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PubMed1993

Effect of FK1052, a potent 5-hydroxytryptamine3 and 5-hydroxytryptamine4 receptor dual antagonist, on colonic function in vivo.

5-Hydroxytryptamine (5-HT) is an important neurotransmitter and hormone/paracrine agent mediating various enteric functions. Its precise physiological and pathophysiological role remains unclear. This study investigated the effects of 5-HT on colonic function and the effects of the newly developed 5-HT3 and 5-HT4 receptor antagonist, FK1052, on colonic responses to 5-HT or stress stimulus in vivo. In conscious rats, both 5-HT and 5-methoxytryptamine significantly increased fecal pellet output and accelerated colonic transit. In contrast, the effect of 2-methyl-5-HT was slight. Although ondansetron and granisetron slightly reduced 5-HT (1 mg/kg s.c.) stimulated colonic transit, FK1052 [(+)-8,9-dihydro-10-methyl-7-[(5-methyl-4-imidazolyl)methyl]pyrido- [1,2-a]-indole-6(7H)-one hydrochloride], at 0.1 mg/kg p.o., inhibited completely the increases in the colonic transit. Furthermore, FK1052, ondansetron and granisetron significantly depressed the increase in fecal pellet output caused by wrap-restraint stress, with ED50 values of 0.21, 3.0 and 1.1 mg/kg p.o., respectively. Intraperitoneal administration of 5-HT and 5-methoxytryptamine, but not 2-methyl-5-HT, produced a dose-related increase in the incidence of diarrhea in fasted mice. 5-HT (0.32 mg/kg i.p.)-induced diarrhea was also inhibited by FK1052, ondansetron and granisetron, with ED50 values of 0.09, 2.3 and 0.88 mg/kg p.o., respectively. These findings suggest that 5-HT3 and 5-HT4 receptors may have an important role in colonic function and FK1052 may have therapeutic potential in the treatment of gastrointestinal dysfunction such as irritable bowel syndrome.

Animals↗

PubMed1996

American trypanosomiasis (Chagas' disease).

Gastrointestinal dysfunction is a major problem for many patients with chronic Chagas' disease, as are cardiac dysrhythmias and cardiomyopathy. The underlying anatomic abnormality in these patients is a denervation of the gastrointestinal tract. This process of nerve destruction usually develops insidiously over many years, and it is highly variable in terms of its extent in individual patients as well as in the segments of the gastrointestinal tract that are most affected. Megaesophagus is the most common manifestation of gastrointestinal Chagas disease, and mechanical dilation of the esophageal sphincter or surgery in advanced cases usually give satisfactory relief of symptoms. Megacolon, particularly of the sigmoid segment, is also common in patients with chronic T. cruzi infections, and its presence can be complicated by fecal impaction or sigmoid volvulus. Patients with advanced megacolon who have resections of the sigmoid colon and most of the rectum generally do well postoperatively.

Chagas Cardiomyopathy↗

PubMed1996

Endotoxin induces biphasic alterations in small intestinal myoelectric activity in fasted newborn piglets.

Previous studies have shown that i.v. endotoxin infusion causes gastrointestinal dysfunction and intestinal injury in piglets. The aim of this study was to investigate the effects of endotoxin on intestinal myoelectric activity in newborn swine and to correlate this with gastrointestinal and hemodynamic events. Three pairs of electrodes were implanted in the jejunal wall of piglets, and after recovery, intestinal myoelectric activity was continuously recorded in the conscious, fasted condition. The intestinal myoelectric activity on the control day showed regular, repeating migrating myoelectric complex (MMC) cycles, each of which was composed of the classic phases I, II, and III. Mean cycle duration was 67.0 +/- 18.7 min (+/- SD), and phase III comprised 9.1 +/- 2.2% of each cycle. On the next day, infusion of 30 micrograms/kg endotoxin caused an initial, prolonged quiescent period and delayed the appearance of the first postendotoxin phase III complex. After the quiescent period, there was a period of irregular spiking activity followed by several shortened MMC cycles (47.9 +/- 22.7 min, p < 0.01 versus control) with a prolongation of the percentage of time spent in phase III (15.4 +/- 11.3%, p < 0.01). Endotoxin thus produced biphasic alterations in intestinal myoelectric activity characterized by an initial quiescence followed by increased gastrointestinal smooth muscle activity. Animals developed diarrhea, hypotension, and tachycardia about 1 h after endotoxin infusion in temporal association with increased spiking activity and MMC cycling. These studies are the first to show this biphasic response to endotoxin.

