1. Patients with PUD that fail to respond to medical therapy
2. Patients with malignant disease

1. B1: the majority of the stomach is removed and the duodenum is anastamosed in end-to-end fashion to the remaining gastric body
2. B2: The remaining gastric body is anastamosed in side-to-side fashion to the jejunum (similar to a Roux-en-y)

• Truncal vagotomy: severs the vagus nerve at the distal esophagus and significantly reduces acid secretion; results in gastric stasis and poor gastric emptying and therefore is combined with gastric drainage procedure (pyloroplasy or gastrojejunostomy)
• Selective vagotomy: divides and severs the vagus nerve branches that supply the parietal cells while preserving those that innervate the antrum and pylorus (thus no gastric drainage procedure is necessary)

• Early satiety
• Dumping syndrome
• Fat maldigestion
• Gastric stasis
• Lactose intolerance

• Early dumping occurs within ~30 minutes of eating when hyperosmotic fluids enter the small bowel and cause rapid fluid shifts
• Symptoms include abdominal cramping, nausea, diarrhea, and palpitations

• Late dumping syndrome occurs up to 3 hours after eating and results from rapid absorption of simple sugars in the small bowel, which triggers an exaggerated release of insulin resulting in reactive hypoglycemia
• Symptoms are similar to those of hypoglycemia and include sweating, dizziness, tachycardia, irritability, hunger, and syncopal symptoms

1. Eat 6 or more small meals per day
2. Eat slowly and chew thoroughly
3. Sit upright while eating
4. Avoid or limit high-sugar foods and beverages
5. Limit fluid consumption at meals
6. Eat a protein-containing food with each meal
7. Choose high-fiber foods when possible

• Accelerated transit time prevents sufficient mixing of foods with digestive enzymes and bile salts
• Decreased enzyme production reduces the ratio of enzymes to food
• Larger-than-normal food particles enter the jejunum, making their degradation by enzymes more difficult

• Addition of exogenous pancreatic enzymes reduces fat excretion
• Prolonged steatorrhea may require monitoring and replacement of fat-soluble vitamins

• Bezoar formation
• Bacterial overgrowth
• Intolerance to solid food

Afferent limb syndrome typically results in pain and cramping as a result of limb distension.

Patients describe relief with vomiting, which temporarily clears or decompresses the afferent limb.

Treatment is generally conservative (as with other types of gastritis) and should include an empiric trial of cholestyramine (which binds bile salts).

Surgical reconstruction can be considered in refractory cases

5 mg/day is recommended for deficiency

A 100 mcg dose in a daily multivitamin is usually sufficient for maintenance

• Distal stomach
• Gallbladder
• Common bile duct
• Portion of the duodenum
• Head of the pancreas

Note: the modern, preferred variation of the procedure preserves the entire stomach, pylorus, and a 2-cm portion of the duodenum

Delayed gastric empyting is the most common complication.

Weight loss, dumping syndrome, DM, and malabsorption due to pancreatic exocrine insufficiency may also occur.

Treating acid hypersecretion with a PPI can improve gastric stagnation.

Prokinetic agents are also common.

Pancreatic enzyme deficiency usually presents with steatorrhea.

Measurements of fecal fat and fecal elastase are used for diagnosis.

• Decreased appetite/anorexia
• Nausea and vomiting
• Bloating
• Fullness (especially in morning after an overnight fast)
• Early satiety
• Halitosis
• Postprandial hypoglycemia

• A 4-hour solid phase gastric scintigraphic study is recommended, as liquid phase emptying can be accelerated in patients with DM or neuropathy.
• Patients must be off motility-slowing agents with a sufficient washout period
• International standards for a low-fat meal are established
• Gastric retention of >10% of test meal at 4 hours is indicative of delayed gastric emptying

• Low fiber
• Ground meats
• Avoidance of fatty foods, raw veggies, and high-fiber fruits

• Iron
• Vitamin B12
• Vitamin D

• Many patients with GP limit iron-rich foods (such as red meat) because of intolerance
• Many GP patients are treated with PPIs for acid reflux, which reduces gastric acidity and prevents conversion of ferric iron to ferrous form
• Elevated gastric pH and poor motility can increase risk of developign small bowel bacterial overgrowth, which can significantly decrease duodenal iron absorption

A patient's diet history can help determine which factors may respond the most to dietary manipulation.

Modifying one or two parameters at a time will prevent overzealous intervention that often results in unnecessary dietary limitations.

