Short bowel syndrome

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Classification according to ICD-10
K91.2 Surgical malabsorption, not elsewhere classified
ICD-10 online (WHO version 2019)

The short bowel syndrome (engl. Short bowel syndrome ) refers to a disease which by the operative removal ( resection large) or congenital absence parts of the small intestine occurs.

Causes of disease (etiology)

Major small bowel surgery may be unavoidable in some diseases, despite their known adverse effects; B. in acute vascular occlusions of the intestine ( mesenteric infarction ), the chronic inflammatory bowel disease Crohn's disease , cancer in the abdomen, after radiation therapy of the abdominal area ( radiation enteritis ) or after injuries with damage to the intestine. In children, entanglements of the intestine ( volvulus ), severe complications in premature birth ( necrotizing enterocolitis ) or congenital malformations ( small intestine atresia , apple peel syndrome , atresia multiplex congenita syndrome ) may require resections of the small intestine. Short bowel syndrome can rarely occur in survivors as part of a syndrome such as Pena Shokeir syndrome I.

Disease development (pathogenesis)

Since the sections of the small intestine ( duodenum , jejunum and ileum with ileocecal valve ) have different functions in digestion and nutrient absorption ( absorption ), very different failures occur when parts of the small intestine are removed. It is not possible to state exactly how much of the small intestine, which is approx. 5–6 meters long, must still be present in a healthy adult in order to ensure a symptom-free absorption of nutrients. If more than 75 percent of the small intestine has been removed, however, there are always restrictions in the absorption of nutrients. The extent of the discomfort depends on:

  • the length and location of the removed part of the small intestine
  • the presence or absence of the valve-like valve between the small and large intestine (ileocecal valve), which serves as a backflow protection and bacterial barrier
  • the functionality of the remaining small intestine and the remaining digestive organs: stomach , pancreas and liver
  • Adaptation processes in the remaining small intestine

Complaints (symptoms)

Patients with short bowel syndrome suffer from frequent, massive diarrhea , fatty stools , a lack of water , macro and micro nutrients ( protein , fat , electrolytes , calcium , magnesium , water and fat-soluble vitamins , especially vitamin B12 ) with the associated deficiency diseases and weight loss .

The diarrhea and fatty stools are caused on the one hand by the fact that water and fat are absorbed (resorbed) less in the remaining small intestine , on the other hand by the fact that the bile acids are no longer sufficiently reabsorbed from the bile when the ileum is removed. In the large intestine, they stimulate the secretion of water and electrolytes , which increases diarrhea.

Removal of the colon flap reinforced the complaints generally, as this is the transit time of the digesta shortened, bacterial overgrowth of the small intestine by colon flora is promoted and the absorption capacity of the small intestine for water and electrolytes reduced approximately by half.

Complications

In addition to the complaints directly affecting the digestive system, short bowel syndrome can lead to other problems. This includes:

  • Overproduction (hypersecretion) of gastric acid , which arises from the fact that inhibiting hormones normally formed in the jejunum cease to exist ( gastric inhibitory polypeptide - GIP, vasoactive intestinal polypeptide - VIP). The increased stomach acid makes diarrhea and fatty stools even worse.
  • Milk sugar (lactose) intolerance due to the elimination of the enzyme lactase found in certain sections of the intestinal mucous membrane . Instead of lactase, the milk sugar is broken down into D- lactate by intestinal bacteria , which on the one hand increases diarrhea and on the other hand can lead to over-acidification of the organism ( metabolic acidosis ).
  • Gallstone formation due to a decrease in the bile acid concentration in the bile , which is caused by the fact that fewer bile acids are absorbed from the food pulp during ileum resection. Since bile acids normally hold cholesterol in solution, the bile tends to precipitate cholesterol stones as the bile acid concentration decreases .
  • Kidney stone formation : Oxalate from food is normally bound to calcium in the intestine, making it insoluble in water and excreted in the stool. In short bowel syndrome, however, calcium binds to fatty acids that are not absorbed by the small intestine, which means that there is more free oxalate, which is absorbed in the still functioning colon and leads to an increase in the oxalate level in the blood (hyperoxalataemia) and urine (hyperoxalaturia). Together with the frequent dehydration, the solubility threshold for oxalate is easily exceeded, and oxalate stones precipitate in the urinary tract.

Treatment (therapy)

The treatment ideally begins before the intestinal operation by compensating for any pre-existing malnutrition or malnutrition by drinking or tube feeding .

Within the first year after the bowel operation, the remaining bowel adapts structurally and functionally to the new circumstances. In order to make maximum use of the remaining resorption capacity, the intestine needs continuous contact with food. Enteral nutrition should therefore be started immediately after the operation .

At the latest when short bowel syndrome develops, the patient receives nutritional therapy tailored to his clinical picture . In the case of pronounced malnutrition, it is necessary to feed artificially , possibly even completely via the bloodstream ( parenteral ).

To prevent deficiency diseases, the blood level of electrolytes, calcium, magnesium, phosphate, zinc, folic acid and vitamin B12 must be monitored and, if necessary, compensated for by increasing the dose. Vitamin B12 must be administered intramuscularly if the last section of the ileum (terminal ileum) where the vitamin is normally absorbed is missing.

Overproduction of gastric acid should be treated with a proton pump inhibitor such as omeprazole . This usually also improves the diarrhea.

In the case of pronounced fatty stools, a diet rich in carbohydrates is indicated. The proportion of medium-chain triglycerides (MCT) in triglycerides should be increased to 50 to 75 percent.

The anion exchanger cholestyramine and the administration of calcium are effective against the formation of gall and kidney stones .

To extend the transit time of the pulp, it can help not to drink during meals.

Overall, the therapy should be adapted as far as possible to the patient's personal situation in order to allow him a maximum quality of life despite the severity of the disease.

Drug therapy has been available for adults with short bowel syndrome since September 2014. The active ingredient teduglutide can improve the ability of the intestines to absorb nutrients and fluids, thus reducing or avoiding the need for parenteral nutrition and hydration.

outlook

In the future, a small bowel transplant may also be one of the therapeutic options for short bowel syndrome. By the beginning of 2003, around 800 patients had been operated on in this way around the world, 50 percent of whom had long-term survival. Of these, 80 percent were no longer dependent on parenteral nutrition and had a good quality of life.

See also

literature

  • P. Layer, U. Rosien: Practical Gastroenterology. 2nd Edition. Urban & Fischer, 2003, ISBN 3-437-23370-X .
  • O. Leiß: Dietetic and drug therapy for short bowel syndrome. In: Journal of Gastroenterology. 07/2005, PMID 16001349 .

Web links

Individual evidence

  1. ↑ PB Jeppesen, M. Pertkiewicz, B. Messing a. a .: Teduglutide reduces need for parenteral support among patients with short bowel syndrome with intestinal failure. In: Gastroenterology. 2012; 143 (6), pp. 1473-1481.
  2. ↑ AR Müller u. a .: Small intestine transplantation - current status and own results . ( Memento of September 27, 2007 in the Internet Archive ) In: Zentralbl Chir. 2003; 128, pp. 849-855.