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DISEASES OF THE LOWER GASTROINTESTINAL TRACT

Winda, Agustus 2012

Diarrhea Definition Diarrhea is defined as an increase in frequency of bowel movements and/or an increase in water content of stools that affects either the consistency or the volume of fecal output. Other definitions describe abnormality in stool production as >200 g/day for adults and >20 g/kg for children. (Donowitz,Kokke and Saidi 1995) Etiology Diarrhea can be classified in several different ways. Diarrhea acute or chronic. Diarrhea can also be classified as either osmotic or secretory. Acute diarrhea is short-term (less than two weeks), whereas diarrhea lasting longer than four weeks is considered chronic. Diarrhea can be associated with a number of health concerns, such as electrolyte imbalances, malabsorption, dehydration, and malnutrition.

Diarrhea Osmotic Osmolality is a measurement of concentration of particles in solution. Normal osmolality of the gastrointestinal tract is approximately 300 mOsm/L. When there is an increase in osmotically active particles in the intestine, the body responds by pulling water into the lumen in an attempt to normalize osmolality. When this occurs, increased water reflux results in what we refer to as osmotic diarrhea. Osmotic diarrhea can be caused by maldigestion of nutrients, excessive sorbitol or fructose intake, enteral feeding, and some laxatives. In general, when the causative agent is removed, osmotic diarrhea will cease. Secretory diarrhea also results from excessive fluid and electrolyte secretions into the intestine. The difference here is that the underlying disease is what causes excessive secretions, not the hyperosmolality. Furthermore, secretory diarrhea does not resolve when the patient is made NPO. Bacterial infections often produce enterotoxins that result in this type of diarrhea. Protozoa, viruses, and other infections can also cause secretory diarrhea.

Travelers diarrhea is a common health problem affecting those who travel to other countries. The major infectious agents resulting in travelers diarrhea are enterotoxigenic Escherichia coli, enteroaggregative E. coli, and Shigella spp, Salmonella, Campylobacter, Yersinia, Aeromonas, and Plesiomonas spp. Other factors that could potentially cause secretory diarrhea include medications, hormone-producing tumors, prostaglandins, and excessive amounts of bile acids or unabsorbed fatty acids in the colon. Antibiotics and other medications may cause diarrhea as a side effect. These medications generally cause diarrhea either by increasing GI motility or by altering the normal flora of the colon. Many gastrointestinal diseases have diarrhea as a common symptom. Examples : Crohns disease, ulcerative colitis, and celiac disease. These diagnoses can also result in malabsorption of lipids and other nutrients, which further contributes to the diarrhea. AIDS enteropathy with HIV infection, thyroid disfunction, and some malignancies.

Clinical Manifestations Diarrhea presents as a change from the normal bowel function. This is generally a watery stool that is increased in frequency. Other characteristics of stool output will vary depending on the etiology of the diarrhea. For example, foul-smeeling, frothy stools are associated with steatorrhea, which means fat in the stool. This would occur with fat malabsorption. Frank blood is bright red blood on the surface of the stool, and represents contamination with blood from the rectum or anus. Occult blood is detected by testing the stool and usually results from bleeding in the lower gastrointestinal tract. Melena is a dark stool and is caused by contamination with blood within the upper GI tract. Hemoglobin from blood contributes to the dark color. Mucus in the stool may also be indicative of secretory diarrhea. High amounts of electrolytes are also consistent with secretory diarrhea. The presence of leukocytes in the stool indicates an inflammatory process such as inflammatory bowel disease

Other clinical manifestations that may occur with diarrhea are abdominal pain and cramping. When defecation relieves cramping, diarrhea is generally from the distal colon. If abdominal pain and cramping continue after defecation, the origin is generally from the small bowel. Other symptoms such as dehydration, weight loss, and electrolyte and acidbase imbalances are dependent on volumes of stool lost and represent one of the most serious consequences of diarrhea. Diagnosis Considerations that will direct diagnostic procedures are the age of the patient, hydration status, the presence of blood in the stool, and whether the patient is immunocompromised. Other important symptoms to note are any recurring characteristics of diarrheal episodes, including time of day or any relationship to food intake. Treatment Restoring normal fluid, electrolyte, and acid-base balance is crucial. This is accomplished through either intravenous therapy or the use of rehydration solutions (Bergogne-Berezin 2000;Guerrant et.al 2001)

Prevention of diarrhea should be a major focus . Recommendations for the prevention of diarrhea worldwide include strategies such as ( Bateman and Mc Gahey 2001): Improving access to clean water and safe sanitation Promoting hygiene education Exclusive breast-feeding Improving weaning practices Immunizing all children, especially against measles Using latrines Keeping food and water clean Washing hands with soap (the babys as well) before touching food Sanitary disposal of stools

Nutrition Therapy Nutritional implications of diarrhea are initially dependent on the volume of gastrointestinal losses and then on the length of the disease course. Large-volume losses can quickly lead to dehydration, and electrolyte and acid-base imbalances. Hyponatremia and hypokalemia are both common with diarrhea. Metabolic acidosis may occur due to excessive loss of bicarbonate ions in stool output. Infants and elderly are at particular risk because their systems are much more sensitive to rapid shifts in both fluids and electrolytes. Maintaining homeostasis is much more difficult for both of these populations, in part due to the inability of their renal systems to act quickly enough for adequate compensation. Chronic diarrhea can cause fluid and electrolyte complications and can result in malnutrition and specific nutrient deficiencies. Diarrhea can affect appetite and thus impair adequate ingestion. Diarrhea also results in decreased transit time, which interferes with the ability of the gastrointestinal tract to perform adequate digestion and absorption.

