Bowel obstruction 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 occurs functionally as a result of abnormal anatomy or mechanically, which may occur acutely or chronically. An obstruction may occur extrinsically, intrinsically or intraluminally including tumors, strictures and foreign bodies. Excessive bowel distention can lead to ischemia, necrosis and perforation.

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.
• 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:

• 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

Gross Pathology

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Microscopic Pathology

• On microscopic histopathological analysis, [feature1], [feature2], and [feature3] are characteristic findings of [disease name].

References

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