Pathophys Burn
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PATHOPHYSIOLOGY OF BURN INJURY Major Burns > 30% BSA
Cell lysis Hemolysis
Hyperkalemia
Hemoglobin/ myoglobin in urine
↑ Capillary permeability
↑Concentration of blood cells
Loss of skin barrier Possible inhalation injury
Thermoregulation problems
Sodium, Water & Protein shift from IVS to ITS
Inflammatory response
Impaired immune response Hyponatremia
↑ Blood viscosity
↓ Circulating blood volume (up to 50%)
Hypoxemia
Shock (hypovol) ↑ Myocardial depressant factor
Massive stress response, sympathetic nervous system activation
↓ Blood pressure
Adrenal corticoid hormones & catecholamine release
Peripheral vasoconstriction
Tachycardia
Hyperglycemia;↑Catabolism; Risk for Curlin’s ulcer; ↑ Metabolism (after burn shock resolves)
Afterload
Dec. Cardiac output Dec. Tissue perfusion
Dec. Renal blood flow
Risk of acute renal failure
Dec. GI blood flow
Anaerobic metabolism
Risk of ileus
Metabolic acidosis
Tissue damage
Potential tissue necrosis
Cellular dysfunction
Cell swelling
Cell lysis Hemolysis
Hyperkalemia
Hemoglobin/ myoglobin in urine
↑ Capillary permeability
↑Concentration of blood cells
Loss of skin barrier Possible inhalation injury
Thermoregulation problems
Sodium, Water & Protein shift from IVS to ITS
Inflammatory response
Impaired immune response Hyponatremia
↑ Blood viscosity
↓ Circulating blood volume (up to 50%)
Hypoxemia
Shock (hypovol) ↑ Myocardial depressant factor
Massive stress response, sympathetic nervous system activation
↓ Blood pressure
Adrenal corticoid hormones & catecholamine release
Peripheral vasoconstriction
Tachycardia
Hyperglycemia;↑Catabolism; Risk for Curlin’s ulcer; ↑ Metabolism (after burn shock resolves)
Afterload
Dec. Cardiac output Dec. Tissue perfusion
Dec. Renal blood flow
Risk of acute renal failure
Dec. GI blood flow
Anaerobic metabolism
Risk of ileus
Metabolic acidosis
Tissue damage
Potential tissue necrosis
Cellular dysfunction
Cell swelling