Nutrition Interventions Current practice recognizes the importance of stimulating the gastrointestinal tract by feeding the patient. This speeds recovery of damaged cells. In addition, clear liquids are typically high in simple carbohydrates, which increase osmolality of the gastrointestinal tract. This actually can make diarrhea worse due to hyperosmolality. Oral rehydration solutions are designed to both restore fluid and electrolyte balance and enhance absorption in the intestinal tract. Infant with diare are of special concern. Their risk of dehydration and electrolyte imbalances are high. It is recommended that infants who breast feed continue to do so. Formulafed infants can be fed half- strength formula. Banana flakes, apple powder, or pectin sources can be added to formula in an attempt to thicken the stool. If the infant has begun solid foods, strained bananas, apple sauce, and rice cereal are the best initial food choices.

In adult and older children, introducing solid foods should begin with a low residu diet. Beginning with starches, and then slowly adding foods as they are tolerated. Use of products with pectin such banana flakes can also assist increasing the consistency of the stool. use of probiotics and prebiotics.(Barbut and Meynard 2002; broussard and Surawics 2004; O Sullivan 2005). These foods and supplements support growth of healthy flora and/or repopulate the intestinal tract with healthy bacteria Probiotics and prebiotics will increase the amount of short-chain fatty acids (SCFA) produced. Recent research indicates SCFA promote water and electrolyte absorption in the colon, which reduces the incidence of diarrhea ( Cummings and Mc Farlane 2002) may play a significant role in reducing diarrhea associated with enteral feeding ( delzenne,cherbut, and nevrinck 2003). Other research has studied the effect of using probiotics and prebiotics as part of the treatment for radiation induced diarrhea, diarrhea secondary to rotavirus, and travelers diarrhea ( De Ross and Katan 2000; Unger et al 2001; Urbancsek et al 2001) .

Constipation
The Rome Consensus Criteria define constipation as a condition where at least two of the following symptoms have occurred in the previous year for at least 12 nonconsecutive weeks (Locke,Pemberton,and Philips
2000;Thompson et.al 2000)

Straining with > of defecations Hard stools in > defecations Sensation of incomplete evacuation or anorectal obstruction in > defecations Manual maneuvers to facilitate > defecations Etiology Constipation can be due to rectal outlet obstruction or other sources of obstruction such as fecal impaction, adhesions, or even the presence of a tumor. Pelvic floor dysfunction ( university of southern california 2003) results not only slowed colonic transit but also storage of fecal contents in the rectum for long periods of time.

Constipation can be secondary to other medical conditions, including scleroderma, amyloidosis, and neurological diseases such as multiple sclerosis (MS) or Parkinsons disease. Constipation can be a side effect of many different classes of medications. These include very common prescription drugs such as calcium channel blockers, antidepressants such as amitriptyline, pain medications such as morphine, diuretics, and antihistamines. Medications that often cause constipation include iron, calcium, and other vitamin supplements, and, for some individuals, even nonsteroidal antiinflammatory drugs Clinical Manifestations Symptoms of constipation include decreased frequency of bowel movements. Bowel movements are often hard and pellet like. Abdominal pain, bloating, and gas are common accompanying symptoms. Treatment Treatment of the underlying etiology will direct medical care for constipation. Common interventions include bowel retraining and use of enemas or cathartic and laxative medications. Other medications involve bulking agents and stool softeners. (Locke,Pemberton,and Philips 2000)

Nutrition Therapy Research regarding nutrition and constipation has concentrated on the role of adequate fiber and fluid intake. The National Health and Nutrition Examination Survey (NHANES) indicated most Americans consume an average 14 to 15 grams of fiber each day (Alaimo et al 1998) When compared to recommendations, most individuals are consuming only 40% to 50% of the recommended intake. Adequate intake of whole grains, fruits, and vegetables has been one of the primary focuses of both the Dietary Guidelines for Americans and the Nutrition Recommendations for Canadians.(Departement of Health and Human Services 2005; Health and Welfare Canada 2005). Inadequate fiber intake has long been associated with many gastrointestinal conditions, including constipation, diverticular disease, and haemorrhoids.

Nutrition Interventions Twenty to thirty-five grams of dietary fiber are recommended For adults each day. Based on caloric intake, this would be approximately 10 to 13 g of dietary fiber per 1000 kcal. For children over the age of 2 years, fiber intake is recommended to be the amount equal to their age plus 5 grams/day (American Dietetic Association
2000,2002).

More recent recommendation suggest adults under the age of 50 should consume 38 grams of fiber per day (Food and Nutrition Board and Institute of
Medicine 2002).

Foods have a mixture of different kinds of fiber, but in general, the recommendations are for a 3:1 ratio of insoluble to soluble fiber. Adequate water intake, minimum of 2000 mL/day (approximately 8 cups/day). Use of probiotic and prebiotics has also been recommended for treatment of constipation. For example, consumption of fructooligosaccharides has been shown to soften feces and to assist in relieving constipation
(Broussard and Surawicz 2004; Brown and Valiere 2004; Garleb et.al 2002; OSullivan 2005).

