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Query: UMLS:C0001339 (acute pancreatitis)
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The present paper described the technique of intravenous hyperalimentation applied to a group of 100 surgical patients. A specially prepared diet supplying a high amount of calories, using hypertonic glucose and supplying nitrogen, using polypeptides or aminoacid solutions, was infused into the superior vena cava. The inhibition of digestive secretions, during the period of hyperalimentation, was used in the management of 19 patients with intestinal and pancreatic fistulae. The general conclusion reached after wide clinical experience was that by supplying energy and nitrogen to a patient in a severe catabolic state, a significant and sometimes dramatic capacity could be developed which allowed him to overcome difficult conditions and even initiated a reversal of the metabolic balance in the direction of anabolism. The regimen should be adopted in the preoperative preparation of debilitated patients; in hypercatabolic states (post-trauma, post-surgery or burns); in gastrointestinal, granulomatous or infectious diseases; in acute pancreatitis; in digestive fistulae; in oncological conditions, and so on. The metabolic and infective complications can be pregressively decreased and eventually prevented by proper handling and strict metabolic monitoring. The use of this hyperalimentation was extremely encouraging, and on many occasions we had the impression that it was life saving.
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PMID:Intravenous hyperalimentation in the management of the critically ill patient, with special reference to abdominal fistulae. 82 16

Three hundred patients with acute pancreatitis have been studied. Pancreatitis was associated with alcoholism in 207, biliary tract disease in 51 and other conditions in 42. Twenty-two patients died, and an additional 34 patients required more than one week of treatment in the intensive care unit. Retrospective analysis of the first 100 patients identified 11 objective findings which correlated with the occurrence of serious illness or death. They were, on admission, age over 55 years, blood glucose level over 200 milligrams per cent, white blood count over 16,000 per cubic millimeter, serum lactic dehydrogenase level over 350 International units per liter and serum glutamic-oxalacetic transaminase level over 250 Sigma Frankel units per cent. During the initial 48 hours of therapy, the findings were hematocrit value decrease over 10 percentage points, serum calcium level below 8 milligrams per cent, base deficit over 4 milli-equivalents per liter, a blood urea nitrogen level increase over 5 milligrams per cent, estimated fluid sequestration over 6 liters and arterial oxygen tension less than 60 millimeters of mercury. Prospective application of these signs in the latter 200 patients permitted the accurate early identification of those with severe pancreatitis. Only one of 162 patients with fewer than three of these early features was seriously ill or died, while 24 of 38 patients with three or more early positive findings were seriously ill or died. The objective early identification of patients with severe pancreatitis permits more vigorous management of this group and also provides a basis for the selection of patients for the evaluation of proposed improved therapies. Percutaneous peritoneal dialysis in severe pancreatitis was evaluated in ten patients, with three or more positive early signs, who were randomly assigned to dialysis or continued conventional care. Morbidity was strikingly reduced in patients who underwent dialysis, and while death or more than nine days of intensive care occurred in two of five patients who did not receive dialysis, all five patients having dialysis recovered after fewer than nine days of intensive care treatment. Serious illness or death occurred in 31 of the first 100 patients but in only 26 of the more recent 200 patients. There has been a similar fall in mortality from 15.0 to 3.5 per cent. Factors which may contribute to this improvment include the objective early identification of patients with severe disease, the avoidance of early laparotomy whenever practical, the prolongation of nasogastric suction until all evidence of pancreatic inflammation has resolved, careful monitoring of respiratory function and early treatment of pulmonary complications and peritoneal dialysis in patients with severe disease.
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PMID:Prognostic signs and nonoperative peritoneal lavage in acute pancreatitis. 94 Oct 75

