Nutritional support for acute pancreatitis

The current review has summarized current data relevant to the nutritional support of patients with acute pancreatitis. Selection of the most appropriate form of nutritional support for patients with acute pancreatitis is intimately linked to a thorough understanding of the effects of various forms of enteral and parenteral nutrition on physiologic exocrine secretory mechanisms. Two basic concepts have emerged from the multiple studies that have addressed these issues to date: 1, enteral feeds should have low fat composition and be delivered distal to the ligament of Treitz to minimize exocrine pancreatic secretion and 2, parenteral substrate infusions, alone or in combinations similar to those administered during TPN, do not stimulate exocrine pancreatic secretion. From a practical standpoint, most patients with acute pancreatitis are diagnosed by nonoperative means and will manifest some degree of paralytic ileus during the early phase of the disease. Therefore, jejunal feeds are usually not a therapeutic option early in the course of this disease. On the basis of the clinical studies reviewed herein we propose general guidelines for the nutritional support of patients with acute pancreatitis: 1, most patients with mild uncomplicated pancreatitis (one to two prognostic signs) do not benefit from nutritional support; 2, nutritional support should begin early in the course of patients with moderate to severe disease (as soon as hemodynamic and cardiorespiratory stability permit); 3, initial nutritional support should be through the parenteral route and include fat emulsion in amounts sufficient to prevent essential fatty acid deficiency (no objective data exist to recommend specific amino acid formulations); 4, patients requiring operation for diagnosis or complications of the disease should have a feeding jejunostomy placed at the time of operation for subsequent enteral nutrition using a low fat formula, such as Precision HN® (Sandoz, 1.3 percent calories as fat), Criticare HN® (Mead Johnson, 3 percent calories as fat) or Vivonex High Nitrogen® (Norwich Eaton, 0.87 percent calories as fat), and 5, oral feedings should be low fat in composition and should be reinstituted using traditional clinical criteria, including the symptoms of the patient, physical examination and computed tomographic appearance of the pancreas (clinicians should bear in mind the well documented exocrine stimulatory effects of even low fat oral feeds and the risks of early refeeding). These general guidelines must be individualized to incorporate what is perhaps the most important clinical variable-the premorbid nutritional state of the patient. Review of the clinical trials examining the efficacy of TPN in acute pancreatitis emphasizes the value of accurate documentation and stratification of patients by severity of disease. As reported, therapies previously regarded as having no role in acute pancreatitis on the basis of studies in patients with mild disease, may have significant benefit when evaluated in patients with moderate to severe disease in whom objective clinical response is much easier to detect. This study is particularly significant because it demonstrated that, not only was objective nutritional benefit seen in patients with acute pancreatitis treated with TPN but, more importantly, failure to reverse the malnutrition seen in these patients increased the risk of mortality for patients with comparable degrees of disease. The optimal nutritional support regimen for patients with moderate to severe acute pancreatitis needs to be defined by further investigation and prospective evaluation. Progress in the treatment and nutritional support of patients with acute pancreatitis will require a better understanding of the underlying metabolic and physiopathologic changes that occur at the cellular level, both in response to the disease itself and in response to the administration of nutritional support. Specific therapies directed at these alterations will be more likely to have an impact on the morbidity and mortality rates of this disease than the multitude of supportive, nonspecific therapies that have, thus far, shown no demonstrable benefit in patients with acute pancreatitis.