Nutrition for Patients with Disorders of the Lower GI Tract and Accessory Organs

Nutrition for Patients with Disorders of the Lower GI Tract and Accessory Organs

Figure 18.1The sites of nutrient absorption.

The lower gastrointestinal (GI) tract consists of the small and large intestines, rectum, and anus. Ninety to 95% of nutrient absorption occurs in the first half of the small intestine (Fig. 18.1). The large intestine absorbs water and electrolytes and promotes the elimination of solid wastes. The accessory organs—liver, gallbladder, and pancreas—play vital roles in nutrient digestion. With many disorders of the lower GI tract and accessory organs, nutrition therapy is used to improve or control symptoms; replenish losses; and promote healing, if applicable. For one GI disorder, celiac disease, nutrition therapy is the sole mode of treatment.

image This chapter presents nutrition therapy for altered bowel elimination, malabsorption syndromes, disorders of the large intestine, and disorders of the accessory organs. Box 18.1 lists nutrition-focused assessment criteria for lower GI disorders.



Criteria for diagnosing constipation include having fewer than three bowel movements per week, passing stools that are hard, and excessive straining during defecation. Inadequate fiber intake, physical inactivity, and low food intake increase the risk of constipation. Constipation can occur secondary to irregular bowel habits, psychogenic factors, chronic laxative use, metabolic and endocrine disorders, and bowel abnormalities (e.g., tumors, hernias, strictures). Certain medications, such as analgesics that contain opiates, antidepressants, diuretics, aluminum hydroxide, and iron and calcium supplements cause constipation. Contrary to popular belief, daily bowel movements are not necessary provided the stools are not hard and dry.

Nutrition Therapy for Constipation

To treat constipation, it is standard practice to recommend that fiber intake be increased. Although a goal of 25 to 38 g/day, which is the Adequate Intake for fiber, may be recommended, those levels are based on the amount of fiber needed to protect against coronary heart disease not for optimal bowel function. The amount of fiber needed to alleviate constipation varies among individuals and is usually determined by trial and error.

Fiber increases stool weight, bulk, and fecal water content and stimulates peristalsis to promote a more rapid transit time. Insoluble fiber is more effective at treating constipation than soluble fiber. Foods with the highest proportion of insoluble fiber are whole grains, wheat bran, and the skins and seeds of fruit and vegetables. Fiber intake is increased by adding fiber-rich foods (e.g., vegetables) and replacing low-fiber foods with higher fiber versions (e.g., replacing white pasta with whole wheat pasta) (Box 18.2). However, most fruits, vegetables, and whole wheat breads provide only 1 to 3 g of fiber per serving. Foods with the highest amount of fiber per serving are high fiber cereals and legumes, which may provide 10 g/serving or up to 8 g/serving, respectively. Fiber supplements may be necessary if adequate fiber cannot be consumed through food.

A gradual increase in fiber is recommended to avoid symptoms of intolerance such as gas, cramping, and diarrhea. If these side effects do occur, they are usually temporary and subside within several days. To achieve maximum benefit, fiber intake should be spread throughout the day.

Probiotics live microorganisms found in food that, when consumed in adequate amounts, are beneficial to health.

Prebiotics nondigestible food components that stimulate the growth of probiotic bacteria within the large intestine.

Other interventions to promote bowel regularity include

  • Ensuring an adequate fluid intake of at least 64 oz/day; without enough water, a high-fiber diet can worsen constipation, abdominal pain, bloating, and gas (Academy of Nutrition and Dietetics [AND], 2016).

  • Increasing aerobic exercise

  • Consuming probiotics or prebiotics daily, such as yogurt containing live bacterial cultures, acidophilus milk, and kefir


Diarrhea is a common symptom of many GI disorders and infectious diseases and is a frequent side effect of chemotherapy and radiation. It is characterized by an increase in the frequency of bowel movements and/or water content of stools, which alters either the consistency or volume of fecal output. A rapid transit time decreases the time available for water, sodium, and potassium to be absorbed through the colon; the result is more water and electrolytes in the stools and the potential for dehydration, hyponatremia, hypokalemia, acid-base imbalance, and metabolic acidosis. Chronic diarrhea can lead to malnutrition related to impaired digestion, absorption, and intake.

