Burn Physiology

Thermal injury triggers systemic microvascular hyperpermeability that drives plasma loss, burn shock, and massive edema, and produces acute lung injury and ARDS even without inhalation injury. Mediators and glycocalyx and endothelial barrier disruption raise transvascular fluid…

A major burn floods the body with reactive oxygen species while depleting its antioxidant reserves. The resulting oxidative damage drives wound progression, edema, lipid peroxidation, and organ injury in lung, kidney, and liver, and the imbalance can be tracked with biomarkers…

Severe burn drives a biphasic immune derangement: an early hyperinflammatory phase superimposed on a prolonged immunoparalysis that suppresses adaptive effector immunity. Monocyte HLA-DR falls as early as 24 hours post-burn and tracks survival; T cells become anergic and…

Major burns drive a systemic inflammatory response (SIRS) that, when severe, progresses to multi-organ dysfunction (MODS) and failure (MOF). MODS and sepsis are the leading late causes of burn death. Larger burns, older age, and inhalation injury are the dominant drivers…

A major burn exports the inflammatory reaction to the whole body, releasing a cascade of cytokines and chemokines (IL-6, IL-8, TNF-alpha, IL-1, IL-10) that rises and falls over a defined time-course. The magnitude tracks burn severity, and several mediators correlate with…