الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
The pathophysiologic mechanisms behind sepsis are intricate and time dependent, making it an ill-defined condition. Mortality rates are still high despite notable advancements in surveillance, diagnosis, and treatment. It can be difficult to give individuals with sepsis or septic shock enough nourishment. Septic shock and sepsis continue to be common disorders linked to increased in-hospital mortality. Patients with septic shock and sepsis have a death rate of 40.4%. A harmful immunological response to an infection, sepsis frequently results in an overpowering reaction that prevents the immune system’s natural ability to restore immune cell homeostasis.
Inflammatory mediators are powerful inducers of catabolism in sepsis; cytokines, for instance, are essential for causing muscle protein oxidation, bone resorption, and adipocyte lipolysis. Moreover, endogenous skeletal muscle protein catabolism due to inflammation can lead to severe muscular atrophy rapidly, particularly in the early stages; it is also linked to immunosuppression, inadequate wound healing, acquired muscle weakness in the intensive care unit (ICU), and other unfavorable consequences. Standard dietary treatments for critically ill individuals are not the same as nutrition therapy for people with sepsis. The reasons for this have not been well investigated, although it might be because of aberrant host reactions brought on by infections, which lead to gradual physiological changes that ultimately reduce metabolic potential by compromising mitochondrial function.
A growing body of research indicates that increasing ketone availability during severe illness may have a protective impact. Ketones are an essential and more efficient energy source than fatty acids or glucose. They may also have signaling properties that provide anti inflammatory effects and trigger healing mechanisms like autophagy and muscle regeneration.
Accordingly, research using animal models of brain damage and sepsis has shown that giving ketones or following a ketogenic diet can be protective. With only a few modest randomized controlled trials (RCTs) indicating better blood glucose control by ketone supplements or ketogenic diets, human evidence is still lacking. Despite the conventional belief that critical illness blunts ketogenesis, a recent pilot crossover RCT found that blood ketone concentrations in critically ill long stay patients increased considerably after four hours of complete fasting.
Additionally, research has shown that in critically ill children and adults, a temporary acceptance of inadequate enteral nutrition during the first week of an intensive care unit (ICU) stay results in a considerable rise in ketogenesis. The early virtual fasting during critical illness that activates ketogenesis was especially prominent in children, where a portion of the intervention’s outcome advantage is also statistically mediated by higher ketone availability.
Since the stomach is the body’s largest immunological organ, events that take place there could have a big impact on systemic immunity. The normal barrier function of the stomach may be significantly impacted by the circulatory irregularities characteristic of sepsis, particularly the decreased oxygen delivery to peripheral tissues. Increased intestinal permeability as a result makes it easier for endotoxins and germs to enter the bloodstream, which may signal the onset of multiple organ dysfunction syndrome.