Acute colonic pseudoobstruction.
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ABSTRACT:
SUBMITTER: Chudzinski AP
PROVIDER: S-EPMC4442725 | biostudies-other | 2015 Jun
REPOSITORIES: biostudies-other
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Project description:BackgroundRoutine colonoscopy is recommended to determine the coexistence of colon cancer after medical treatment for colon diverticulitis. However, in the case of uncomplicated diverticulitis diagnosed by computed tomography, the clinical relevance of routine follow-up colonoscopy has recently been debated. Yet, the role of follow-up colonoscopy for right colon diverticulitis, which tends to develop at a younger age than left colon diverticulitis, has not been specifically evaluated. Therefore, we aimed to evaluate the incidence of right colon cancer or colonic adenomatous polyps, detected by routine colonoscopy, after conservative management of acute uncomplicated right colon diverticulitis.MethodsPatients with uncomplicated right colon diverticulitis (modified Hinchey stage Ia) diagnosed by computed tomography imaging, between 2011 and 2017, and who underwent follow-up colonoscopy surveillance after treatment were included. The primary outcome was the incidence of colon cancer, with the detection rate of adenoma being the secondary outcome. Information for analysis was retrieved retrospectively from patients' medical records.ResultsThe study group included 330 consecutive patients, with a mean age of 41.9 years, and 51.9% being men. For the primary outcome, the rate of colon cancer on follow-up colonoscopy was 0.3% (1/330 cases). The rate of adenoma detection was 20.9% (69/330 cases) and advanced adenoma (> 10 mm in diameter; or exhibiting a > 25% villous component or severe dysplasia), including colon cancer, was observed in 9 patients (2.7%).ConclusionsIn patients with acute uncomplicated right colonic diverticulitis, routine colonoscopy after conservative treatment may be necessary because although the colon cancer detection rate is low, it is possible to detect advanced colon adenoma.
| S-EPMC7913260 | biostudies-literature
Project description:Background and purposeAcute colonic pseudo-obstruction (ACPO) is a common but understudied complication in neurocritically ill patients. The acetylcholinesterase inhibitor neostigmine can be used to treat ACPO in patients who do not respond to conventional treatment. This study investigated the effectiveness and adverse events when using neostigmine to manage ACPO in neurocritically ill patients.MethodsThis retrospective study investigated patients with ACPO who were treated using neostigmine in the neurological intensive-care units at two centers between March 2017 and August 2020. Neostigmine was administered intravenously or subcutaneously (at doses ranging from 0.25 mg to 2 mg) according to the protocols at the two centers. The outcomes were bowel movements and the changes in colon diameters on abdominal radiographs. Safety events such as bradycardia, vomiting, salivation, and sweating were evaluated.ResultsThis study included 31 subjects with a mean age of 46.8 years (65.4% males). All patients had a bowel movement at a median of 120 minutes after administering neostigmine. The colon diameter decreased by a median of 17.5 mm (paired t-test: p<0.001) regardless of the dose and treatment protocols. Multilevel analysis confirmed that the mean colon diameter decreased from 66 mm pretreatment to 47.5 mm posttreatment (p<0.001), with an intraclass correlation coefficient of 13%. Three patients (9.7%) exhibited hypersalivation, sweating, bradycardia, and vomiting. Bradycardia (heart rate, 42 beats/minute) occurred in one patient (3.2%), and was successfully managed by injecting atropine.ConclusionsNeostigmine injection is a safe and effective treatment option for ACPO in neurocritically ill patients who fail to respond to conservative management.
| S-EPMC8490912 | biostudies-literature
Project description:Diverticular disease incidence is increasing up to 65% by age 85 in industrialized nations, low fiber diets, and in younger and obese patients. Twenty-five percent of patients with diverticulosis will develop acute diverticulitis. This imposes a significant burden on healthcare systems, resulting in greater than 300000 admissions per year with an estimated annual cost of $3 billion USD. Abdominal computed tomography (CT) is the diagnostic study of choice, with a sensitivity and specificity greater than 95%. Unfortunately, similar CT findings can be present in colonic neoplasia, especially when perforated or inflamed. This prompted professional societies such as the American Society of Colon Rectal Surgeons to recommend patients undergo routine colonoscopy after an episode of acute diverticulitis to rule out malignancy. Yet, the data supporting routine colonoscopy after acute diverticulitis is sparse and based small cohort studies utilizing outdated technology. While any patient with an indication for a colonoscopy should undergo appropriate endoscopic evaluation, in the era of widespread use of high-resolution computed tomography, routine colonic endoscopic evaluation following resolution of acute uncomplicated diverticulitis poses additional costs, comes with inherent risks, and may require further study. In this manuscript, we review the current data related to this recommendation.
