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Burns part 2 - pathophysiology

part 2 for summary of burns
Course

Integrated pathophysiology for nurses (HTHSCI 3PA2A)

162 Documents
Students shared 162 documents in this course
Academic year: 2022/2023
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BURN PATHOPHYSIOLOGY - OVERVIEW

  • Burn injuries causes both local and systemic response

  • Local responses described as 3 zones of burn:

    • Zone of coagulation (necrosis)
      • Tissue necrosis is irreversibly lost due to coagulation of skin proteins
      • Evidenced by clotted blood and thrombosed blood vessels
    • Zone of stasis (injury)
      • Located deep and peripheral to the necrosis zone
      • Area at risk due to decreased blood flow but potentially salvageable if perfusion is maintained and infection or edema is prevented
    • Zone of hyperemia
      • Peripheral to and below the zone of stasis
      • Characterized by minimal cellular injury with increased blood flow and should recover unless an invasive infection or profound tissue inflammation occurs
  • When burn injuries occur, local mediators (histamine, serotonin, kinins, arachidonic acid metabolites, complement, cytokines, catecholamines) are released by the body

  • These local mediators cause vasodilation and increase capillary permeability allowing plasma proteins to escape the intravascular space - This increases tissue oncotic pressure (pulls water towards higher concentrations of proteins) and creates local tissue edema. - A burn injury is also associated with increased levels of profound vasoconstrictor thromboxane A2, which may compromise perfusion, decreasing blood flow thus enlarging the zone of stasis and creating a larger burn injury - The coagulation system (blood clotting) is activated concurrently, causing platelet aggregation (clustering of platelets to form a plug to stop bleeding). - Neutrophils and macrophages release multiple cytokines to promote wound healing - Together, all of these intense inflammatory responses lead to vascular stasis and rapid tissue edema BURN PATHOPHYSIOLOGY

  • The release of cytokines and other inflammatory mediators at the site of injury has systemic effects once the burn reaches 30% of total body surface area. Thus Causing alterations in organ function remote from site of injury

- SYSTEMIC CHANGES:

  • Cardiovascular changes:
    • Increased capillary permeability causing loss of intravascular proteins and fluids into the interstitial compartment
    • Peripheral and splanchnic (stomach, intestine, liver..) vasoconstriction occurs
    • Decreased Myocardial contractility due to release of tumor necrosis factor alpha (TNF alpha)
    • ^these changes along with fluid loss from burn wound, results in systemic hypotension (low bp) and end organ hypoperfusion (decreased blood flow and oxygen delivery to organs/tissues)
  • Respiratory changes
    • Inflammatory mediators cause bronchoconstriction and in severe burns, adult respiratory distress syndrome can occur (ARDS)
  • Metabolic changes
    • Includes increase of basal metabolic rate (energy needed) up to 3x it's original rate
    • ^this coupled with splanchnic hypoperfusion (reduced blood flow to abdominal organs), necessitates early and aggressive enteral feeding to decrease catabolism (breakdown of tissues/muscle proteins) and maintain gut integrity
  • Immunologic changes
    • Immunologic changes leads to non-specific down regulation of the immune response, affecting cell mediated and humoral pathways
    • Non-specific down regulation of cell mediated and humoral pathways (diminished production and effectiveness of antibodies)

*basal metabolic rate: amount of calories body needs for life sustaining functions *enteral feeding: thru the nose *catabolism: breakdown of complex molecules like organ tissues or muscle proteins *splanchnic perfusion: describes blood flow to abdominal gastrointestinal organs (stomach, liver, spleen, pancreas, small/large intestine) *non-specific down regulate: decreased surface receptors for neurotransmitters= decreased cell sensitivity Humoral response: production and action of antibodies by B cells to neutralize and eliminate foreign substances and pathogens circulating in the body fluids

SPECIAL CONSIDERATIONS FOR PEDIATRIC AND GERIATRIC POPULATIONS

  • Pediatric:
    • Sustains more injuries than adults due to their thin skin
    • They have proportionally larger body surface area in relation to their height/weight = greater risk for fluid and heat loss - Large body surface to mass ratio
    • Achieving a delicate balance between dehydration and overhydration is important
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Burns part 2 - pathophysiology

Course: Integrated pathophysiology for nurses (HTHSCI 3PA2A)

162 Documents
Students shared 162 documents in this course
Was this document helpful?
BURN PATHOPHYSIOLOGY - OVERVIEW
- Burn injuries causes both local and systemic response
- Local responses described as 3 zones of burn:
- Zone of coagulation (necrosis)
- Tissue necrosis is irreversibly lost due to coagulation of skin proteins
- Evidenced by clotted blood and thrombosed blood vessels
- Zone of stasis (injury)
- Located deep and peripheral to the necrosis zone
- Area at risk due to decreased blood flow but potentially salvageable if
perfusion is maintained and infection or edema is prevented
- Zone of hyperemia
- Peripheral to and below the zone of stasis
- Characterized by minimal cellular injury with increased blood flow and
should recover unless an invasive infection or profound tissue
inflammation occurs
- When burn injuries occur, local mediators (histamine, serotonin, kinins, arachidonic
acid metabolites, complement, cytokines, catecholamines) are released by the body
- These local mediators cause vasodilation and increase capillary permeability allowing
plasma proteins to escape the intravascular space
- This increases tissue oncotic pressure (pulls water towards higher concentrations
of proteins) and creates local tissue edema.
- A burn injury is also associated with increased levels of profound
vasoconstrictor thromboxane A2, which may compromise perfusion,
decreasing blood flow thus enlarging the zone of stasis and creating a larger burn
injury
- The coagulation system (blood clotting) is activated concurrently, causing platelet
aggregation (clustering of platelets to form a plug to stop bleeding).
- Neutrophils and macrophages release multiple cytokines to promote wound
healing
- Together, all of these intense inflammatory responses lead to vascular stasis and
rapid tissue edema
BURN PATHOPHYSIOLOGY
- The release of cytokines and other inflammatory mediators at the site of injury has
systemic effects once the burn reaches 30% of total body surface area. Thus
Causing alterations in organ function remote from site of injury