Osmotic diarrhea occurs when there is an increase in particles in the intestine, which draws water in to dilute the high concentration. The causes of osmotic diarrhea include maldigestion of nutrients (e.g., lactose intolerance), excessive intake of sorbitol or fructose, dumping syndrome, tube feedings, and some laxatives. It is cured by treating the underlying cause.

Secretory diarrhea is related to an excessive secretion of fluid and electrolytes into the intestines. Bacterial, viral, protozoan, and other infections cause secretory diarrhea, as do some medications and some GI disorders, such as Crohn disease and celiac disease. An excessive amount of bile acids or unabsorbed fatty acids in the colon can also cause secretory diarrhea. If the cause is infection, antibiotics are the primary component of treatment. Symptoms may be treated with medications that decrease GI motility or thicken the consistency of stools, such as the soluble fiber psyllium (Metamucil).

Antibiotic-acquired diarrhea is caused by the disruption in GI microbiota as a side effect of antibiotic therapy. Symptoms range from mild and self-limiting to severe, particularly in Clostridium difficile infections (Hempel et al., 2012).

Nutrition Therapy for Diarrhea

Nutrition therapy for diarrhea is largely supportive and depends on the severity of diarrhea and the underlying cause. Maintaining or restoring fluid and electrolyte balance is the primary focus. Mild diarrhea lasting 24 to 48 hours usually requires no nutrition intervention other than encouraging a liberal fluid intake to replace losses. Oral rehydration solutions, such as Pedialyte and Rehydralyte, may be used. Clear liquids are avoided because they have high osmolality related to their high sugar content, which may promote osmotic diarrhea. For more serious cases, intravenous (IV) therapy is used to replace fluid and electrolytes.

On a short-term basis, a low-fiber diet (Box 18.3) that is also low in fat and lactose may help decrease bowel stimulation. Food and beverages that stimulate GI motility are avoided. High-potassium foods are encouraged. Banana flakes, apple powder, or other sources of pectin may be added to foods to help thicken the consistency of stools (AND, 2016).

Probiotics may help lessen diarrhea, especially diarrhea related to use of antibiotics. A systematic review and metaanalysis found moderate quality evidence that suggests probiotics are safe and effective for preventing C. difficile-associated diarrhea (Goldenberg et al., 2013). Because it is not known which strains or doses of probiotics may be most beneficial, it may be prudent to obtain probiotics from food sources, such as yogurt, kefir, and acidophilus milk, instead of supplements. Patients with intractable diarrhea may need complete bowel rest (i.e., total parenteral nutrition or TPN).

Lactose the disaccharide (double sugar) in milk composed of glucoses and galactose.


Malabsorption a broad term that describes altered or inadequate nutrient absorption from the GI tract.

Malabsorption occurs secondary to nutrient maldigestion or from alterations to the absorptive surface of the intestinal mucosa. Generally, malabsorption related to maldigestion involves one or few nutrients, whereas malabsorption that stems from an altered mucosa is more generalized, resulting in multiple nutrient deficiencies and weight loss. Symptoms of malabsorption vary with the underlying disorder, ranging from minimal to widespread and serious. Malabsorption may be suspected in patients who have weight loss, growth failure, postprandial abdominal pain, bloating, and flatulence. Watery diarrhea and distention are symptoms of malabsorption from carbohydrate maldigestion (e.g., lactose intolerance), whereas the passage of less frequent stools that are oily, bulky, and foul-smelling is a symptom of malabsorption related to fat maldigestion (e.g., pancreatitis). The excretion of fat in the stools means that essential fatty acids, fat-soluble vitamins, calcium, and magnesium are also lost through the stools. Nutrient deficiencies can cause metabolic complications, such as osteomalacia and bone pain related to the deficiencies of calcium, vitamin D, and magnesium. Appetite may be poor and nutrient needs may be elevated for healing. The risk for malnutrition can be high.

