Case-10-12 Celiac Disease – Medical Nutrition Therapy: A Case-Study Approach : Book Guide

This Document Contains Cases 10 to 12 Case 10 – Celiac Disease I. Understanding the Disease and Pathophysiology 1. What is the etiology of celiac disease? Is anything in Mrs. Talbot’s history typical of patients with celiac disease? Explain. The prevalence of celiac disease appears to be increasing. What does the current literature suggest as contributors to this change in celiac disease prevalence? • The etiology of celiac disease originates from genetic (DQ2- and/or DQ8-HLA genes), environmental, and autoimmune factors that are triggered by the body’s abnormal reaction to the gliadin component of gluten and that result in an inflammatory response damaging the intestinal mucosa. • Gluten is found in wheat barley, rye, and malt. Generally, gluten is the term used to encompass all autoimmune-causing prolamins (i.e. gliadin, hordein, secalin). • Many people with celiac disease have minimal symptoms for lengthy periods and often go undiagnosed. • In adults, it is more common in women and is often diagnosed after a pregnancy or another stressful event. • Current data suggest that many more people have celiac disease than what was previously thought. • It has been estimated that the prevalence may be as high as 1 case in every 200 persons. • Mrs. Talbot presents with: ○ Joint pain ○ Diarrhea • Abdominal pain ○ Fetal loss It is suggested that the increasing prevalence may be in part due to increasing availability and reliability of serological testing. Still, this cannot entirely account for the increased prevalence, which has been estimated at being 4 times greater in the U.S. than even 50 years ago. Additional research to assist in the explanation includes a focus on increased wheat consumption and actual changes in wheat hybridization over the past 50 years. 2. tTG antibodies are used in serological testing to diagnose celiac disease. Each test is sensitive and specific for the antibody it measures. The tTG test has a sensitivity of more than 90%. What does this mean? It also has a specificity of more than 95%. What does this mean? • >90% sensitivity means the test yields few false negative results • > 95% specificity means the tests yields few false positive results 3. Mrs. Talbot presents with some nondescript symptoms of celiac disease. List the nongastrointestinal as well as the gastrointestinal clinical manifestations of celiac disease. • Nongastrointestinal symptoms: ○ Dermatitis herpetiformis ○ Infertility or fetal loss ○ Anemia ○ Dementia ○ Folate or iron deficiency ○ Spinocerebellar syndrome ○ Neuropathy ○ Tetany ○ Osteoporosis ○ Arthralgia ○ Developmentally synchronous dental enamel defects ○ Fatigue ○ Osteomalacia ○ Seizures ○ Depression ○ Glycemic control more difficult • Gastrointestinal symptoms: ○ Steatorrhea ○ Duodenal obstruction ○ Osmotic diarrhea ○ Elevated transaminase concentrations ○ Secretory diarrhea ○ Recurrent pancreatitis ○ Weight loss ○ Occult blood ○ Constipation ○ Enteropathy-associated T cell lymphoma ○ Bloating • Gas ○ Abdominal pain ○ Failure to thrive ○ Vomiting ○ Dyspepsia 4. Biopsy of the small intestine continues to be the “gold standard” for diagnosis of celiac disease. Briefly describe the procedure. Multiple biopsies are taken so that an accurate diagnosis can be made from the distal duodenum and proximal jejunum via endoscopy while the patient is conscious but sedated with evidence of: • Villous atrophy • Crypt hyperplasia • Lymphocytic and plasma cell infiltrate in the lamina propria 5. How does celiac disease damage the small intestine? • The autoimmune reaction that occurs when gluten is eaten damages intestinal villi. • Damaged villi do not effectively absorb nutrients. • Without functioning villi, they will flatten and malnutrition will occur. • The anatomy of a normal small intestine is composed of villi or finger-like projections throughout the lumen. • Exposure to gliadin—a component of gluten—results in an inflammatory process that damages the small intestine, resulting in decreasing villus height. • A flat mucosa with villus atrophy indicates the absorptive surface of the small intestine is nonexistent. • Between each pair of adjacent villi is the area called the crypt, which is a small glandular tube at the base of the villus. • Absorptive cells or enterocytes enter the villus from the crypt. • Reduced absorptive surface area and loss of digestive enzymes follows damage to the enterocytes. • Adequate villus height and normal proliferation of enterocytes are significantly affected by nutritional status. • If a patient is malnourished or adequate fuel is not available to the small intestine, the villi shorten and the replication of enterocytes is decreased. II. Understanding the Nutrition Therapy 6. Gluten restriction is the major component of the medical nutrition therapy for celiac disease. What is gluten? Where is it found? • Gluten is a term for all of the prolamin protein components including: gliadin, hordein, and secalin, found in the grains of wheat, barley, and rye, respectively. • This means any food containing wheat, rye, or barley must be eliminated from the diet. • Convenience foods or any commercial products that use thickeners or fillers made from these grains cannot be consumed either (ex: hot dogs, French fries, Communion wafers, gravy, candy, malted products, and beer). In the US, most thickeners or fillers use corn rather than wheat but it is also important to assure safety. 7. Can patients on a gluten-free diet tolerate oats? • Restriction of oats is controversial primarily because the processing and manufacturing of oats may expose this grain to other grains processed in the same facilities. • It is generally recommended to restrict initially and then attempt to add back after symptoms have resolved. • It is recommended that initial intake be limited to ½ c. daily. • Restriction to 50 grams of safe (no more than 20 ppm gluten) dry oats per day (1 cup cooked) has been suggested to be safe in several studies • It is also recommended to find out where oat products were manufactured and to avoid any grains from bulk bins. • Gluten-free oats manufactured on dedicated equipment (and thus not in danger of cross-contamination) are available and can be selected. 