Electrocoagulation Of Vascular Abnormalities Of The Large Bowel
John P. Papp in Endoscopie Control of Gastrointestinal Hemorrhage, 2019
Hypo-oxygenation is postulated to result from the associated cardiac, vascular, or pulmonary disease. Heart and peripheral vascular disease would decrease available oxygen to peripheral tissues by decreasing blood flow. Long-standing hypertension with arteriosclerosis and diabetes mellitus, with its involvement of the microcirculation, may produce the same effect. Chronic obstructive pulmonary disease would decrease available oxygen to peripheral tissues by desaturation of hemoglobin. Localized hypoxemia of the microcirculation would lead to capillary proliferation and dilation, eventually leading to a clinically recognizable vascular abnormality. This is seen in Takayasu’s arteritis, where it can cause a proliferative response around the optic disc downstream from a vascular occlusion. Perhaps an angiogenesis factor is being produced by the local ischemia. Ischemic necrosis or mechanical abrasion of the surface of the lesion would result in gastrointestinal bleeding. The lesions tend to form in the mucosa of the gastrointestinal tract because its contents have a very low partial pressure of oxygen, which exacerbates the local hypoxemia already produced by the associated disease. Anatomy, physiology, and vascular supply of the cecum all probably contribute to it being the most frequent site of involvement. The cecum is the widest point of the lower intestinal tract. It is physiologically normal for the cecum to contain a large, anaerobic mass of feces. The combined oxygen requirements of the metabolically active mucosa and adjacent oxygen sink should produce an area of high-oxygen need. The vascular supply of the cecum may also be a factor in producing localized ischemia, since cecal arteries are end arteries and the most distal branches of the superior mesenteric. Therefore, the cecum can be viewed as a large oxygen sink at the end of a long and precarious vascular supply. This is inconsequential in healthy, young people, but in elderly patients with cardiac, vascular, or pulmonary disease, it could lead to a localized area of chronic mucosal hypo-oxygenation and subsequent vascular proliferation. This theory explains why acquired vascular abnormalities affect the mucosa of the gastrointestinal tract, especially the cecum, and why they are associated with cardiac, vascular, and pulmonary disease. There are important implications if this theory can be proven to be true. Presently, there is no recognized demonstrable lesion of ischemic bowel disease short of infarction. Acquired mucosal vascular abnormalities of the cecal area may represent such a lesion.
Appendiceal Cancer
Dongyou Liu in Tumors and Cancers, 2017
The human appendix is a narrow pouch of tissue extending from the cecum located in the lower right-hand abdominal area. It measures about 10 cm in length and 0.6 cm in diameter. Structurally, the appendix is composed of four layers: mucosa, submucosa (with masses of lymphoid tissue), muscularis externa, and serosa. The mucosa of the appendix is studded with pits (called the crypts of Lieberkuhn), which are lined by a single layer of columnar cells. The crypts also contain mucus-producing, large clearer cells (or goblet cells). At the base of the crypts are intestinal stem cells, with the capacity to differentiate into columnar cells (entrocytes), goblet cells, neuroendocrine cells, and Paneth cells. The appendix differs from the colon in having a very large number of lymphoid aggregates in the submucosa. These aggregates produce secretory IgA antibodies to assist in detoxification within the gut. The mucus and antibodies produced by the appendix are subsequently pushed into the cecum by peristalsis. Although adenoma is often limited to the mucosa of the appendix and does not produce murin, some neoplasms show adenomatous growths with mucin dissection beyond the muscularis mucosa (so-called broad front invasion), mural perforation, or even peritoneal dissemination (as in the case of pseudomyxoma peritonei, PMP). The 2010 WHO classification recognizes three categories of mucinous neoplasms: mucinous adenoma (restricted to mucosa, no extra-appendiceal mucin, not associated with PMP, nonrecurrent), low-grade appendiceal mucinous neoplasm (LAMN; non-invasive glands beyond appendix, extra-appendiceal mucin, associated with low-grade PMP, recurrent), and appendiceal adenocarcinoma (invasive glands beyond appendix, extra-appendiceal mucin, associated with high-grade PMP, 10-year survival <10%) [1,2].