The goal of nutrition therapy for malabsorption syndromes is to control steatorrhea, promote normal bowel elimination, restore optimal nutritional status, and promote healing, when applicable. Nutrition therapy is individualized according to symptoms and complications; possible diet modifications appear in Table 18.1. Specific malabsorption syndromes are discussed in the following sections—namely, lactose intolerance, inflammatory bowel disease (IBD), celiac disease, and short bowel syndrome.

Steatorrhea excess fat in the stools that are loose, foamy, and foul-smelling.

Lactose Malabsorption

Lactose malabsorption refers to impaired lactose digestion related to reduced activity of lactase, the enzyme that splits lactose into its component simple sugars glucose and galactose. Without adequate lactase, lactose reaches the large intestine where microbiota ferment the sugar, which may produce bloating, cramping, flatulence, and diarrhea. Particles of undigested lactose increase the osmolality of intestinal contents, increasing the likelihood of osmotic diarrhea. Symptoms range from mild to severe, depending on the amount of lactase actually produced and the amount of lactose consumed.

Lactose malabsorption caused by a complete lack of lactase—congenital lactase deficiency—is rare. The most frequent cause of lactose malabsorption is lactase nonpersistence, a common condition in which lactase activity is low in most of the world’s adults, particularly in adults of Asian, Native American, and African descent (Heaney, 2013). Lactase nonpersistence is not synonymous with lactose intolerance, which by definition requires evidence of lactose malabsorption and the development of symptoms, which is not currently done in practice (Misselwitz et al., 2013).

In comparison to lactase nonpersistence, Caucasians from Northern Europe or Northern European descent retain high lactase levels during adulthood, which is termed lactase persistence. Both lactase persistence and nonpersistence are normal human conditions (Misselwitz et al., 2013).

Lactose malabsorption may also occur secondary to GI disorders that alter the integrity and function of intestinal villi cells, where lactase is secreted. For instance, people with IBD lose lactase activity when the disease is active and sometimes for a prolonged period afterward. The loss of lactase may also develop secondary to malnutrition because the rapidly growing intestinal cells that produce lactase are reduced in number and function. Symptoms tend to be more severe and occur more quickly after eating lactose than when lactose malabsorption is caused by lactase nonpersistence.

Lactose Malabsorption incomplete digestion of lactose.

Lactase Nonpersistence reduced activity of lactase at the jejunal brush border, which is common in the majority of human adults. Low lactase activity may cause symptoms after lactose is consumed.

Lactose Intolerance GI symptoms of lactose malabsorption that occur after a blinded, placebo-controlled lactose challenge.

Lactase Persistence persistence of a high level of lactase into adulthood which enables adequate digestion of larger amounts of lactose.

Nutrition Therapy for Lactose Malabsorption

Nutrition therapy for lactose malabsorption is to reduce lactose to the maximum amount tolerated by the individual, which is dose-related (Box 18.4). People with lactose nonpersistence may be asymptomatic when they consume doses less than 4 to 12 g of lactose (e.g., 1/3 to 1 cup of milk) or when lactose is consumed as part of a meal. Chocolate milk may be better tolerated than plain milk, although the reason is unclear (Heaney, 2013). A proven way to improve lactose tolerance is to gradually increase milk intake: Add a half-glass of milk to 1 meal on the first day, a half-glass to each of 2 meals on the second day, and continue the gradual daily increase
(Hertzler & Savaiano, 1996). This strategy promotes the development of intestinal microbiota that contains its own lactase, thereby building tolerance over time. Another strategy that may improve tolerance is to use probiotics that favor colonization with lactase-containing organisms (Heaney, 2013). For people who want to consume milk or lactose-containing foods beyond their limit, lactose-reduced milk and lactase enzyme tablets or liquid may be used.

