Third degree - Extends through dermis to underlying SQ
- Fourth degree - extend to underlying muscle or fascia
- Fifth degree - Extends to bone
What occur when the skin 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 halves of the trunk 18% each
What are the three zones when evaluating tissue injury secondary to thermal burns?
- 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 interstital pressure from increased capillary permeabiltiy. Tissues in this zone may be saved or may deteriorate
- Zone of hyperaemia - Primary zone of the inflammatory response
What causes vasodilation as an acute response to a burn injury?
- Postganglionic autonomic stimulation
- Upregulation of NO 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 Hb)
- Hydrogen cyanide ( binds mitochondrial cytochrome oxidase, disrupting electron transport and preventing cellular respiration)
- Inorganic acids (intensely irritating cauding 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 oedema
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 increase because of myosin-mediated contraction of vascualr endothelial cells and direct damage to endothelial cells
Mediated by complement, histamine and oxygen free radicals from the burn site
When does generalise oedema and hypovolaemia peak?
Within the first 12 hours
What are the main source 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 NO from myenteric plexus)