Changes In Intestinal Motility Research Articles

Su1190 Effect of Gastrointestinal Barrier Protection on Sepsis-Induced Changes of Intestinal Motility, Inflammation and Colonic Permeability

Su1190 Effect of Gastrointestinal Barrier Protection on Sepsis-Induced Changes of Intestinal Motility, Inflammation and Colonic Permeability

Once-daily prolonged release tacrolimus in liver transplantation: Experts' literature review and recommendations.

The efficacy and safety of tacrolimus (Tac) twice daily (bid) and once a day (qd) formulations are considered to be similar. However, the available information regarding initiation of Tac qd is sparse, and practical information is lacking. On the basis of a literature review, clinical efficacy, and safety trials, French experts in the liver transplantation field were asked to highlight pharmacokinetic (PK) differences between both formulations to assess efficacy and safety of the qd formulation in the context of de novo initiation or conversion and to provide their recommendations for initiation and day-to-day management of Tac qd. The same efficacy and safety profile is found for both immediate-release and prolonged-release Tac. PK differences carry on absorption because of the difference in formulations but not on metabolism or excretion. Tac qd offers a better reproducibility in exposure than Tac bid but is associated with an increased risk of disturbed absorption in case of a change in intestinal motility. The same therapeutic drug monitoring with Tac qd and bid could be applied, based on minimal concentration (trough level; C(min)), as there is a similar strong correlation between C(min) and the area under the curve (AUC) for both formulations. Different protocols for Tac qd initiation were described through numerous studies, except for early conversion: initiation on day 0, using 0.10 to 0.20 mg/kg/day as monotherapy, or lower dosages in case of concomitant immunosuppressant treatment or poor graft quality; early conversion from day 5 to 6 months, preferably before hospital discharge, using a 1 to 1.3 mg/kg/day schedule and with first C(min) assessment 48 hours after the conversion; and later conversion (>6 months posttransplantation) using a milligram-to-milligram dosage schedule, and with dose adjustment based on weekly C(min) measurement. Experts underline that an increase in treatment adherence was expected using Tac qd in liver recipients. In conclusion, Tac qd has the same efficacy and safety profile as Tac bid. De novo introduction or later conversion are well documented but could differ from day-to-day practice.

Oclusão/sub-oclusão intestinal recorrente no período neonatal: displasia ou imaturidade intestinal?

Introduction: Changes in intestinal motility may be due to primary or secondary causes, the most serious clinical manifestation is intestinal pseudo-obstruction. However, in the neonatal period this may be due to abnormalities of intestinal innervation and / or varying degrees of immaturity of ganglion cells. Clinical Case: A preterm infant 26 weeks of gestation presented, at the 43rd day of life a clinical picture suggestive of necrotizing enterocolitis type IIA, which was not confirmed. In the following months she presented with successive subocclusive and occlusive intestinal episodes, ending in ileostomy. The anatomopathological examination revealed some myenteric and submucosal plexus (with increase in the number of ganglion cells) and some larger nodes than usual. The subsequent clinical course was favorable with good weight gain requiring, however, transient artificial nutritional support; reconstitution of intestinal transit occurred after 21 months. Discussion/Conclusions: The authors present this case of intestinal neuronal dysplasia emphasizing the favorable prognosis associated with intestinal growth and maturity with age.

Management of diverticular disease.

Diverticular disease is a common condition in Western countries and the incidence and prevalence of the disease is increasing. The pathogenetic factors involved include structural changes in the gut that increase with age, a diet low in fibre and rich in meat, changes in intestinal motility, the concept of enteric neuropathy and an underlying genetic background. Current treatment strategies are hampered by insufficient options to stratify patients according to individual risk. One of the main reasons is the lack of an all-encompassing classification system of diverticular disease. In response, the German Society for Gastroenterology and Digestive Diseases (DGVS) has proposed a classification system as part of its new guideline for the diagnosis and management of diverticular disease. The classification system includes five main types of disease: asymptomatic diverticulosis, acute uncomplicated and complicated diverticulitis, as well as chronic diverticular disease and diverticular bleeding. Here, we review prevention and treatment strategies stratified by these five main types of disease, from prevention of the first attack of diverticulitis to the management of chronic complications and diverticular bleeding.