Malabsorption Definition Malabsorption is a general term referring to malabsorption of fat, carbohydrate, or protein as a result of maldigestion or from damage to the anatomy and physiology of the small intestine. Etiology Damage to the anatomy and physiology of the small intestine due to disease is the most common cause of malabsorption. Conditions such as celiac disease, Crohns disease, and even proteincalorie malnutrition result in decreased villous height, decreased enzyme production, and subsequen malabsorption and/or maldigestion. Dysfunction of the accessory organs of digestion (liver, pancreas, and gallbladder) may also serve as the origin of the maldigestion. Decreased transit time, as seen in diarrhea or from surgical changes in the anatomy, also can result in either maldigestion or malabsorption.

Pathophysiology Nutrient digestion and absorption are dependent on normal anatomy; normal physiology with adequate production of enzymes, hormones, and other secretions such as bile; and appropriate motility. FAT MALABSORPTION The digestion and absorption process for lipid or fat is the most complex, and therefore the easiest to disrupt. Fat malabsorption is called steatorrhea literally meaning fat in the stool. Digestion and absorption of fat requires adequate colipase and pancreatic lipase, adequate emulsifierbilefrom the liver and gallbladder, and adequate secretion through the common bile duct and pancreatic ducts. Motility needs to be normal due to the lengthy process lipid has to undergo from micelle to chylomicron for absorption. When any of these processes is disrupted, fat remains in the stool and travels undigested and unabsorbed to the large intestine.

Fat-soluble vitamins are malabsorbed as well. An additional concern for fat malabsorption is the potential presence of excess oxalate. Excessive amounts of oxalate have been linked to development of urothiasis or kidney stones. Hyperoxaluria (excessive oxalate in the urine) is responsible for about 30% of kidney stones and is considered to be the most common cause. Persons with fat malabsorption will experience abdominal pain, cramping, and diarrhea. Stools produced will be frothy, foul-smelling, and greasy in appearance. CARBOHYDRATE MALABSORPTION The most common example of carbohydrate malabsorption is lactose malabsorption,commonly referred to as lactose intolerance. When there is inadequate lactase available for digestion, or if anatomy or motility does not allow adequate exposure to lactase, lactose will travel to the large intestine undigested and unabsorbed.

Bacteria in the large intestine will cause the lactose to undergo fermentation, which creates increased gas and abdominal cramping. Undigested lactose also pulls additional water into the large intestine, contributing to abdominal cramping and resulting diarrhea.

PROTEIN MALABSORPTION Protein malabsorption is most commonly referred to as proteinlosingenteropathy. Excessive protein is lost in the stool, and the patient will experience reduced serum levels of proteins and an increasing amount of peripheral edema due to the reduced oncotic pressure. Treatment Appropriate treatment for malabsorption will depend on the nutrient that is malabsorbed and the underlying disease causing malabsorption. NUTRITION THERAPY FOR FAT MALABSORPTION Restriction of fat to 25 to 50 grams per day is a standard first step in reducing the symptoms of fat malabsorption. Medium-chain triglyceride (MCT) supplements can be used to increase caloric intake. MCT is absorbed directly into the circulatory system from the small intestine and does not require the normal lipid digestion and absorption processes that long-chain fatty acids require.

NUTRITION THERAPY FOR LACTOSE MALABSORPTION Lactose is the simple carbohydrate found in milk and dairy products. Lactose is also found as an ingredient in many other food products in which it is often used as a filler. Milk provides approximately 11 grams of lactose per cup. Other dairy products have varying amounts, with ice cream having approximately 9 grams per cup and cheese having 1 to 2 grams per ounce. Restriction of all milk and dairy products is the major step to treat lactose malabsorption - individuals do vary on amounts of lactose they can tolerate. Celiac Disease Definition Celiac disease (CD) , previously referred to as gluten- sensitive enteropathy, gluten intolerance, or non-tropical sprue, is a complex disease whose etiology originates from both genetic and autoimmune factors. In this disease, exposure gluten results in damage to the intestinal mucosa. Other diseases or conditions associated with CD are type 1 diabetes mellitus and thyroid dysfunction as well as dermatitis and muscle and

Etiology The damage to the intestinal mucosa observed in CD, occurs when the small intestine is exposed to the prolamin fraction-gliadin and other protein components of gluten. Gluten is found in wheat, rye, malt, barley, and, in smaller amounts, in oats. Pathophysiology When the small intestine is exposed to certain sequences of amino acids found in the prolamin fraction of wheat (gliadin), rye (secalin), and barley (hordein), there appears to be both a toxic and inflammatory response.(Thompson 2003). This response damages villi; height is reduced, and they are flattened in appearance. Lack of surface area and reduction of enzyme production cause both malabsorption and maldigestion. Celiac disease is often accompanied by other systemic autoimmune disorders, including type 1 diabetes mellitus, thyroid disease, systemic lupus erythematous, primary biliary cirrhosis, rheumatoid arthritis, Sjgrens syndrome.

