The cornerstone of management of acute pancreatitis has been pancreatic rest, as the presence of food in the proximal gut is the most potent stimulus for trypsin synthesis and secretion, and continued trypsin synthesis can be expected to perpetuate the inflammatory response. Further studies have shown that acute pancreatitis is one of the most catabolic of illnesses [18, 19]. Consequently, the maintenance of pancreatic rest through starvation is a less than ideal option as an adequate supply of amino acids is essential for the repair process. The development of PN was heralded as a potential major breakthrough as, for the first time, feeding could be maintained without stimulating the pancreas. We, and others, have shown in human studies that PN is efficacious in meeting nutritional requirements without stimulating the pancreas . Unfortunately, its use was also associated with an alarming increase in metabolic (namely, hyperglycemia) and septic complications. Indeed, one study showed that PN use worsened outcome when compared to no feeding at all . The explanation is complex. First, PN and bowel rest probably exacerbate the intestinal and distant organ dysfunction that characterizes acute pancreatitis. Kudsk's studies in rats showed that PN and bowel rest result in atrophy of the mucosa and the gut immune system, with suppression of Th-2 responses and activation of adhesion molecules, which leads to neutrophil priming and migration to distant targets, such as the lung, producing a 'first hit' phenomenon . This is remarkably similar to what is found in the acute pancreatitis-associated gut injury shown in Fig. 5.2. Other studies have shown that IL-6 is the mediator of gut barrier dysfunction , and both acute pancreatitis and PN induce intestinal IL-6 production [22, 24]. The use of PN (i.e., failure to feed patients enterally) further reduces motility and blood flow, increases the risk of small bowel bacterial overgrowth with antegrade colonization with colonic organisms and increases mucosal permeability as discussed above, thus exacerbating the pathophysiological response to acute pancreatitis [25, 26]. This may be of critical importance, as the organisms most commonly responsible
Relative Insulin Insufficiency in Acute Pancreatitis
J Blood glucose J Blood insulin
J Blood glucose J Blood insulin
for pancreatic infections are of colonic origin , and endotoxemia commonly accompanies severe disease . Second, the presence of a central vein catheter in PN-fed patients provides an open conduit for nosocomial infection. Third, intravenous feeding invariably results in hyperglycemia in patients with severe acute pancreatitis because (1) the glycemic effect of glucose administered parenterally is greater than if it is given enterally , (2) acute pancreatitis impairs pancreatic endocrine function resulting in a relative insulin deficiency  and (3) the acute inflammatory response and secretion of counter-regulatory hormones increases endogenous glucose production and creates insulin resistance  (Fig. 5.3).
Recent studies have clearly demonstrated that hyperglycemia worsens outcome in any form of critical illness . In hyperglycemia, leukocyte function is impaired and intestinal motility reduced, leading to increased infection risk from enteric pathogens . Consequently, it is likely that the potential benefits of PN on 'resting' the pancreas are overshadowed by its detrimental effects on intestinal function and mucosal integrity, and by its septic and metabolic complications.
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