Activity Cycles↗

PubMedDate not supplied

Nutritional management in cystic fibrosis--an alternative perspective in gastrointestinal function.

The gastrointestinal problems in cystic fibrosis (CF) may limit energy and nutrient availability and also cause symptoms such as abdominal pain and disturbed bowel habit which may further suppress appetite or alter the diet. Taken together this may lead to an inadequate supply of energy and nutrients to meet the nutritional requirements of the individual resulting in restricted growth or weight loss. A failure to optimize the digestive and absorptive capacity of the gastrointestinal tract places greater emphasis upon nutritional management by food intake alone. Practitioners need to focus more on gastrointestinal dysfunction in CF and its impact upon food intake in order to improve the efficacy of nutritional management. Refined stable isotopic tracers allow further exploration of the pathophysiology of the gastrointestinal tract in terms of nutrient availability. In clinical practice, a closer assessment of gastrointestinal function is supported by the use of simple, noninvasive tools which, both objectively and systematically, characterize those patients who have problems.

Cystic Fibrosis↗

PubMed2001

Parenteral nutrition support after bone marrow transplantation: comparison of total and partial parenteral nutrition during the early posttransplantation period.

OBJECTIVE: Bone marrow transplantation (BMT) usually is indicated if the patient's malignant disease involves the marrow or if hazard to the normal marrow is the limiting factor in the aggressive treatment of disease. The success of BMT depends on a complete team with all the resources needed to ensure optimal results. Aggressive nutrition support after BMT is very important. Adequate parenteral nutrition, total (TPN) or partial, followed by enteral nutrition according to the patient's gastrointestinal function is the important principle. METHODS: Between 1996 and 2000, 60 patients, 46 male and 14 female, received BMT in Chang Gung Memorial Hospital. Their ages ranged from 6 to 54 y. Standard TPN was used in 40 patients after BMT, and partial parenteral nutrition was used in the remaining 20 patients. TPN was enriched with branched-chain amino acids (BCAA) when the patient's liver functions were impaired, and cyclic TPN was shifted when the patient's liver functions persistently deteriorated. RESULTS: Most patients improved their nutrition status and increased their body weights, especially those receiving TPN. The patients receiving partial parenteral nutrition decreased their visceral proteins significantly during the course of parenteral nutrition. The BCAA-TPN can maintain a patient's visceral protein better than standard TPN. Only two patients expired because of graft rejection and sepsis; their body weights and nutrition status showed deterioration despite aggressive nutrition support. CONCLUSIONS: We conclude that the nutrition support for patients with BMT is related to the success of marrow transplantation. Parenteral nutrition support, especially with TPN, is important because of frequent gastrointestinal dysfunction during the posttransplantational period, and it is better at maintaining the nutrition status and body weights of patients after BMT. An oral diet can be resumed after the patient's gastrointestinal function has improved and it can be tolerated.

Adolescent↗

PubMed1976

The pancreatic involvement in disseminated "collagen" disorders. Studies of pancreatic secretion in patients with scleroderma and Sjögren's "disease".