8. Are there any known health benefits of following a gluten-free diet if a person does not have celiac disease? No, adherence to a gluten-free dietary pattern may result in a diet low in: • Carbohydrates • Iron • Folate • Niacin • Zinc • Fiber • B12 • Calcium • Phosphorus 9. Can patients with celiac disease also be lactose intolerant? • Lactase is available for digestion of lactose at the brush border of the enterocyte. • When this brush border is damaged—in this case from celiac disease—it is not uncommon for patients to experience secondary lactose intolerance (hypolactasia). • Until the villi have had an opportunity to heal, lactose may need to be restricted. 10. There is a high prevalence of anemia in individuals with celiac disease. How can this be explained? What tests are used for anemia? • When the lining of the small intestine is damaged with celiac disease, the amount of iron absorbed is inadequate, resulting in iron-deficiency anemia. • Researchers have also found an unexpectedly high prevalence of anemia not exclusively owing to iron deficiency. ○ It is often referred to as “anemia of chronic inflammation” and is characteristically seen in individuals with long-standing chronic inflammation. ○ The immune system’s response to this inflammation can hinder the body’s production of red blood cells. • The test most commonly used is a complete blood count CBC), in which blood components are counted and analyzed. ○ WBC ○ RBC ○ Hgb ○ Hct ○ MCV ○ MCH ○ MCHC ○ RBC distribution ○ Platelet count ○ Transferrin ○ Ferritin ○ Iron ○ TIBC ○ Iron saturation ○ Vitamin B12 ○ Folate III. Nutrition Assessment 11. Calculate this patient’s total energy and protein needs. Energy needs: (Harris Benedict) REE = 655.1 + 9.6 W (kg) + 1.9 S (cm) - 4.7 A (yrs) REE = 655.1 + 9.6 x 56.8 kg + 1.9 x 160.02 cm - 4.7 x 26 yrs REE = 1372.9 ≈ 1400 kcal TEE = 1372.9 x 1.3 (PA) x 1.1 (SF) = 1963.3 ≈ 1950 kcal; range of 1900-2000 kcal/day OR American Chest Physician’s nomogram: 25-30 kcal/kg: 1420 – 1704 kcal Protein needs: 56.8 kg x 1.0-1.2 g/kg = 57-68 g/day 12. Evaluate Mrs. Talbot’s laboratory measures for nutritional significance. Identify all laboratory values that are indicative of a potential nutrition problem. Hgb, Hct, ferritin, RBC, and prealbumin are low. Transferrin is high. 13. Are the abnormalities identified in question #12 related to the consequences of celiac disease? Explain. Anemia (iron-deficiency) is a consequence of celiac disease. Also, the diminished prealbumin associated with her weight loss is a consequence of poor intestinal absorption of nutrients. 14. Are any symptoms from Mrs. Talbot’s physical examination consistent with her laboratory values? Explain. • Pale skin and sclera are consistent with her laboratory values diagnostic for anemia. • Her measured weakness (strength 4/5) is also consistent with laboratory values of decreased Hgb and Hct. IV. Nutrition Diagnosis 15. Select two nutrition problems and complete the PES statement for each. Following are PES statements that students can complete given the possible diagnoses noted above: • Food- and nutrition-related knowledge deficit related to lack of prior nutrition-related education as evidenced by history of daily wheat-based bread and questionable gluten-containing commercial food (ex. soup) consumption. • Undesirable food choices related to lack of prior exposure to accurate nutrition-related information as evidenced by 24-hour recall. • Inadequate mineral intake (iron) related to food- and nutrition-related knowledge deficit and malabsorption due to celiac as evidenced by low Hgb, Hct and ferritin laboratory values, elevated transferrin, an estimated inadequate iron intake from 24-hr recall (15 mg), and a low consumption of meats. V. Nutrition Intervention 16. For each of the PES statements that you have written, establish an ideal goal (based on the signs and symptoms) and an appropriate intervention (based on the etiology). • Food- and nutrition-related knowledge deficit ○ Goal: Verbalizes willingness to learn about appropriate diet modifications. ○ Intervention: Advise and educate Mrs. Talbot about whole and enriched gluten-free grains and products so her diet will not be low in iron, folate, niacin, zinc, and fiber. • Undesirable food choices ○ Goal: Demonstrates ability to apply food- and nutrition-related information. ○ Intervention: Advise and educate Mrs. Talbot about gluten-free dietary patterns. • Inadequate mineral intake (iron) ○ Goal: Iron nutriture is at normal levels ○ Intervention: Advise and educate Mrs. Talbot about good sources of dietary iron. These sources may include animal meats, beans, fish, fortified cereal and oatmeal, and spinach. 17. What type of diet would you initially prescribe, considering the possibility that Mrs. Talbot has suffered intestinal damage? • Gluten restriction will need to begin immediately and continue throughout life. • Mucosal damage can appear within just a few hours of exposure to gliadin. • Oats should be avoided until gastrointestinal symptoms are stabilized from her gluten-free diet VI. Nutrition Monitoring and Evaluation 18. Evaluate the following excerpt from Mrs. Talbot’s food diary. Identify the foods that might not be tolerated on a gluten-/gliadin-free diet. For each food identified, provide an appropriate substitute. Cornflakes Check label – may contain gluten in the caramel coloring. Substitutions include: puffed corn, puffed rice, rice flakes. Look for Gluten free label designation. Milk/Chocolate milk Soy milk or lactose-free milk until GI tract has healed and it is verified that patient is not lactose intolerant. Adding chocolate syrup should be fine (double check nutrition label). Banana OK. Coffee Should be fresh brewed, not flavored or instant. Half and Half Avoid due to dairy/lactose content (though, it may be tolerated due to the small amount used). Consider non-dairy creamers. Hot dog on bun Fresh meat, fish, poultry (e.g., sliced chicken or turkey) with rice or potatoes. French fries May be contaminated with gluten via fryer oil. Some frozen French fries are also coated with flour. Check label for gluten free designation. Consider baked or homemade mashed potatoes instead. Stir-fry chicken nuggets with soy sauce Chicken nuggets are breaded and contain gluten. Check the label of the soy sauce - may contain gluten. Substitution may be grilled chicken with gluten-free soy sauce. Mixed vegetables OK. Rice OK. Pudding Check label. Good substitution would be tapioca. Iced tea OK. Gluten-free graham crackers OK. Peanut butter OK. Cookie dough ice cream Contains wheat. Consider vanilla or chocolate ice-cream (double check label for gluten). 