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Enteral insulin-like growth factor-I augments intestinal disaccharidase activity in piglets receiving total parenteral nutrition.

BACKGROUND: Partial enteral nutrition is administered to infants on parenteral nutrition to stimulate intestinal function. Herein, the hypothesis that supplementation of partial enteral nutrition with insulin-like growth factor-I would augment intestinal development was investigated. METHODS: One-day-old piglets (n = 29) were randomly assigned to five dietary treatment groups: 100% of energy as enteral formula, 100% of energy as total parenteral nutrition, or 80% parenteral nutrition/20% enteral formula supplemented with either 0, 0.2, or 1 mg/kg insulin-like growth factor-I for 7 days. Weight gain, intestinal weight, morphology, protein, and DNA content and disaccharidase activity and mRNA expression were assessed. RESULTS: Parenterally fed piglets had similar whole body weight gain and serum hormone concentrations but reduced intestinal mucosal weight, villus height, and sucrase and lactase activity compared with 100% enterally fed pigs. Partial enteral nutrition alone increased mucosal weight and protein content, villus height, and disaccharidase activity compared with 100% parenterally fed piglets. No effect of the lower dose of insulin-like growth factor-I (0.2 mg/kg per day) was observed, but supplementing partial enteral nutrition with 1 mg insulin-like growth factor-I/kg further increased villus width and cross-sectional area and disaccharidase activity compared with partial enteral nutrition alone. Lactase mRNA expression was not affected by insulin-like growth factor-I, suggesting that the primary site of regulation of lactase by insulin-like growth factor-I occurs after transcription. CONCLUSIONS: Enteral insulin-like growth factor-I augmented intestinal morphology and disaccharidase activity in parenterally fed piglets over that observed with partial enteral nutrition alone. Thus enteral insulin-like growth factor-I may represent an efficacious clinical adjunct to promote intestinal development of parenterally fed neonates.

Animals↗

Acute abdominal pain in systemic lupus erythematosus: focus on lupus enteritis (gastrointestinal vasculitis).

OBJECTIVE: To determine the causes of acute abdominal pain in systemic lupus erythematosus (SLE) and to compare the clinical and laboratory data, especially antiphospholipid antibodies and the SLE Disease Activity Index (SLEDAI), between lupus enteritis (gastrointestinal vasculitis) and acute abdominal pain without lupus enteritis in patients with SLE. METHODS: A retrospective study was carried out for all patients admitted with SLE from 1993 to March 2001. The SLEDAI and laboratory data were collected at the time of diagnosis of SLE and at the time of acute abdominal pain. Lupus enteritis (gastrointestinal vasculitis) was diagnosed by clinical investigation and abdominal computed tomographic findings. RESULTS: Chart review identified 175 patients (20 male, 155 female) who had been admitted with SLE. Of these patients, 38 (22%) presented with acute abdominal pain. Lupus enteritis was the most common cause of acute abdominal pain. Patients were divided into three groups: group 1: lupus enteritis (n=17), group 2: acute abdominal pain without lupus enteritis (n=21), and group 3: SLE without acute abdominal pain (n=137). There was no difference in age and sex among the three groups. Antiphospholipid, anti-RNP, anti-Sm, anti-Ro, and anti-La antibodies did not differ among the three groups. There was no difference in the SLEDAI at the time of diagnosis and at the time of acute abdominal pain between groups 1 and 2. Complement, erythrocyte sedimentation rate, C reactive protein, and anti-dsDNA measured at the time of acute abdominal pain did not differ between groups 1 and 2. A drop in the white blood cell count at the time of abdominal pain was more prominent in group 1 than group 2. In lupus enteritis, the jejunum and ileum were the sites most commonly affected. Rectal involvement was rare. Even though four patients relapsed, all the patients with lupus enteritis, including those who relapsed, responded well to corticosteroid. CONCLUSION: Lupus enteritis is the most common cause of acute abdominal pain in SLE. All patients with lupus enteritis responded well to a high dose of a corticosteroid without surgical intervention. The SLEDAI and laboratory data, except leucopenia, do not correlate with the occurrence of lupus enteritis.

Abdominal Pain↗

Reduction in diarrhea incidence by soluble fiber in patients receiving total or supplemental enteral nutrition.