In this study of 66 patients with Sjögren's syndrome and/or scleroderma abnormal pancreatic secretory patterns were observed in 43 patients, 17 of 23 with Sjögren's and 19 of 31 with scleroderma. Pancreatic insufficiency was often associated with depressed gastric secretion and/or abnormal gallbladder function. While in both disorders digestive complaints are attributable to one or more dysfunctions, the pathogenetic factors in scleroderma appear to be more varied and require careful investigation for complete elucidation. Antibiotics, antimetabolites and steroid therapies are also additional causal factors involved in the initiation of gastrointestinal dysfunction and pathology.

Gallbladder↗

PubMed2001

Myenteric plexus of obese diabetic mice (an animal model of human type 2 diabetes).

The myenteric plexus of the gastrointestinal tract was investigated in the obese diabetic mouse, an animal model of human type 2 diabetes. Sections were immunostained by the avidin-biotin complex method, using a general nerve marker, protein gene product 9.5 (PGP 9.5), as well as antibodies to several important neurotransmitters. Computerized image analysis was used for quantification. When diabetic mice were compared with controls, no difference was found in the density of PGP 9.5-immunoreactive (IR) nerve fibres in antrum, duodenum or colon. In antrum and duodenum, diabetic mice showed a decreased number of vasoactive intestinal peptide (VIP)-IR neurons in myenteric ganglia as well a decreased relative volume density in myenteric plexus (though not significantly in antrum, p=0.073). No difference was found regarding VIP-IR nerves in colon. The volume density of nitric oxide synthase (NOS)-IR nerve fibres was decreased in antrum and duodenum of diabetic mice, whereas no difference was found in colon. The density of galanin-IR nerve fibres was decreased in duodenum. Whereas neuropeptide Y (NPY)- and vesicular acetylcholine transporter (VAChT)-IR nerve fibres was increased in density in colon of diabetic mice, no difference was found in antrum and duodenum. Regarding substance P, there was no difference between diabetic and control mice in antrum, duodenum or colon. The present study shows that gut innervation is affected in this animal model of human type 2 diabetes. It is possible that the present findings may have some relevance for the gastrointestinal dysfunctions seen in patients with type 2 diabetes.

Animals↗

PubMed2005

Novel and established markers of cobalamin deficiency: complementary or exclusive diagnostic strategies.

New developments in diagnostic markers and a better understanding of the limitations of traditional diagnostic strategies have allowed diagnosis of earlier stages and atypical forms of cobalamin deficiency. Still, there are no generally accepted guidelines for the definition, diagnosis, treatment, and follow-up of cobalamin deficiency. The new trend toward defining cobalamin deficiency purely on the basis of biochemical test outcomes in the absence of overt clinical signs and symptoms could, however, be problematic and may result in overdiagnosis and overtreatment. Use of metabolic markers for the assessment of cobalamin deficiency allows the demonstration of tissue deficiency, but the establishment of the cause of deficiency should also be part of the diagnostic approach. Four groups of diagnostic tests are currently available and these include total cobalamin and cobalamin fractions (such as holo-transcobalamin), tests of gastrointestinal dysfunction, tests of metabolic function, and different gene tests. Among the available tests, only homocysteine, methylmalonic acid, holo-transcobalamin, and possibly methylcitric acid are considered to be useful in clinical practice to add to cobalamin. Gastrointestinal function tests may identify the cause of cobalamin deficiency, whereas the diagnostic usefulness of genetic testing needs to be evaluated. This article provides an overview of recent developments and a reappraisal of novel and established diagnostic markers for cobalamin deficiency.

Biomarkers↗

PubMed2001

Synthesis and evaluation of novel 2-oxo-1,2-dihydro-3-quinolinecarboxamide derivatives as potent and selective serotonin 5-HT4 receptor agonists.

