Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection (Sepsis-3, 2016). The pathophysiological cascade involves: infection triggers release of pathogen-associated molecular patterns (PAMPs: endotoxin/LPS from gram-negative bacteria, lipoteichoic acid from gram-positive) that activate innate immune cells via pattern recognition receptors (TLR-4, TLR-2). Subsequent release of pro-inflammatory cytokines (TNF-alpha, IL-1, IL-6) causes systemic inflammatory response: vasodilation (decreased SVR → hypotension), capillary leak (third-spacing → tissue edema), endothelial activation (microthrombosis → DIC, organ ischemia), and mitochondrial dysfunction (impaired cellular oxygen utilization even with adequate delivery — cytopathic hypoxia). Multi-organ dysfunction manifests as: cardiovascular (distributive shock — warm, vasodilated → then cold, vasoconstricted), pulmonary (ARDS), renal (AKI from hypoperfusion and nephrotoxic mediators), hepatic (ischemic hepatitis, coagulopathy), hematologic (DIC — thrombocytopenia, prolonged PT/aPTT, elevated D-dimer), and neurological (septic encephalopathy). The Sequential Organ Failure Assessment (SOFA) score quantifies organ dysfunction across 6 systems (respiratory, cardiovascular, hepatic, renal, coagulation, neurological); an increase of ≥2 SOFA points from baseline in the setting of infection defines sepsis. Quick SOFA (qSOFA) screens for sepsis outside the ICU: RR ≥22, altered mentation, SBP ≤100....