Short bowel syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Sadaf Sharfaei M.D.[2]
Overview
Short bowel syndrome occurrs as a result of bowel resection following various diseases of the gut such as Crohn's disease, malignancies, ischemia, and trauma. Short bowel syndrome occurs when the length of the small intestine is less than 2 meters and requires nutritional therapy to prevent malnutrition. Post bowel resection, adaptation might occur which includes structural, motility and functional changes in the remaining intestine. Changes usually start in the first 24 hours following bowel resection and last for about two years. Adaptation depends upon multiple factors including individual, intestinal and therapeutic measurements. Following bowel resection, adaptation occurs in three phases including acute, adaptive, and maintenance phases. Successful adaptation depends on the length of remaining intestine, portion of the resected intestine, and early introduction of nutrition therapy. The term total intestinal adaptation is used when the patient is weaned from parenteral nutrition. The main reason for malabsorption following bowel resection is reduced absorptive capacity of the small intestine due to loss of surface area. On gross and microscopic examination, the resected bowel segment may show the underlying causes including Crohn's disease, malignancies or ischemia.
Pathophysiology
Physiology
The small intestine has an average length of 5.5-6 meters and is responsible for digestion and absorption of food and nutrients. Three portions of small intestine are duodenum, jejunum, and ileum. There is an anatomic gradient for absorption throughout the gastrointestinal tract.[2][3]
- Duodenum is the first part of the intestine located after the stomach and receives partially digested acidic chyme from the stomach. Brunner's glands, which secrete alkaline rich mucin are also found in the duodenum. This alkaline rich mucin plays a protective role against the acidic contents received from the stomach.
- The jejunum (second portion of small intestine) is responsible for absorption of nutrients. The inner surface of the jejunum is covered with villi, which increase the surface area of tissue available to absorb nutrients from the gut contents. The villi in the jejunum are much longer than in the duodenum or ileum. It has many large circular folds in its submucosa called plicae circulares, which increase the surface area for nutrient absorption.
- The ileum (third portion of small intestine) is responsible for absorption of vitamin B12 and bile salts and whatever products of digestion that were not absorbed by the jejunum. Its surface is made up of folds, mainly villi and microvilli. Therefore the ileum has an extremely large surface area both for the adsorption of enzymes and for the absorption of products of digestion. The diffuse neuroendocrine system (DNES) cells that line the ileum contain protein and carbohydrate digesting enzymes (gastrin, secretin, cholecystokinin), which are responsible for the final stages of protein and carbohydrate digestion.
Pathogenesis
- Short bowel syndrome is the result of bowel resection following Crohn's disease, malignancies, ischemia, and trauma.[4]
- The small intestine has a very good adaptation following bowel resection of up to half of the small bowel length. However, a small intestine length less than 2 meters is considered as short bowel syndrome and requires nutritional therapy to prevent malnutrition.[5]
Post bowel resection adaptation
- Adaptation is the specific ability of the intestine to increase its capacity to absorb nutrients following loss of its surface area and length.[6][7]
- There will be structural, motility and functional changes in the remaining intestine to compensate its loss.[2][5]
- Changes usually starts in the first 24 hours following bowel resection.[8]
Change | Main features |
---|---|
Structural changes |
|
Motility changes | |
Functional changes |
|
- Adaptation depends on multiple factors including individual, intestinal and therapeutic measurements.[6]
- Adaptation usually occurrs during the first two years after the bowel resection.
- Successful adaptation depends on the length of remaining intestine, portion of the resected intestine, early introduction of nutrition therapy. Total intestinal adaptation defines as when patient is weaned from parenteral nutrition.[9]
- Following the bowel resection, adaptation occurs in three phases including acute, adaptive, and maintenance phases.[10]
Intestinal adaptation | ||
---|---|---|
Phase | Duration | Main feature |
Acute phase | 1 to 3 months |
|
Adaptive phase | 1 to 2 years |
|
Maintenance phase | Following adaptive phase |
|
- There are factors which stimulate the intestinal adaptation, including:[11]
- Oral nutrients
- Soluble fibres such as polysaccharides present in pectin and soy
- Hydrolysed or whole protein formula
- Polyamines
- Long-chain triglycerides and short-chain fatty acids
- Glucagon-like peptide 2 (GLP-2)
- Secretin
- Cholecystokinin
- Neurotensin
- Insulin-like growth factor I
- Glutamine
- There are factors which decrease the intestinal adaptation, including:
- Starvation
- Absence of luminal nutrients
- Absence of pancreato-biliary secretions
- Monosaccharides
Malabsorption
- The main reasons for malabsorption following bowel resection include:
- Reduced absorption capacity of the small intestine due to loss of surface area, leading to:
- Loss of fluid and dehydration
- Electrolyte imbalance
- Loss of Macronutrients including carbohydrates, lipids and proteins
- Disturbance in production of enzymes and hormones, leading to:
- Diarrhea
- Steatorrhea
- Loss of vitamins
- Resection of specific sites, leading to:
- Loss of absorption of vitamin B12 and bile salts
- Reduced capacity of fluid retention
- Loss of ileocecal valve, leading to:
- Small bowel bacterial overgrowth
- Increased gastric and intestinal transit
- Compromised production of gastrointestinal regulators including cholecystokinin, secretin, gastric inhibitory polypeptide and peptide YY, leading to:
- Increased gastric and intestinal transit
- Hypergastrinemia
- Reduced absorption capacity of the small intestine due to loss of surface area, leading to:
Associated Conditions
Short bowel syndrome might be associated with following pathologies:
- Mesenteric vascular events including thrombosis or occlusion of the superior mesenteric artery or vein
- Crohn's disease
- Malignancy
- Radiation enteritis
- Volvulus
- Adhesions
- Jejunoileal bypass surgery to treat obesity
- Trauma to the small intestine
- Internal hernia
Gross Pathology
- On gross pathology, the resected bowel may show the underlying causes including Crohn's disease, malignancies or ischemia.
