Toxic epidermal necrolysis (TEN) in the ICU setting requires understanding of the massive pathophysiological derangements caused by >30% BSA epidermal loss. The immunological mechanism involves CD8+ cytotoxic T lymphocytes and NK cells releasing granulysin, the key mediator of widespread keratinocyte apoptosis, along with perforin/granzyme B and Fas-FasL-mediated death signaling. The full-thickness epidermal necrosis creates pathophysiology analogous to a major burn: (1) Massive insensible fluid losses — evaporative water loss from denuded dermis is 3-4 L/day for 50% BSA involvement, causing hypovolemia, hemoconcentration, and prerenal AKI; (2) Thermoregulatory failure — loss of the epidermal barrier eliminates insulation, causing hypothermia; ambient temperature must be maintained at 28-32°C; (3) Protein catabolism — protein loss through wound exudate is substantial (up to 20-30% of total body protein), requiring aggressive nutritional support; (4) Infection susceptibility — the skin barrier is the primary defense against microbial invasion; loss creates portal of entry for bacteria; sepsis is the leading cause of death in TEN (accounting for 40-50% of TEN mortality). Multiorgan involvement occurs in severe TEN: hepatic (transaminase elevation in 10-30%), pulmonary (tracheobronchial mucosal sloughing causing respiratory...