Prolonged Orocecal Transit Time Enhances Serum Bile Acids Through Bacterial Overgrowth, Contributing Factor to Gallstone Disease

Gallstones (GS) are associated with slow intestinal transit but the effect of altered transit time on physiological changes in gastrointestinal tract among GS patients is poorly understood. To investigate the association of gallstone disease with change in intestinal motility and how motility alters serum bile acid (SBA) levels. A total of 333 subjects were enrolled, of which 183 were GS patients and 150 age-matched and sex-matched controls. Intestinal transit time was assessed by measuring orocecal transit time (OCTT). Breath tests were used to evaluate OCTT and small intestinal bacterial overgrowth (SIBO). Total SBA levels were measured by enzymatic colorimetric assay. A linear regression analysis was performed to look for interrelationship between OCTT and SBA levels. Orocecal transit time was significantly delayed (P<0.001) in GS patients (134.8±30.64 min) compared with controls (85.35±19.81 min). SIBO was observed to be significantly higher (P<0.01) in patients (15%) compared with controls (0.7%). OCTT was further delayed significantly (P<0.01) in GS patients with SIBO (165.6±33.9 min) compared with patients lacking SIBO. Total SBA levels were found to be significantly higher (P<0.05) in GS patients (5.3±2.7 μmol/L) compared with controls (3.7±1.8 μmol/L). SBA levels were also significantly higher (P<0.05) in SIBO-positive GS patients (6.4±2.8 μmol/L) compared with SIBO-negative patients (4.8±2.4 μmol/L). There was positive correlation between OCTT and SBA levels in SIBO-positive patients. The findings indicate that delayed OCTT leads to SIBO and thus enhance SBA levels in etiology underlying GSs.

Gut Microbial Products Regulate Murine Gastrointestinal Motility via Toll-Like Receptor 4 Signaling

Altered gastrointestinal motility is associated with significant morbidity and health care costs. Toll-like receptors (TLR) regulate intestinal homeostasis. We examined the roles of TLR4 signaling in survival of enteric neurons and gastrointestinal motility. We assessed changes in intestinal motility by assessing stool frequency, bead expulsion, and isometric muscle recordings of colonic longitudinal muscle strips from mice that do not express TLR4 (Tlr4(Lps-d) or TLR4(-/-)) or Myd88 (Myd88(-/-)), in wild-type germ-free mice or wild-type mice depleted of the microbiota, and in mice with neural crest-specific deletion of Myd88 (Wnt1Cre(+/-)/Myd88(fl/fl)). We studied the effects of the TLR4 agonist lipopolysaccharide (LPS) on survival of cultured, immortalized fetal enteric neurons and enteric neuronal cells isolated from wild-type and Tlr4(Lps-d) mice at embryonic day 13.5. There was a significant delay in gastrointestinal motility and reduced numbers of nitrergic neurons in TLR4(Lps-d), TLR4(-/-), and Myd88(-/-) mice compared with wild-type mice. A similar phenotype was observed in germ-free mice, mice depleted of intestinal microbiota, and Wnt1Cre(+/-)/Myd88(fl/fl) mice. Incubation of enteric neuronal cells with LPS led to activation of the transcription factor nuclear factor (NF)-κB and increased cell survival. Interactions between enteric neurons and microbes increases neuron survival and gastrointestinal motility in mice. LPS activation of TLR4 and NF-κB appears to promote survival of enteric neurons. Factors that regulate TLR4 signaling in neurons might be developed to alter gastrointestinal motility.

Mast cells drive mesenteric afferent signalling during acute intestinal ischaemia

