Bowel obstruction pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
It is thought that bowel obstruction may | It is thought that bowel obstruction may occur functionally as a result of abnormal anatomy or mechanically, which may occur acutely or chronically. An obstruction that occurs functionally or mechanically can be classified as extrinsic, intrinsic or intraluminal including tumors, strictures and foreign bodies. Excessive bowel distention can lead to ischemia, necrosis and perforation. A functional obstruction may be due to a number of genetic defects including trisomy 21 and the RET proto-oncogene mutation. Associated conditions include post-operative adhesions, complicated hernias, gastrointestinal cancers and endometriosis. Gross pathology may demonstrate adhesions, narrow lumens and volvulus. Microscopic pathology may show evidence of fibrosis, necrosis and ischemia. | ||
==Pathophysiology== | ==Pathophysiology== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Hadeel Maksoud M.D.[2]
Overview
It is thought that bowel obstruction may occur functionally as a result of abnormal anatomy or mechanically, which may occur acutely or chronically. An obstruction that occurs functionally or mechanically can be classified as extrinsic, intrinsic or intraluminal including tumors, strictures and foreign bodies. Excessive bowel distention can lead to ischemia, necrosis and perforation. A functional obstruction may be due to a number of genetic defects including trisomy 21 and the RET proto-oncogene mutation. Associated conditions include post-operative adhesions, complicated hernias, gastrointestinal cancers and endometriosis. Gross pathology may demonstrate adhesions, narrow lumens and volvulus. Microscopic pathology may show evidence of fibrosis, necrosis and ischemia.
Pathophysiology
Pathogenesis
- Normally, the small intestine functions to pass gastrointestinal contents for absorption. The large surface area provided by the villi, plicae circularis and valvulae conniventes allow for this exchange to happens.[1][2][3]
- In addition, the small bowel is free of microbes, in comparison to the large bowel that houses commensal flora that facilitate digestion and vitamin synthesis, namely vitamin K.
- Continuous transit throughout the bowel is important to prevent bowel dilatation, ischemia and necrosis.
- Obstruction of the bowel can occur functionally (due to abnormal anatomy) or mechanically, which can be acute or chronic.
- Obstructions can be extrinsic, intrinsic or intraluminal obstruction.
- Extrinsic obstructions can happen as the result of a tumor, post-operative adhesions or hernias.
- Intrinsic obstructions can happen as a result of a tumor, stenosis or hematoma.
- Intraluminal obstructions are sometimes referred to intramural obstructions and include, foreign bodies, intussusception and gallstones.
- However an obstruction occurs, proximal to the blockage there will be a dilated segment, whilst distal to the obstruction the segment of bowel will collapse as the contents cannot pass.
- Bowel distention occurs as air that is swallowed and gases produced by the commensal flora begins to accumulate.
- Eventually, the bowel wall becomes edematous and fluid gathers inside the lumen of the bowel. This disrupts the absorptive properties of the gut.
- Some fluid may be lost to the peritoneal cavity, moreover, the proximal obstruction causes severe emesis which will lead to further loss of fluid that contains several electrolytes. This process may result in metabolic alkalosis and hypovolemia.
- The obstruction also causes the normally sterile proximal bowel to become overgrown with bacteria and vomitus may contain feces.
- When a massive dilation of the bowel occurs, the vessels that perfuse the walls of the bowel become compressed and will not be able to supply the bowel loop adequately, which leads to ischemia.
- If ischemia is not reversed within a timely manner, then necrosis, volvulus and perforation may ensue.
Genetics
The development of congenital bowel obstruction is the result of multiple genetic mutations:[4][5][6][7]
- Chromosome 21 trisomy can lead to imperforate anus and duodenal atresias in 50% of babies with down syndrome.
- Chromosome 7 mutation locus leads to cystic fibrosis that predisposes to a thickened meconium which may lead to an intraluminal obstruction of the terminal ileum and microcolon.
- Hirschsprung disease is associated with several gene mutations:
- The RET proto-oncogene located on chromosome 10q11.21 that interacts with the EDNRB protein located on chromosome 13.
- Mutations in the RET and 3p21, 9q31, and 19q12 genes leads to failure of migration of the enteric neural crest cells.
- Hirschsprung syndromes are associated with PHOX2B homeobox gene mutations.