BACKGROUND: Gastrointestinal side effects, particularly diarrhea, are still the main reasons for discontinuation of enteral nutrition. Although the causes of diarrhea are diverse, the enteral nutrition solution is frequently suspected of playing a leading role in causing diarrhea. METHODS: Our randomized, prospective, double-blind trial with 100 patients assessed the effects of feeding a standard diet (Nutrodrip Standard) vs the same diet supplemented with 20 g of soluble fiber, containing partially hydrolyzed guar gum (Sunfiber), per 1000 mL. Thirty patients received total enteral nutrition postoperatively, and 70 patients received enteral supplementation. RESULTS: The patients receiving total enteral nutrition with soluble fiber had decreased diarrhea but increased flatulence. In none of these patients did enteral feeding have to be discontinued because of gastrointestinal side effects, whereas in four patients who were on a standard diet, enteral feeding had to be interrupted because of diarrhea (p < .05). Similar observations were made in patients receiving enteral supplementation. In both groups, the incidence of diarrhea decreased significantly with the soluble fiber diet compared with the standard diet (6 vs 15, p < .05). CONCLUSIONS: Enteral feeding with a formula supplemented with partially hydrolyzed guar gum reduces the incidence of diarrhea in patients receiving total enteral nutrition as well as in those receiving enteral supplementation, regardless of the cause of diarrhea. The increased hydrogen production and the significantly higher rate of flatulence are likely to result from fermentation of the soluble fiber in the colon, with concomitant production of short-chain fatty acids, which leads to increased absorption of short-chain fatty acids, sodium, and water by the colonocytes. This effect, together with the observed cholecystokinin-mediated decrease in colonic transit time with partially hydrolyzed guar gum, may explain the reduction in the incidence of diarrhea in this study.

Aged↗

Subcutaneously implanted enteral nutrition port.

BACKGROUND: Patients who have undergone esophagectomy with extensive lymph node dissection under thoracolapalotomy for advanced esophageal carcinomas frequently need long-term nutrition support because of their inadequate oral intake. We have used tube enterostomy feeding for these patients not only immediately after the operations but also at home to prevent the development of malnutrition. Patients who receive long-term tube enterostomy feeding often suffer from skin problems around the enteral nutrition catheters. Once the catheter is removed, the patient with anticipated malnutrition is subsequently unable to receive beneficial enteral nutrition. We have developed a new enteral access system that is placed subcutaneously. This subcutaneously implanted enteral nutrition port makes possible intermittent and long-term enteral nutrition support not only for the postoperative period but also for home care. METHODS: This system consists of the port (Infuse-a-Port, SMAP15 Snaplock Macro-Port Venous Access System; Strato Medical Co) and the enteral nutrition tube (Enteral Tube 8F, 75 cm; Zeon Co). This system was applied to seven patients who had undergone esophagectomy. The port was placed on the lower chest subcutaneously, and the catheter was placed through the gastric tube and duodenum up to the jejunum. After the operation, a 20-gauge port needle was placed, and enteral nutrition formula (Enterued; Termo Co) was started with the enteral nutrition pump. RESULTS: No complications (eg, infection of skin, obstruction of tube) were observed from the postoperative period through the home care stage. The observation period for this implanted system ranged from 2 to 12 months. The patients were able to avoid the malnutrition anticipated after the extensive operations and continued to receive nutrition support safely and effectively at home. CONCLUSION: This new nutrition support system is safe and efficient for patients who anticipate long-term enteral nutrition support. A subcutaneously implanted enteral nutrition port makes possible intermittent and long-term nutrition support without patient discomfort and inconvenience.

Enteral Nutrition↗

Distinct subpopulations of enteric neuronal progenitors defined by time of development, sympathoadrenal lineage markers and Mash-1-dependence.