Clinical anatomy of the newborn
Prem Puri in Newborn Surgery, 2017
The anterior surface of the stomach is overlapped by the left lobe of the liver, which extends almost to the spleen. The capacity of the neonatal stomach is 30–35 mL at term but reaches 100 mL by the fourth week. Gastric emptying is relatively slow and poorly coordinated in the first few weeks. The small bowel of the newborn is distributed more horizontally because of the shape of the abdominal cavity. The mean length of the small intestine from the duodenojejunal flexure to the ileocecal junction is around 160 cm when measured at term along its antimesenteric border in vivo 39 but considerably longer when measured at autopsy.40In normal infants, the duodenojejunal flexure lies to the left of the midline, most often at the level of the L1 vertebra, although this level is variable.41The superior mesenteric artery typically lies to the left of the superior mesenteric vein. This vascular relationship is often abnormal in patients with intestinal malrotation, although abnormal orientation of these vessels can be seen in some healthy individuals and a normal relationship may sometimes exist in patients with intestinal malrotation.42The mean in vivo length of the colon from the ileocecal junction to the upper rectum is 33 cm at term.39The cecum and ascending and descending colon are proportionately shorter than in the adult, and the transverse colon, sigmoid colon, and rectum proportionately longer. The cecum tapers to a proportionately large appendix with a relatively wide orifice. The anal canal has well-defined anal columns and prominent anal sinuses43; stasis within these sinuses is a putative cause of perianal sepsis, particularly in male infants.44Neonatal small bowel has few circular folds (valvulae conniventes), and the neonatal colon has no haustra. This makes it difficult to distinguish the small and large bowel on plain abdominal radiographs. Their relative position (central versus peripheral) and caliber are a guide, but a contrast study may be required to accurately differentiate small and large bowel pathology.
Effects of Microbial Contamination on the Cecum Enlargement of Germfree Rats
Published in Scandinavian Journal of Gastroenterology, 1970
B. E. Gustafsson, T. Midtvedt, K. Strandberg
Gustafsson, B. E., Midtvedt, T. & Strandberg, K. 1970. Effects of Microbial Contamination on the Cecum Enlargement of Germfree Rats. Scand. J. Gastroent. 5, 309-314. Strips from germfree rat ceca were less sensitive to acetylcholine and serotonin than strips from conventional rats. Other smooth muscle organs of the germfree rat did not show a low muscular sensitivity to these agents. The effects of ‘conventionalization’ were different in young and old rats. Cecum contents were fully reduced in both age groups; cecum wall was fully reduced in young but only partially in old rats. The cecum muscular sensitivity remained unchanged in old but was ‘conventionalized’ in young rats. Monocontamination of germfree rats with Cl. difficile gave a partial reduction of the cecum contents and wall; the muscular sensitivity remained unchanged.
Removal of the cecum affects intestinal fermentation, enteric bacterial community structure, and acute colitis in mice
Published in Gut Microbes, 2018
Kirsty Brown, D. Wade Abbott, Richard R. E. Uwiera, G. Douglas Inglis
ABSTRACT The murine cecum is a major site of fermentation of dietary materials, and production of short chain fatty acids (SCFAs). To examine the role that the cecum plays in acute bacterial infection in mice, the cecum was surgically removed, and changes in bacterial communities and production of SCFAs were analyzed relative to surgical sham animals. To incite bacterial colitis, mice were orally challenged with Citrobacter rodentium. The impact of butyrate administered directly into the colon was also examined. Concentrations of SCFAs in feces were substantially lower in mice with an excised cecum. Bacterial communities were also less diverse in cecectomized mice, and densities of major SCFA-producing taxa including bacteria within the Ruminococcaceae and Lachnospiraceae families were reduced. Colonization of the intestine by C. rodentium was not affected by removal of the cecum, and the bacterium equally incited acute colitis in mice with and without a cecum. However, cecectomized mice exhibited lower body weights at later stages of infection indicating an impaired ability to recover following challenge with C. rodentium. Furthermore, removal of the cecum altered immune and inflammatory responses to infection including increased inflammatory markers in the proximal colon (Tnfα, Il10, βd1), and heightened inflammatory response in the proximal and distal colon (Ifnγ, Tnfα, Relmβ). Exogenous administration of butyrate was insufficient to normalize responses to C. rodentium in cecectomized mice. The murine cecum plays a critical role in maintaining intestinal health, and the murine cecectomy model may be a useful tool in elucidating key aspects of intestine-pathogen-microbiota interactions.
Studies on Cecum Digestion
Published in Journal of the Agricultural Chemical Society of Japan, 1960
Ichiro Yoshihara, Makoto Kandatsu
For the study of cecum digestion, the movement of cecal contents in the rabbit with abdominal window was studied by injecting 35S-barium sulfate into the cecum. The fecal output and the distribution of radioactivity in cecum, indicated that the hard and soft feces in the rabbit are formed from the same cecal contents. A new assumption was thus suggested to explain the formation of the hard and soft feces.
Related Knowledge Centers
- Large Intestine
- Colon
- Rectum
- Small Intestine
- Ileum
- Peritoneum
- Human Gastrointestinal Tract