A series of 8'-substituted N-(endo-8-azabicyclo[3.2.1]oct-3-yl)-1-isopropyl-2-oxo-1,2-dihydro-3-quinolinecarboxamides were synthesized. The 5-HT4 receptor agonistic activity was evaluated using the isolated guinea pig ileum preparation. Of the compounds synthesized, N-(endo-8-(3-hydroxypropyl)-8-azabicyclo[3.2.1]oct-3-yl)-1-isopropyl-2-oxo-1,2-dihydro-3-quinolinecarboxamide (15a, TS-951) exhibited the most potent serotonin 5-HT4 receptor agonistic activity. This compound had a high affinity for the serotonin 5-HT4 receptor although it had no affinities for other broad spectrum receptors. Furthermore, it remarkably enhanced gastrointestinal motility in conscious fed dogs without unfavorable effects that non-selective serotonin 5-HT4 receptor agonist has. TS-951 may be useful in improving gastrointestinal dysfunction.

Amides↗

PubMed1993

Simian immunodeficiency virus infection of the gastrointestinal tract of rhesus macaques. Functional, pathological, and morphological changes.

Gastrointestinal dysfunction and wasting are frequent complications of human immunodeficiency virus (HIV) infection. Nutrient malabsorption, decreased digestive enzymes and HIV transcripts have been documented in jejunal mucosa of HIV-infected patients; however, the pathogenesis of this enteropathy is not understood. Rhesus macaques infected with simian immunodeficiency virus (SIV) also exhibit diarrhea and weight loss; therefore, we investigated the use of this animal model to study HIV-associated intestinal abnormalities. A retrospective study of intestinal tissues from 15 SIV-infected macaques was performed to determine the cellular targets of the virus and examine the effect of SIV infection on jejunal mucosal morphology and function. Pathological and morphological changes included inflammatory infiltrates, villus blunting, and crypt hyperplasia. SIV-infected cells were detected by in situ hybridization in stomach, duodenum, jejunum, ileum, cecum, and colon. Using combined immunohistochemistry and in situ hybridization, the cellular targets were identified as T lymphocytes and macrophages. The jejunum of SIV-infected animals had depressed digestive enzyme activities and abnormal morphometry, suggestive of a maturational defect in proliferating epithelial cells. Our results suggest that SIV infection of mononuclear inflammatory cells in intestinal mucosa may alter development and function of absorptive epithelial cells and lead to jejunal dysfunction.

Animals↗

PubMed2002

Antibody-mediated gastrointestinal dysmotility in scleroderma.

BACKGROUND & AIMS: Defects in enteric excitatory neurotransmission have been proposed to underlie the gastrointestinal dysmotility associated with scleroderma (systemic sclerosis). This study investigated whether patients with scleroderma produce antibodies that inhibit M3-muscarinic or neurokinin receptor-mediated intestinal contractions, either directly or via an effect on L-type voltage-gated calcium channels (VGCCs). METHODS: Responses of mouse colon longitudinal muscle to stimulation by the muscarinic agonist carbachol (1-300 micromol/L) and neurokinin-1 and -2 receptor agonists were measured in the absence and presence of serum (2%) or immunoglobulin G (IgG) (0.3-1.0 mg/mL) from patients with scleroderma, those with other autoimmune disorders, and healthy controls. The role of L-type VGCCs in carbachol- and tachykinin-evoked contractions was assessed using nicardipine. RESULTS: M3-muscarinic receptor-mediated contractions were inhibited by Ig fractions from 7 of 9 patients with scleroderma (limited and diffuse forms), 4 of 4 patients with primary Sjögren's syndrome, and 3 of 3 patients with secondary Sjögren's syndrome. Ig fractions from healthy controls did not inhibit the M3-muscarinic receptor-mediated contractions. Inhibition by Ig was concentration-dependent; a maximum inhibition of approximately 40% occurred at 0.6 mg/mL IgG. Both M3-muscarinic and neurokinin receptor-mediated contractions were L-type VGCC dependent. Patient sera had no effect on responses to neurokinin receptor stimulation, demonstrating the lack of antibodies inhibiting L-type VGCCs. CONCLUSIONS: Functional antibodies specifically inhibiting M3-muscarinic receptor-mediated enteric cholinergic neurotransmission may provide a pathogenic mechanism for the gastrointestinal dysfunction seen in patients with scleroderma.

