{Reference Type}: English Abstract
{Title}: [Pathophysiology of septic shock].
{Author}: Chiscano-Camón L;Plata-Menchaca E;Ruiz-Rodríguez JC;Ferrer R;
{Journal}: Med Intensiva (Engl Ed)
{Volume}: 46
{Issue}: 0
{Year}: 2022 Apr
暂无{DOI}: 10.1016/j.medine.2022.03.010
{Abstract}: Sepsis and septic shock result from an inadequate host response to an infection, which causes organ dysfunction. The progression of this condition is manifested by the occurrence of successive clinical stages, resulting from the systemic inflammatory response secondary to the activation of different inflammatory mediators, leading to organ dysfunction. There is a high burden of evidence on the role of endotoxin in the pathogenesis of sepsis and its crucial role in triggering the inflammatory response in sepsis caused by gram-negative bacteria. The coagulation cascade activation in sepsis patients is part of the host's adaptive immune response to infection. The endothelium is the main target in sepsis, which is metabolically active and can.