Clinical Manifestations Classic clinical symptoms of CD include diarrhea, abdominal pain and cramping, bloating, and gas production. Other symptoms that can occur in the absence of GI problems include bone and joint pain, muscle cramping, fatigue, peripheral neuropathy, seizures, skin rash, and mouth ulcerations. Prognosis and Treatment The only current treatment for CD is nutrition therapy consisting of a glutenfree diet. After avoidance of all gluten, villous height generally returns to normal. As the anatomy returns to normal, maldigestion and malabsorption resolve. The most common reasons for nonresponsive CD were unknown gluten contamination and the presence of coexisting diseases such as pancreatic insufficiency, irritable bowel syndrome as well as the presence of malignancies. Nutrition Therapy Nutritional consequences of CD are dependent on the extent of malabsorption present. Severe malabsorption will results in significant weight loss, vitami and mineral deficiencies, and, ultimately, protein-

Nutrition therapy will be consistent with the level of damage to the intestinal mucosa and the degree of malabsorption. Most often, the individual diagnosed with CD will need to initially begin on nutrition therapy using a low- residu, low- fat, lactose free, gluten- free diet. A low- fat diet of approximtely 45 to 50 grams/day can assist in minimizing symtoms of steatorrhea. Lactase deficiency will be common in this disorder due to damaged villi and enzyme secretion. As villi are regenerated and absorptive capability returns, these nutrients (fiber, lactose and fat) can be added back to the diet slowly and usually does not require a lifelong restriction. On the other hand, gluten does require a lifelong restriction. The patient will need to avoid all foods and other products that contain wheat, rye, barley, and malt. Restriction of oats is still controversial, but most recent research has indicated individuals may tolerate oats, as long as the oats are from a pure, uncontaminated source.( Thompson 2003)

The major controversy regarding use of oats is contamination within oat products by wheat, barley, or rye. Thompson recommended that oats should be limited to cup per day, and that step should be taken reduce the chance of contamination. This would include, in part, contacting manufacturers regarding the methods of production and avoiding products sold in bulk bis (Thompson 2003).

Irritable Bowel Syndrome Definition Throughout the last century, varying names such as spastic colon, irritable colon syndrome, and neurogenic mucous colitis have been given to this syndrome. Currently, irritable bowel syndrome (IBS) is defined using the rome II criteria, that for at least 12 weeks (they need not be consecutive weeks) and in the past 12 months, the individual has experienced abdominal pain that has at least two of the following three criteria ; (1) pain relieved defecation, (2) onset associated with change in frequency of stool (3) onset associated with change in form of stool. Subtypes of IBS include conditions that primarily involve diarrhea, conditions that primarily involve constipation alternate
(Adeniji,Barnett and DiPalma 2004;Thompson et.al 2000; Holten,Wetherington, and Bankston 2003).

Certain red-flag symtomps should be eliminated prior to diagnosis of IBS. These symptoms may actually signal other conditions. They include age at onset over 50, progresively severe symptoms, symptoms at night that wake the patient, persistent diarrhea, bleeding, anemia, weight loss, vomiting, fever, or a family history of colon cancer. Etiology IBS historically has been designated as a functional disorder. It is not a psychosomatic disorder, although its symptoms can be aggravated by stress, anxiety, depression, or emotional trauma. The spesific cause of IBS is unknown , but etiological factors may include increased levels serotonin, an elevated inflammatory response to infection, and an increased sensitivity of the enteric nervous system that cause abnormal motility and pain. There are often conditions associated with IBS, which include anxiety, panic, mood, and somatization disorders.

Pathophysiology The pathophysiology of IBS is complex and, as previously stated, not completely understood. In IBS, abnormal motility is considered to be one of the major factors involved in symptoms of abdominal pain and altered bowel habits (lyford
et.al 2002).

Individuals with IBS have been found to have an increased sensitivity to stimulation of the gastrointestinal tract. This means the same stimuli in normal patients do not result in symptoms that patients with IBS experience: abdominal pain, urgency, diarrhea, or constipation. When IBS patients were evaluated using balloon-distention, they experienced abdominal pain and gastrointestinal symptoms at much lower levels of distention than controls
(American College of Gastroenterology Functional Gastrointestinal Disorders Task Force 2002; Cash 2004).

Other studies have observed development of IBS after infectious enteritis. Specific organisms that have been documented include Blastocystis hominis, Campylobacter, Salmonella, and parasites such as Trichinella spiralis.
( Gomez-Escuder2003)

Clinical Manifestations Abdominal pain, alteration in bowel habits or motility, gas, and flatulence as well as some upper GI symptoms (reflux and noncardiac chest pain) are major symptoms for IBS. Abdominal pain can be acute and relieved by defecation. At the same time, some patients with IBS experience constant, chronic abdominal pain. Alterations in bowel habits are seen in both major types of IBS constipation and diarrhea. In some patients, both constipation and diarrhea are experienced. In people with IBS, there appears to be an increased sensitivity to certain foods such as lactose, wheat, or high- fiber foods, which results in an exaggreated response to these nutrients.

Treatment For those patients with IBS-D, antidiarrheal agents can be used. These medications assist by decreasing motility and increasing consistency of the stool. Other treatment for IBS include behavioral therapies (hypnosis, relaxation techniques, guided imagery), antibiotics, probiotics and nutrition therapy
(Beradi 2004;Crowell 2004) (American Dietetic Association 1996, 1997).

Nutrition Therapy Symptoms of IBS can lead to changes in oral intake that lead to nutrient deficiencies, potential underweight, and malnutrition. Once a baseline nutritional history has been established, the RD and patient can begin to identify any needed changes in diet. Overall nutritional adequacy should be addressed first. Many patients with IBS tend to eat erratically due to their gastrointestinal symptoms, and often eating is associated with a high level of anxiety and stress. Establishing a regular eating pattern that does not exacerbate symptoms is a crucial initial step.

