SHORT BOWEL SYNDROME
Short bowel syndrome refers to the clinical consequences of massive small bowel resection, with or without some additional loss of large intestine. Short bowel syndrome frequently results when 75% or more of the small intestine is resected.
Reasons for massive bowel resection include intussusception, intestinal infarction secondary to strangulation or vascular thrombosis, loss of blood supply due to injury, and intestinal neoplasia. Clinical manifestations of short bowel syndrome persist when the remaining intestine is unable to undergo adequate compensatory changes. SIBO may also become a significant complicating factor, especially if the ileocolic valve is removed.Affected patients usually have unrelenting small bowel diarrhea and progressive weight loss in the face of a ravenous appetite. It should be noted, however, that not all patients that lose a large amount of small intestine have signs of short bowel syndrome. It is not always the amount of bowel loss that determines whether or not a patient will be affected. The response to bowel loss is often unpredictable. Clinically, sometimes a patient will do surprisingly well when it was anticipated that the prognosis would be poor, and in other cases a patient will do unexpectedly poorly. Several important factors are involved in determining clinical course. These include the following:
1. Status of the ileocolic valve (symptoms are consistently worse if the valve is lost)
2. The extent and site of bowel resection
3. The functional capacity of the remaining bowel and other digestive organs
4. The degree of adaptation that subsequently occurs in the remaining small and large intestine
The ileocolic valve is important for preventing SIBO, and it may also play an important role in slowing small intestinal transit time.
Maldigestion and malabsorption are prominent features of short bowel syndrome.
Factors causing malabsorption include decreased absorptive surface area; reduced transit time, which results in inadequate intestinal mucosa-nutrient contact time; decreased bile salt reabsorption, especially if the ileum is lost, resulting in decreased fat absorption; and decreased fatty acid absorption, which results in impairment of colonic water absorption.Maldigestion results from decreased nutrient contact time with digestive enzymes; deficiency of cholecystokinin and secretin in patients with significant resection of duodenum and jejunum, which subsequently causes decreased release of pancreatic and biliary exocrine secretions; and loss of important mucosal brush border digestive enzymes, which follows massive bowel resection. Gastric acid hypersecretion may also occur after massive small bowel resection, for unknown reasons. Consequences of acid hypersecretion may include inactivation of pancreatic lipase and increased osmolarity in the small intestinal lumen.
The degree of adaptation that occurs in the small intestine is an important factor in determining whether or not a patient will be able to recover sufficiently to maintain adequate fluid balance and body weight. Over time following massive bowel resection, compensatory changes that increase the absorptive surface of the remaining intestine occur. The fact that it takes time for compensation to occur is an important clinical point, because it is important that a decision resulting in too early euthanasia of a patient not be made too hastily. These include increased bowel diameter, lengthening of villi, and crypt enlargement to maximize the number of mucosal cells per unit length of gut. One of the most important factors in promoting adaptation is the presence of intraluminal nutrients (long-chain triglycerides or long- chain free fatty acids have been shown to have the greatest trophic effect, but any nutrient may promote a stimulatory effect). Pancreaticobiliary secretions, GI and other hormones, and prostaglandin E2 also play a role in stimulating bowel adaptation.
Corticosteroids probably do not have any significant effect on promoting bowel adaptation.Clinical Signs
In patients that have undergone extensive resection, persistent diarrhea that is often watery in nature is the predominant early sign. Dehydration and electrolyte deficiencies can readily occur. Postoperative treatment is directed at preventing these factors from becoming significant. Malabsorption predominates during the ensuing weeks, and major weight loss and nutritional deficiencies develop. Later, as intestinal adaptation begins to occur, body weight frequently stabilizes, although at levels that are mildly to moderately below preresection levels. Diarrhea and steatorrhea persist in most patients. In some patients, especially those that have lost the ileocolic valve, steatorrhea and malabsorption continue to be severe and the prognosis for stabilization becomes very poor.
Treatment
The primary goal of medical therapy for patients with short bowel syndrome involves providing adequate nutritional support and controlling diarrhea through use of antidiarrheal agents. Gastric acid hypersecretion can be an important causative factor of diarrhea and should be controlled with H2-receptor antagonists (e.g., famotidine). Intestinal bacterial overgrowth is managed with antibiotics (metronidazole and amoxicillin or enrofloxacin are often used initially; metronidazole and/or tylosin are often used if long-term antibiotics are required). It is sometimes useful to provide pancreatic enzyme replacement therapy (e.g., Pancrezyme). If diarrhea is persistently watery, an antidiarrheal agent such as loperamide is used. The dose for dogs is 0.05 to 0.1 mg/lb orally two to three times daily. Loperamide can be used in cats at 0.025 to 0.04 mg/lb every 12 hours. In some patients, it may be necessary to use loperamide on a long-term basis.