| S-EPMC4168084 | biostudies-literature
Project description:OBJECTIVES:A healed intestinal mucosa is the aim of therapy in acute ulcerative colitis (UC). Disruption of mucosal wound healing may lead to severe complications including intestinal fibrosis. This study examined mucosal gene expression in the healing process of acute UC with a special focus on known mediators of fibrosis. METHODS:Endoscopic biopsies from patients with acute, moderate to severe UC were analyzed with a quantitative polymerase chain reaction array for 84 genes involved in fibrosis pathways. All patients were treated with infliximab (anti- tumor necrosis factor). Biopsies were taken before therapy and when disease remission was reached, defined as a Mayo score of ≤2, with an endoscopic subscore of 0 or 1. A healthy control group was included. Immunostaining of matrix metallopeptidase 9 and smooth muscle actin was performed. RESULTS:Mucosal biopsies from acute UC (n = 28), remission UC (n = 28), and healthy controls (n = 13) were analyzed. Fibrosis and extracellular matrix-associated genes were upregulated in the endoscopically healed UC mucosa vs controls, with collagen type III alpha 1 chain, actin alpha 2, lysyl oxidase, TIMP metallopeptidase inhibitor 3, and caveolin 1 uniquely showing no overlap with acute disease. Pro- and antifibrotic mediators (interleukin [IL]13 receptor subunit alpha 2, IL1B, IL10, tumor necrosis factor, snail family transcriptional repressor 1, and C-C motif chemokine ligand 2) were upregulated in both acute and healed UC compared with controls. An attenuated pattern of the canonical transforming growth factor beta (TGFB) pathway was observed in acute UC and to a lesser extent in the healed mucosa, except for TGFB2, which was enhanced. DISCUSSION:The endoscopically healed mucosa of UC showed a persisting dysregulation of fibrosis-associated mediators compared with controls, including extracellular matrix remodeling, profibrotic cytokines, and TGFB signaling pathways.
| S-EPMC6884345 | biostudies-literature
Project description:The use of colonic stenting with elective surgery has been suggested as an alternative management for acute malignant colonic obstruction, as emergency surgery has a high risk of morbidity and mortality.
However, the available body of literature addressing their benefit in this setting is contradictory.
The purpose of this study is to determine the efficacy and safety of colonic stenting with elective surgery versus emergency surgery in the management of acute malignant colonic obstruction.
| 2155828 | ecrin-mdr-crc
Project description:Central to inflammatory bowel disease (IBD) pathogenesis is loss of mucosal barrier function. Emerging evidence implicates extracellular adenosine signaling in attenuating mucosal inflammation. We hypothesized that adenosine-mediated protection from intestinal barrier dysfunction involves tissue-specific signaling through the A2B adenosine receptor (Adora2b) at the intestinal mucosal surface. To address this hypothesis, we combined pharmacologic studies and studies in mice with global or tissue-specific deletion of the Adora2b receptor. Adora2b(-/-) mice experienced a significantly heightened severity of colitis, associated with a more acute onset of disease and loss of intestinal epithelial barrier function. Comparison of mice with Adora2b deletion on vascular endothelial cells (Adora2b(fl/fl)VeCadCre(+)) or intestinal epithelia (Adora2b(fl/fl)VillinCre(+)) revealed a selective role for epithelial Adora2b signaling in attenuating colonic inflammation. In vitro studies with Adora2b knockdown in intestinal epithelial cultures or pharmacologic studies highlighted Adora2b-driven phosphorylation of vasodilator-stimulated phosphoprotein (VASP) as a specific barrier repair response. Similarly, in vivo studies in genetic mouse models or treatment studies with an Adora2b agonist (BAY 60-6583) recapitulate these findings. Taken together, our results suggest that intestinal epithelial Adora2b signaling provides protection during intestinal inflammation via enhancing mucosal barrier responses.
| S-EPMC4598274 | biostudies-literature
Project description:BackgroundInflammatory Bowel Disease (IBD) is characterized by overt inflammation of the intestine and is typically accompanied by symptoms of bloody diarrhea, abdominal pain and cramping. The Colonic Migrating Motor Complex (CMMC) directs the movement of colonic luminal contents over long distances. The tri-nitrobenzene sulphonic acid (TNBS) model of colitis causes inflammatory damage to enteric nerves, however it remains to be determined whether these changes translate to functional outcomes in CMMC activity. We aimed to visualize innate immune cell infiltration into the colon using two-photon laser scanning intra-vital microscopy, and to determine whether CMMC activity is altered in the tri-nitro benzene sulphonic (TNBS) model of colitis.MethodsEpithelial barrier permeability was compared between TNBS treated and healthy control mice in-vitro and in-vivo. Innate immune activation was determined by ELISA, flow cytometry and by 2-photon intravital microscopy. The effects of TNBS treatment and IL-1? on CMMC function were determined using a specialized organ bath.ResultsTNBS colitis increased epithelial barrier permeability in-vitro and in-vivo. Colonic IL-1? concentrations, colonic and systemic CD11b+ cell infiltration, and the number of migrating CD11b+ cells on colonic blood vessels were all increased in TNBS treated mice relative to controls. CMMC frequency and amplitude were inhibited in the distal and mid colon of TNBS treated mice. CMMC activity was not altered by superfusion with IL-1?.ConclusionsTNBS colitis damages the epithelial barrier and increases innate immune cell activation in the colon and systemically. Innate cell migration into the colon is readily identifiable by two-photon intra-vital microscopy. CMMC are inhibited by inflammation, but this is not due to direct effects of IL-1?.