Table 18.1 Nutrition Therapy for Malabsorption Symptoms


Dietary Interventions



Small, frequent meals

To maximize intake

Oral nutrition supplements

Liquid supplements are easy to consume, are nutritionally dense, and leave the stomach quickly.

Enteral nutrition if anorexia is severe and/or prolonged

To meet calorie and nutrient needs until the patient is able to consume an adequate oral intake


Low-fiber diet

To minimize stimulation to the bowel

Ensure adequate fluid and electrolytes.

Increased losses of fluid and electrolytes in the stool

Avoid lactose.

Lactase activity may be lost during acute episodes of malabsorption due to altered integrity and function of intestinal villi cells; lactase deficiency may persist into remission.

Nutrient deficiencies

Nutrient-dense diet

To replenish losses, facilitate healing, and meet increased needs related to the metabolism of a high-calorie, high-protein diet.

Vitamin supplements; may need water-soluble forms of the fat-soluble vitamins

Dietary sources may not be adequate to meet need.

Water-soluble forms do not require normal fat absorption to be absorbed, as do fat-soluble vitamins in their natural form.

Oral or parenteral vitamin B12

Bacterial overgrowth, pancreatic insufficiency, and ileal disease or resection impair vitamin B12 absorption.

Calcium supplements

Serum calcium may be low related to low serum albumin or calcium malabsorption related to poor vitamin D absorption or the binding of calcium with unabsorbed fats to form unabsorbable soaps.

Other mineral supplements

Magnesium levels are often low in some malabsorption syndromes; losses of zinc are high in patients with fistulas.


Limit fat.

To avoid aggravating fat malabsorption

MCT oil may be used for calories.

MCT oil is absorbed without undergoing digestion.

Tissue damage (e.g., resulting from inflammation or surgery) and/or weight loss

Increase calories (2000-3500 cal/day).

Increase protein (1.0-1.5 g/kg/day).

Calories and protein are needed to facilitate healing and restore weight.

Formation of calcium oxalate kidney stones related to binding of calcium to fat instead of oxalate, leaving increased amount of oxalate available for absorption into the blood

Increase fluids.

To dilute the urine

TFN, medium chain triglycerides.

For patients with GI disorders, a lactose-restricted diet is indicated at least until the disorder is resolved and sometimes for a prolonged period thereafter. Because lactose is used as an ingredient in many foods and drugs, a lactose-free diet is not realistic.

Inflammatory Bowel Disease

IBD, including Crohn disease (CD) and ulcerative colitis (UC), is a group of chronic immune disorders of unclear etiology, although a combination of genetic and environmental factors may be involved (Massironi et al., 2013). CD and UC are characterized by cycles that alternate between active and quiescent states; they share common symptoms and treatments (Table 18.2). Very limited data suggest diet plays a role in the onset and course of IBD; however, the association has not been clearly demonstrated (T. Yamamoto, 2013).

Malnutrition occurs in both CD and UC patients, during active or quiescent states (Alastair, Emma, & Emma, 2011). Malnutrition may be caused by poor intake, poor digestion, increased requirements related to systemic inflammation, malabsorption due to chronic inflammation, drug-nutrient interactions, and, in patients with CD, previous surgical resection of the bowel (Massironi et al., 2013). Evidence-based diet recommendations do not exist for patients with IBD, other than to follow a healthy and varied diet (Massironi et al., 2013).

Nutrition Therapy for Crohn Disease

Because CD primarily affects the small bowel, it is more likely than UC to cause nutritional complications, such as protein-calorie malnutrition and micronutrient deficiencies. Nutrition plays a pivotal role in treatment, even though there is a lack of solid evidence to formulate strong dietary recommendations (A. Cohen et al., 2013). Nutrition interventions are based on the presence and severity of symptoms, the presence of complications, and the nutritional status of the patient (see Table 18.1). Restrictions are kept to a minimum to encourage an adequate intake. Nutrition therapy varies over the course of the disease.

