Case  #3 Answers:

Answer 1
A general rule of thumb is that if the patient has at least three feet of small bowel, especially if that bowel has been reanastamosed to the colon, there is a very good chance that the patient can be weaned off long term parenteral nutrition. In a process called adaptation the villi of the remaining small bowel elongate and begin to branch effectively increasing the absorptive capacity of the small bowel. However, this process is a slow one and occurs over the course of one to two years. During that time, the patient will likely need to be supported by parenteral nutrition.

After the post-operative period the factors for eventual transition to enteral support will need to be considered. For example, challenging the gut with complex carbohydrates (as opposed to using elemental or semi-elemental diets) is important in promoting adaptation. Some studies suggest that glutamine supplementation will help with this adaptation process. Of note, this process of adaptation is more effective in the ileum than the jejunum. Thus, as the patient begins to take in more calories orally, caloric delivery from the parenteral source can be decreased slowly and the patient needs to be observed for weight maintenance. If successful, this needs to be repeated until the patient is no longer dependent on parenteral calories. Equally, if not more significant, is attention to the fluid status of the patient as well as to the delivery of vitamin B12, fat soluble vitamins, and essential fatty acids, the absorption of which will be extremely inefficient in this patient given the resection of the terminal ileum and consequent contraction of the bile acid pool.

Answer 2
Fluid and electrolyte disturbances are particularly challenging in patients with short bowel syndrome. In the proximal small bowel, sodium is co-transported with either amino acids or glucose, and water is absorbed passively. However, the intracellular junctions in the proximal gut are "leaky" and if luminal osmolality is high the water will leak back out into the lumen. Similarly, if luminal osmolality is very low, sodium will return to the gut lumen. Usually, the distal small bowel and colon remedy this. These cells have "tight" intracellular junctions and have sodium-potassium pumps that actively pump luminal sodium into the cell without needing a concentration gradient. Water follows passively, but unlike the situation in the proximal gut, the tight intracellular junctions do not allow for passive diffusion back out into the intestinal lumen.

Additionally, the proximal bowel has a more rapid intrinsic rhythmicity than the distal bowel. In other words movement of intraluminal contents is much more rapid in the jejunum compared to the ileum and is slowest in the colon. By removing the distal small bowel, an intrinsic "break" has been removed which will lead to faster intestinal transit. This will diminish contact time between luminal contents and mucosa and result in decreased absorption. Finally, in the normal setting, when the ileum is perfused by either a high fat or hyperosmotic solution it sends a message to the proximal gut to slow motility. This "ileal break" is also lost with resection of the ileum. All these factors, make management of fluid and electrolytes in the short bowel patient very difficult.

Answer 3
In response to intestinal resection there is resultant release of trophic hormones, which can result in gastric acid hypersecretion. This can lead to peptic ulceration. Fortunately this affect is usually transient and is easily remedied by the use of H2 blockers in the alimentation solution.

In addition, as discussed previously, the ileum is the site of resorption of bile acids. With loss of the ileum, there is an interruption of the enterohepatic circulation, the pathway that brings absorbed bile acids back to the liver for reutilization. Subsequently, the bile salt concentration in bile falls as the liver is unable to pace production of bile acids with their loss. This results in a decrease in the concentration of chenodeoxycholic acid, which consequently increases endogenous cholesterol synthesis. Bile acids act as solvents in the gallbladder, maintaining cholesterol in solution, as their concentration falls, cholesterol begins to precipitate from solution resulting in gallstone formation. It is unclear if any dietary changes will impact on stone formation.

Hyperoxaluria can also occur in patients with short bowel syndrome. Ingested oxalate is usually bound to calcium, which impedes its absorption.. In short bowel, much of the luminal calcium becomes bound to unabsorbed free fatty acids leaving oxalate unbound. Additionally, bile acids lost into the colon increase the colon's permeability to oxalate. These two factors result in increased oxalate absorption which subsequently precipitate in the kidney resulting in formation of oxalate stones. Treatment involves following a low oxalate diet, taking cholestyramine to bind bile acids and using citrate to prevent stone formation.

Finally, patients with short bowel syndrome can present with syndrome of slurred speech, ataxia, and altered affect simulating the "drunk state". This is caused by colonic fermentation of unabsorbed carbohydrates. One of the fermentation products is d-lactate and absorption of this metabolite can cause the syndrome. Using a lower carbohydrate diet usually readily treats this.

In the 4ICU, Kim Davis, MD provides a review of Nutrition Support with TPN guidelines for Stress.

Activities that incorporate patient evaluation with staff support:

Identify a case of excessive elevated blood glucose, blood glucose level >200 mg/dl, in a patient on TPN or TF. What was the etiology? Overfeeding, stress, lack of ability to utilize substrates, lack of insulin, or insulin resistance.....

Identify a case of refeeding syndrome. For example, decreased phosphorus, potassium, and magnesium after initiating nutrition support.

Identify a case of enteral feeding intolerance, such as high residuals, regurgitation, aspiration, diarrhea, or frequent discontinuation of feedings (due to testing procedures, intolerance, or blockage.)

Identify a patient who required a percutaneous gastrostomy tube and their requirements for placement and possible complications.

After identifying cases as described above, contact the Clinical Nutrition Unit at extension 6-4304 to review them with a team member (dietitian and/or pharmacist).