Acute intestinal ischaemia stimulates visceral afferent nerves but the mechanisms responsible for this excitation are not fully understood. Mast cells may participate in this process as they are known to signal to mesenteric afferents during intestinal anaphylaxis and contribute to early inflammation and neuronal damage in response to cerebral ischaemia. We therefore hypothesised that mast cells are early responders to acute intestinal ischaemia and their activation initiates rapid signalling to the CNS via the excitation of mesenteric afferents. Primary afferent firing was recorded from a mesenteric nerve bundle supplying a segment of jejunum in anaesthetized adult rats. Acute focal ischaemia was produced by clamping theme senteric vessels for 8 min, and reperfusion followed removal of the vessel clip. Two episodes of ischaemia–reperfusion (I–R) separated by a 30 min interval were performed. Drugs or their vehicles were administered 10 min before the 2nd I–R episode. Ischaemia caused a reproducible, intense and biphasic afferent firing that was temporally dissociated from the concomitantly triggered complex pattern of intestinal motor activity. The L-type calcium channel blocker, nifedipine, significantly attenuated this afferent firing by a mechanism independent of its action on intestinal tone. Ischaemia-induced afferent firing was also abrogated by the mast cell stabilizer, doxantrazole, and the H1 histamine receptor antagonist, pyrilamine. In contrast, the nicotinic receptor antagonist, hexamethonium, and the N-type calcium channel toxin, ω-conotoxin GVIA, each reduced the ischaemia-evoked motor inhibition but not the concurrent afferent discharge. Similarly, the cyclooxygenase inhibitor, naproxen, had no effect on the ischaemic afferent response but reduced the intestinal tone shortly from the onset of ischaemia to the early period of reperfusion. These data support a critical role for mast cell-derived histamine in the direct chemoexcitation of mesenteric afferents during acute intestinal ischaemia, whereas enteric reflex mechanisms and cyclooxygenase products contribute primarily to ischaemia-induced changes in intestinal motility. Therefore, targeting mast cells may provide benefits in patients with abdominal pain resulting from an ischaemic insult to the gastrointestinal tract.

Postnatal development of myenteric neurochemical phenotype and impact on neuromuscular transmission in the rat colon

Profound changes in intestinal motility occur during the postnatal period, but the involvement of the enteric nervous system (ENS), a key regulator of gastrointestinal (GI) motility, in these modifications remains largely unknown. We therefore investigated the postnatal development of the ENS phenotype and determined its functional repercussion on the neuromuscular transmission in the rat colon. Sprague-Dawley rats were euthanized at postnatal day (P) 1, P3, P5, P7, P14, P21, and P36. Whole mounts of colonic myenteric plexus were stained with antibodies against choline acetyltransferase (ChAT), neuronal nitric oxide synthase (nNOS), and HuC/D. Colonic contractile response induced by electrical field stimulation (EFS) was investigated in organ chambers in absence or presence of N-nitro-l-arginine methyl ester (l-NAME) and/or atropine. In vivo motility was assessed by measurement of the colonic bead latency time. Randomly occurring ex vivo contractions appeared starting at P5. Starting at P14, rhythmic phasic contractions occurred whose frequency and amplitude increased over time. In vivo, bead latency was significantly reduced between P14 and P21. Ex vivo, EFS-induced contractile responses increased significantly over time and were significantly reduced by atropine starting at P14 but were sensitive to l-NAME only after P21. The proportion of ChAT-immunoreactive (IR) neurons increased time dependently starting at P14. The proportion of nNOS-IR neurons increased as early as P5 compared with P1 but did not change afterward. Our data support a key role for cholinergic myenteric pathways in the development of postnatal motility and further identify them as putative therapeutic target for the treatment of GI motility disorders in the newborn.

The validation of an invitro colonic motility assay as a biomarker for gastrointestinal adverse drug reactions

Motility-related gastrointestinal adverse drug reactions (GADRs), such as constipation and diarrhea, are some of the most frequently reported adverse events associated with the clinical development of new chemical entities, and for marketed drugs. However, biomarkers capable of detecting such GADRs are lacking. Here, we describe an in vitro assay developed to detect and quantify changes in intestinal motility as a surrogate biomarker for constipation/diarrhea-type GADRs. In vitro recordings of intraluminal pressure were used to monitor the presence of colonic peristaltic motor complexes (CPMCs) in mouse colonic segments. CPMC frequency, contractile and total mechanical activity were assessed. To validate the assay, two experimental protocols were conducted. Initially, five drugs with known gastrointestinal effects were tested to determine optimal parameters describing excitation and inhibition as markers for disturbances in colonic motility. This was followed by a “blinded” evaluation of nine drugs associated with or without clinically identified constipation/diarrhea-type GADRs. Concentration–response relationships were determined for these drugs and the effects were compared with their maximal free therapeutic plasma concentration in humans. The assay detected stimulatory and inhibitory responses, likely correlating to the occurrence of diarrhea or constipation. Concentration-related effects were identified and potential mechanisms of action were inferred for several drugs. Based on the results from the fourteen drugs asssessed, the sensitivity of the assay was calculated at 90%, with a specificity of 75% and predictive capacity of 86%. These results support the potential use of this assay in screening for motility-related GADRs during early discovery phase, safety pharmacology assessment.

Transrectal ultrasonographic diagnosis of jejunoileal intussusception in a cow.

