孕产妇脓毒症的发病机制与病理生理学特点OA

Maternal sepsis is one of the top three leading causes of global maternal morbidity and mortality.It is characterized by an insidious onset and rapid progression.Sepsis is fundamentally defined as life-threatening organ dysfunction caused by a dysregulated host response to infection,and its pathophysiological progression encompasses sequential cascade reactions ranging from loss of control of localized infection,a systemic inflammatory cytokine storm and immune suppression to endothelial glycocalyx degradation,microvascular thrombosis and shock.To accommodate fetal growth and parturition,the maternal body undergoes profound physiological remodeling across the immune,cardiovascular,coagulation,respiratory,and urinary systems.When sepsis occurs,pregnancy-specific Th2-biased immune tolerance,hyperdynamic and low-resistance circulation,and a physiological hypercoagulable state may mask the early clinical warning signs of septic shock,significantly increasing the difficulty in diagnosis,precise treatment,and bundle management.This article aims to elucidate the pathophysiological mechanisms of sepsis and elaborate on the unique evolution processes of maternal vasodilation,increased vascular permeability,coagulation disorders,and multiorgan hypoperfusion.The ultimate objective is to lay a solid pathophysiological theoretical foundation for understanding the severity and treatment complexity of maternal sepsis.