19. Mrs. Talbot asks what steps she should take to keep herself from being exposed to gluten in her kitchen since her family does not have celiac disease. What advice would you give her? Are there other potential environmental sources of gluten that you would alert Mrs. Talbot to? • Store gluten-containing and gluten-free foods in separate areas • Use separate gluten-free labeled equipment (e.g. toaster) • Prepare gluten-free foods first (e.g. boil gluten-free pasta first) • When going to restaurants, do your research and ask the waiting staff about how the food is prepared and if any sources of gluten are involved. Ask to speak with the chef/manager if necessary. • Environmental sources of gluten can occur when crumbs or remnants of gluten-containing food products contaminate gluten-free food • Gluten may be in medications (e.g. excipients/fillers) Case 11 – Irritable Bowel Syndrome (IBS) I. Understanding the Disease and Pathophysiology 1. IBS is considered to be a functional disorder. What does this mean? How does this relate to Mrs. Clarke’s history of having a colonoscopy and her physician’s order for a hydrogen breath test and measurements of anti-tTG? • IBS is a functional disorder, which means that other GI diseases that present with similar symptoms (celiac, Crohn’s, infectious diarrhea, etc.) are ruled out before diagnosing the patient with irritable bowel syndrome. • A colonoscopy is an endoscopic exam of the colon, or the large intestine. This exam would see diverticulitis or polyps, which are pre-cancerous growths that may develop into colon cancer. Mrs. Clarke’s colonoscopy was normal, indicating that diverticulosis, diverticulitis, and ulcerative colitis/Crohn’s disease (inflammatory bowel diseases) are ruled out. In addition, the colonoscopy is a part of screening to rule out colon cancer. • The hydrogen breath test is used to detect lactose malabsorption or small intestinal bacterial overgrowth. Lactose malabsorption is often associated with IBS. Baseline hydrogen on the breath is measured. The patient then consumes 25-50 g of lactose and breath hydrogen concentration is measured after 3-8 hours. >20 ppm indicates lactose malabsorption. Depending on the outcome of the scheduled hydrogen breath test, positive results may aid in assistance with nutrition therapy. • Anti-tTG are antibodies associated with celiac disease (CD). The identification of antibodies is commonly used to diagnose CD. A negative result for these antibodies would rule out CD for Mrs. Clarke. Celiac disease is also associated with IBS so the American College of Gastroenterology recommends that all patients be screened for celiac disease as a component of differentiating the diagnosis from IBS. 2. What are the Rome III criteria that were used as part of Dr. Mohammed's diagnosis? Using the information from Mrs. Clarke’s history and physical, determine how Dr. Mohammed made his diagnosis of IBS. • The American College of Gastroenterology (ACG) uses the Rome III criteria to diagnose IBS. The basis for these criteria, according to the ACG, is that IBS experts have met in Rome for the past 15 years to decide what methods are best used to diagnose IBS. • Rome III as diagnostic criteria are accurate about 65-100% of the time, according to the ACG. • The Rome III criteria include: • Recurrent abdominal pain or discomfort at least 3 months in the last year with two or more of the following: • Improvement of pain with defecation • Onset associated with change in frequency of stool • Onset associated with change in appearance of stool • Physician has ruled out other inflammatory and GI disorders with similar symptoms • Other symptoms may include: • Altered bowel habits or motility (*key symptom) • Diarrhea • Constipation • Mixed—pt. experiences both constipation and diarrhea • Lower abdominal pain (*key symptom) • Flatulence • Gas • Upper GI symptoms including: • Reflux • Chest pain (non-cardiac) • The physician was able to diagnose Ms. Clarke with IBS because: ○ She experiences both bouts of constipation and diarrhea for many years ○ She complains of "several accidents", being unable to make it to the restroom on time ○ She endures daily abdominal pain ○ Lately several episodes of diarrhea daily (may be evident due to dry mucous membranes - dehydration) ○ Hyperactive bowel sounds 3. Discuss the primary factors that may be involved in IBS etiology. You must include in your discussion the possible roles of genetics, infection, and serotonin. • Unknown cause • Genetic predisposition: Genes that control serotonin receptors may make certain people more prone to IBS • Gender: Affects more women than men • Altered immune response stimulated by food sensitivity • Patients may be able to identify certain foods that exacerbate symptoms • Fermentable oligosaccharides, disaccharides, monosaccharides, and polyols or sugar alcohols (FODMAPs) may play a role in the development of IBS • Altered microbial environment in the colon ○ Abnormal colonic fermentation (partial digestion of food in the large intestine that may lead to excessive gas production as a by-product) ○ Includes small intestine bacterial overgrowth • Elevated inflammatory response to gastroenteritis (infection) • Specific bacteria documented with gastroenteritis in the development of IBS: • Salmonella • Blastocystis hominis • Campylobacter • Parasites like Trichinella spiralis • Heightened or abnormal communication between GI tract and muscle • Increased sensitivity to the enteric system that changes motility ○ Stimuli that most people would not react to cause symptoms of urgency, diarrhea, or constipation in IBS patients ○ Stress and other psychological factors may exacerbate symptoms • Commonly associated with celiac disease, Inflammatory bowel disease - not causes but these often co-exist with IBS. • Abnormal release, transport, or recognition of serotonin ○ 95% of serotonin is found in the GI tract, and serotonin can be either stimulatory or inhibitory to the GI tract, which is why people may have diarrhea, constipation, or a mix with IBS. ○ Serotonin can either cause stimulation of acetylcholine, which causes muscle contraction, or it can cause release of nitric oxide, which relaxes smooth muscle in the GI tract. ○ Altered serotonin levels are well documented in IBS patients. • Documented reduced levels of serotonin in IBS-C patients • Documented elevated levels of serotonin in IBS-D • Although there is documentation, the