Enteric and sympathetic neurons have previously been proposed to be lineally related. We present independent lines of evidence that suggest that enteric neurons arise from at least two lineages, only one of which expresses markers in common with sympathoadrenal cells. In the rat, sympathoadrenal markers are expressed, in the same order as in sympathetic neurons, by a subset of enteric neuronal precursors, which also transiently express tyrosine hydroxylase. If this precursor pool is eliminated in vitro by complement-mediated lysis, enteric neurons continue to develop; however, none of these are serotonergic. In the mouse, the Mash-1-/- mutation, which eliminates sympathetic neurons, also prevents the development of enteric serotonergic neurons. Other enteric neuronal populations, however, including those that contain calcitonin gene related peptide are present. Enteric tyrosine hydroxylase-containing cells co-express Mash-1 and are eliminated by the Mash-1-/- mutation, consistent with the idea that in the mouse, as in the rat, these precursors generate serotonergic neurons. Serotonergic neurons are generated early in development, while calcitonin gene related peptide-containing enteric neurons are generated much later. These data suggest that enteric neurons are derived from at least two progenitor lineages. One transiently expresses sympathoadrenal markers, is Mash-1-dependent, and generates early-born enteric neurons, some of which are serotonergic. The other is Mash-1-independent, does not express sympathoadrenal markers, and generates late-born enteric neurons, some of which contain calcitonin gene related peptide.

Animals↗

Enteral nutrition in clinical practice.

Enteral nutrition has, at long last, found its place in the modulation of disease. Because of its importance in terms of both anabolic and catabolic processes, today's clinician must have a working knowledge of the types of enteral formulations, their delivery and the therapeutic considerations (particularly concomitant medications) that impact on the safety and efficacy of enteral nutrition. The advantages and disadvantages of this therapeutic intervention must be carefully weighed by the clinician, in concert with sound medical principles. Despite the widespread belief that enteral nutrition is superior to parenteral nutrition in humans, data does suggest that there is little difference between the two. Also, associated costs of enteral nutrition in contrast to parenteral nutrition need to be reappraised based on more invasive enteral access and falling parenteral nutrition prices. Although the enteral route is presumed to be the best feeding modality, the clinician must be ever vigilant about the shortcomings of using the gut, especially in the setting of severe inflammation, stenosis or sepsis. The best feeding modality, then, must blend a knowledge of the patients' anatomy, physiology, and disease with considerations of enteral access, timing of delivery, complications, and a myriad of other therapeutic variables (to include concurrent medication administration) that impact on the enteral feeding regimen. This article reviews the basic principles of enteral nutrition in clinical practice. It describes nutritional assessment, routes of administration, selection of feeding formulas based on nutritional needs, interactions with medications, as well as possible complications of enteral feeding.

Cost-Benefit Analysis↗

Breed-related risk factors for canine parvovirus enteritis.

Case records of 305 dogs with canine parvovirus (CPV) enteritis, seen at the Veterinary Hospital of the University of Pennsylvania from July 1, 1981 to Aug 31, 1982, were selected on the basis of admitting diagnoses or signs of diarrhea and vomiting. The case records were subdivided into 3 diagnostic categories, based on final diagnoses and laboratory test results. There were 96 dogs with definite CPV enteritis, 139 with possible CPV enteritis, and 70 with unlikely CPV enteritis. These cases were then stratified by animal's age (less than or equal to 6 months or greater than 6 months) and specific hospital service (medicine or emergency). A control group was selected from all canine case records from the Veterinary Hospital of the University of Pennsylvania for conditions other than the criteria used in selecting the case group. Approximately 2 hospital patients were selected for each CPV enteritis case by frequency matching for hospital service and age. The proportion of dogs with definite CPV enteritis that had each of the clinical signs that were studied was greater than that of dogs in the other CPV enteritis diagnostic categories. The overall survival rate for dogs with definite CPV enteritis was 64.0%; survival was not associated with any given clinical sign of disease. Odds ratios (OR) for the risk of CPV enteritis were calculated for breeds with 3 or more dogs with definite CPV enteritis. The Doberman Pinschers (OR = 3.1), Rottweilers (OR = 6.0), and English Springer Spaniels (OR = 8.1) had a significantly increased risk of CPV enteritis.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗

Colonization of the bowel by the precursors of enteric glia: studies of normal and congenitally aganglionic mutant mice.

