Septic Shock

Excerpt

Sepsis syndromes span a clinical continuum with variable prognoses. Septic shock, the most severe complication of sepsis, carries high mortality. In response to an inciting agent, pro-inflammatory and anti-inflammatory arms of the immune system are activated in concert with the activation of monocytes, macrophages, and neutrophils that interact with the endothelium through pathogen recognition receptors to elaborate cytokines, proteases, kinins, reactive oxygen species, and nitric oxide. As the primary site of this response, the endothelium not only suffers microvascular injury but also activates the coagulation and complement cascades, which further exacerbate vascular injury, leading to capillary leak. This cascade of events is responsible for the clinical signs and symptoms of sepsis and progression from sepsis to septic shock. The ability to balance pro-inflammatory responses to eradicate the invading microorganism with anti-inflammatory signals set to control the overall inflammatory cascade ultimately determines the degree of morbidity and/or mortality experienced by the patient. Judicious and early antimicrobial administration, sepsis care bundle use, and early goal-directed therapies have significantly and positively impacted sepsis-related mortality. However, early identification remains the best therapeutic tool for sepsis treatment and management.