Microscopic Pathology
- On microscopic histopathological analysis, the resected bowel may show the underlying causes including Crohn's disease, malignancies or ischemia.
References
- ↑ "File:Diagram of the small bowel 01 CRUK 045.svg - Wikimedia Commons".
- ↑ 2.0 2.1 Tappenden KA (2014). "Pathophysiology of short bowel syndrome: considerations of resected and residual anatomy". JPEN J Parenter Enteral Nutr. 38 (1 Suppl): 14S–22S. doi:10.1177/0148607113520005. PMID 24500909.
- ↑ Thomson, Alan B.R.; Drozdowski, Laurie; Iordache, Claudiu; Thomson, Ben K.A.; Vermeire, Severine; Clandinin, M. Tom; Wild, Gary (2003). Digestive Diseases and Sciences. 48 (8): 1546–1564. doi:10.1023/A:1024719925058. ISSN 0163-2116. Missing or empty
|title=
(help) - ↑ Sundaram A, Koutkia P, Apovian CM (2002). "Nutritional management of short bowel syndrome in adults". J. Clin. Gastroenterol. 34 (3): 207–20. PMID 11873098.
- ↑ 5.0 5.1 Eça, Rosário; Barbosa, Elisabete (2016). "Short bowel syndrome: treatment options". Journal of Coloproctology. 36 (4): 262–272. doi:10.1016/j.jcol.2016.07.002. ISSN 2237-9363.
- ↑ 6.0 6.1 Warner, Brad W. (2013). "Adaptation: Paradigm for the gut and an academic career". Journal of Pediatric Surgery. 48 (1): 20–26. doi:10.1016/j.jpedsurg.2012.10.014. ISSN 0022-3468.
- ↑ Rowland, Kathryn J.; McMellen, Mark E.; Wakeman, Derek; Wandu, Wambul S.; Erwin, Christopher R.; Warner, Brad W. (2012). "Enterocyte expression of epidermal growth factor receptor is not required for intestinal adaptation in response to massive small bowel resection". Journal of Pediatric Surgery. 47 (9): 1748–1753. doi:10.1016/j.jpedsurg.2012.03.089. ISSN 0022-3468.
- ↑ Matarese LE, O'Keefe SJ, Kandil HM, Bond G, Costa G, Abu-Elmagd K (2005). "Short bowel syndrome: clinical guidelines for nutrition management". Nutr Clin Pract. 20 (5): 493–502. doi:10.1177/0115426505020005493. PMID 16207689.
- ↑ Wall, Elizabeth A. (2013). "An Overview of Short Bowel Syndrome Management: Adherence, Adaptation, and Practical Recommendations". Journal of the Academy of Nutrition and Dietetics. 113 (9): 1200–1208. doi:10.1016/j.jand.2013.05.001. ISSN 2212-2672.
- ↑ Misiakos EP, Macheras A, Kapetanakis T, Liakakos T (2007). "Short bowel syndrome: current medical and surgical trends". J. Clin. Gastroenterol. 41 (1): 5–18. doi:10.1097/01.mcg.0000212617.74337.e9. PMID 17198059.
- ↑ Vanderhoof JA, Young RJ (2003). "Enteral and parenteral nutrition in the care of patients with short-bowel syndrome". Best Pract Res Clin Gastroenterol. 17 (6): 997–1015. PMID 14642862.
- ↑ "File:ResectedIleum.jpg - Wikimedia Commons". External link in
|title=
(help) - ↑ "File:Crohn Jejunum.PNG - Wikimedia Commons".