The terminal portion of the ls/ls mouse is congenitally aganglionic because the precursors of enteric neurons fail to enter this region. This animal was studied in order to gain insight into the origin of enteric glia and into the process by which the precursors of these cells colonize the gut. In control (CD-1) mice, immunoreactivity of the glial marker, glial fibrillary acidic protein, appeared for the first time in the fetal bowel at day E16 and, in adults, was much more intense within intraenteric neural elements than in nerves outside the bowel. Glial fibrillary acidic protein developed in tissue cultures of fetal intestine explanted before the protein appeared in situ, and before the bowel became innervated by extrinsic nerves; thus, the precursors of cells able to elaborate glial fibrillary acidic protein must have been present, but unrecognizable, in the original explants. This explant assay demonstrated that these glial precursors were present in all regions of the bowel of control mice, but not in the presumptive aganglionic bowel of ls/ls mice. The nerves (of extrinsic origin) in the aganglionic tissue of ls/ls mice showed a high level of immunoreactive glial fibrillary acidic protein; nevertheless, their ultrastructure was typical of peripheral nerve, not enteric plexus, and they contained Schwann cells, not enteric glia. These observations support the view that enteric glia are derived from the single wave of neural crest colonists that populates the enteric nervous system before the gut receives its extrinsic innervation. These glial precursors, like neuronal precursors, tend to be excluded from the presumptive aganglionic ls/ls bowel. In contrast, Schwann cells grow into the abnormal ls/ls gut with the extrinsic innervation. The enteric microenvironment appears to promote the expression of glial fibrillary acidic protein in both enteric glia and Schwann cells; however, even within the bowel, Schwann cells retain their characteristic morphology. It is thus probable that the normal enteric nervous system contains supporting cells of separate lineages, enteric glia and Schwann cells.

Animals↗

How preliminary data affect people's stated willingness to enter a hypothetical randomized controlled trial.

PURPOSE: To explore how preliminary trial data affect the general public's stated willingness to enter a randomized clinical trial. METHODS: We asked 165 prospective jurors to imagine that their physicians wanted them to enroll in a clinical trial. We then presented them with scenarios portraying preliminary trial results--for example, 9 out of 10 patients get better with drug A and 5 out of 10 get better with drug B--and asked after each scenario, whether they would choose to be part of the trial. We designed the scenarios to test how stated willingness to enter the trial would be influenced by: 1) the difference in effectiveness of the 2 treatments based on the patients enrolled thus far; and 2) by the chance that the difference in effectiveness was random (i.e., the P value). The subjects' willingness to enter the trial at various decision points was analyzed using logistic regression. RESULTS: Fewer subjects were willing to enter the trial as preliminary data indicated either an increasing difference in the effectiveness of the two treatments or an increasing statistical significance of that difference. For example 75% of subjects were willing to enter the research trial before any preliminary data were presented, but this number fell to 49% when subjects were presented with preliminary data showing that 9 out of 10 patients improved with one treatment and 5 out of 10 with the other. Multivariable logistic regression revealed that higher P values (odds ratio = 4.29; P < 0.001; 95% CI: 2.22-8.28) and smaller differences in effectiveness (odds ratio = 0.02; P < 0.001; 95% CI: 0.00-0.07) implicit in preliminary data presented to subjects made subjects less likely to agree to enter clinical trials. After adjustment for other relevant variables, male gender was associated with increased willingness to enter the trial. CONCLUSION: A subjects' willingness to enter the hypothetical trial was influenced by preliminary data. Fewer subjects were willing to enter the trial as the differences in benefit between 2 treatment groups increased. However, the majority of subjects were willing to enter the hypothetical trial even when preliminary evidence strongly favored one treatment over another. Given the importance of informed consent in entering patients in clinical trials, these results should be confirmed in actual trial settings.

Adult↗

Home parenteral and enteral nutrition in cancer patients.