Aged↗

PubMed1998

Exposure to ionizing radiation modifies circulating gastrin levels and gastrointestinal endocrine cell densities in the rat.

PURPOSE: Gastrointestinal functions, controlled partly by gut peptides, are disturbed by ionizing radiation exposure. The effect of whole-body irradiation on circulating gastrin levels, densities of gastrointestinal endocrine cells and gastric acid secretion was investigated. MATERIALS AND METHODS: Rats were exposed to 2 or 6 Gy gamma-radiation. They were killed 3 or 7 days later and compared with shams. Plasma gastrin and basal acid output were measured. Endocrine cells were identified by argyrophilia or immunohistochemistry and their densities estimated. RESULTS: Radiation exposure significantly increased gastrinaemia and gastric acid output at the times studied (p<0.05-p<0.001). Endocrine cells displayed different sensitivities to irradiation. In the gastric mucosa, a 6 Gy dose induced a decrease in fundic argyrophil cell, antral gastrin and somatostatin cell densities, always accentuated 7 days after irradiation, while in the intestinal mucosa it induced an increase, with highest values often at 7 days post-irradiation (p<0.01-p<0.001). This was true for neurotensin cells in the jejunum and ileum, substance P cells in ileum and enteroglucagon cells in the descending colon. CONCLUSIONS: Whole-body irradiation in rats significantly alters plasma gastrin levels, and several gut endocrine cell densities. This has repercussions on hormonal function, such as that exerted on acid secretion, and may explain gastrointestinal dysfunction observed following radiation exposure.

Animals↗

PubMed2002

Endothelin A-receptor blockade in experimental diabetes improves glucose balance and gastrointestinal function.

Secondary complications of diabetes mellitus often involve gastrointestinal dysfunction. In the experimental Goto Kakizaki rat, a model of Type II diabetes, hyperglycaemia and reduced glucose clearance is associated with elevated plasma endothelin (ET)-1 levels and selective decreases in nitric oxide synthase in circular muscle, longitudinal muscle and neuronal elements of the gastrointestinal tract. Functionally, this is accompanied by decreased nitrergic relaxatory responses of jejunal longitudinal muscle to tetrodotoxin-sensitive electrical field stimulation. Long-term treatment with a selective ET A-type receptor antagonist, markedly reduced hyperglycaemia and restored plasma glucose clearance rates towards normal. This was associated with a restoration of N(G)-nitro-L-arginine methyl ester-sensitive relaxatory responses of jejunal longitudinal muscle to electrical field stimulation. The results indicate that beneficial effects of ETA receptor blockade on gastrointestinal function may result from an improvement in insulin sensitivity with concomitant reduction of the severity of hyperglycaemia. ETA receptor blockade may represent a new therapeutic principle for improving glucose tolerance in Type II diabetes and could be beneficial in alleviating or preventing hyperglycaemia-related secondary complications in this condition.

Animals↗

PubMed1997

Intractable diarrhoea associated with secondary amyloidosis in rheumatoid arthritis.

