Early and innovative interventions for severe sepsis and septic shock: taking advantage of a window of opportunity

Abstract

The pathogenic, diagnostic and therapeutic landscape of sepsis is no longer confined to the intensive care unit: many patients from other portals of entry to care, both outside and within the hospital, progress to severe disease. Approaches that have led to improved outcomes with other diseases (e.g., acute myocardial infarction, stroke and trauma) can now be similarly applied to sepsis. Improved understanding of the pathogenesis of severe sepsis and septic shock has led to the development of new therapies that place importance on early identification and aggressive management. This review emphasizes approaches to the early recognition, diagnosis and therapeutic management of sepsis, giving the clinician the most contemporary and practical approaches with which to treat these patients.

Figures

Box 1

Fig. 1: Endothelial disruption and the inflammatory response. The platelets (green bodies), endothelial cells (purple), macrophages (light blue cell with dark centres), polymorphonuclear cells (pink with 3 inner lobes) and cytokines (small pellets) are inflammatory mediators. Adapted with permission from Matuschak GM. Continuous central venous and pulmonary artery oxygen saturation monitoring in the critically ill. Crit Care Med 1996;24:1769-71.

Fig. 2: Oxygen transport and utilization.

Fig. 4: The pathogenesis of cardiovascular insufficiency.

Fig. 3: The clinical utility of venous oxygen saturation (SvO2 or ScvO2).

Fig. 5: Treatment options in sepsis. CVP = central venous pressure, MAP = mean arterial pressure, ScvO2 = central venous oxygen saturation, Hct = hematocrit.