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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.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Nutritional support for acute pancreatitis. 151 64

Some surgeons avoid placing a jejunostomy in patients with complications, fearing either exacerbation of the disease during enteral feedings or complications from the jejunostomies. Eleven patients with hemorrhagic pancreatitis (four), pancreatic abscess (five), or infected pseudocyst (two) underwent placements of needle (five) or Red Robinson (six) jejunal catheters during laparotomy. Five patients had been given 30.8 +/- 16 liters of TPN over 25 +/- 12 days preoperatively. Only two patients received TPN postoperatively because of progressive sepsis with enteral intolerance to feedings. One of these patients developed a jejunal leak near the placement of the Red Robinson catheter. Both patients died of complications from their pancreatic disease. The remaining nine patients received 35.6 +/- 8.6 liters of enteral feedings over 31 +/- 6.8 days before resuming oral intake. Glucosuria and hyperglycemia were common, but easily managed. No catheters were lost, and diarrhea necessitating slowing and diluting the diet was unusual after the first week. Enteral feeding did not elevate amylase values. Therefore, jejunal feedings can be given safely in patients with severe acute pancreatic disease to provide prolonged nutrition without aggravating the disease.
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PMID:Postoperative jejunal feedings following complicated pancreatitis. 210 78

Acute pancreatitis often results in a hyperdynamic, consumptive state. Hallmarks of this condition are decreased peripheral resistance with increased cardiac output. Hemodynamic and cardiovascular changes are accompanied by metabolic alterations. Increased protein catabolism, increased ureagenesis, glucose intolerance, increased lipolysis, and reduced servoregulation are metabolic changes commonly seen in this syndrome. To preserve organ structure and function, biochemical processes must be metabolically supported. Substrate needs change as stress level increases. The per cent of total calories provided as protein must increase. Branched-chain-enriched amino acid solutions have been shown to improve nitrogen utilization in hypermetabolic patients and may therefore be beneficial for the patient with acute pancreatitis. Glucose utilization decreases and free fatty oxidation increases. A mixed fuel system that provides fat, protein, and glucose is suggested for these patients. IV fat has been shown to be a safe energy substrate for patients with pancreatitis in the absence of hyperlipidemia. Failure to use fat as an energy substrate in conjunction with TPN may result in hepatic steatosis and excess carbon dioxide production. The decision of whether to use the parenteral or enteral route to nutritionally support the patient with pancreatitis remains controversial. TPN may allow maintenance of pancreatic rest. The role of enteral feedings is less clear. However, it has been shown that the further down the alimentary tract the feeding is infused, the less pancreatic stimulation occurs. Therefore, it seems wise to support the patient with TPN during severe acute pancreatitis. Jejunal enteral feedings should be initiated as a transitional feeding when the acute inflammatory episode begins to subside.
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PMID:Nutritional support in acute pancreatitis. 250 54

The clinical course of 19 patients with pancreatic phlegmon, as diagnosed by computed tomography (CT) and clinical criteria, was assessed retrospectively and compared to that of eight patients with pancreatic abscess diagnosed either at surgery or with percutaneous aspiration. Controls consisted of 55 patients with uncomplicated acute pancreatitis without CT scans and 11 patients with acute pancreatitis in whom CT scans were negative or only consistent with acute pancreatitis (no phlegmon). The age, sex, and presumed etiology of the pancreatitis were not significantly different in the four groups. Patients with phlegmon had a higher incidence of severe pancreatitis as defined by Ranson's criteria, presence of an abdominal mass, as well as a longer duration of fever, abdominal pain and leukocytosis than controls without CT scans. With the exception of a palpable abdominal mass and fever lasting over five days, the results were similar when comparing the phlegmon group and controls with CT scans, although the severity of the disease and prolonged abdominal pain tended to be increased in the former patients. There was no statistically significant difference in clinical or laboratory criteria between the phlegmon and abscess groups, although the latter group had longer hospital stays and periods with no oral intake (npo). Management of patients with phlegmon tended to include TPN, longer npo periods, antibiotics, and longer hospital stay than in controls without CT scans. Controls with CT scans were managed similarly to the phlegmon group because of prolonged amylase elevation and abdominal pain. Percutaneous aspiration was successful in differentiating abscess from phlegmon in five of six cases. Major complications were rare in the phlegmon group and spontaneous resolution was the rule. Pancreatic phlegmon is a distinct clinical/radiologic entity which may be very difficult to differentiate clinically from pancreatic abscess. Early percutaneous thin-needle aspiration of the inflammatory mass (under CT guidance) seems to be the diagnostic procedure of choice. Management is nonsurgical unless complications arise. The role of TPN and antibiotics is unknown, and controlled studies of these therapeutic approaches in pancreatic phlegmon are needed.
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PMID:Pancreatic phlegmon. Clinical features and course. 402 9

During the 22nd week of her first pregnancy, a 28-year-old woman developed an attack of acute pancreatitis 10 months after pancreatoduodenectomy for chronic pancreatitis of alcoholic origin. She received total parenteral nutrition without complications for 83 days until the cesarean delivery of a child weighing 2,120 g. During that time, clinical, biological, and echographic signs of pancreatitis progressively disappeared. The favorable outcome for both mother and fetus suggests that prolonged TPN may be a useful measure in the management of severe digestive disease occurring during pregnancy.
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PMID:Prolonged total parenteral nutrition in a pregnant woman with acute pancreatitis. 642 23