OBJECTIVE: To examine the clinical characteristics of intractable diarrhoea associated with secondary amyloidosis in rheumatoid arthritis (RA). METHODS: Of 179 RA patients with biopsy confirmed secondary amyloidosis, 24 cases (23 women and one man) with intractable diarrhoea lasting for more than one month were retrospectively evaluated. RESULTS: The mean (SD) duration of diarrhoea was 87 (64) days. Prodromal symptoms of gastrointestinal dysfunction (n = 21) and impaired peristalsis (n = 16) were observed. Laboratory data showed hypoproteinaemia (4.7 (0.85) g/dl) caused by malabsorption or protein loss and high values of C reactive protein (17.0 (9.3) mg/dl). Recurrence of intractable diarrhoea (n = 4) and transition from intractable diarrhoea to other gastrointestinal problems of amyloidosis (ischaemic colitis (n = 2) and intestinal pseudo-obstruction (n = 4)) were observed. In 19 patients (25 episodes) the duration of intravenous hyperalimentation at remission (18 episodes) was 68 (52) days. Corticosteroid pulse therapy was administered to 10 patients (11 times) and the time elapsed from the end of corticosteroid pulse therapy to the end of diarrhoea was 18 (14) days. One and five year survival rates after the onset of intractable diarrhoea were 73.4% and 38.9%. Seven of 13 patients (54%) had died as a result of infectious diseases. CONCLUSION: Intractable diarrhoea associated with secondary amyloidosis in RA is a serious clinical entity and the prognosis is poor. Although it is assumed that intravenous hyperalimentation treatment and corticosteroid pulse therapy are favourable regimens for intractable diarrhoea, the patients should be monitored for possible infectious complications.

Adult↗

PubMed1999

Gastrointestinal abnormalities in children with autistic disorder.

OBJECTIVES: Our aim was to evaluate the structure and function of the upper gastrointestinal tract in a group of patients with autism who had gastrointestinal symptoms. STUDY DESIGN: Thirty-six children (age: 5.7 +/- 2 years, mean +/- SD) with autistic disorder underwent upper gastrointestinal endoscopy with biopsies, intestinal and pancreatic enzyme analyses, and bacterial and fungal cultures. The most frequent gastrointestinal complaints were chronic diarrhea, gaseousness, and abdominal discomfort and distension. RESULTS: Histologic examination in these 36 children revealed grade I or II reflux esophagitis in 25 (69.4%), chronic gastritis in 15, and chronic duodenitis in 24. The number of Paneth's cells in the duodenal crypts was significantly elevated in autistic children compared with non-autistic control subjects. Low intestinal carbohydrate digestive enzyme activity was reported in 21 children (58.3%), although there was no abnormality found in pancreatic function. Seventy-five percent of the autistic children (27/36) had an increased pancreatico-biliary fluid output after intravenous secretin administration. Nineteen of the 21 patients with diarrhea had significantly higher fluid output than those without diarrhea. CONCLUSIONS: Unrecognized gastrointestinal disorders, especially reflux esophagitis and disaccharide malabsorption, may contribute to the behavioral problems of the non-verbal autistic patients. The observed increase in pancreatico-biliary secretion after secretin infusion suggests an upregulation of secretin receptors in the pancreas and liver. Further studies are required to determine the possible association between the brain and gastrointestinal dysfunctions in children with autistic disorder.

Autistic Disorder↗

PubMedDate not supplied

[Duodenal stenosis secondary to tuberculosis. Case presentation and review of the literature].

Infections caused by tuberculosis reached epidemic dimensions in the middle of the last century. Unexpectedly in the present, a growing number of new cases has been detected each year, reaching alarming figures, according to the World Health Organization. One of the most infrequent manifestations is intestinal tuberculosis, specially the one that affects duodenum and as a complication, stenosis. Its diagnosis is difficult because of similarity of this pathology with other gastrointestinal dysfunctions. Medical and surgical treatments have been proposed to afford a solution to this pathology. Due to its rareness, and the diagnostic difficulty and controversy in its treatment, we present the case of a patient diagnosed with duodenal stenosis caused by tuberculosis who was treated at the Gastrointestinal Surgery Service in our hospital.

Adult↗

PubMedDate not supplied

How age changes the content of neuroendocrine peptides in the murine gastrointestinal tract.

