Infection occurs in 15% to 40% of admissions to the intensive care unit (ICU); mortality ranges from 10% to 80%. The EPIC (European prevalence of infection in intensive care) European study, with 10,038 patients, found that 21% of patients enter intensive care: 65% with pneumonia, 17% with urinary infection, and 12% with bacteremia. The most frequently found germs were the following: enterobacteria (34%), Staphylococcus aureus (30%), and Pseudomonas aeruginosa (30%). The risk factors observed in the study were the following: prolonged stay, mechanical ventilation, trauma, central venous catheter, and urinary catheter. Only 50% of blood growths were positive in sepsis patients.1

https://link.springer.com/content/pdf/10.1007%2F978-1-4757-3824-7_1.pdf

Physiopathology of Sepsis

In recent years, multiple organ dysfunction syndrome (MODS) has been studied extensively because of its relationship to adverse outcome in sepsis. In fact, the dysfunction of organs such as the lung, the kidney, the brain, the liver, the hematopoetic and the cardiovascular system have been incorporated into scoring systems such as the sequential organ function assessment (SOFA) score, APACHE II and III. In addition, effort has been made to understand intestinal dysfunction in critical illness. The ‘gut origin’ theory of MODS posits that a loss of gut barrier function results in translocation of bacteria or endotoxin, thus initiating or perpetuating sepsis.

Pancreatic Dysfunction in Critical Illness

Multiple organ dysfunction syndrome (MODS) continues to be a source of excessive morbidity and mortality in the critically ill population [1]. While the pathogenesis of MODS remains to be fully elucidated, a popular approach to explain its development is the ‘gut origin’ theory. This proposes that a variety of local and/or systemic insults result in depression of the intestine’s physiological function, specifically the loss of its protective barrier function [2]. This leads to increased translocation, the passage of viable bacteria and/or endotoxin across the intestinal epithelium to mesenteric lymph nodes and portal blood [3]. Such gut-derived bacteria or endotoxin could then trigger, exaggerate, and perpetuate the systemic inflammatory response that occurs in MODS. It is this concept that has prompted some to refer to the gut as the ‘motor’ of MODS [4].

Intestinal Microcirculation: Changes in Sepsis and Effect of Vasoactive Manipulation

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Intestinal Microcirculation: Changes in Sepsis and Effect of Vasoactive Manipulation