If the treatments listed above are not considered reasonably effective, several other maneuvers can be tried.
Research work published in Japan in 1992 suggested that ursodeoxycholate (UDCA) is beneficial in some dogs with short bowel syndrome. The study involved resection of 75% of the small intestine in healthy beagle dogs followed by separation of the dogs into one of three treatment groups:1. 300 mg UDCA plus 0.375 μg of vitamin D3 every other day
2. 0.375 μg vitamin D3 every other day
3. Control group, no drug therapy
Dogs medicated with UDCA experienced significant improvements in body weight, fecal characteristics, and overall nutritional status. The beneficial effect of UDCA may be in prolongation of intestinal transit time. Other investigators have also found that UDCA has an inhibitory effect on GI smooth muscle.
Finally, use of a hydrophilic laxative may help decrease fluidity of the existing bowel content and increase fecal bulk. Among the compounds that may be tried are methylcellulose (Citrucel), psyllium (Metamucil, Siblin), Karaya gum, and calcium polycarbophil (Fiberall, Fiber Con). Calcium poly- carbophil reportedly absorbs 60 to 100 times its weight in water.
The ideal form of nutritional support during the early postoperative period is total parenteral nutrition (TPN) (see Chapter 12). TPN is routinely used in humans with short bowel syndrome to maintain caloric intake, electrolyte balance, and acid-base balance for as long as 1 to 2 months of the initial phase of therapy. This is not feasible in most veterinary patients.
Partial parenteral nutrition can also be used to help provide adequate early nutritional support. ProcalAmine (McGaw, Inc) is a protein-sparing product that is very convenient for use in clinical practice because no mixing or additives are required. It is a combination of 3% amino acids, 3% glycerol, and electrolytes. If infused at maintenance rates (30 ml/lb/day), this product provides approximately 20% of a patient's caloric needs and 0.6 to 0.9 g/lb/day of protein. ProcalAmine contains inadequate sodium (35 mEq/L) and chloride (41 mEq/L) for total maintenance requirements.
Addition of 65 ml of 7.2% hypertonic saline to a liter of ProcalAmine increases electrolyte levels sufficiently (sodium, 115 mEq/L). ProcalAmine does contain adequate potassium (24 mEq/L). A peripheral vein can be used. ProcalAmine is hypertonic, and the catheter site should be watched carefully for any evidence of phlebitis. Catheters are not left in place any longer than 60 to 72 hours.Limited oral intake is instituted as soon as possible after surgery to begin stimulation of intestinal adaptation. Elemental or polymeric diets are often fed in the initial phase. Long-term feeding involves diets that are low in fat and highly digestible. Small amounts should be fed frequently (three to four meals per day). Vitamin B12 (cobalamin) as well as fat-soluble vitamins should be supplemented indefinitely.
If intestinal adaptation occurs, a stable body weight and a reasonable stool consistency can be maintained on a long-term basis. Some patients, however, never stabilize despite all treatment efforts and careful dietary manipulation, and their prognosis becomes poor. The prognosis seems to be better in patients that are aggressively managed in the early stages. Because it can be very difficult to predict accurately how well a patient with short bowel syndrome will respond to therapy, every effort should be made to maintain treatment for a reasonable period of time before euthanasia is recommended.
Careful consideration about how much bowel will be resected should be given at the time of surgery. Prevention of situations that may end with development of short bowel syndrome begins with avoiding unnecessarily extensive resection of small intestine, considering conservative resection of ischemic bowel with the option of follow-up surgery if necessary, and making every effort to leave the duodenum and ileocolic valve intact. Early diagnosis and timely surgical intervention in situations that might end up requiring intestinal resection are extremely important in minimizing the amount of intestine that will need to be removed.
More on the topic SHORT BOWEL SYNDROME:
- Short bowel syndrome
- SHORT BOWEL SYNDROME
- References
- Index
- Diagnosis
- VOMITING
- INFLAMMATORY BOWEL DISEASE
- DISEASES OF THE COLON WITH DIARRHEA AS THE PRINCIPAL SIGN
- Acute Abdomen in Ruminants
- Obstructive Intestinal Diseases