The clinical outcomes of 2968 patients with active cancer receiving home nutrition support are described. Of these patients 1672 were receiving home parenteral nutrition and 1296 were receiving home enteral nutrition. The outcomes of these active cancer patients are compared to those of 123 radiation enteritis ("cured" cancer) and 480 Crohn's disease patients receiving home parenteral nutrition and 918 noncancer dysphagic patients receiving home enteral nutrition. This longitudinal clinical information was reported to the North American Home Parenteral and Enteral Nutrition Patient Registry between 1985 and 1990. Evidence indicates that the number of home parenteral and enteral nutrition patients has increased nationally by about 25% each year between 1989 and 1990. In a subsample of 37 home nutrition support programs that have consistently reported their data to the registry since 1985, more than 90% of their program growth was accounted for by new patients with active cancer. This is now the largest single diagnosis of patients starting home parenteral and enteral nutrition. The mean survival time of cancer patients is 6 months after starting home parenteral and enteral nutrition, but 25% live beyond a year and 20% resume full oral nutrition. Although most active cancer patients experience only partial rehabilitation, for those patients with longer survival, rehabilitation is more complete. The outcome is relatively better for children and for patients whose neoplasm is leukemia, lymphoma, small bowel, or liver. In comparison, 96% of home parenteral nutrition Crohn's patients, 80% of home parenteral nutrition radiation enteritis patients, and 60% of home enteral nutrition noncancer dysphagic patients survive at least 1 year. Adult active cancer home parenteral and enteral nutrition patients do not have a greater incidence of therapy-related readmissions than other patient groups, however, their overall rehospitalization rate is much more frequent. This article discusses factors that may have contributed to this growth in home nutrition support in active cancer patients. It attempts to clarify where this therapy is clearly justified and where more information is needed. It emphasizes some of the special issues that need to be addressed in treating these vulnerable patients.

Enteral Nutrition↗

Minimal enteral nutrition for promoting feeding tolerance and preventing morbidity in parenterally fed infants.

BACKGROUND: Because of concern that feedings may increase the risk of necrotizing enterocolitis, some high-risk infants have received prolonged periods of parenteral nutrition without enteral feedings. Providing minimal enteral feedings during this period of parenteral nutrition was developed as a strategy to enhance feeding tolerance and decrease time to reach full feedings. OBJECTIVES: For high-risk neonates receiving parenteral feedings, to assess the effect of minimal enteral nutrition (MEN) compared to no enteral nutrient intake on measures of feeding tolerance and neonatal outcome. SEARCH STRATEGY: Searches were performed of the Oxford Database of Perinatal Trials, MEDLINE, abstracts and conference proceedings, references from relevant publications in the English language, and studies identified by personal communication. SELECTION CRITERIA: Only randomized or quasi-randomized clinical trials were considered. Trials were included if they enrolled high-risk infants randomly assigned to receive minimal enteral feedings (defined as dilute or full strength feedings providing <= 25 kcal/kg/d for >= 5d) or no enteral nutrient intake (no feedings or water only). DATA COLLECTION AND ANALYSIS: The two reviewers reached consensus for inclusion of trials. Data regarding clinical outcomes were extracted and evaluated by the two reviewers independently of each other. Authors were contacted as needed and feasible to clarify or provide missing data. The specific data that were needed were requested in writing. MAIN RESULTS: Among infants given minimal enteral nutrition (MEN), there was an overall reduction in days to full enteral feeding, total days that feedings were held, and total hospital stay. There was no discernible effect on necrotizing enterocolitis. REVIEWER'S CONCLUSIONS: The evidence of benefit from MEN in these analyses is not convincing for a variety of reasons--the inherent difficulty of assessing enteral feedings in high-risk infants, the small size and methodologic limitations of the studies to date, unexplained heterogeneity with respect to some of the apparent benefits, the potential for bias to affect the findings in unblinded studies, and the unexcluded possibility that MEN might increase necrotizing enterocolitis. For these reasons, it is unclear whether MEN should be used in lieu of an equal period of time without enteral feedings.

Enteral Nutrition↗

Sacral neural crest cells colonise aganglionic hindgut in vivo but fail to compensate for lack of enteric ganglia.