• Patients with chronic intestinal pseudo-obstruction
• End-stage scleroderma
• Dysmotility disorders that include both the small bowel and stomach

• Gastric acid
• Intestinal peristalsis
• Ileo-cecal valve
• Bile acids
• The enteric immune system
• Pancreatic enzyme secretion

SBBO increases SCFA production, which can result in decreased luminal pH, denatured intestinal enzymes, and increase in overall osmotic load.

The result is rapid gut transit, maldigestion, and malabsorption.

• Gas
• Bloating
• Abdominal distension/discomfort
• Nausea
• Diarrhea
• Weight loss
• Overall decline in nutrition status

• Hydrogen breath test (preferred)
• Radio-labeled carbon incorporated into xylose
• Ileal aspirate and culture (gold standard but invasive)

It is not uncommon for clinicians to empirically treat for SBBO based on symptoms.

• Diarrhea (steatorrhea)
• Weight loss
• Fe anemia
• Fat-soluble vitamin deficiencies

• Unexplained Fe deficiency
• Dermatitis herpetiformis
• Rising serum transaminases
• Problems with fertility

• Serological testing used as screening tool
• Positive serological test is followed up with small bowel biopsy (gold standard)

• Collagenous sprue
• Ulcerative jejunitis
• Small bowel T-cell lymphoma

EE is not significantly elevated in patients with inactive Crohn's.

In active Crohn's, REE is increased but total energy expenditure is not significantly elevated (likely due to patients being sedentary during flares)

Polymeric is as effective as elemental/semi-elemental.

Reduced fat may offer greater tolerance compared with formulas that have large amounts of LCTs. Formulas with large amounts of MCTs are as effective as reduced fat formulas.

Crohn's disease increases risk of hyperhomocysteinemia due to decreased serum levels of B12 and folate

Ileal resections increase risk of B12 deficiency, while use of methotrexate and/or decreased intake of leafy green veggies increases risk of folate deficiency.

Patients with high-output EC fistulas and those with frequent diarrhea are at risk of zinc deficiency

Those with zinc deficiency should receive supplemental zinc.

Folic acid adequacy is particularly relevant for UC because of its link to cancer prevention (patients with long-standing dz are at risk of colon cancer)

Folate supplementation may have a protective role

Phase 1 occurs right after surgery and is characterized by hypersecretion of gastric fluids and significant fluid losses. PN and fluid resuscitation is necessary during this period.

Phase 2 occurs over the next 2 years. The gut goes through a period of accomodation when absorptive capacity (and ability to get nutrients from EN) increases

Phase 3 occurs after 2 years. Further adaptation of the gut is not possible and nutrition support must be tailored to meet patient's needs

In general, patients with >70-90 cm of small bowel and an intact colon are able to gain autonomy from total PN

Patients need ~130-150 cm of small bowel when the colon is removed

• Increase nutrient and fluid absorption by slowing intestinal transit time
• Control gastric acid hypersecretion
• Enhance mixing of pancreatic enzymes and bile salts
• Avoid osmotic agents
• Treat bacterial overgrowth when necessary
• Use of ORS to avoid dehydration

Octreotide can reduce GI fluid output in patients with output driven by secretory processes.

Disadvantages are that it is expensive, it must be given subcutaneously, and tachyphylaxis (diminished effects from medication) develops quickly.

Cholestyramine binds to bile salts and prevents reabsorption.

If SBS patients lose <100 cm of functional distal ileum, then the remaining bowel can adequately absorb bile salts for reuse. Cholestyramine can be helpful for these patients.

If patients lose >100 cm of functional distal ileum, then they have difficulty reabsorbing bile salts. Replacement of the lost bile salts by the liver can be inadequate, resulting in inadequate fat absorption. Cholestyramine rapidly depletes the bile salt pool in these patients and can exacerbate diarrhea.

• Normally, calcium binds to oxalate, forming an unabsorbable complex that is excreted in the stool
• In the presence of steatorrhea, free fatty acids have a higher affinity for calcium, resulting in the oxalate being absorbed
• The absorbed oxalate eventually binds to calcium in the kidney, resulting in kidney stone formation

A urine output of >1200 mL/d is the most important intervention to avoid kidney stone formation.

Diets low in oxalate and oral calcium supplementation may also be helpful.

• Length of bowel resected
• Length of bowel remaining
• Presence or absence of terminal ileum
• Amount of remaining colon

Patients with a colon should have a lower-fat, high carbohydrate diet

Patients without a colon benefit from a higher-fat, lower-carbohydrate diet to reduce fluid losses

Many patients infuse their PN over 10-12 hours overnight, allowing time off during the day for activities?

Infusion rates of 250-350 mL/hr are not uncommon in home setting

24-hour urine output should be monitored to avoid kidney stone formation (<1 L/day = bad)

Periodic assessment of vitamin and mineral indices should be monitored