Abstract

The initial instantaneous pain after a burn injury results from skin nociceptors, including thermoreceptors that respond to heat, mechanoreceptors that respond to mechanical distortion, and chemical stimuli both exogenous (such as hydrofluoric acid) and endogenous (inflammatory mediators).2 These mediators include histamine, prostaglandins, thromboxane, bradykinin, serotonin, catecholamines, platelet aggregation factor, angiotensin II, vasopressin, oxygen radicals, and corticotropin-releasing factor. They cause surrounding tissue hypoperfusion and capillary vasoconstriction, leading to disruption of deep skin structures.