| S-EPMC6014673 | biostudies-literature
Project description:Background and study aims Through advanced endoscopic clipping techniques, endoscopic treatment of both diagnostic and therapeutic acute iatrogenic colonic perforations has been shown effective. The main purpose of this study was to compare the management of acute iatrogenic perforations (AIPs) of the colon before and after the introduction of advanced clipping techniques. Methods We conducted a retrospective study from July 1996 to February 2020. The period was divided into two sub periods, Period 1: from July 1996 to December 2012 and Period 2: from January 2013 to March 2020. All AIPs occurring during a colonoscopy and detected during or immediately (< 4 hours) after the procedure, were included in the study. Results The total number of colonoscopies performed at our hospital was 33055 and 36831 during Periods 1 and 2 respectively. Fifteen perforations were observed in Period 1 and 11 in Period 2. The rate of surgery was 93.3 % % (14/15) in Period 1 and 27.2 % (3 /11) in Period 2 ( P < 0.01). The mean hospital stay in Period 1 was 6.9 days and 4 in Period 2 ( P < 0.01). Conclusions Data from this historical cohort have clearly shown a decrease in the surgery rate and the length of hospitalization of AIPs in Period 2 compared to Period 1.
| S-EPMC8159597 | biostudies-literature
Project description:BackgroundAcute colonic diverticulitis (ACD) complications arise in approximately 8% to 35% patients and the most common ones are represented by phlegmon or abscess, followed by perforation, peritonitis, obstruction, and fistula. In accordance with current guidelines, patients affected by generalized peritonitis should undergo emergency surgery. However, decisions on whether and when to operate ACD patients remain a substantially debated topic while algorithm for the best treatment has not yet been determined. Damage control surgery (DCS) represents a well-established method in treating critically ill patients with traumatic abdomen injuries. At present, such surgical approach is also finding application in non-traumatic emergencies such as perforated ACD. Thanks to a thorough systematic review of the literature, we aimed at achieving deeper knowledge of both indications and short- and long-term outcomes related to DCS in perforated ACD.MethodsWe performed a systematic literature review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyzes (PRISMA) guidelines. Pubmed/MEDLINE, Embase, Scopus, Cochrane Library, and Web of Science databases were used to search all related literature.ResultsThe 8 included articles covered an approximately 13 years study period (2006-2018), with a total 359 patient population. At presentation, most patients showed III and IV American Society of Anesthesiologists (ASA) score (81.6%) while having Hinchey III perforated ACD (69.9%). Most patients received a limited resection plus vacuum-assisted closure at first-look while about half entire population underwent primary resection anastomosis (PRA) at a second-look. Overall morbidity rate, 30-day mortality rate and overall mortality rate at follow-up were between 23% and 74%, 0% and 20%, 7% and 33%, respectively. Patients had a 100% definitive abdominal wall closure rate and a definitive stoma rate at follow-up ranging between 0% and 33%.ConclusionDCS application to ACD patients seems to offer good outcomes with a lower percentage of patients with definitive ostomy, if compared to Hartmann's procedure. However, correct definition of DCS eligible patients is paramount in avoiding overtreatment. In accordance to 2016 WSES (World Society of Emergency Surgery) Guidelines, DCS remains an effective surgical strategy in critically ill patients affected by sepsis/septic shock and hemodynamical unstability.
| S-EPMC7710165 | biostudies-literature
Project description:The primacy of the gastrointestinal (GI) tract in dictating the outcome of graft-versus-host disease (GVHD) is broadly accepted; however, the mechanisms controlling this effect are poorly understood. Here, we demonstrate that GVHD markedly enhances alloantigen presentation within the mesenteric lymph nodes (mLNs), mediated by donor CD103(+)CD11b(-) dendritic cells (DCs) that migrate from the colon under the influence of CCR7. Expansion and differentiation of donor T cells specifically within the mLNs is driven by profound levels of alloantigen, IL-12, and IL-6 promoted by Toll-like receptor (TLR) and receptor for advanced glycation end products (RAGE) signals. Critically, alloantigen presentation in the mLNs imprints gut-homing integrin signatures on donor T cells, leading to their emigration into the GI tract where they mediate fulminant disease. These data identify a critical, anatomically distinct, donor DC subset that amplifies GVHD. We thus highlight multiple therapeutic targets and the ability of GVHD, once initiated by recipient antigen-presenting cells, to generate a profound, localized, and lethal feed-forward cascade of donor DC-mediated indirect alloantigen presentation and cytokine secretion within the GI tract.
| S-EPMC4516799 | biostudies-literature