The next goal is to focus on increasing fiber intke to approximately 25 grams/day. Higher fiber intakes may not be initially tolerated adequate fluid is also necessary as fiber intake is increased.(Nobak et.al 2000). Both prebiotics and probiotics have received attention for their potential use in IBS. adding these foods and supplements may be beneficial in the overall MNT plan Due to problems with gas and flatulence, providing recommendations to relieve these symptoms will also be beneficial. Avoiding foods that produce gas and taking steps to decrease swallowed air will decrease gas production

Inflammatory Bowel Disease Definition Inflammatory bowel disease (IBD) is characterized as an autoimmune, chronic inflammatory condition of the gastrointestinal tract. IBD is actually the general term for either of two diagnoses: ulcerative colitis (UC) and Crohns disease. These diagnoses are very similar but have very distinct differences. Etiology The complete etiology for both Crohns disease and UC is unknown at this time. it is understood that multiple factors play a role in these conditions.(Thompson Chagoyan 2005). These may include environmental factors such as smoking, infectious agents, intestinal flora, and physiological changes in the small intestine from which an abnormal inflammatory response is triggered. There is a strong genetic association for IBD. There is a positive family history in approximately 5% to 15% of patients with IBD. In identical twins, the incidence of IBD is 44% versus only 3.8% in fraternal twins.

Clinical Manifestations Patients with UC present with signs and symptoms including abdominal pain, bloody diarrhea, and tenesmus (urgency for defecation). Patients with severe disease often are febrile, are tachycardic, and have diarrhea that contains pus and mucus. Disease activity is rated using the Truelove and Witts Criteria (Truelove and witts 1995). Treatment Treatments for both UC and Crohns disease include antibiotics, immunosuppressive medications, immunomodulators, and biologic therapies as well as surgical intervention.(Hanuver and Sandborn 2001) Medical treatment for ulcerative colitis historically has used combinations of both antibacterial coverage with sulfapyridine and anti-inflammatory 5 aminosalicylic acid Immunomodulators work to inhibit inflammatory cell proliferation by interrupting cellular RNA and by inhibiting the overall immune response. These medications include azathioprine (AZA) and 6-mercaptopurine (6MP).

Corticosteroids work to inhibit the overall inflammatory response and are commonly used to treat UC. Antibiotics are used in UC only when there is an acute infection. Surgical intervention is required in both UC and Crohns disease in over 60% of patients. The most common procedure in UC is a total colectomy, and in Crohns disease, the ileostomy. Surgery is performed due to nonresponsive disease and due to acute complications such as perforation, obstruction, or abscess. These surgical procedures will be described in greater detail later in this chapter in the section Common Surgical Interventions for the Lower GI Tract.

Nutrition Therapy Nutrition implications. Patients with IBD are at significant nutritional risk. It is estimated that from 60% to 75% of patients with Crohns disease experienc malnutrition. (Krok and Lichenstein 2003). Both Crohns disease and UC have dramatic effects on nutritional status and often require nutritional support during periods of exacerbation.These diagnoses affect normal digestion and absorption; may increase caloric, protein, and micronutrient requirements; can result in protein-energy malnutrition; and additionally may require nutrition therapy to minimize symptoms. Nutrition therapy may also be implicated in treatment of the disease process. When infection is present or when the patient is febrile, energy needs are increased. Protein needs are increased, in some cases up to 150% of normal requirements.This is due, in part, to increased protein losses in inflammatory exudate. Micronutrients, especially iron, zinc, magnesium, and electrolytes, are at risk for deficiencies due to their losses in blood and diarrhea.

IBD is common in both children and young adults. Meeting nutritional needs of the growing child or adolescent poses its own challenge. It is crucial for nutrition therapy to be designed to ensure adequate nutrients to support growth and development. Since the mainstay of treatment for IBD involves multiple medications and often surgery, these nutritional risks compound those of the disease process. use of corticosteroids can result in hyperglycemia, nitrogen wasting, and increased risk of osteoporosis. use of sulfasalazine, which interferes with folate metabolism . Surgery increases calorie and protein requirements and additional nutrients are needed to support wound healing.

NUTRITION THERAPY DURING EXACERBATION OF DISEASE During acute exacerbations of both UC and Crohns disease, the extent of diarrhe output, and bleeding will the level of direct the level of nutrition intervention. For fulminant disease, parenteral nutrition support or enteral nutrition with a chemically defined formula will probably be necessary. Most research indicates parenteral nutrition is not necessarily advantageous, and the gastrointestinal tract can benefit from exposure to enteral nutrition (Dominioni 2003). Glutamine and arginine supplementation may assist with modifying inflammatory response in the disease process (Akisu et.al 2003; Kanauchi et al
2003; Panigrahi et al 1997; Van der Hulst et al 1993).

Energy needs for adults can be estimated using the Harris- Benedict or Miffl in-St. Jeor ,equation with appropriate stress factor (1.31.5). The amount of prior weight loss and the presence of infection will support the need for higher energy provision. To meet growth needs of infants, children, and adolescents, specific attention to their unique requirements is important. As much as 120 kcal/kg for infants and 80 kcal/kg for adolescents may be required (see Chapter 5). If available, indirect calorimetry provides the most reliable indicator of energy needs in the hospitalized patient.

Energy needs for adults can be estimated using the Harris- Benedict or Miffl in-St. Jeor equation with appropriate stress factor (1.31.5). The amount of prior weight loss and the presence of infection will support the need for higher energy provision. To meet growth needs of infants, children, and adolescents, specific attention to their unique requirements is important. As much as 120 kcal/kg for infants and 80 kcal/kg for adolescents may be required If available, indirect calorimetry provides the most reliable indicator of energy needs in the hospitalized patient. Estimation of protein requirements will be based on the presence of any lean body mass wasting and biochemical parameters measuring protein status such as prealbumin and albumin. Protein needs may be as high as 1.5 to 1.75 g protein/kg for adults and 2.0 to 2.5 g/kg for infants, children, and adolescents.