Transrectal ultrasonographic diagnosis of jejunoileal intussusception in a cow.

Changes in intestinal motility and in the myenteric plexus in a rat model of intestinal ischemia–reperfusion

Background/Purpose Early histologic changes induced by intestinal ischemia–reperfusion injury (IIRI) have been extensively studied using animal models. However, information regarding late effects on intestinal motility is lacking. The aim of this study was to investigate the late effects of IIRI on myenteric plexus histology and intestinal motility. Materials and Methods Thirty-two postweaning male mice weighing between 58 and 103 g were divided randomly into 4 groups: Control (unoperated), Sham (celiotomy), 30-minute ischemia (celiotomy and superior mesenteric artery ischemia for 30 minutes), and 45-minute ischemia (celiotomy and superior mesenteric artery ischemia for 45 minutes). Postoperative intestinal motility was assessed by weighing total fecal output for 24 hours on the 3rd, 7th, 14th, and 21st day after surgery. Segments of duodenum, jejunum, and ileum were examined at light microscopy for changes in the myenteric plexus. Results Three weeks after IIRI, the ganglion cells from the myenteric plexus appeared in light microscopy, spongy or foamy, containing many vacuoles in their cytoplasm. The neuronal nucleus became irregular, with degenerative signs. These alterations did not occur among animals from the control or sham groups. Although the animals of the 45-minute ischemia group showed a significant drop in fecal output in the 21st postoperative day, this appeared to have no effect on weight gain. Conclusions The results suggest that intestinal ischemia–reperfusion causes late neuronal damage. These changes resulted in alterations of intestinal motility, which, within the conditions of the present study, had no repercussion on general weight gain.

From molecules to motion: altering neuronal ion channel function can lead to changes in intestinal motility

From molecules to motion: altering neuronal ion channel function can lead to changes in intestinal motility

Age-related changes in the gastrointestinal tract: a functional and immunohistochemical study in guinea-pig ileum

It is known that there is an age-related increase in gastrointestinal diseases. However, there is a lack of studies dealing with the correlation between age-related changes in function and intrinsic innervation in the gastrointestinal tract. The purpose of this work was to study this subject in the guinea pig ileum, whose functional and structural features are well known in the young age. Ileal longitudinal muscle — myenteric plexus (LMMP) preparations were obtained from 3-to 24-month-old guinea pigs. Both functional and immunohistochemical techniques were applied. The force of the contraction elicited by excitatory stimuli (electrical stimulation, acetylcholine, substance P, and opioid withdrawal) increased in parallel with an age-dependent reduction in the density of excitatory motor neurones to the longitudinal muscle, whereas other subpopulations of neurones, including inhibitory motor neurones, decreased much more slowly. Although the increase in responsiveness could be related to the age/weight-related increment in muscle bulk, some compensatory modifications to the lowered density of excitatory neurones could also be involved. On the other hand, the acute inhibitory response to morphine remained unaltered in old animals, whilst in vitro tolerance was lower. These results suggest that although age-dependent neuronal loss does not cause dramatic changes in intestinal motility, it is a factor that could contribute to disturbing normal responsiveness and, perhaps, underlie the higher frequency of gastrointestinal diseases encountered in the elderly.

Changes in intestinal motility, visceral sensitivity and minor mucosal inflammation after fasting therapy in a patient with irritable bowel syndrome

