Burn injuries result in both local and systemic responses

Pathophysiology – Local response

Jackson’s Burn wound model is made up of 3 zones (figure 3). This helps us to understand the pathophysiology of a burn injury.

  • Zone of Coagulation: occurs at the point of maximum damage i.e. the nearest point to the heat source. There is irreversible tissue necrosis here due to coagulation of proteins.
  • Zone of Stasis:surrounding the zone of coagulation, this area is characterised by decreased tissue perfusion. It is damaged but potentially viable. If the burn is managed correctly it has the potential to be salvaged, otherwise it could evolve into an area of necrosis.
  • Zone of Hyperaemia: the outermost zone as its name suggests is where there is increased tissue perfusion. This is a reversible zone.
Figure 3

Pathophysiology – Systemic

  • The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 20- 30% of total body surface area.
  • Cardiovascular changes – Capillary permeability is increased, leading to loss of intravascular proteins and fluid into the interstitial compartment. Peripheral and splanchnic vasoconstriction occurs. Myocardial contractility is decreased. These changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end-organ hypoperfusion.
  • Respiratory changes – Inflammatory mediators cause bronchoconstriction, and in severe burns, adult respiratory distress syndrome can occur.
  • Metabolic changes – The basal metabolic rate increases up to three times its original rate. This, coupled with splanchnic hypoperfusion, necessitates early and aggressive enteral feeding to decrease catabolism and maintain gut integrity.
  • Immunological changes – Non-specific down regulation of the immune response occurs, affecting both cell mediated and humoral pathways.
Figure 4: Systemic effects of a burn injury
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