- The following protein mutations may also lead to Hirschsprung disease:
- Chromosome 5 - GDNF protein
- Chromosome 20 - EDN3 protein
- Chromosome 22 - SOX10 protein
- Chromosom 1 - ECE1 protein
- Chromosome 19 - NTN protein
- Chromosome 2 - SIP1 protein
Associated Conditions
- Conditions associated with extrinsic bowel obstruction include:[8][9][10][11]
- Adhesions
- Hernia
- Volvulus
- Endometriosis
- Conditions associated with intrinsic bowel obstruction include:
- Large and small bowel cancers
- Cystic fibrosis
- Hirschsprung disease
- Down's syndrome
- Strictures:
- Anatomical
- Inflammatory
- Ischemic
- Radiation
- Conditions associated with intraluminal bowel obstruction include:
- Gastrointestinal foreign body
- Intussusception
- Gallstones
- Constipation
- Bezoar
- Volvulus
- Hematoma
Gross Pathology
- On gross pathology, adhesions, volvulus, narrow lumen with proximal dilatations and exudate are characteristic findings of bowel obstruction.[11]
Microscopic Pathology
- On microscopic histopathological analysis, fibrosis, necrosis, and ischemia are characteristic findings of bowel obstruction.[11]
References
- ↑ Wright HK, O'Brien JJ, Tilson MD (1971). "Water absorption in experimental closed segment obstruction of the ileum in man". Am. J. Surg. 121 (1): 96–9. PMID 5540839.
- ↑ Noer RJ, Derr JW, Johnston CG (1949). "The Circulation of the Small Intestine: An Evaluation of its Revascularizing Potential". Ann. Surg. 130 (4): 608–21. PMC 1616446. PMID 17859455.
- ↑ Markogiannakis H, Messaris E, Dardamanis D, Pararas N, Tzertzemelis D, Giannopoulos P, Larentzakis A, Lagoudianakis E, Manouras A, Bramis I (2007). "Acute mechanical bowel obstruction: clinical presentation, etiology, management and outcome". World J. Gastroenterol. 13 (3): 432–7. PMC 4065900. PMID 17230614.
- ↑ Mitul AR (2016). "Congenital Neonatal Intestinal Obstruction". J Neonatal Surg. 5 (4): 41. doi:10.21699/jns.v5i4.472. PMC 5117264. PMID 27896149.
- ↑ Huis M, Stulhofer M, Szerda F, Vukić T, Bubnjar J (2006). "[Obstruction icterus--our experience]". Acta Med Croatica. 60 (1): 71–6. PMID 16802577.
- ↑ BODIAN M, WHITE LL, CARTER CO, LOUW JH (1952). "Congenital duodenal obstruction and mongolism". Br Med J. 1 (4749): 77–9. PMC 2022519. PMID 14896034.
- ↑ Dalla Vecchia LK, Grosfeld JL, West KW, Rescorla FJ, Scherer LR, Engum SA (1998). "Intestinal atresia and stenosis: a 25-year experience with 277 cases". Arch Surg. 133 (5): 490–6, discussion 496–7. PMID 9605910.
- ↑ Miller G, Boman J, Shrier I, Gordon PH (2000). "Natural history of patients with adhesive small bowel obstruction". Br J Surg. 87 (9): 1240–7. doi:10.1046/j.1365-2168.2000.01530.x. PMID 10971435.
- ↑ Barkan H, Webster S, Ozeran S (1995). "Factors predicting the recurrence of adhesive small-bowel obstruction". Am. J. Surg. 170 (4): 361–5. PMID 7573729.
- ↑ Butt MU, Velmahos GC, Zacharias N, Alam HB, de Moya M, King DR (2009). "Adhesional small bowel obstruction in the absence of previous operations: management and outcomes". World J Surg. 33 (11): 2368–71. doi:10.1007/s00268-009-0200-6. PMID 19756860.
- ↑ 11.0 11.1 11.2 Beardsley C, Furtado R, Mosse C, Gananadha S, Fergusson J, Jeans P, Beenen E (2014). "Small bowel obstruction in the virgin abdomen: the need for a mandatory laparotomy explored". Am. J. Surg. 208 (2): 243–8. doi:10.1016/j.amjsurg.2013.09.034. PMID 24565365.