1.
The systemic inflammation hypothesis: Towards a new paradigm of acute decompensation and multiorgan failure in cirrhosis.
Arroyo, V, Angeli, P, Moreau, R, Jalan, R, Clària, J, Trebicka, J, Fernández, J, Gustot, T, Caraceni, P, Bernardi, M, et al
Journal of hepatology. 2021;(3):670-685
Abstract
Acute decompensation (AD) of cirrhosis is defined by the development of ascites, hepatic encephalopathy and/or variceal bleeding. Ascites is traditionally attributed to splanchnic arterial vasodilation and left ventricular dysfunction, hepatic encephalopathy to hyperammonaemia, and variceal haemorrhage to portal hypertension. Recent large-scale European observational studies have shown that systemic inflammation is a hallmark of AD. Here we present a working hypothesis, the systemic inflammation hypothesis, suggesting that systemic inflammation through an impairment of the functions of one or more of the major organ systems may be a common theme and act synergistically with the traditional mechanisms involved in the development of AD. Systemic inflammation may impair organ system function through mechanisms which are not mutually exclusive. The first mechanism is a nitric oxide-mediated accentuation of the preexisting splanchnic vasodilation, resulting in the overactivation of the endogenous vasoconstrictor systems which elicit intense vasoconstriction and hypoperfusion in certain vascular beds, in particular the renal circulation. Second, systemic inflammation may cause immune-mediated tissue damage, a process called immunopathology. Finally, systemic inflammation may induce important metabolic changes. Indeed, systemic inflammatory responses are energetically expensive processes, requiring reallocation of nutrients (glucose, amino acids and lipids) to fuel immune activation. Systemic inflammation also inhibits nutrient consumption in peripheral (non-immune) organs, an effect that may provide one mechanism of reallocation and prioritisation of metabolic fuels for inflammatory responses. However, the decrease in nutrient consumption in peripheral organs may result in decreased mitochondrial production of ATP (energy) and subsequently impaired organ function.
2.
Use of Enteral Nutrition for Gastrointestinal Bleeding Prophylaxis in the Critically Ill: Review of Current Literature.
Newberry, C, Schucht, J
Current nutrition reports. 2018;(3):116-120
Abstract
PURPOSE OF REVIEW This review provides a comprehensive overview of the etiology of stress-related mucosal disease, current acid suppression therapy recommendations, and the role enteral nutrition may play in disease prevention. RECENT FINDINGS Recent literature indicates enteral nutrition may prevent complications of stress-related mucosal disease by increasing splanchnic blood flow, enhancing gastrointestinal motility, and promoting cellular immunity and integrity through local nutrient delivery. Stress-related mucosal disease is a common complication of hospitalization in the critically ill which may lead to overt gastrointestinal bleeding and enhanced mortality. High-risk patients have historically been prescribed acid suppression therapy, though enteral nutrition may also have a role in disease mitigation.