Journal of Gastroenterology and HepatologyVolume 21, Issue 6 p. 1078-1079 Changes in intestinal motility, visceral sensitivity and minor mucosal inflammation after fasting therapy in a patient with irritable bowel syndrome Michiko Kano, Michiko Kano Departments of Behavioral Medicine, Psychosomatic Medicine andSearch for more papers by this authorShin Fukudo, Shin Fukudo Departments of Behavioral Medicine, Psychosomatic Medicine andSearch for more papers by this authorMotoyori Kanazawa, Motoyori Kanazawa Departments of Behavioral Medicine, Psychosomatic Medicine andSearch for more papers by this authorYuka Endo, Yuka Endo Psychosomatic Medicine andSearch for more papers by this authorHiroyuki Narita, Hiroyuki Narita Department of Psychiatry, Yokohama City University School of Medicine, Yokohama, JapanSearch for more papers by this authorDaisaku Tamura, Daisaku Tamura Psychosomatic Medicine andSearch for more papers by this authorMichio Hongo, Michio Hongo Comprehensive Medicine, Tohoku University School of Medicine, Sendai andSearch for more papers by this author Michiko Kano, Michiko Kano Departments of Behavioral Medicine, Psychosomatic Medicine andSearch for more papers by this authorShin Fukudo, Shin Fukudo Departments of Behavioral Medicine, Psychosomatic Medicine andSearch for more papers by this authorMotoyori Kanazawa, Motoyori Kanazawa Departments of Behavioral Medicine, Psychosomatic Medicine andSearch for more papers by this authorYuka Endo, Yuka Endo Psychosomatic Medicine andSearch for more papers by this authorHiroyuki Narita, Hiroyuki Narita Department of Psychiatry, Yokohama City University School of Medicine, Yokohama, JapanSearch for more papers by this authorDaisaku Tamura, Daisaku Tamura Psychosomatic Medicine andSearch for more papers by this authorMichio Hongo, Michio Hongo Comprehensive Medicine, Tohoku University School of Medicine, Sendai andSearch for more papers by this author First published: 24 May 2006 https://doi.org/10.1111/j.1440-1746.2006.03513.xCitations: 3Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume21, Issue6June 2006Pages 1078-1079 RelatedInformation

Long‐lasting changes in small intestinal transport following the recovery from Trichinella spiralis infection

Changes in intestinal motility and visceral sensitivity are found after resolution of acute enteric inflammation. The study investigates whether a transient nematode-induced intestinal inflammation may result in long-lasting remodelling of epithelial transport. Ferrets infected with Trichinella spiralis or sham-infected animals were euthanized on day 10, 30 or 60 postinfection (PI) and the jejunum was isolated. The net transport of electrolytes was measured electrophysiologically as transmucosal short-circuit current (I(sc)) and responses to electrical field stimulation (EFS: 1-32 Hz) or secretagogues were investigated. Myeloperoxidase (MPO) activity, a marker of mucosal inflammation, was maximal during the enteric stage of T. spiralis infection (day 10 PI) and returned to normal on days 30 and 60 PI. Mucosal inflammation caused a reduction in basal I(sc), increased electrical conductance (G) and decreased the maximal responses to EFS, carbachol or histamine. On days 30 and 60 PI the inflammation resolved and basal electrogenic transport appeared normal; however, the secretion induced by EFS, carbachol or histamine remained suppressed. Moreover, EFS-induced responses were shifted from predominantly cholinergic in controls to non-cholinergic in the infected animals. The results suggest that a transient small intestinal inflammation causes a long-term remodelling of epithelial function.

Effects of probiotic bacteria on gastrointestinal motility in guinea-pig isolated tissue

To evaluate the intestinal motility changes evoked by 8 bacterial strains belonging to Bifidobacterium, Lactobacillus and Streptococcus genera within the probiotic preparation VSL#3. Ileum and proximal colon segments isolated from guinea-pigs were used as a study model. Entire cells and cell fractions (cell debris, cell wall fraction, cytoplasmatic fraction, proteinaceous and non-proteinaceous cytoplasmatic components) of VSL#3 strains and, as controls, Escherichia coli, Salmonella aboni and Bacillus licheniformis were tested in this in vitro model. Among the bacterial cell fractions tested, only the cytoplasmatic fraction modified intestinal motility. Lactobacillus strains stimulated the contraction of ileum segment, whereas all probiotic strains tested induced proximal colon relaxation response. The non-proteinaceous cytoplasmatic components were responsible for the colon relaxation. The results obtained in this study suggest that the proximal colon relaxation activity showed by the probiotic bacteria could be one of the possible mechanisms of action by which probiotics exert their positive effects in regulating intestinal motility.

Immune‐mediated alteration in gut physiology and its role in host defence in nematode infection

Activation of the mucosal immune system of the gastrointestinal tract in nematode infection results in altered intestinal physiology, which includes changes in intestinal motility and mucus production. These changes are considered to be under direct immunological control rather than a non-specific consequence of the inflammatory reaction to the infective agent. However, little is known about the immunological basis for the changes in intestinal physiology accompanying nematode infection, or the precise role of these changes in host defence, which remains an important area to explore. In this review we describe the mechanisms by which the immune response to nematode infection influences the changes in two major cells of intestinal physiology, namely smooth muscle and goblet cells, and how these changes in intestinal physiology contribute to the host defence. Data clearly demonstrate that the T helper (Th) 2 type immune response generated by nematode infection plays an important role in the development of infection-induced intestinal muscle hypercontractility and goblet cell hyperplasia and that these immune-mediated changes in intestinal physiology are associated with worm expulsion. These observations strongly suggest that intestinal muscle contractility, goblet cell hyperplasia and worm expulsion share a common immunological basis and may be causally related. These data not only provide insights into host defence in nematode infection in the context of muscle function and goblet cell response, but also have broad implications in elucidating the pathophysiology of a wide range of gastrointestinal disorders associated with altered gut physiology.

