Septic Shock

Overview
  • Septic Shock is a subtype of shock initiated by infection with microbes. From a clinical perspective, sepsis transitions to "Septic Shock" when septic hypotension can no longer be corrected by fluid infusion.
Etiology
  • Infection by any class of microbes can cause septic shock although bacteria are the most common, especially gram negative bacteria. Hematogenous infection is not essential, as the inflammatory mediators which result in shock can be systemically released from localized foci of infection.
Pathogenesis
  • The hallmark of Septic Shock is a severe, inappropriate reduction in systemic vascular resistance caused by widespread arteriolar vasodilation. This vasodilatory phenomenon appears to be due the release of enormous amounts of inflammatory cytokines such as TNF-alpha by innate immune cells which recognize microbial molecules. Importantly, cytokine-induced vasodilation appears to be largely refractory to endogenous vasoconstricting processes such as activation of the SNS and thus processes of Systemic Arterial Pressure - Autonomic Control. Release of inflammatory cytokines also appears to induce endothelial injury which can lead to DIC. Ultimately, systemic hypoperfusion can lead to multi-organ failure and death.