SqJpyMMM I Op Mrtt Wtfftl UWIift Table 1 Basic medical management of severe acute pancreatitis

Sedatives and non-morphine-based analgesics are often required for agitation and pain. Epidural analgesia has the advantage of increasing splanchnic and pancreatic blood flow, which is often rapidly impaired in the setting of severe acute pancreatitis. Theoretically, it may limit the progression toward pancreatic necrosis and prevent bacterial translocation from the digestive tract.

As morbidity caused by early remote organ dysfunction has been controlled by advances in intensive care, bacterial contamination of pancreatic necrosis has emerged as the major determinant of mortality. Early prophylactic antibiotics and selective digestive decontamination have been shown to reduce the incidence of pancreatic infection. It seems wise to consider both measures in view of the 40 per cent incidence of early bacterial contamination of necrosis, the mechanisms underlying bacterial invasion of necrotic areas, and the potential for further bacterial/endotoxin translocation. Considering their penetration into pancreatic tissues, the microbial spectrum most prevalent in infected necrosis, and the potential to achieve therapeutic and antimicrobial activity in the pancreas, quinolones or imipenem may be used as first-line agents.

Aggressive nutritional support has become standard therapy, since constant features of severe acute pancreatitis include the inability of the gastrointestinal tract to function effectively for long periods and a concurrent increase in the basal metabolic rate caused by the inflammatory process. In addition, there is a high prevalence of premorbid nutritional depletion. The impact on the primary disease process by suppressing pancreatic secretion with total parenteral nutrition remains controversial and probably of little concern. Nutritional support should be initiated early in the course of the attack; this may be given parenterally as intravenous substrate infusions including fat emulsions do not stimulate exocrine pancreatic secretion. Lipids are usually well tolerated and contribute towards the caloric substrate needed to meet the increased energy needs of these glucose-intolerant patients. However, intravenous lipid solutions should not be given to either the rare patient with hypertriglyceridemia-induced acute pancreatitis or those with lipemia. Triglyceride levels usually fall quickly when oral intake is withheld and insulin administered. Plasma exchange should be undertaken in refractory cases with marked hypertriglyceridemia.

Both gastric/duodenal feeding and enteral fat stimulate exocrine pancreatic function which may be deleterious with respect to the pathophysiology of severe acute pancreatitis. Enzyme output appears to be proportional to the fat content in the diet and to duodenal inflow of nutrients. In patients requiring surgery for complications of severe acute pancreatitis, nutritional support can be given through a feeding jejunostomy with a semi-elemental diet incorporating medium-chain triglycerides. Early placement of a nasojejunal tube may be a valid, yet unsubstantiated, alternative to allow early enteral feeding and gut decontamination in these patients. Proper positioning of the tube, careful exclusion of jejunoduodenal reflux, and prevention of duodenal injury are prerequisites for the use of this technique. Nevertheless, early jejunal feeding improves nitrogen-caloric balance, helps to preserve or restore the integrity of the gut-blood barrier by providing luminal nutrients to the mucosa, and is of immunotherapeutic benefit in those patients at risk of developing bacterial translocation and multiple organ failure. The value of diets supplemented with enterocyte or colonocyte substrates such as arginine, glutamine, and short-chain fatty acids remains to be determined. Low-fat oral feeds should be reinstituted carefully after completion of the acute phase of the attack.

Acute pancreatitis should be regarded as the disease prototype that generates multisystem organ failure even in the absence of sepsis. Consequently, intensive care support of these patients shares many common therapeutic features with other acute illnesses requiring intensive care unit (ICU) admission. Circulatory shock, acute respiratory failure, renal dysfunction, and metabolic derangements involving glucose and calcium homeostasis, hepatic function, and the hematopoietic system all mandate appropriate therapy and ICU support.

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