The vagal neural crest is the origin of majority of neurons and glia that constitute the enteric nervous system, the intrinsic innervation of the gut. We have recently confirmed that a second region of the neuraxis, the sacral neural crest, also contributes to the enteric neuronal and glial populations of both the myenteric and the submucosal plexuses in the chick, caudal to the level of the umbilicus. Results from this previous study showed that sacral neural crest-derived precursors colonised the gut in significant numbers only 4 days after vagal-derived cells had completed their migration along the entire length of the gut. This observation suggested that in order to migrate into the hindgut and differentiate into enteric neurons and glia, sacral neural crest cells may require an interaction with vagal-derived cells or with factors or signalling molecules released by them or their progeny. This interdependence may also explain the inability of sacral neural crest cells to compensate for the lack of ganglia in the terminal hindgut of Hirschsprung's disease in humans or aganglionic megacolon in animals. To investigate the possible interrelationship between sacral and vagal-derived neural crest cells within the hindgut, we mapped the contribution of various vagal neural crest regions to the gut and then ablated appropriate sections of chick vagal neural crest to interrupt the migration of enteric nervous system precursor cells and thus create an aganglionic hindgut model in vivo. In these same ablated animals, the sacral level neural axis was removed and replaced with the equivalent tissue from quail embryos, thus enabling us to document, using cell-specific antibodies, the migration and differentiation of sacral crest-derived cells. Results showed that the vagal neural crest contributed precursors to the enteric nervous system in a regionalised manner. When quail-chick grafts of the neural tube adjacent to somites 1-2 were performed, neural crest cells were found in enteric ganglia throughout the preumbilical gut. These cells were most numerous in the esophagus, sparse in the preumbilical intestine, and absent in the postumbilical gut. When similar grafts adjacent to somites 3-5 or 3-6 were carried out, crest cells were found within enteric ganglia along the entire gut, from the proximal esophagus to the distal colon. Vagal neural crest grafts adjacent to somites 6-7 showed that crest cells from this region were distributed along a caudal-rostral gradient, being most numerous in the hindgut, less so in the intestine, and absent in the proximal foregut. In order to generate aneural hindgut in vivo, it was necessary to ablate the vagal neural crest adjacent to somites 3-6, prior to the 13-somite stage of development. When such ablations were performed, the hindgut, and in some cases also the cecal region, lacked enteric ganglionated plexuses. Sacral neural crest grafting in these vagal neural crest ablated chicks showed that sacral cells migrated along normal, previously described hindgut pathways and formed isolated ganglia containing neurons and glia at the levels of the presumptive myenteric and submucosal plexuses. Comparison between vagal neural crest-ablated and nonablated control animals demonstrated that sacral-derived cells migrated into the gut and differentiated into neurons in higher numbers in the ablated animals than in controls. However, the increase in numbers of sacral neural crest-derived neurons within the hindgut did not appear to be sufficiently high to compensate for the lack of vagal-derived enteric plexuses, as ganglia containing sacral neural crest-derived neurons and glia were small and infrequent. Our findings suggest that the neuronal fate of a relatively fixed subpopulation of sacral neural crest cells may be predetermined as these cells neither require the presence of vagal-derived enteric precursors in order to colonise the hindgut, nor are capable of dramatically altering their proliferation or d

Animals↗

The effect of continuous enteral nutrition on gastric acidity in humans.

The effect of continuous intraduodenal enteral nutrition on gastric pH was compared with the effects of fasting and of parenteral and standard nutrition control regimens containing equal amounts of carbohydrate, protein, and lipid. Eleven healthy volunteers underwent four 24-hour intragastric pH-metry studies; serum glucose, calcium, immunoreactive insulin and gastrin levels were determined during fasting and enteral and parenteral regimens. Median 24-hour gastric pH during enteral nutrition (group median pH 1.4) was lower than during parenteral nutrition (pH 1.9; P = 0.0039 vs. enteral) but was not different from fasting (pH 1.4) or standard nutrition (pH 1.6) values. Median 24-hour serum glucose levels during enteral nutrition (group median, 4.8 mmol/L) were higher than during fasting (4.0 mmol/L; P = 0.00098 vs. enteral) and lower than during parenteral nutrition (5.3 mmol/L; P = 0.0039 vs. enteral). Median 24-hour serum insulin levels during enteral nutrition (group median, 22.9 mU/L) were higher than during fasting (group median, 9.2 mU/L; P = 0.00098 vs. enteral) but similar to levels during parenteral nutrition (23.3 mU/L). Neither median 24-hour gastrin levels nor calcium levels were affected by any nutrition regimen. Thus, continuous enteral nutrition produces gastric pH values similar to those seen with fasting or standard nutrition, suggesting that, under most physiological conditions, gastric acidity is subject to close feedback control. Parenteral nutrition increases gastric pH, suggesting that systemic nutrients may influence this feedback mechanism.

