Читать книгу Clinical Pancreatology for Practising Gastroenterologists and Surgeons - Группа авторов - Страница 137

Nutritional intervention in the treatment of acute pancreatitis (AP) is a continually evolving topic. It is clear that the triggering insult and sentinel event of inflammation involve the pancreas directly, with the process of inflammation and necrosis within the gland serving as a key source for the overall systemic inflammatory response syndrome (SIRS). However, the downstream effects include large fluid losses from third‐spacing, redistribution of blood away from the splanchnic circulation, autoregulatory abnormalities, and vasoconstriction of mesenteric afferent arterioles infusing the pancreas and causing classic ischemia/reperfusion injury [1,2]. The ensuing ischemia can damage the intestinal mucosa [2], with oxidative stress and activation of inflammatory cytokines and release of lysosomes causing increased intestinal permeability [1]. Furthermore, slowing of gut motility due to intestinal ischemia/reperfusion injury can result in small intestinal bacterial overgrowth, intestinal dysbiosis, and bacterial translocation [1].

Although the initial sentinel event is important, subsequent damage to the intestinal mucosa resulting in intestinal injury and breakdown of mucosal barrier defenses can have a significant impact on overall disease severity [3]. Maintaining the intestinal mucosal barrier is important in the process of treating AP, and can be considered a logical part of the treatment strategy. Nutritional support is a necessary step in maintaining intestinal mucosal barrier health, and has become a focus in the treatment of AP. Nutritional management is not only important in sustaining mucosal immunity, but also important because AP is a highly metabolic disease process with activation of an inflammatory cascade that leads to catabolic stress, formation of reactive oxygen species, and activation of immune responses that can rapidly overwhelm innate immune regulation and inherent antioxidant capacity [4–6]. AP is associated with the typical metabolic pattern of SIRS, with elevated protein catabolism, a marked inflammatory state, and deranged glucose metabolism [7,8]. If AP is complicated by sepsis, protein catabolism is further enhanced, with high net nitrogen losses; negative nitrogen balance is associated with increased mortality [7,9]. In severe necrotizing pancreatitis, 80% of all patients are catabolic [10], with high energy expenditure and enhanced protein catabolism [11]. Furthermore, nutrient digestion and absorption can be impaired during AP, and without nutritional support patients may rapidly develop severe malnutrition, water retention, and decreased muscle function [12,13]. Because of their increased energy expenditures, all patients with pancreatitis should be classified as having a moderate to high nutritional risk [14,15]. Nutritional assessment of these patients within the first 24–48 hours of admission is required to formulate a plan for the appropriate nutritional intervention [16].

Despite the clear importance of nutrition in AP, the historic focus of nutrition and feeding during AP aimed to “rest the pancreas” by providing nil by mouth, thereby removing the food‐induced stimulation of exocrine pancreatic secretion. This approach would presumably reduce enzyme‐driven inflammation, and/or address intolerance to feeding by mouth via fasting or administering total parenteral nutrition (TPN). Over the past two decades, there has been a shift in the nutritional management of all critically ill patients, including AP patients, toward early feeding, either by mouth or enteral tube feeding if oral intake is not possible due to abdominal pain or nausea. Results on early feeding (initiated within 24–36 hours of admission) in AP have demonstrated lower risk of multiple organ failure (MOF), operative interventions, systemic infections, septic complications, and mortality compared to standard therapy (no enteral/parenteral nutrition) or delayed enteral nutrition (EN) [17]. Randomized clinical trials and meta‐analysis [18] have demonstrated the superiority of EN over TPN with regard to reducing complications, cost, and mortality in predicted severe and necrotizing types of AP, and possibly in mild AP. EN, as compared with TPN, decreases systemic infections, MOF, need for surgical intervention, and mortality [4,19]. The overall focus has shifted toward protecting the gut mucosal barrier by initiating enteral feeding, either orally or by enteral tube. Enteral feeding maintains villous height and the CD4/CD8 ratio in mesenteric lymph nodes, spleen, and peripheral blood when compared with TPN‐fed controls [20]. TPN results in rapid and severe atrophy of gut‐associated lymphoid tissue and increased occurrence of bacterial translocation [21]. Consequently, the reliance on TPN has decreased in response to an increased awareness of attendant problems, such as catheter‐related sepsis, high cost of treatment, electrolyte and metabolic disturbances, villous atrophy, and gut barrier failure with promotion of bacterial translocation, systemic sepsis, and MOF [22].