If oral intake can be initiated, a low-residue, lactose-free diet with small, frequent meals is best tolerated. If steatorrhea is present, then fat should be reduced with added MCT or an MCT-containing supplement to assist with meeting energy requirements. As the patient responds to medical therapy, adding small amounts of fiber and then lactose as the patient can tolerate will advance the diet. Other foods that may need to be initially restricted may be gas-producing foods, spicy or fried foods, caffeinated beverages, or any other food the individual patient identifies as problematic. The addition and advancement of an oral diet will need to be highly individualized. Some research has indicated that there is no improvement in complication rates when comparing a low- residue diet to a reguler diet in patients with Crohns (Levenstein et.al 1985).

All patients should receive a multivitamin that meets the RDA or AI for all nutrients. Patients with IBD are at higher risk for deficiencies of vitamin B12 and iron. In a normal small intestine, the ileum has specific receptor sites that allow for B12 absorption. Therefore, disease affecting the ileum specifically can potentially result in B12 deficiency. Supplementation of B12 to prevent pernicious anemia can be accomplished using nasal gel or oral tablets, or by intramuscular injection.( little 1999; Eiden 2003). Micronutrient requirements are additionally increased during exacerbations of disease. It is recommended that additional supplementation should include zinc (12 to 15 mg/liter of stool output); calcium (10 to 25 mEq/day); magnesium (15 to 30 mEq/day); and copper (0.5 to 1.5 mg/day).( Eiden 2003;
Jeejeehboy 2002)

Research has shown patients with Crohns disease have lower serum levels of antioxidants (vitamin E, vitamin C, and betacarotene). (Krok and lichenstein 2003) . It is thought that this might contribute to higher levels of oxidative stress in this disease. Higher levels of antioxidants may be warranted, but specific levels have not been established at this time; nor is it clear that supplement forms produce the same effect as foods. The most convincing evidence for the relationship between antioxidants and disease prevention has been in epidemiologic studies where strong associations have been demonstrated between dietary sources of fruits and vegetables and disease risk (Mc Dermott 2000). Patients with IBD may avoid fruits and vegetables due to their disease symptoms and perceived intolerance to these foods.

NUTRITION THERAPY FOR REHABILITATION DURING PERIODS OF REMISSION Maximizing energy and protein intake to facilitate rehabilitation should be the primary goal. Weight gain within a normal healthy range combined with physical activity will ensure rebuilding of protein stores and muscle mass. Depending on the extent of disease and the response to treatment, specific dietary modifications will need to be individualized. It is always a goal to normalize dietary patterns and encourage a variety of all foods as the patient is able to tolerate them. Consumption of foods high in antioxidants (for example, carotenoids, vitamin E, vitamin C, and selenium) and omega-3 fatty acids has been associated with protection against inflammation.

These would include fruits, vegetables, vegetable oils, nuts, and fishes such as tuna and salmon. Although some reports have indicated that glutamine, short-chain fatty acids, antioxidants, and immunonutrition with omega-3 fatty acids are an important therapeutic alternative in the management of inflammatory bowel diseases, the reported beneficial effects have yet to be translated into clinical practice.
The real efficacy of these nutrients still needs further evaluation through prospective and randomized trials (Campos et al 2003)

Foods high in oxalate may increase risk for urolithiasis or kidney stones, which can occur in IBD. These foods include, for example, cocoa, tea, wheat germ, strawberries, nuts, spinach, beets and baked beans, peanut butter, tofu, and high doses of vitamin C supplements (>2 g/day). As has been previously discussed in this chapter, use of probiotics and prebiotics enhances the normal flora of the GI tract. Several recent studies have indicated consumption of foods and supplements with probiotics and prebiotics has been associated with decreased symptoms for patients with IBD (Galves,Rodriguez Cabeas,
and Zarzuelo 2005; Gassull 2005; Guarner 2005; Shanahan 2004; Schultz and Sartor 2000).

Diverticulosis/Diverticulitis Definition Diverticulosis is defined as the abnormal presence of outpockets or pouches on the surface of the small intestine or colon. Meckels diverticulum is a type of diverticulosis present at birth. Meckels diverticula are usually found near the ileocecal valve and may cause gastrointestinal bleeding or obstruction for the newborn. Etiology Evidence suggest development of diverticulosis is related to low fiber intake, history of constipation, and the resulting long-term increased colonic pressure. Recently it has been proposed that low fiber intake also contributes to the incidence od diverticulosis ( Floch and Bina 2004; Ye,
Losada and West 2005).

Factors that may increase risk for development of diverticulosis include obesity, decreased physical activity, steroids, alcohol and caffeine intake, and cigarette smoking.( Aldoori et al 1995,1998).