exact role of serotonin in IBS is not understood • Altered GI mucosal permeability may be caused by these previously discussed triggers and lead to inflammation and an altered perception of pain. 4. Mrs. Clarke’s physician prescribed two medications for her IBS. What are they and what is the proposed mechanism of each? She discusses the potential use of Lotronex if these medications do not help. What is this medication and what is its mechanism? Identify any potential drug-nutrient interactions for these medications. First medication: Elavil (25 mg daily) i. Mechanism: a. Antidepressant b. Changes neurotransmitter levels in the brain, particularly serotonin-norepinephrine reuptake inhibitor. Since serotonin may have a role in IBS, changes in serotonin levels resulting from use of this medication may have a secondary effect on IBS. ii. Drug-nutrient interactions: a. Cannot take with alcohol; should tell doctor if you drink an excessive amount of alcohol b. Cannot take with MAOIs c. Cannot take with epinephrine (may cause high blood pressure) d. Changes in appetite e. Constipation f. Nausea g. Vomiting h. Avoid St. John's Wort i. Avoid excessive amounts of caffeine Second medication: Metamucil (1 T in 8 oz. of liquid twice daily) i. Mechanism: Laxative, psyllium bulking agent; soluble fiber forms gel in the colon, retains water, and increases peristalsis. ii. Drug-nutrient interactions: a. Diarrhea, cramping b. Malabsorption of nutrients due to decreased transit time Lotronex: i. Mechanism: a. Specifically for women whose main IBS problem is diarrhea b. Used to treat diarrhea, pain, cramps, and the feeling of an urgent need to have bowel movements caused by irritable bowel syndrome c. Serotonin-antagonist. Blocks 5-HT3 serotonin receptor to decrease action of serotonin, reduce abdominal pain, and change motility of the intestine. d. The indication is restricted to those patients for whom the benefit-to-risk balance is most favorable (may cause severe constipation or ischemic colitis). ii. Drug-nutrient interactions: a. Avoid eating grapefruit or grapefruit juice b. Constipation II. Understanding the Nutrition Therapy 5. For each of the following foods, outline the possible effect on IBS symptoms: a. lactose Lactose malabsorption often co-exists with a diagnosis of IBS. Often times with IBS, there may be abnormal colonic flora. In addition, in this case, there is an increase in GI motility since the patient is experiencing diarrhea. Therefore, lactose does not have the opportunity to be adequately digested and absorbed before reaching the large intestine. Fermentation of lactose occurs in the large intestine, which increases abdominal cramping and gas production. Therefore, the symptoms of IBS are exacerbated when lactose is consumed in certain patients. This is why the patient had a hydrogen breath test. b. fructose Fructose relates to IBS because it is a potential food trigger that may exacerbate symptoms. Fructose is part of the FODMAP group and it is a hyperosmolar substrate. The hyperosmolality of malabsorbed fructose causes a rapid shift of water to the GI tract, which increases motility and may potentially cause diarrhea, which is seen in this case. This is why the patient was given the FODMAP assessment, to identify potential food triggers that may make symptoms worse. Fructose may not be well absorbed, which increases fermentation in the colon, leading to worse symptoms associated with IBS. c. sugar alcohols Similar to fructose, an excessive amount of sugar alcohols such as sorbitol, mannitol, and xylitol can contribute to diarrhea. Sugar alcohols, or polyols, are also part of the FODMAP group, which are poorly digested and increase fermentation, leading to excessive by-products and abdominal cramping. 6. What is FODMAP? What does the current literature tell us about this intervention? • FODMAP are groups of foods that are poorly digested and absorbed and contribute to fermentation in the large intestine, which may cause abdominal pain, cramping, diarrhea, flatulence and gas. • FODMAP stands for fermentable oligosaccharides, disaccharides, monosaccharides, and polyols (sugar alcohols). • The current thought regarding this intervention is that it is effective in some patients to exclude these foods in order to identify consistent trigger foods. Several recent studies have demonstrated a significant reduction in IBS symptoms with the FODMAP diet. • Right now, diet histories and diet recalls should be evaluated and should be used to help identify particular food triggers that may exacerbate symptoms. 7. Define the terms prebiotic and probiotic. What does the current research indicate regarding their use for treatment of IBS? What guidance would you give Mrs. Clarke for choosing a probiotic? • Prebiotics: food sources that contain substances that stimulate the beneficial flora of the large intestine. In other words, prebiotics are the food for the beneficial bacteria in the colon. Examples: oligosaccharides, inulin • Probiotics: microorganism-containing products that are manufactured and sold as food products and supplements. These foods contain actual live microorganisms that have proved to be beneficial for the gut flora. They help improve the microbial balance, which potentially is off balance in IBS patients. • Currently, research supports the use of prebiotics and probiotics in IBS patients to help establish a population of beneficial microbial flora to help with fermentation. However, the ideal dosage or amount has not been determined through research because it is a newer therapy for IBS patients. These are not considered to be a primary treatment option or standard of care, but considering their general safety, supplementing the diet with probiotics may be considered. Examples of recommended sources include: Yogurt, kefir, cheeses • Suggesting Mrs. Clarke to continue consuming her yogurt if she enjoys it is appropriate. 3/4 cup of Greek yogurt can provide up to 1 billion bacterial colonies. • If the patient does not like foods that contain probiotic cultures, a dietary supplement like Culturelle© or Align© may be suggested. III. Nutrition Assessment 8. Assess Mrs. Clarke’s weight and BMI. What is her desirable weight? • BMI: 703  191 lbs./65 in./65 in.= 31.8 or ~32. This classifies her as obese. • IBW: 100 + (5 in.)  (5 lbs.) = 125 lbs. • % IBW: 191 lbs./125 lbs.  100 = 153% of IBW 9. Identify any abnormal laboratory values measured at this clinic visit and explain their significance for the patient with IBS. • Glucose (high): Glucose may be elevated due to underlying diabetes. • HbA1c (high): 6.1% is consistent with a diagnosis of diabetes mellitus. • Cholesterol (high): The value is 201, which is just above the upper threshold and not a huge concern or a huge factor in the nutritional intervention for IBS, except that perhaps the patient may be advised to decrease fat intake, especially saturated fat intake. • Triglycerides (high): High, potentially due to excessive dietary fat intake. High dietary fat intake may contribute to IBS symptoms. • HDL-C (low): Not directly related to her IBS symptoms, but does place her at a greater risk for CVD (along with the other abnormal lipid values) 10. List Mrs. Clarke’s other medications and identify the rationale for each prescription. • Omeprazole: for history of GERD. It is a proton pump inhibitor, which blocks acid production, decreasing gastric acidity. This is prescribed to reduce symptoms of GERD but may also help with IBS, as GERD symptoms (upper GI) can be associated with IBS, such as chest pain or heartburn or abdominal pain. • Levothyroxine: used to treat hypothyroidism, it is a synthetic version of the thyroid hormone, which increases the metabolic rate and is important for growth and bone health. Rationale: patient has hypothyroidism. • Vitamin D/calcium supplements: rationale for usage is to compensate for other drugs such as omeprazole, which inhibits calcium absorption; supplementation may be necessary to preserve bone health. • Lomotil: helps with diarrhea, which patient has recently had several episodes of. 11. Determine Mrs. Clarke’s energy and protein requirements. Be sure to explain what standards you used to make this estimation. • Energy: 22-25 kcal/kg IBW to facilitate weight loss 1250 -1420 kcal May also use Mifflin St. Jeor equation to determine energy requirements. • Protein: 0.8 g/kg body weight 0.8 g/kg  IBW (57 kg) = 45.6. Increasing protein may help increase satiety and aid in weight reduction. 1.0 g/kg  57 kg = 57 g. 46-57 g protein 12. Assess Mrs. Clarke’s recent diet history. How does this compare to her estimated energy and protein needs? Identify foods that may potentially aggravate her IBS symptoms. • Mrs. Clarke’s current diet is adequate and varied. • She does consume foods that may increase gas production such as asparagus, lentils, and kidney beans. • She does identify eating foods from the FODMAP list “often,” which may increase fermentation and contribute to her symptoms of IBS. FODMAP foods Mrs. Clarke eats include: 1. Asparagus 2. Lentils 3. Kidney beans 4. Milk 5. Sugary foods such as cookies cake, ice cream, etc. 6. Peaches, dried fruits 7. Sugar-free candies which may contain sugar alcohols • Her snack foods are usually high in fat, which may also contribute to IBS, although it seems that the patient is working toward change. These foods high in fat may be contributing to elevated cholesterol and triglyceride levels as well. • Patient seems to be exceeding caloric needs for weight loss, although calorie consumption is hard to compare to needs since portions of her diet recall were not given. • Patient seems to be consuming adequate protein based on meat and legume consumption from dietary recall. • Patient consumes quite a bit of sugar alcohols which may be contributing to symptoms. IV. Nutrition Diagnosis 13. Prioritize two nutrition problems and complete the PES statement for each. 1. Inappropriate fiber intake related to nutrition-related knowledge deficit as evidenced by patient’s reports of confusion concerning adequate fiber intake. 2. Nutrition-related knowledge deficit related to FODMAP food consumption as evidenced by FODMAP assessment with frequent consumption of asparagus, sugar alcohols, high-sugar foods, and lentils. 3. Obesity related to consumption of snack foods high in fat as evidenced by BMI > 30 (BMI of 32). V. Nutrition Intervention 14. The RDN that counsels Mrs. Clarke discusses the use of an elimination diet. How may this be used to treat Mrs. Clarke’s IBS? • Elimination diets are used to determine certain foods that may be contributing to IBS symptoms of abdominal pain, bloating, diarrhea, etc. • These diets eliminate all possible foods related to the patient’s symptoms. These may be common foods containing substances that have adverse effects such as lactose. Other common eliminations are fructose and sugar alcohols. Use of typical high-FODMAP foods may help guide the process. • Each food is added back one at a time to see which foods are associated with the onset of IBS symptoms. 15. The RD discusses the use of the FODMAP assessment to identify potential trigger foods. Describe the use of this approach for Mrs. Clarke. How might a food diary help her determine which foods she should avoid? • Foods such as fruit juices, dried fruits, wheat-based foods, high-fat foods, cruciferous vegetables (broccoli, cauliflower, Brussel sprouts, cabbage, etc.), artificial sweeteners, fructose, and legumes (kidney beans, lentils) would be eliminated as these are examples of foods that increase fermentation in the large intestine, which exacerbates symptoms. • The FODMAP assessment pinpoints specific food groups that have been shown to increase gas production or fermentation. This is a more specific elimination diet. • A food diary can help the patient see patterns in food consumption and corresponding symptoms. A patient should note what they eat and when their symptoms are severe or when symptoms occur. This will help distinguish which foods are related to IBS symptoms as the patient will be able to observe any correlations between foods eaten and occurrence of symptoms. 