Different methods available for investigating patients for pancreatic disease are discussed. They first include measurement of pancreatic enzymes in biological fluids. Basal amylase and/or lipase in blood are truly diagnostic in acute pancreatitis but their utility is low in chronic pancreatic diseases. Evocative tests have been performed to increase the sensitivity of blood enzyme measurement. The procedure is based on enzyme determination following administration of pancreozymin and secretin, and offers a valuable aid in diagnosis of chronic pancreatitis and cancer of the pancreas. They are capable of discerning pancreatic lesions but are not really discriminatory because similar changes are observed in both diseases. The measurement of urinary enzyme levels in patients with acute pancreatitis is a sensitive indicator of disease. The urinary amylase excretion rises to abnormal levels and persists at significant values for a longer period of time than the serum amylase in acute pancreatitis. The fractional urinary amylase escretion seems to be more sensitive than daily urinary measurement. The pancreatic exocrin function can be assessed by examining the duodenal contents after intravenous administration of pancreozymin and secretin. Different abnormal secretory patterns can be determinated. Total secretory deficiency is observed in patients with obstruction of excretory ducts by tumors of the head of the pancreas and in the end stage of chronic pancreatitis. Low volume with normal bicarbonate and enzyme concentration is another typical pattern seen in neoplastic obstruction of escretory ducts. In chronic pancreatitis the chief defect is the inability of the gland to secrete a juice with a high bicarbonate concentration; but in the advanced stage diminution of enzyme and volume is also evident. Diagnostic procedures for pancreatic diseases include digestion and absorption tests. The microscopic examination and chemical estimation of the fats in stool specimens in different conditions of intake are still important screening tests. Isotopic estimates of steatorrhea and distinction between labeled triolein and oleic acid absorption do not provide greater diagnostic discrimination than traditional procedures. 131I labeled proteins permit a good evaluation of a negative nitrogen balance. Sophisticated procedures to estimate exocrine pancreatic insufficiency are based on the study of endoluminal digestive processes at several times and different level of the small intestine. They permite esclusion of extrapancreatic factors interfering in digestion and absorption functions. The endocrin pancreatic function is evaluated by mean of oral tolerance test an radioimmunoassay of blood insulin. It is generally agreed that "diabetes" caused by insulin deficiency and digestion and absorption defects are the result of diffuse pancreatic destruction. Many methods are now available investigating patients with pancreatic disease but the single use of one of them is never satisfactory...
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PMID:[Clinical significance of the tests used in the diagnosis of pancreatic diseases]. 99 11

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

The influence of total parenteral nutrition (TPN) was studied in 67 patients with severe acute pancreatitis having three or more criteria according to Ranson (mean +/- SD = 3.8 +/- 0.21). Although TPN has been reported to not be of benefit in the progress and severity of the disease, we have found that the time TPN is started is important in influencing the course of the disease and in the development of local complications, as well as in the mortality rate. Patients whose TPN was started within the first 72 hours of the disease had a 23.6% complication rate and 13% mortality, in comparison with patients whose TPN was started later in the course of the disease, who had a 95.6% complication rate (p less than 0.01) and a mortality rate of 38% (p less than 0.03). The nutritional status of the patients during TPN administration of 28.4 days was maintained either steady or was improved, as assessed by nitrogen balance, serum levels of transferrin (p less than 0.05), and albumin (p less than 0.05). The administration of fat solution, either to prevent essential fatty acid deficiency or to provide part of the caloric requirements, was found to cause neither clinical nor laboratory worsening of the disease. All pancreatic fistulae that developed during the course of the disease spontaneously closed in patients receiving TPN without operation in a mean period of 33.3 days, and all pseudocysts subsided in an average of 18.3 days. Those who died (overall mortality rate 24%) had had uncontrollable sepsis, which resulted in hypercatabolism and multiple system organ failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Total parenteral nutrition in severe acute pancreatitis. 157 3

A three-and-a-half-year-old boy was transferred to our hospital under the impression of Reye's syndrome. The laboratory data showed hypoglycemia, hyperammonemia and elevated serum transaminases. A remarkable high serum amylase level of 2,223 IU/L and CAm/CCr of 36% was noted. A blood urea nitrogen level of 143 mg/dl was found on the third day and a creatinine level of 8.7 mg/dl on the fourth day. Disseminated intravascular coagulopathy (DIC) and systemic candidal infection complicated his final course. He died after intensive treatment for eleven days. Hemorrhagic pancreatitis and fatty change of the liver were noted at autopsy. Disseminated candidal invasion was noted within the kidneys, cerebrum, and lungs. Tonsillar herniation, systemic candidiasis and bronchopneumonia were believed to be the causes of his death. It is extremely rare for all three complications, acute pancreatitis, acute renal failure and DIC, to occur in Reye's syndrome at the e time.
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PMID:An autopsy case of Reye's syndrome associated with acute pancreatitis, acute renal failure and disseminated intravascular coagulopathy. 198 77

