Sepsis and septic shock are complex medical conditions characterized by a dysregulated systemic inflammatory response to microbial infection, leading to organ injury and potentially fatal complications. The mortality rates for sepsis have declined to 15–25%, while septic shock, defined by hyperlactatemia and hypotension requiring vasopressor therapy, has an in-hospital mortality rate of 30–50%. Early recognition and adherence to best practices have improved outcomes, but the disease remains a significant challenge due to its chronic nature and associated long-term sequelae. The pathophysiology of sepsis involves multiple components, including inflammation, immune suppression, endothelial barrier dysfunction, and coagulation. Inflammation is initiated by the activation of the innate immune system, leading to the expression of pro-inflammatory cytokines and chemokines. Immune suppression occurs both early and late in the sepsis response, characterized by chronic inflammation and tissue damage. Endothelial barrier dysfunction results in increased permeability and leakage of fluids and proteins, contributing to multi-organ failure. Coagulation is disrupted, leading to a hypercoagulable state with microvascular thrombi and fibrin deposition. Diagnosis of sepsis and septic shock relies on clinical signs, symptoms, and laboratory abnormalities, rather than a single diagnostic test. Biomarkers like procalcitonin have shown some utility in distinguishing sepsis from non-infectious critical illness and guiding antibiotic therapy. Prevention focuses on reducing infection rates, particularly in high-risk populations, through good clinical practices and infection control measures.Sepsis and septic shock are complex medical conditions characterized by a dysregulated systemic inflammatory response to microbial infection, leading to organ injury and potentially fatal complications. The mortality rates for sepsis have declined to 15–25%, while septic shock, defined by hyperlactatemia and hypotension requiring vasopressor therapy, has an in-hospital mortality rate of 30–50%. Early recognition and adherence to best practices have improved outcomes, but the disease remains a significant challenge due to its chronic nature and associated long-term sequelae. The pathophysiology of sepsis involves multiple components, including inflammation, immune suppression, endothelial barrier dysfunction, and coagulation. Inflammation is initiated by the activation of the innate immune system, leading to the expression of pro-inflammatory cytokines and chemokines. Immune suppression occurs both early and late in the sepsis response, characterized by chronic inflammation and tissue damage. Endothelial barrier dysfunction results in increased permeability and leakage of fluids and proteins, contributing to multi-organ failure. Coagulation is disrupted, leading to a hypercoagulable state with microvascular thrombi and fibrin deposition. Diagnosis of sepsis and septic shock relies on clinical signs, symptoms, and laboratory abnormalities, rather than a single diagnostic test. Biomarkers like procalcitonin have shown some utility in distinguishing sepsis from non-infectious critical illness and guiding antibiotic therapy. Prevention focuses on reducing infection rates, particularly in high-risk populations, through good clinical practices and infection control measures.