16. Mrs. Clarke is interested in trying other types of treatment for IBS including acupuncture, herbal supplements, and hypnotherapy. What would you tell her about the use of each of these in IBS? What is the role of the RDN in discussing complementary and alternative therapies? • There is mixed evidence as to whether acupuncture and hypnotherapy are effective complementary therapies for IBS patients. Some patients report feeling better while it does not work for others. Providing guidance on evaluating information is an important aspect of nutrition education. • The role of the RDN is to determine the nutritional intervention for IBS. This puts an emphasis on treating IBS by identifying certain trigger foods that may be associated with its symptoms. • The RDN could refer the patient to a specialist in these alternative therapies, but since RDNs only share information that is evidence-based, these forms of treatment may be out of standards of practice for the RDN. VI. Nutrition Monitoring and Evaluation 17. Write an ADIME note for your initial nutrition assessment with your plans for education and follow-up. Alicia Clarke (Nutrition consult for IBS) 7-10-12 A: 42 YOWF Dx: irritable bowel syndrome-Diarrhea (D); PMH: history of constipation and diarrhea, obesity, GERD, and hypothyroidism Meds: Omeprazole 50 mg twice daily; Levothroxine 25 mcg; vitamin D 600 IU; 800 mg calcium; Lomotil prn. Elavil (25 mg daily), Metamucil (1 T in 8 oz. of liquid twice daily) Skin: warm, dry Abdomen: hyperactive bowel sounds x4; no organomegaly or masses - lower abdominal tenderness. Labs: glu 115, Chol 201, Tg 171, HDL 42, HbA1C 6.1%, Urinalysis: WNL Height: 5’ 5” (65in.), Weight: 191 lbs. BMI: 32 (obese), IBW 125 +/- 10#, 153% IBW Estimated energy requirements: 1250 -1420 kcal (22-25 kcal/kg IBW to facilitate weight loss) Estimated protein requirements: 46-57 g per day Diet Hx: diet reveals many fermentable oligosaccharides, disaccharides, monosaccharides, artificial sweeteners, and sugar alcohols are consumed (FODMAP assessment analysis). Snacks are high in fat as evidenced by cookies, cake, and ice cream. “Often” consumption of gas-producing foods including: asparagus, kidney beans, lentils, fruit juice, dried fruit, artificial sweeteners, and fructose, which may contribute to IBS symptoms. Daily high fiber sources include wheat, dried fruit, kidney beans, and lentils. D: Nutrition-related knowledge deficit related to FODMAP food consumption as evidenced by FODMAP assessment with frequent consumption of asparagus, sugar alcohols, high-sugar foods, and lentils. I: Goal: Identify food triggers that make symptoms worse and alleviate symptoms. pt. will focus on elimination diet and re-introduction over 6-8 week trial. pt. will be educated on the FODMAP foods to identify which foods may contribute to symptoms. pt. will consider adding probiotics such as cheese, kefir, or yogurt to diet. pt. may consider continuing weight reduction to improve overall health. M/E: pt. will keep a food diary for six weeks to identify food patterns. Pt. should note when symptoms occur to identify food triggers. Pt. should note episodes of diarrhea. Symptoms will be monitored as pt. eliminates FODMAP foods from diet over a period of time. Referral to primary MD regarding HgbA1c and risk of diabetes. Case 12 – Inflammatory Bowel Disease: Crohn’s Disease I. Understanding the Disease and Pathophysiology 1. What is inflammatory bowel disease? What does current medical literature indicate regarding its etiology? Inflammatory bowel disease (IBD) is a chronic relapsing inflammatory condition involving the gastrointestinal tract; the term IBD encompasses the two specific diagnoses of Crohn’s disease and ulcerative colitis (UC). IBD is thought to involve the activation of T cells (by macrophages) to produce a T H1 immune response (cytokine production) that causes a vicious cycle of chronic inflammation. The mucosal damage from the abnormal immune response can allow the translocation of luminal contents past the tight junctions. This can allow the body to produce antigens to these "leaked in" contents. . The etiology of IBD is still unclear, but it is believed that various environmental factors may be involved as “triggers” for the inflammatory response of the disease; genetics also play an important role in the etiology of the disease. Certain genes are linked to the dysregulation of the gastrointestinal immune response and microbiome and therefore certain individuals are more susceptible than others to develop IBD. IBD has been found to be more prevalent among individuals of Caucasian and Ashkenazi Jewish descent. However, because all genetically susceptible individuals do not develop IBD, and because of the speed at which IBD incidence has increased in certain regions of the world, genetics cannot be the sole factor in the etiology of IBD. Proposed theories regarding the environmental factors associated with IBD involve the hygiene hypothesis, Helicobacter pylori, family size and birth order, urban environment, etc. Smoking, oral contraceptives, appendectomy, diet, breastfeeding, and nonsteroidal anti-inflammatory drugs (NSAIDs). 2. Mr. Page was initially diagnosed with ulcerative colitis and then diagnosed with Crohn’s. How could this happen? What are the similarities and differences between Crohn’s disease and ulcerative colitis? • UC and CD are very similar, but can be distinguished from one another by the following: Symptoms Complications Antibody testing Imaging and biopsy results Crohn’s disease Ulcerative colitis Symptoms • Blood &/or mucus in stool • Abdominal pain & cramping • Fever • Wt loss • Chronic diarrhea • Anorexia • Malnutrition • Delayed growth in adolescents • Bloody diarrhea with mucus • Abdominal &/or rectal pain • Fever • Wt loss • Possibly constipation & rectal spasm • Arthritis • Dermatological changes • Ocular manifestations Complications • Malabsorption • Malnutrition • Abdominal fistulas & abscesses • Intestinal obstruction • Bacterial overgrowth (blind loop syndrome) • Gallstones • Perianal disease • Neoplasia • Urinary tract infections • Kidney stones • Thromboembolic complications • Affects any part of the GI tract (from mouth to anus) and may have a "skipping" pattern • Severe bleeding • Toxic colitis • Toxic megacolon • Strictures • Perforation • Colonic structures • Dysplasia • Carcinoma • Intolerance to immunosuppression • Affects the colon and rectum only (continuous) Diagnosis • Clinical presentation – CDAI score • Abdominal ultrasound • MRI • CT • Antiglycan antibodies (ASCA/ANCA) • Calprotectin, lactoferrin, & polymorphonuclear neutrophil elastase • Abdominal ultrasound • MRI • CT • Antiglycan antibodies (ASCA/ANCA) • Calprotectin, lactoferrin, & polymorphonuclear neutrophil elastase 3. What did you find in Mr. Page’s history and physical that is consistent with his diagnosis of Crohn’s? Explain. There are multiple aspects of Mr. Page’s history and physical that are consistent with his diagnosis of Crohn’s. Mr. Page had a fever, which is common in Crohn’s; his fever is most likely due to the infection and inflammation that he is experiencing and can indicate the period of exacerbation of the disease. Mr. Page presented with abdominal pain, which can be due to increased air in the GI tract as well as the bowel obstruction. Abdominal pain and cramping are common in patients with Crohn’s. Diarrhea is also common in patients with Crohn’s, and Mr. Page reported that he is experiencing increased diarrhea. The weight loss of 26-28 pounds is also consistent with Mr. Page’s diagnosis of Crohn’s and is most likely due to his increased requirements and decreased oral intake as well as the constant diarrhea. 