BACKGROUND: Motility disorders in the gastrointestinal tract increase with ageing, and colorectal carcinoma is a tumor of the middle-aged and elderly. Gastrointestinal secretion, absorption, motility, cell proliferation, local immune defense and blood flow are all regulated by the neuroendocrine peptides. It is conceivable that gastrointestinal disorders at an advanced age may be accompanied by changes in this regulatory system. OBJECTIVE: To ascertain possible age-related changes in neuroendocrine peptides in a rodent animal model. METHODS: The concentrations of various neuroendocrine peptides were determined by radioimmunoassays in tissue extracts from the antrum, duodenum and colon of mice in four different age groups: 1, 3, 12 and 24 months. The neuroendocrine peptides investigated were: secretin, gastric inhibitory polypeptide (GIP), gastrin, motilin, peptide YY (PYY), somatostatin, vasoactive intestinal polypeptide (VIP), substance P, neuropeptide Y (NPY), galanin and neurotensin. RESULTS: Antrum: Concentrations of somatostatin, VIP and substance P decreased significantly in 1-month-old mice (but that of neurotensin increased) compared with 3-month-old mice. In 12-month-old and 24-month-old mice, concentrations of gastrin, somatostatin, VIP, substance P, NPY, galanin and neurotensin all decreased vis-à-vis 3-month-old mice. Duodenum: Whereas the levels of secretin, GIP and neurotensin increased, those of gastrin, motilin, somatostatin, VIP, substance P, NPY and galanin decreased in 1-month-old mice vis-à-vis 3-month-old mice. In both 12-month-old and 24-month-old mice, the concentrations of secretin and GIP increased, compared with those of 3-month-old mice. The levels of gastrin, motilin, somatostatin, VIP, NPY and galanin decreased in both 12-month-old and 24-month-old mice vis-à-vis 3-month-old mice. Substance P and neurotensin concentrations decreased in 12-month-old mice, but not in 24-month-old mice. Colon: In 1-month-old mice the levels of PYY, somatostatin, VIP, substance P and galanin decreased vis-à-vis 3-month-old mice. In 12-month-old mice, the concentrations of PYY, somatostatin, VIP, NPY, galanin and neurotensin decreased compared with those in 3-month-old mice. In 24-month-old mice, the VIP level decreased, whereas the substance P level increased. CONCLUSION: The changes in neuroendocrine peptides observed in the gastrointestinal tract of this murine animal model could be of some relevance for the increased gastrointestinal dysfunction in the elderly human. They may also be involved in the development of colorectal cancer.

Aging↗

PubMed2003

Tube feeding in mechanically ventilated critically ill patients: a prospective clinical audit.

BACKGROUND: When and whether early enteral nutrition (EN) benefits critically ill patients is debatable. This prospective clinical audit aimed to evaluate the feasibility of an early EN protocol and to identify factors that may hinder EN delivery in critically ill patients. METHODS: Thirty-six medical patients with severe respiratory failure under invasive ventilation and scheduled to receive early EN, with a length of ICU stay >72 hours, were included. As asserted by the Society of Critical Care Medicine, 8% of patients were priority 1, 72% priority 2, and 20% priority 3 for intensive therapeutic and vital support interventions. RESULTS: Overall, because of gastrointestinal complications, only 39% of the prescribed EN was administered; only 8 (22%) patients did tolerate EN within the first 48 hours after admission and did achieve their minimum nutritional requirements. The most frequent complication (78%) was high volume of gastric residuals followed by abdominal distention (61%), both associated with hemodynamic instability (HI). Gastrointestinal dysfunction was associated with high Acute Physiologic and Chronic Health Evaluation II score (p = .01), total calorie intake (p = .02), total carbohydrate intake (p = .02), HI (p = .03), malnutrition (p = .04), volume of IV saline (p = .04), and concurrent vasoactive drug administration (p = .05). CONCLUSIONS: This audit in extremely severe intensive care patients identified several factors that impair gastrointestinal function and preclude EN at any stage, namely early EN. Nutrition management must take into account concurrent therapies, given their potential interference with nutrition and organ function.

Journal Article↗