Clinical meaning
Major burn injury (> 20% TBSA) triggers a systemic capillary leak syndrome driven by massive inflammatory mediator release: histamine from mast cell degranulation increases capillary permeability, prostaglandins (PGE2, PGI2) cause vasodilation, complement activation (C3a, C5a) amplifies inflammation, and oxygen free radicals damage endothelial cell membranes. This creates 'capillary leak' where protein-rich plasma shifts from the intravascular space into the interstitium, producing massive edema (both in burned and unburned tissue in large burns). The Starling equation governs this fluid movement: increased capillary hydrostatic pressure and decreased reflection coefficient (allowing protein escape) overwhelm the opposing oncotic gradient. Cardiac output drops precipitously in the first 24 hours due to: (1) decreased preload from intravascular volume depletion, (2) direct myocardial depressant factor release from burned tissue, and (3) increased afterload from catecholamine-driven vasoconstriction. The Parkland formula (4 mL x kg x %TBSA) calculates estimated crystalloid needs for the first 24 hours. Lactated Ringer's (LR) is the preferred crystalloid because normal saline's supraphysiological chloride content (154 mEq/L vs plasma 98-106 mEq/L) causes hyperchloremic metabolic acidosis when infused in large volumes -- this worsens the already-present lactic acidosis from tissue hypoperfusion. LR's lactate (28 mEq/L) is converted to bicarbonate in the liver, providing a mild buffering effect. Capillary integrity typically restores by 18-24 hours post-burn, at which point colloid administration (albumin 5%) becomes effective because the protein will remain intravascular rather than leaking into the interstitium.