Septic shock is an inflammatory state resulting from the systemic response to bacterial infection. In septic shock, there is critical reduction in tissue perfusion. Acute failure of multiple organs can occur. Treatment is aggressive fluid resuscitation, antibiotics, surgical excision of infected or necrotic tissues and drainage of pus, supportive care, and sometimes intensive control of blood glucose and administration of corticosteroids and activated protein C. Overall mortality in patients with septic shock averages 40%.
The pathogenesis of septic shock includes the production of proinflammatory mediators, including tumor necrosis factor and IL-1. These cytokines cause neutrophil-endothelial cell adhesion, activate the clotting mechanism, and generate microthrombi. They also release numerous other mediators, including leukotrienes, lipoxygenase, histamine, bradykinin, serotonin, and IL-2. These are opposed by anti-inflammatory mediators, such as IL-4 and IL-10, resulting in a negative feedback mechanism.
The administration of ancillary IL-1 receptor antagonist on the outcome of septic shock in patients receiving maximal medical therapy for their underlying disease was evaluated.