When CD is active, patients may benefit from

  • A low-fiber diet to minimize bowel stimulation (see Box 18.3)

  • Limiting fat if steatorrhea is present

  • Increasing protein and calories to facilitate healing

  • Restricting the intake of lactose, fructose, and sorbitol if diarrhea is present

  • Consuming small, frequent meals to help maximize intake

Table 18.2 Comparison Between Crohn Disease and Ulcerative Colitis

Crohn Disease

Ulcerative Colitis

Area affected

Can occur anywhere along the GI tract but most commonly occurs in the ileum and colon

Confined to the rectum and colon

Disease pattern

Inflammation is discontinuous, with normal tissue between patches of inflamed tissue.

All layers of the bowel are affected.

Inflammation is continuous, beginning at rectum and usually extending into the colon.

Affects only the mucosal layer

Main symptoms

Diarrhea, abdominal pain, weight loss

Diarrhea, abdominal pain, rectal bleeding

Weight loss, fever, and weakness are common when most of the colon is involved.


Fistulas, abscesses

Stricture of the ileum

Bowel perforation

Bowel obstructions may occur from scar tissue formation.

Toxic megacolon

Increased risk of intestinal cancer

Tissue erosion and ulceration

Toxic megacolon

Greatly increased risk of cancer

Nutritional complications

Impaired bile acid reabsorption may cause malabsorption of fat, fat-soluble vitamins, calcium, magnesium, and zinc.

Malnutrition may occur from nutrient malabsorption, decreased intake, or intestinal resections.

Anemia related to blood loss or malabsorption

Vitamin B12 deficiency related to B12 malabsorption from the ileum due to inflammation

Anemia related to blood loss

Dehydration and electrolyte imbalances related to diarrhea

Protein depletion from losses through inflamed tissue

Medical treatment

Antidiarrheals, immunosuppressants, immunomodulators, biologic therapies, and anti-inflammatory agents

Antidiarrheals, immunosuppressants, and anti-inflammatory agents

Surgical intervention

Most common procedure is ileostomy; disease often recurs in the remaining intestine.

Most common procedure is total colectomy; surgery prevents recurrence.

Patients are often reluctant to eat because they associate eating with pain and diarrhea. Enteral nutrition (EN) may be used for supplemental or complete nutrition. Because EN is at least as effective as parenteral nutrition (PN) but with lower costs and fewer side effects, the use of PN is limited to a small group of IBD patients for whom EN has failed or is contraindicated (Massironi et al., 2013).

Nutrition Therapy for Ulcerative Colitis

Dietary modifications for UC are based on symptoms and complications. When the disease is active, symptoms of bleeding and diarrhea are treated with an increased intake of fluid, electrolytes, protein, and calories. A low-fiber diet minimizes stimulation to the bowel. Other diet modifications that may be appropriate depending on symptoms and complications are outlined in Table 18.1.

Nutrition Therapy During Inflammatory Bowel Disease Remission

For both CD and UC, dietary restrictions are liberalized during periods of remission. Patients tend to have strong beliefs about the role of diet in the cause of IBD and in improving or worsening their symptoms (Hou, Lee, & Lewis, 2014). Box 18.5 lists food items that patients commonly believe worsen or improve their IBD (A. Cohen et al., 2013). Unfortunately, items from each of the food groups have been noted to worsen symptoms and so the list does not provide generalizable information to benefit others (Hou et al., 2014). Keeping a food diary to monitor tolerance and identify specific triggers may help manage symptoms.

A number of defined dietary regimens are promoted in lay literature as being beneficial in managing IBD based on theories of how food interacts with the body (Hou et al., 2014). The Specific Carbohydrate Diet (SCD), the Fermentable Oligo-, Di-, and Monosaccharides (FODMAP) diet, and the Paleolithic (Paleo) diet are among the regiments advocated for IBD.
Little evidence exists for the efficacy of these diets. Prospective randomized controlled trials are needed to clarify the role of diet in IBD.

