Pathophysiology
Burn injury results in a local inflammatory response. In larger burns there is a systemic inflammatory response. The lungs may be doubly compromised by smoke inhalation and the venous affluent returning from circulation through the burned skin. Following a major burn injury, heart rate and peripheral vascular resistance increase. This is due to the release of catecholamines from injured tissues, and the relative hypovolemia that occurs from fluid volume shifts. Initially cardiac output decreases. At approximately 24 hours after burn injuries, cardiac output returns to normal if adequate fluid resuscitation has been given. Following this, cardiac output increases to meet the hypermetabolic needs of the body.
The effects of high temperature on tissue include speeding chemical reactions and unfolding (denaturing) proteins.
Heat stimulates pain fibers and alters protein structure in the burn area. Stimulated pain fibers release neuropeptides. Altered proteins activate complements. Complements in turn coat these altered proteins and degranulate mast cells. Complement-coated proteins attract neutrophils which also degranulate to release free radicals and proteases causing further damage. Mast cells upon degranulation release tumor necrosis factor – α (TNF – α, primary cytokine). TNF – α is chemotactic to other inflammatory cells (TNF – α acts as a chemokine in this way) which release secondary cytokines. These secondary cytokines increase permeability of blood vessels in the burn area. This causes exudation of proteins and fluid into the adjacent interstitial tissue. Red cells are not extravasated. This results in increase in the oncotic pressure in the interstitium. The volume of fluid loss is directly proportional to the burn area. If burn area is 10% to 15% of the total body surface area (TBSA), then the consequent fluid loss may cause circulatory shock. If it is more than 25% of TBSA, then inflammation occurs even in the blood vessels remote to the burn, causing greater fluid loss.
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