Neurokinin NK1 and NK3 receptors as targets for drugs to treat gastrointestinal motility disorders and pain.

NK1 and NK3 receptors do not appear to play significant roles in normal GI functions, but both may be involved in defensive or pathological processes. NK1 receptor antagonists are antiemetic, operating via vagal sensory and motor systems, so there is a need to study their effects on other gastro-vagal functions thought to play roles in functional bowel disorders. Interactions between NK1 receptors and enteric nonadrenergic, noncholinergic motorneurones suggest a need to explore the role of this receptor in disrupted colonic motility. NK1 receptor antagonism does not exert consistent analgesic activity in humans, but similar studies have not been carried out against pain of GI origin, where NK1 receptors may have additional influences on mucosal inflammatory or "irritant" processes. NK3 receptors mediate certain disruptions of intestinal motility. The activity may be driven by tachykinins released from intrinsic primary afferent neurones (IPANs), which induce slow EPSP activity in connecting IPANs and hence, a degree of hypersensitivity within the enteric nervous system. The same process is also proposed to increase C-fibre sensitivity, either indirectly or directly. Thus, NK3 receptor antagonists inhibit intestinal nociception via a "peripheral" mechanism that may be intestine-specific. Studies with talnetant and other selective NK3 receptor antagonists are, therefore, revealing an exciting and novel pathway by which pathological changes in intestinal motility and nociception can be induced, suggesting a role for NK3 receptor antagonism in irritable bowel syndrome.

Problemas de utilización de medicamentos en pacientes enterostomizados

The practice of intestinal stoma, transitory or permanent, has a series of implications of a physiological, pharmacological, psychological and communitarian character that must be attended to in an integral and individualised way for each patient. Frequently, the ostomised patient is subjected to pharmacological therapy. However, the foreseeable effect of the medicines administered can be affected by factors related to the stoma. Thus, descriptions have been made of extensive resections of ileum that affect the process of the oral absorption of medicines, especially in pharmaceutical forms of enteric covering, delayed release and pills. This would mean access of the unabsorbed portion of the active principle to the collecting device through the faeces and a possible alteration of the duration and intensity of the pharmacological effect. On the other hand, pharmaco surveillance studies have revealed that numerous active principles produce changes in intestinal motility, either on the basis of its fundamental mechanism of action (laxatives, anti-diarrhoea, prokinetics), or as a collateral or secondary effect (antiacids, antidepressants, antihistamines, opioid analgesics). The appearance of constipation and, especially, of diarrhoea can be disturbing and worrying for ostomised patients, and particularly grave in ileostomised patients, due to the dehydration to which it can give rise. Similarly, changes in the colour and odour of faeces, secondary to the administration of medicines (ferrous salts, aluminium hydroxide, bismuth compounds) can needlessly alarm the patients who detect them in the ostomy collecting device (pouch). All these factors can create difficulties for the adhesion of the patient to the proscribed treatment and, as a result, affect its success. However, they can be avoided, corrected or justified with good counselling by the health professionals involved in caring for enterostomized patient.

Síndrome de ogilvie poscesárea

Ogilvies syndrome, or acute colonic pseudo-obstruction, is a change in intestinal motility which is characterized by progressive dilatation of the large intestine with no evidence of mechanical obstruction. The physiopathology of this entity is unknown and it is frequently to be found associated with caesarean section, and also normal deliveries. Diagnosis is made by the clinical presentation, and simple abdominal radiography. El síndrome de Ogilvie o seudoobstrucción colónica aguda es un trastorno de la motilidad intestinal, que se caracteriza por dilatación progresiva del intestino grueso, sin evidencia de obstrucción mecánica. Se desconoce la fisiopatología de esta entidad y es frecuente encontrarla asociada a cesáreas e incluso partos eutócicos. El diagnóstico se establece por el cuadro clínico y los hallazgos de la radiografía simple de abdomen.