4. Crohn’s patients often have extraintestinal symptoms of the disease. What are some examples of these symptoms? Is there evidence of these in his history and physical? • Extraintestinal symptoms include: ○ Osteopenia and osteoporosis ○ Dermatitis ○ Rheumatological conditions such as ankylosing spondylitis ○ Ocular symptoms ○ Hepatobiliary complications • Anemia • Mr. Page appears to be experiencing anemia. 5. Mr. Page has been treated previously with corticosteroids and mesalamine. His physician had planned to start Humira prior to this admission. Explain the mechanism for each of these medications in the treatment of Crohn’s. Identify any drug-nutrient interactions for each. • Corticosteroids: Anti-inflammatory; reduction of lymphocytes; increased neutrophils; decreased production of prostaglandins. • Drug-nutrient interactions: hyperglycemia, nitrogen wasting, and increased risk of osteoporosis (increased excretion of calcium). May result in hypokalemia, as well. • Mesalamine: Also known as 5-aminosalicylic acid/5-ASA. Anti-inflammatory—inhibits cyclooxygenase, which reduces synthesis of prostaglandins. • Drug-nutrient interactions: none • Humira: Anti-TNF antibody that inhibits TNF-α, which reduces the inflammatory response. • Drug-nutrient interactions: none 6. What laboratory values are consistent with an exacerbation of his Crohn’s disease? Identify and explain these values. Fecal calprotectin (Cal), lactoferrin (Lf), and polymorphonuclear neutrophil elastase (PMN-e) levels correlate with inflammation and can be used to indicate an exacerbation of Crohn’s disease. PMN-e is an enzyme released from polymorphonuclear leukocytes involved in the body’s non-specific immune response; it is released early in infection and helps destroy offending organisms. On a side note, some suggest PMN-e content may be linked to genetics, which is interesting considering the genetic component of IBD. Calprotectin correlates significantly with endoscopic colonic inflammation and lactoferrin correlates with histologic inflammation. Because colorectal neoplasia and GI infection also can increase levels of fecal calprotectin, it should be used with caution. However, research is continuing in the practical use of this marker for clinicians as it appears to be as good as the CDAI for indicating Crohn’s disease activity. Other laboratory values consistent with an exacerbation of Crohn’s disease include antisacchromyces antibodies (ASCA), which are often used to differentiate Crohn’s from ulcerative colitis. Interleukins and tumor necrosis factor are markers for IBD; these serum cytokines may be elevated in an exacerbated state of Crohn’s. C-reactive protein and erythrocyte sedimentation rate (ESR) are acute-phase reactants that could be elevated as well, but these do not always indicate intestinal inflammation. Severe exacerbations of Crohn’s disease will also commonly show low albumin levels, which are consistent with inflammation and poor protein/calorie intake. Elevated WBC levels are consistent with the inflammation of exacerbated Crohn’s. 7. Is Mr. Page a likely candidate for short bowel syndrome? Define short bowel syndrome, and provide a rationale for your answer. Short bowel syndrome results when a large portion (>50%) of the small intestine is resected or an individual presents with significant signs of malabsorption and/or is unable to maintain fluid and electrolyte status. The likelihood that an individual will develop short bowel syndrome depends on which sections of the small intestine have been resected, presence of the ileocecal valve, and health of the remaining portions of the small intestine. It is difficult to predict Mr. Page’s postoperative course. The small intestine is about 20 feet, or 610 cm, long. Thus, Mr. Page lost about 33% of his small intestine with this surgery. Because 50% or more has to be removed before its ability to function normally is significantly reduced, Mr. Page should be able to recover to normal functionality. Also, Mr. Page still has his ileocecal valve, which controls transit time through the small intestine. If this is absent, transit time is decreased and the contact time needed for digestion and absorption is affected. The major concern for Mr. Page is the effect of Crohn’s disease on the remaining small bowel and his state of malnutrition preoperatively. 8. What type of adaptation can the small intestine make after surgical resection? The small bowel is remarkably adaptive (villi height and crypt depth can increase to accommodate for lost surface area). Usually, when less than 50% of the small intestine is resected, normal digestion and absorption can be expected. Success of adaptation is related directly to the health of the remaining small intestine. Mr. Page has had extensive Crohn’s disease for several years so it may prove difficult to predict his tolerance to this extensive surgery. II. Understanding the Nutrition Therapy 9. Mr. Page underwent resection of 200 cm of jejunum and proximal ileum. The ileocecal valve was preserved. Mr. Page did not have an ileostomy, and his entire colon remains intact. How long is the small intestine, and how significant is this resection? The entire small intestine is approximately 15-16 feet (4.6-4.9 m) long. The first 9-11 inches is the duodenum. The second portion of the small intestine is the jejunum, which is approximately 9-10 feet in length. The ileum is the final portion of the small intestine and is approximately 4 feet in length. 200 cm (2 m) is approximately 44% of his entire small intestine. Usually, when less than 50% of the small intestine is resected, normal digestion and absorption can be expected. 10 What nutrients are normally digested and absorbed in the portion of the small intestine that has been resected? Most digestion and absorption of macronutrients occurs within the duodenum and the first three feet of the jejunum. Almost all vitamins and minerals are also absorbed in the proximal jejunum. One exception is vitamin B12, which is absorbed in the distal ileum. Mr. Page has lost the lower portion of his jejunum and the proximal ileum. The remaining portions of the small bowel, if fully functional, should be able to compensate for the resection. Full adaptation for normal digestion and absorption should theoretically be possible. 