Pathophysiology Diverticula do occur in the small intestine but are most common in the colon. Factors that affect integrity of the mucosa of the colon appear to contribute to development of the diverticula. The aging process and differences within parts of the colon may account for the pattern of development that has been observed. Specific pathophysiology indicates that within two or more of the muscular bands (taeniae coli) contract at the same time. This hinders motility of the colon, and thus its ability to move waste products. Fecal matter becomes trapped and exerts excessive pressure against the wall of the colon. This pressure causes development of small pouches on the wall of the colon, which are referred to as diverticula.(Beitz 2004; West and Losada 2004) Constipation increases colonic pressure through the excessive straining involved in bowel movements. This further increases the probability for development of diverticula.(Stollman and Raskin 1999)

Diverticulitis is acute inflammation of the diverticula. Food stuffs and bacteria can collect in diverticula and the mucosa can become infected. Further complications can include development of bleeding, abscess, obstruction, fistula, or perforation.(American Society of Colon and Rectal
Surgeon 2000)

Clinical Manifestations Diverticulosis is asymptomatic for most individuals. Diverticula are usually only diagnosed when other tests such as a colonoscopy identify them. In approximately 20% of individuals, complications from diverticula, including diverticulitis, may develop. Signs and symptoms of diverticulitis can include fever, abdominal pain, gastrointestinal bleeding, and elevated white blood cell count. Radiology testing (ultrasound and CT scan) may be used to diagnose diverticulitis. Test results can demonstrate thickened walls of the colon, abscess, or inflammation (American Society of Colon and Rectal Surgeon 2000)

Treatment Treatment for diverticulosis involves only nutrition therapy, with a specific focus on fiber intake, and use of probiotic and prebiotic supplementation. Treatment for acute diverticulitis begins with making the patient NPO with complete bowel rest until symptoms (bleeding and/or diarrhea) subside. Antibiotics are used to treat any infection. The most common antibiotic regimens involve treatment for Gram negative rods and anaerobes.
(American Society of Surgeon Colon dan Rectal 2000;Stoolman and Raskin 1999).

For those patients with complications (such as abscess or sepsis), surgical resections may be necessary. Nutrition Therapy Research indicates that dietary habits may be strongly linked to the etiology of diverticulosis. Nutrition therapy should then focus on those nutrition interventions that could impact disease course. The patient with diverticulosis is not at any more risk for malnutrition than any other individual. The presence of diverticulitis with infection and inflammation does impact nutritional requirements if this condition is prolonged or if other complications, such as sepsis, occur.

Nutrition Intervention Nutrition therapy to treat and prevent diverticulosis will include a high-fiber diet of 6 to 10 grams above and beyond the recommendations of 25 to 35 grams/day.It is common practice to avoid nuts, seeds, and hulls, which are sharp enough, hard enough, or large enough to irritate or get caught in diverticula. This will prevent opportunity for these foodstuffs to lodge in diverticula and pottentially result in diverticullitis. Foods to omit include caraway seeds, nuts, popcorn hulls, and sunflower, pumpkin, and sesame seeds.A food with small seeds such as a tomato, squash, cucumber, strawberry, or rapsberry is ussuallly tolerated. Many patients, especially the elderly, will need to use a fiber supplement if they are unable to consume adequate fiber from foods. The patient with acute diverticulitis will be progressed from bowel rest to clear liquids. The patient can then move toward a low-residue diet until inflammation and bleeding are no longer a risk.

Nutrition Therapy for Ileostomy and Colostomy When a certain part of the intestinal tract is removed, normal physiology and function of that portion is lost to the individual. This loss of function will produce changes in motility, in absorption, and in how waste products are handledall of which potentially can impact nutritional status. Resections of the terminal ileum and loss of the ileocecal valve tend to result in significant fluid, electrolyte, vitamin, and mineral deficiencies. The ileocecal valve controls the rate of movement from the small intestine to the large; hence, when it is absent, motility is much faster, interrupting normal absorption.

Nutrition Intervention Goals for nutrition therapy include decrease risk of obstruction, maintain normal fluid and electrolyte balance, reduce excessive fecal output and minimize gas and flatulence (to reduce odor and inflation of the appliance).(American dietetic association 2000). After surgery, the patient will be transitioned to an oral diet.

This begins with clear liquids and progresses as tolerated to a low-residue diet with four to six small feedings each day. Foods that may not be completely digested and that can cause stoma obstruction should be avoided for the first 6 to 8 weeks after surgery. These include tough fibrous meats; vegetables such as spinach, corn, and peas; dried fruits such as raisins; fruit skins and seeds; and popcorn. The patient will need to be instructed to eat slowly, chew thoroughly, and drink adequate fluids. Generally, oral intake should resemble the regular diet, meeting all nutritional needs by the eighth week postoperatively. If the patient experiences excessive or watery fecal output, the amount of insoluble fiber should be reduced while increasing the amount of soluble fiber. Applesauce, bananas, tapioca, potatoes, oatmeal, oat bran, rice, and pasta may help decrease diarrhea. Use of yogurt, parsley, and buttermilk may decrease gas and odor.

Recent research has focused on absorption of vitamin and minerals in the diets for patients with colostomy. It was that most vitamins, minerals, and phytochemicals appear to have adequate absorption in this population.
(Chen et.al 2004; Faulks et.al 2004).

Livny and colleagues did find beta-carotene was best absorbed from cooked carrots rather than raw carrots in these patients.( Livny 2003). However, since most patients intake and tolerance varies widely, a general multivitamin is recommended. Vitamin B12 supplementation may also be required.

Short Bowel Syndrome Definition Short bowel syndrome (SBS) (also known as short gut syndrome) results from a large resection of the small intestine. Spesific definitions vary, but Buchman (2004) describes the most important concerns of this condition: patients who are the greatest nutritional and dehydration risk generally have less than 115 cm of residual small intestine in the absence of colon in continuity or less than 60 cm of residual small intestine with colon in continuity (Buchman 2004). Patient with less than 100 cm of residual jejenum often have a net secretory response to food and may actually secrete more fluid than they ingest. The American Gastroenterologi and Association states in its clinical guidelines that Short bowel syndrome occur when, after surgery or congenitally, a patient is left with less than 200 cm of functional small intestine Those patients who also experience resections of the large intestine will have additional symptoms that contribute to complications of their SBS.

