Acute burn blisters have excited much interest among clinical investigators and have been the subject of intensive study. Their pathogenesis has long been understood as the straightforward consequence of thermal tissue injury but their pathobiology has been shown to be complex. Analyses of blister fluid have demonstrated a panoply of biologically active substances, including enzymes,1,2 enzyme inhibitors,3,4 inflammatory mediators,5-7 cytokines,8 factors that suppress both granulocyte and lymphocyte function,9-12 and factors that promote fibroblast growth and function,13 all of which could contribute to the physiologic consequences of burn injury. Thus, their clinical importance has been emphasized, and their treatment has been the subject of lively debate.14 In sharp contrast with acute burn blisters, delayed postburn blisters have been largely ignored. They are rarely reported or studied, and their pathogenesis remains undefined. As the term implies, delayed blistering is a phenomenon that occurs after initial
Compton CC. The Delayed Postburn Blister: A Commonplace but Commonly Overlooked Phenomenon. Arch Dermatol. 1992;128(2):249–252. doi:10.1001/archderm.1992.01680120121016
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