Adult↗

Variation in enteral nutrition delivery in mechanically ventilated patients.

OBJECTIVE: We determined the variability in enteral feeding practices in mechanically ventilated patients in four adult intensive care units of a tertiary-care, referral hospital. METHODS: Patients who had been mechanically ventilated for at least 48 h and received enteral nutrition were prospectively followed. RESULTS: Fifty-five of 101 consecutive mechanically ventilated patients received enteral nutrition; in 93% of patients, feedings were infused into the stomach. Patients who were cared for in the medical intensive care unit, where a nutritional protocol was operational, received enteral nutrition earlier in their ventilatory course (P=0.004) and feedings were advanced to target rates faster (P=0.043) than those who received care in other units. The number (P=0.243) and duration (P=0.668) of interruptions in feeding did not differ by patient location. On average, patients received only 50% to 70% of their targeted caloric goals during the first 6 days of enteral nutrition. Most feeding discontinuations (41%) were secondary to procedures. Gastrointestinal intolerances, including vomiting, aspiration, abdominal distention, and increased gastric residuals, were uncommon despite allowing gastric residuals up to 300 mL. CONCLUSIONS: The practice of providing enteral feeds to mechanically ventilated patients varies widely, even within one hospital. A protocol enhanced early initiation of enteral feeds and advancement to target feeding rates but did not alter the number or duration of interruptions in enteral feedings. Procedures represented the most common reason for stopping enteral feeds, and gastrointestinal intolerances (vomiting, aspiration, and increased gastric residuals) caused few feeding interruptions. The gastric route was safe and well tolerated for early enteral feeding in most mechanically ventilated patients.

Adolescent↗

Enteral nutrition prolongs delayed gastric emptying in patients after Whipple resection.

BACKGROUND: Delayed gastric emptying is one of the most frequent postoperative complications after Whipple resection. In the present study we evaluated the role of enteral nutrition in the development of delayed gastric emptying after Whipple resection. PATIENTS AND METHODS: Between January 1996 and June 1998, 64 patients (30 female, 34 male) underwent a classic (n = 27) or pylorus-preserving (n = 37) Whipple resection. Two patients were excluded; 30 patients received enteral and 32 patients received no-enteral nutrition. RESULTS: Delayed gastric emptying occurred significantly more in patients with enteral (17 of 30, 57%) than in patients with no-enteral nutrition (5 of 32, 16%) (P <0.01). Consequently, patients in the enteral nutrition group had a nasogastric tube for a significantly (P<0.01) longer period and had a significantly (P<0.01) longer hospital stay than patients in the no-enteral nutrition group. There were no differences in the frequency of occurrence of other postoperative complications between patients with enteral and no-enteral nutrition. CONCLUSION: In patients undergoing a Whipple resection, enteral nutrition is associated with a higher frequency of delayed gastric emptying with no advantages regarding other postoperative complications and should therefore be restricted to specific indications.

Adult↗

Postoperative enteral versus parenteral nutrition in malnourished patients with gastrointestinal cancer: a randomised multicentre trial.

BACKGROUND: Although current opinion favours the use of enteral over parenteral nutrition, the clinical benefits of early postoperative nutrition in patients undergoing elective surgery have never been clearly shown. We aimed to test the hypothesis that postoperative enteral nutrition is better (fewer postoperative complications) than parenteral nutrition containing similar energy and nitrogen amounts (112 kJ kg(-1) day(-1) and 1.4 g aminoacid kg(-1) day(-1)). METHODS: We did a randomised multicentre clinical trial in patients with gastrointestinal cancer who were malnourished and candidates for major elective surgery. 159 patients were assigned to enteral nutrition and 158 to parenteral nutrition. The primary endpoint was the occurrence of postoperative complications, and secondary endpoints were length of postoperative hospital stay, adverse effects, and treatment crossover. Analysis was by intention to treat. FINDINGS: Postoperative complications occurred in 54 (34%) patients fed enterally versus 78 (49%) fed parenterally (relative risk 0.69, 95% CI 0.53-0.90, p=0.005). Length of postoperative stay was 13.4 days and 15.0 days in the enteral nutrition and parenteral nutrition groups, respectively (p=0.009). Adverse effects occurred in 56 (35%) patients fed enterally versus 22 (14%) patients fed parenterally (2.50, 1.61-3.86, p<0.0001). 14 (9%) patients on enteral nutrition had to switch to parenteral nutrition, whereas none of those fed parenterally crossed over to enteral feeding. INTERPRETATION: We conclude that early enteral nutrition significantly reduces the complication rate and duration of postoperative stay compared with parenteral nutrition, although parenteral nutrition is better tolerated than enteral nutrition.