A patient with a history of diabetes, coronary artery disease, stroke, previous renal transplantation, and multiple hospital admissions for recurrent pancreatitis was transferred to the hospital from a chronic care facility because of fever and severe epigastric discomfort. At the time of admission, she was receiving hyperalimentation through a central venous TPN catheter. Multiple blood cultures obtained on the first and second hospital days yielded pure cultures of the yeast, Pichia ohmeri. The patient developed acute renal failure, and despite high-dose amphotericin B therapy, ultimately expired.
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PMID:Pichia ohmeri fungemia. 957 30

A 4-month-old boy presented with 9 days of abdominal distension. The abdomen was tense, distended, and nontender, with a fluid wave. Hypoalbuminemia, hyponatremia, high lipase, normal amylase, high ascitic fluid: lipase, amylase, and serum-ascites albumin gradient < 1.1 were present. Abdominal CT showed large ascites, edema, and pancreatic cyst. No improvement was noted with bowel rest, TPN, albumin, furosemide, octreotide, and paracentesis. Endoscopic retrograde cholangiopancreatography showed disrupted pancreatic duct and a cyst. Pancreatic duct stenting was complicated by early outward migration of the stent and was thus ineffective. An exploratory laporatomy revealed a cyst. Cystogastrostomy resolved the pancreatitis and ascites. The patient was discharged off TPN and tolerating enteral nutrition. Pancreatic ascites is rare, producing few or no symptoms in infants. In conclusion, our patient may have had viral pancreatitis, complicated by a disrupted duct and/or ruptured pseudocyst with ascites formation. Medical management was ineffective. Surgery appears to have been curative.
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PMID:Pancreatic ascites in an infant: lack of symptoms and normal amylase. 1456 Sep 86

Severe acture pancreatitis (SAP), a multisystem disease, is characterized by multiple organ system failure and additionally by local pancreatic complications such as necrosis, abscess, or pseudocyst. The rate of mortality in SAP, which is about 20% of all cases of acute pancreatitis (AP), may be as high as 25%, as in infected pancreatic necrosis. The factors that influence mortality in different degrees are various. Etiology for the episode, age, sex, race, ethnicity, genetic makeup, severity on admission, and the extent and nature of pancreatic necrosis (sterile vs. infected) influence the mortality. Other factors include treatment modalities such as administration of prophylactic antibiotics, the mode of feeding (TPN vs. enteral), ERCP with sphincterotomy, and surgery in selected cases. Epidemiological studies indicate that the incidence of AP is increasing along with an increase in obesity, a bad prognostic factor. Many studies have indicated a worse prognosis in idiopathic AP compared to pancreatitis induced by alcoholism or biliary stone. The risk for SAP after ERCP is the subject of extensive study. AP after trauma, organ transplant, or coronary artery bypass surgery is rare but may be serious. Since Ranson reported early prognostic criteria, a number of attempts have been made to simplify or add new clinical or laboratory studies in the early assessment of severity. Obesity, hemoconcentration on admission, presence of pleural effusion, increased fasting blood sugar, as well as creatinine, elevated CRP in serum, and urinary trypsinogen levels are some of the well-documented factors in the literature. The role of appropriate prophylactic antibiotic therapy although still is highly controversial, in properly chosen cases appears to be beneficial and well accepted in clinical practice. Early enteral nutrition has gained much support and jejunal feeding bypassing the pancreatic stimulatory effect of it in the duodenum is desirable in selected cases. The limited role for endoscopic sphincterotomy in patients with demonstrated dilated CBD with impacted stone and evidence of impending cholangitis is well documented. Surgery in AP other than for removal of the gallbladder is often limited to infected pancreatic necrosis, pseudocysts, and pancreatic abscess and in some cases of traumatic pancreatitis with a ruptured duct system. The progress in the understanding of the role of cytokines will over us opportunities to use immunomodulatory therapies to improve the outcome in SAP.
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PMID:Factors influencing mortality in acute pancreatitis: can we alter them? 1663 13

In patients with Crohn's disease and ulcerative colitis parenteral nutrition (PN) is indicated when enteral nutrition is not possible or should be avoided for medical reasons. In Crohn's patients PN is indicated when there are signs/symptoms of ileus or subileus in the small intestine, scars or intestinal fistulae. PN requires no specific compounding for chronic inflammatory bowel diseases. In both diseases it should be composed of 55-60% carbohydrates, 25-30% lipids and 10-15% amino acids. PN helps in the correction of malnutrition, particularly the intake of energy, minerals, trace elements, deficiency of calcium, vitamin D, folic acid, vitamin B12, and zinc. Enteral nutrition is clearly superior to PN in severe, acute pancreatitis. An intolerance to enteral nutrition results in an indication for total PN in complications such as pseudocysts, intestinal and pancreatic fistulae, and pancreatic abscesses or pancreatic ascites. If enteral nutrition is not possible, PN is recommended, at the earliest, 5 days after admission to the hospital. TPN should not be routinely administered in mild acute pancreatitis or nil by moth status <7 days, due to high costs and an increased risk of infection. The energy requirements are between 25 and 35 kcal/kg body weight/day. A standard solution including lipids (monitoring triglyceride levels!) can be administered in acute pancreatitis. Glucose (max. 4-5 g/kg body weight/day) and amino acids (about 1.2-1.5 g/kg body weight/day) should be administered and the additional enrichment of TPN with glutamine should be considered in severe, progressive forms of pancreatitis.
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PMID:Gastroenterology - Guidelines on Parenteral Nutrition, Chapter 15. 2004 77