Etiology Surgical resections of the small intestine and colon due to disease and trauma can result in extensive loss of surface area of the small intestine and colon. Without normal anatomy and physiology, malabsorption of nutrients, fluids, and electrolytes will result Pathophysiology Several factors will determine the prognosis of this condition: extent of remaining small intestine, presence of the colon, presence of the ileocecal valve, health of the remaining gastrointestinal tract, and any comorbid conditions the individual may have. Though each case is highly individualized, most research agrees that a resection of more than 70% of the GI tract will result in severe nutritional and metabolic complications. (American Gastroenterological Association 2003; Buchman
2004; Lykins and Stockwell 1998).

The postoperative period for SBS generally follows three distinct phases. The first period ranges anywhere from 7 to 10 days and is characterized by extensive fluid and electrolyte losses within large volumes of diarrhea. During this phase, patients are dependent on parenteral nutrition, which not only provides required nutrients but manages fluid and electrolyte balance.

The second postoperative phase may last for several months and is characterized by reduction in diarrhea volumes with the initial stages of adaptation of the remaining bowel. It is during this phase that enteral nutrition can be introduced with a gradual transition to an oral diet. ( ReesParrish 2005).

During the third phase, there is continued adaptation of the remaining bowel. There is some evidence the intestinal tract increases in both length and diameter with additional increase in villous height. This time frame varies, but may range from 1 to 2 years. ( Buchman 2004). The amount of remaining bowel determines the extent of this condition. Loss of the ileum prevents B12 absorption and reabsorption of bile salts. Reduction in bile salts further contributes to fat malabsorption. No other part of the intestinal tract can compensate for these losses. The ileocecal valve not only controls intestinal motility but also prevents translocation of bacteria from the colon to the small intestine. When this control is lost, nutritional and metabolic complications are much more prominent.

Vitamin and mineral losses are major issues in SBS. When there is fat malabsorption, there is an inability to absorb adequate amounts of vitamins A, D, E, and K. These will need to be supplemented appropriately, and levels within the body will need to be evaluated. Other nutrients often deficient include sodium, magnesium, iron, zinc, selenium, and calcium, because they are often lost in the large volumes of diarrhea.(Rees- Parrish 2005) Treatment Initially, medical treatment will focus on managing fluid and electrolyte balance. This is generally managed by parenteral nutrition and intravenous support initially, and then as the patient is able, by oral rehydration solutions. Motility is controlled by medications used to treat symptoms of diarrhea. Nutrition Therapy Maintenance of nutritional and hydration status is critical for individuals with SBS. Aggressive nutrition support and careful progression to an oral diet require careful attention by the entire health care team.

Nutrition Intervention Immediately postoperatively, patients will receive total parenteral nutrition. Prescription for this therapy will be based on energy, protein, and micronutrient requirements. As diarrhea begins to decrease (anywhere from 2 to 6 weeks postoperatively), oral diets can begin.( Sundaram,
Koutkia, and Apovian 2002).

Many patients require combinations of parenteral, enteral, and oral nutrition support in order to accommodate degrees of malabsorption and patient requirements for nutrition and fluids. Sugar-free, isotonic clear liquids should be the first items offered. Diet is then progressed slowly to a low residue, low-fat, lactose-free, low-oxalate diet. Caffeine and alcohol should not be initially consumed. Alcohol sugars such as xylitol, mannitol, and sorbitol are usually not tolerated. Insoluble fiber is generally not tolerated initially, but sources of soluble fiber may actually assist in promoting mucosal health. Soluble fiber, like other sources of prebiotics, assists in production of shortchain fatty acids that are a primary fuel for the colon.

One item at a time is added to the diet to ensure tolerance. If GI symptoms are exacerbated, the food added should be removed from the diet. It may be added again at a later date, depending on the patients adaptation after surgery. Lykins and Stockwell suggest it may be best to retry categories of restricted foods even as long as 6 months, since bowel adaptation can take as long as 1 to 2 years (Lykins and Stockwell 1998). Many patients with SBS are discharged on home parenteral nutrition (PN) or home enteral nutrition support (EN) in addition to the limited oral diet. PN or EN is usually cycled over 10 to 12 hours at home, which will allow a patient to resume normal activity. Bacterial Overgrowth Definition Bacterial overgrowth syndrome results from cross-contamination of bacteria from the colon to the small intestine. This may be a result of surgery, disease, or trauma to the GI tract.

Pathophysiology In this condition, motility of the gastrointestinal tract is delayed due to disease, surgery, or trauma, and stasis develops. There is a high risk for development of small bowel bacterial overgrowth for those individuals with short bowel syndrome. Bacteria numbers increase and begin to compete with the host for nutrients. Malabsorption, maldigestion, and malnutrition can result. ( Parisi et al 2003; Singh and Toskes 2003) Clinical Manifestations Signs and symptoms are similar to all conditions of malabsorption. Diarrhea, steatorrhea, anemia, and weight loss all may be present in this condition. Treatment Bacterial overgrowth syndrome is treated by both correcting the underlying cause and administering broad spectrum antibiotics. ( Singh and Toskes
2003)

Nutrition Therapy Nutrition therapy will be consistent with the level of malabsorption that is present. Nutrients most commonly malabsorbed (fat and lactose) should be eliminated from the diet initially until the underlying condition is

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