Comorbidity↗

Enteral tube feeding in a cohort of chronic hemodialysis patients.

Malnutrition affects up to half of all chronic dialysis patients and is an important predictor of mortality, but the efficacy of interventions designed to improve the nutritional status of dialysis patients has been poorly studied. Specifically, although enteral tube feeding is often cited as an important option in the treatment of malnourished dialysis patients, there are few studies examining the effectiveness and complications of enteral tube feedings in adults on dialysis. We performed a retrospective analysis of a small cohort (n = 10) of chronic hemodialysis patients who received enteral tube feeding as all or part of their nutrition between January 1 and May 1, 1999, with follow-up through May 1, 2000, to assess the efficacy and complications of enteral tube feeding. Six patients received feeding via a peritoneoscopically placed (PEG) tube, 3 via nasogastric (NG) tube, and 1 patient was switched from PEG to NG feeding after an exit site infection developed at her PEG site. Seven patients received enteral feeding because of swallowing difficulties occurring after a cerebrovascular accident. Four patients were fed via enteral tube temporarily (</=4 months); the range of time on enteral feeding was 0.5 to 36 months. Five patients died by study end; only 1 recovered and no longer required enteral feeding. Patients were well dialyzed (median urea reduction rate, 73%). A significant improvement in serum albumin was seen (initial median albumin, 2.8, versus final median albumin, 3.4 g/dL, P =.04). Hypophosphatemia occurred in 8 of the 10 patients, and the nadir median phosphorus level was 1.95 mg/dL. One patient died as a result of an infected PEG. We conclude that enteral tube feeding is an important tool in the treatment of malnourished chronic hemodialysis patients and deserves formal study. Hypophosphatemia commonly occurs, and phosphorus levels should therefore be followed closely when initiating tube feedings in hemodialysis patients. In some cases, a nonrenal enteral formula may be useful for avoiding hypophosphatemia in these patients.

Adult↗

Minimal enteral nutrient requirements for intestinal growth in neonatal piglets: how much is enough?

BACKGROUND: Parenterally nourished preterm infants commonly receive minimal enteral feedings, the aim being to enhance intestinal function. Whether this regimen increases intestinal growth has not been established. OBJECTIVE: Our objective was to determine the minimal enteral nutrient intakes necessary to stimulate and to normalize neonatal intestinal growth. METHODS: Intestinal growth and cell proliferation were quantified in neonatal pigs given equal amounts of an elemental nutrient solution for 7 d. Different groups (n = 5-7 per group) received 0%, 10%, 20%, 40%, 60%, 80%, or 100% of total nutrient intake enterally, with the remainder given parenterally. RESULTS: In the jejunum, wet weight, protein mass, and villus height were significantly greater at enteral intakes >40%. Stimulation of ileal protein mass required a higher enteral intake (60%). In both segments, abrupt increases in DNA mass, crypt depth, ornithine decarboxylase activity, and crypt cells in S-phase occurred between enteral intakes of 40% and 60%. Circulating concentrations of glucagon-like peptide-2 and peptide YY, but not gastrin, increased significantly between enteral intakes of 40% and 60% and closely paralleled indexes of cell proliferation. CONCLUSIONS: The minimal enteral nutrient intake necessary to increase mucosal mass was 40% of total nutrient intake, whereas 60% enteral nutrition was necessary to sustain normal mucosal proliferation and growth. Our results imply that providing <40% of the total nutrient intake enterally does not have significant intestinal trophic effects.

Animals↗