The predictive value of eight clinical variables and 20 analytical variables on mortality was retrospectively analyzed in 61 patients with severe acute pancreatitis, fulfilling at least three Ranson criteria, admitted to the ICU between 1977 and 1987. The mean age of the series was 57 +/- 16.6 years. Twenty seven were males and 34 females. The mortality rate was 60%. Univariate analysis demonstrated that the variables with greater predictive value of mortality were: age, days of hospitalization, presence of associated diseases, plasma lactodehydrogenase, more than 10% hematocrit decrease during the first 48 hours, plasma ureic nitrogen on admission and a value greater than 1.8 mmol/l during the first 48 hours, calcemia, arterial oxygen pressure, plasma albumin, and prothrombin time. A logistic regression multivariate analysis disclosed that the variables with independent predictive value of mortality were: age, serum ureic nitrogen, calcemia, arterial oxygen pressure, plasma albumin, and hematocrit decrease after 48 hours. When the patients were grouped according to the presence of less than three, three, four or more than four of these risk factors (being, the average the cutting point) we obtained a good prognostic discriminative power since the mortality in those groups was 0, 30%, 60%, and 100%, respectively.
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PMID:[Predictive factors of mortality in a series of 61 patients with severe acute pancreatitis]. 777 43

The use of total parenteral nutrition (TPN) in the treatment of 73 patients with acute severe pancreatitis was prospectively studied during a two year period. Patients were divided into three groups on the basis of calorie substrate used. Glucose and twice weekly lipid infusion (glucose based) were used in 60 per cent; 27 per cent required daily lipid infusion (lipid based), and 13 per cent received no lipid because of pre-existing hyperlipemia or thrombocytopenia (no lipid). Nutritional indices (albumin, transferrin and total lymphocyte count) were initially abnormal in more than 80 per cent of patients, and 50 per cent had three or more of Ranson's criteria. After TPN, 81 per cent had improved nutritional indices, and none had hypertriglyceridemia or aggravation of pancreatitis develop. Patients who received lipid based or no lipid had higher insulin requirements (p less than 0.01) than those receiving mainly glucose. Mortality was increased tenfold (2.5 versus 21.4 per cent, p less than 0.01) in patients who did not achieve positive nitrogen balance. We conclude that TPN, either lipid or glucose based, is a safe and effective therapy to reverse the malnutrition of acute pancreatitis and that failure to achieve positive nitrogen balance is associated with increased mortality.
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PMID:Total parenteral nutrition and alternate energy substrates in treatment of severe acute pancreatitis. 249 6

In this study we investigated the effect of a total parenteral nutrition supplemented with synthetic dipeptides on plasma and muscle amino acid metabolism in four patients with acute pancreatitis. We infused an amino acid solution containing alanylglutamine, glycylglutamine, glycylvaline, glycylisoleucine, glylcylleucine, and glycyltyrosine for a period of five days in daily dosages of 10.3, 22.1, 68.8, 37.2, 42.5, and 15.7 mmol, respectively. The plasma levels remained below 100 mumol/L for all infused dipeptides. The plasma concentrations of alanylglutamine were not measurable. Mean peptide urine excretion remained below 5%, with the exception of glycylglutamine (8.5% +/- 5.1%). Arteriovenous concentration differences of the dipeptides across the leg were not significantly different from zero, indicating that the infused dipeptides have no important role in the nitrogen exchange of skeletal muscle. A marked intracellular glutamine deficiency in skeletal muscle was found in all four patients (5.1 +/- 0.6 mmol/L v 19.5 +/- 0.8 in healthy subjects) before infusion. Intracellular glutamine concentration was significantly higher after the infusion period (5.1 +/- 0.7 v 9.5 +/- 1.8 mmol/L, P greater than .05), but no normalization of the intracellular glutamine levels was achieved by the infusion of the two glutamine-containing peptides. We conclude that peptides are well metabolized as substrates for parenteral nutrition in catabolic patients. Furthermore, the infusion of glutamine peptides caused a significant increase in intracellular glutamine levels; however, the dosage of glutamine peptides was too low to normalize the muscular glutamine concentrations.
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PMID:Infusion of dipeptides as nutritional substrates for glutamine, tyrosine, and branched-chain amino acids in patients with acute pancreatitis. 250 85

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


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