Celiac Disease

Celiac disease is a genetic autoimmune disorder characterized by chronic inflammation of the proximal small intestine mucosa related to a permanent intolerance to certain gluten-forming proteins found in wheat, barley, and rye. When ingested, these proteins trigger an immune response that damages the villi that line the mucosa of the small intestine. Loss of absorptive surface area and a decrease in digestive enzymes lead to malabsorption of macro- and micronutrients, resulting in diarrhea, flatulence, weight loss, vitamin and mineral deficiencies, iron deficiency anemia, and loss of bone. People at risk of celiac disease are those who have an autoimmune disease (e.g., type 1 diabetes), Down syndrome, or a first-degree relative with celiac disease.

Dermatitis Herpetiformis a chronic inflammatory skin disease characterized by groups of red, raised blisters that itch and burn.

Symptoms and their severity vary widely among individuals, depending on the patient’s age and the duration and extent of the disease. Children typically exhibit GI symptoms such as chronic diarrhea, steatorrhea, flatulence, abdominal pain, bloating, weight loss, irritability, and failure to thrive. Adults may also present with GI symptoms and with non-GI symptoms such as abnormal liver function tests, unexplained iron deficiency anemia, bone disease, dermatitis herpetiformis, and peripheral neuropathy.

GI symptoms alone cannot accurately differentiate celiac disease from other common GI disorders (Rubio-Tapia, Hill, Kelly, Calderwood, & Murray, 2013). A positive celiac disease-specific serology in patients with villous atrophy identified by small intestine biopsy is needed to confirm the diagnosis (Leffler & Schuppan, 2010). Ideally, testing for celiac disease occurs before a gluten-free diet is implemented. However, because of media attention on gluten-free diets, people often adopt the diet without an objective celiac disease diagnosis (Oxentenko & Murray, 2015).

Nonceliac gluten sensitivity (NCGS) is a condition in which people do not have the diagnostic features of celiac disease but develop celiac-like symptoms in response to eating gluten. Symptoms alone cannot reliably differentiate celiac disease from NCGS because symptoms overlap between the two conditions (Lundin & Alaedini, 2012). Although knowledge about NCGS is still growing, it appears that it does not have a strong genetic basis, is not associated with malabsorption or nutritional deficiencies, and is not associated with an increased risk for autoimmune disorders or intestinal malignancy (Rubio-Tapia et al., 2013). Treatment is a gluten-free diet, although it is not known if long-term strict avoidance
of all gluten is necessary because NCGS may be transient (Fasano, Sapone, Zevallos, & Schuppan, 2015).

Nutrition Therapy for Celiac Disease

The only effective treatment for celiac disease is a life-long gluten-free diet (Box 18.6). “Gluten-free” actually means gluten intake so low it does not cause harm because complete elimination is not possible due to contamination of foods with small amounts of gluten. Although the exact daily amount of gluten that poses no harm is not known, less than 10 mg/day is probably unlikely to cause damage in most patients (Oxentenko & Murray, 2015). The U.S. Food and Drug Administration (FDA) requires that foods labeled as “gluten-free” contain less than 20 ppm of gluten (FDA, 2013).

Over time, a gluten-free diet leads to repair of intestinal damage and resolution of symptoms and increases in body weight and bone mineralization. Failure to adhere to the diet increases the risk for malignancies such as small bowel adenocarcinoma, cancer of the esophagus, and B-cell and T-cell non-Hodgkin lymphomas, especially T-cell lymphomas (Ludvigsson, 2012). Biopsies are the only way to confirm healing of the intestine. In a U.S. study, the median time from beginning the gluten-free diet to achieving mucosal healing was 3 years (Rubio-Tapia et al., 2013). In some patients, intestinal healing does not occur despite the absence of symptoms and normal serology (Rubio-Tapia et al., 2013).

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Nov 8, 2018 | Posted by in NURSING | Comments Off on Nutrition for Patients with Disorders of the Lower GI Tract and Accessory Organs

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