What is Sepsis: Introduction & Learning Objectives






				What is Sepsis Introduction

				Infection has killed more soldiers in war than gunfire. Although the age of infectious diseases has all but passed in the western world, infection and the means by which the body deals with it remain our principle foes in intensive care units. You cannot understand critical care if you do not understand the disease syndrome that we call “sepsis”. This term, and its sister – “systemic inflammatory response syndrome (1)” describe a pathologic process involving widespread release of inflammatory mediators, with or without infection, leading to organ injury. Sepsis is, unquestionably, the most challenging problem encountered in intensive care There is something dark and mysterious about systemic sepsis. Newcomers to intensive care are often overwhelmed by the way in which two different patients, with completely different injuries, can have similar responses to those injuries. For example a patient involved in a major motor vehicle accident can develop the same lung injury and the same hypotensive state as a patient with fecal peritonitis. Likewise, two patients with the same injury, for example pancreatitis, may have completely different systemic manifestations. One patient may be sick for a few days; another may develop multi organ failure and die The reason for this is that the host response to both infectious and non infectious injuries is similar (2); the clinical signs are essentially the same. This inflammatory response is determined, qualitatively and quantitatively, by genetic and environmental factors. Inflammation, rather than infection, is the major cause of tissue damage in critical illness. Death in critical illness is due to overwhelming systemic inflammation which degrades the patient’s organ systems and obliterates the physiologic reserve. Two major injuries occur in sepsis: 1. Widespread release of cytokines and cytotoxic enzymes that damages the endothelium, the lining of blood vessels, turning (more or less) water tight blood vessels into sieves – allowing large amounts of protein rich fluid to leak into the lax subcutaneous tissues, causing tissue edema and intravascular dehydration. 2. Damage to the lining of blood vessels causes activation of the coagulation cascade and initial intravascular deposition of thrombus (before clotting factors are used up and the patient bleeds). The result of intravascular thrombosis and hypotension is ischemic injury to many of the body’s organs. In this tutorial we will explore the terminology used to describe sepsis; the mechanisms by which the inflammatory response is created and amplified; the hemodynamic and systemic problems associated with sepsis, the modulation of these responses and potential methods for reducing the inflammatory response. We will conclude by piecing together systemic inflammation and multi-organ failure. Learning Objectives To define what is meant by “sepsis” To understand the mechanism behind systemic inflammation. To illustrate the interaction between inflammation and coagulation. To identify the importance of the microcirculation. To explore the genesis of multi-organ failure. References CLICK HERE FOR REFERENCES


				THIS TUTORIAL BY PATRICK NELIGAN MD, UNIVERSITY OF PENNSYLVANIA
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