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Abstract
Septic shock, the most severe complication of sepsis, is a deadly disease. In recent
years, exciting advances have been made in the understanding of its pathophysiology
and treatment. Pathogens, via their microbial-associated molecular patterns, trigger
sequential intracellular events in immune cells, epithelium, endothelium, and the
neuroendocrine system. Proinflammatory mediators that contribute to eradication of
invading microorganisms are produced, and anti-inflammatory mediators control this
response. The inflammatory response leads to damage to host tissue, and the anti-inflammatory
response causes leucocyte reprogramming and changes in immune status. The time-window
for interventions is short, and treatment must promptly control the source of infection
and restore haemodynamic homoeostasis. Further research is needed to establish which
fluids and vasopressors are best. Some patients with septic shock might benefit from
drugs such as corticosteroids or activated protein C. Other therapeutic strategies
are under investigation, including those that target late proinflammatory mediators,
endothelium, or the neuroendocrine system.