Ch 81 Burns Flashcards
What are the 4 aetiological classifications of burns?
Thermal
Chemical
Electrical
Radiation
What are the 5 degrees of thermal burns?
- First degree - Superficial, only epidermis effected. 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, is irreversibly injured
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, viable and heal if no further injury is sustained.
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
- -Damaged tissue and inflammatory cells sources of chemokines that initiate the inflammatory response, including endotoxin, prostaglandin E2, histamine
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
Systemic Response to Thermal Burn Injury (9)
- Smoke Inhalation
- Hypovolemia, Vascular Dysfunction, and Generalized Edema
- Myocardial Effects
- Gastrointestinal System
- Renal System
- Hematopoietic System
- Immune System
- Neurologic System
- Metabolic and Endocrine Changes
Pulmonary System: Smoke Inhalation
- Smoke inhalation: complex pathophysiologic changes in many organ systems dt local and systemic inflammatory response to smoke exposure and the failure of oxygen delivery at the tissue level
Pulmonary
- Smoke exposure consists of two components: thermal and toxic.
- former component is usually limited to the upper airways
- majority of the injury from smoke inhalation is caused by toxicity
List the main toxins associated with smoke inhalation (3)
- 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)
Carbon monoxide effects (3)
(1) preferentially binding to hemoglobin (forming carboxyhemoglobin), thereby reducing its oxygen-carrying capacity;
(2) carboxyhemoglobin (COHb) > leftward shift of the oxyhemoglobin dissociation curve and reducing DO2
(3) binding of carbon monoxide with myoglobin to reduce oxygen availability to muscle
level of oxyhemoglobin (oxygen saturation) will be progressively overestimated as the level of carboxyhemoglobin increases
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 changes result in the development of acute respiratory distress syndrome?
What are the main effectors causing the changes resulting in ARDS (6)? and where from? (3)
- Pulmonary oedema
- atelectasis,
- decreased alveolar ventilation
- deactivation of pulmonary surfactant
- decreased lung compliance
effectors:
activated neutrophils,
eicosanoids,
cytokines,
nitric oxide,
free radicals
substance P
main sources:
1. smoke-damaged lungs;
2. burn-injured tissues;
3. gastrointestinal tract (via lymphatics).
What is the pathophysiology of systemic vascular permeability in response to a major burn injury?
mediated by (3)
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
Systemic extravasation > generalized edema and hypovolemia ensue as protein-rich fluid accumulates in the interstitial space.
When does generalise oedema and hypovolaemia peak?
Within the first 12 hours
What are the main source of fluid loss in burn patients causing hypovolaemia?
Extravasation
Evaporative (3-20 times greater)
What are the main cause of myocardial effects of burn patients?
Decreased left ventricular contractility
- increase of myocyte intracytoplasmic Ca
- oxidative injury to the sarcoplasmic reticulum induces Ca2+ leakage into the cytoplasm and reduces sarcoplasmic reticulum reuptake
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)
- liver is also affected: burns cause increased oxidative stress in hepatocytes
Management of severe burn injuries with novel
treatment techniques including maggot debridement and applications of acellular fish skin grafts
and autologous skin cell suspension in a dog
Dawson 2022
50% of total body surface area
aggressive multimodal analgesia, systemic support, and a combination of novel debridement and reconstructive techniques.
novel treatments including applications of widespread acellular fish (cod) skin graft and autologous skin cell suspension.
reconstruction phase began by preconditioning a right caudal superficial epigastric flap during debridement and skin stretching devices were employed.