11. Are there nutrition recommendations that could impact the inflammatory mechanisms of Mr. Page's disease process? How might these recommendations be different than those aimed at controlling symptoms of his Crohn's disease such as diarrhea, gas, or abdominal pain? Certain nutrients, such as omega 3 fatty acids, may provide an anti-inflammatory benefit. Furthermore, increasing fiber and avoiding concentrated sweets and red meat, may promote the growth of beneficial microbiota. These dietary recommendations are consistent with the meal pattern associated with the Mediterranean diet. Very few controlled nutrition studies have examined this effect of diet and Crohn’s disease. Consumption of high-fiber foods (e.g. vegetables, fruits, whole-grains) may be problematic due to strictures or during periods of exacerbation. Nutrition recommendations will need to be individualized with consideration of disease process, current symptoms, previous surgeries and response to medications. III. Nutrition Assessment 12. Evaluate Mr. Page’s %UBW and BMI. Ht. 69#; Current wt. 140#; UBW 166-168#; 84% UBW; BMI: 20.7 Mr. Page has experienced a 17% weight loss in the previous six months. Any change greater than 10% is considered to place him at significant nutritional risk. His BMI is within normal limits. Though this measurement assesses disease risk from obesity, the lower BMI is consistent with his obvious low body fat secondary to his significant weight loss. The most important factor for Mr. Page is this significant unintentional weight loss. 13 Calculate Mr. Page’s energy and protein requirements. Harris-Benedict Equation: REE = 66.5 + 13.8 x W (kg) + 5.0 x S (cm) - 6.8 x A (yrs) REE = 66.5 + 13.8 x 63.6 kg + 5.0 x 175.26 - 6.8 35 yrs REE = 1582 ≈ 1600 kcal/day TEE = 1582 x 1.2 (PA) x 1.3 (IF) = 2467.9 ≈ 2450 kcal/day or 2300-2600 kcal/day Or 30-35 kcal/kg (ASPEN guidelines): 30-35 kcal/kg  63.6 kg = 1908-2227 kcal or 1900-2200 kcal/day Protein requirements can be estimated using either 1.2-1.5 g/kg 1.2-1.5 g/kg: = 76-95 grams 14. Identify any significant and/or abnormal laboratory measurements from both his hematology and his chemistry labs. Explain possible mechanisms for the abnormal labs. Lab Patient’s value Normal value Relationship to diagnosis Albumin 3.2 g/dL 3.5-5.5 g/dL Decreased visceral protein stores due to hepatic reprioritization during acute inflammatory response. Prealbumin 16 mg/dL 18-35 mg/dL Decreased visceral protein stores due to hepatic reprioritization during acute inflammatory response. ASCA Positive Negative Antibody consistent with Crohn’s disease. C-reactive protein 22 mg/dL 7 days and patient is malnourished); recovery time; functional status of the gastrointestinal tract (including clinical condition—hemodynamically stable, soft/bowel sounds); access for parenteral support; and ability to tolerate the fluid volume required for PN. Enteral nutrition should be used, unless contraindications exist (e.g. severe GI bleed, distal high output fistulas >500 mL/day, mechanical obstruction, intractable diarrhea, etc.). 17. The members of the nutrition support team note his serum phosphorus and serum magnesium are at the low end of the normal range. Why might that be of concern? • Those levels may fall dramatically as Mr. Page receives nutrition support (due to refeeding syndrome). • They will need to be maintained in order to prevent electrolyte imbalances. 18. What is refeeding syndrome? Is Mr. Page at risk for this syndrome? How can it be prevented? • Refeeding syndrome is a term used to describe metabolic changes that occur as a result of repletion of malnourished individuals. Refeeding syndrome occurs after a period of starvation to which the body has adapted by metabolizing fat for energy instead of carbohydrate. When a carbohydrate-rich diet is reintroduced, thiamin, phosphorous, potassium, and magnesium are swiftly removed from the bloodstream into the cells for anabolism. • This may result in electrolyte imbalances and shifts of fluid balance that accompany these changes. This can lead to heart failure and edema, acidosis, hyperventilation, and neurological dysfunction. • Mr. Page is at risk due to his malnutrition, metabolic stress, and levels of electrolytes. • Prevention of refeeding can be prevented by following these steps: 1. Obtain and correct baseline electrolytes (supplement K, Phos, Mg). 2. Initiate nutrition support with caution and at a low and slow rate (e.g., 15-20 kcal/kg or <BEE  1.0). 3. Increase caloric intake gradually. 4. Monitor electrolytes closely (q 12 hr; 2/day) for at least the first 3-5 days until Mr. Page is stable at his full caloric target. 19. Mr. Page was placed on parenteral nutrition immediately postoperatively, and a nutrition support consult was ordered. Initially, he was prescribed to receive 200 g dextrose/L, 42.5 g amino acids/L, and 30 g lipid/L. His parenteral nutrition was initiated at 50 cc/hr with a goal rate of 85 cc/hr. Do you agree with the team’s decision to initiate parenteral nutrition? Will this meet his estimated nutritional needs? Explain. Calculate: pro (g); CHO (g); lipid (g); and total kcal from his PN. • Mr. Page was certainly malnourished prior to surgery. • His surgery places his gastrointestinal function at risk. Mr. Page will be NPO for some time. • The decision to use parenteral nutrition is correct. • This formula prescription provides 2346 kcal and 86.7 g protein. • This is slightly higher in both energy and protein than the lower calculated energy needs and will sufficiently nourish him. Note: Calculations of parenteral nutrition are as follows: • 2436 kcal  64 kg = 36.7 kcal/kg • 86.7 g amino acids  64 kg = 1.4 g protein/kg • Dextrose: 200  3.4 = 680 kcal/L. Total volume is 2040 mL, which would provide 1387.2 kcal. 408 g dextrose  64 kg = 6.375 g/kg/day  1000 mg/g  1 day/1440 min = 4.4 mg dextrose/min (4.3-7.2 mg/kg/min guideline for critically ill/stressed patients) • Lipid: 30 g lipid/L @ 11 kcal/g: 673.2 kcal 20. For each of the PES statements you have written, establish an ideal goal (based on the signs and symptoms) and an appropriate intervention (based on the etiology). • Increased nutrient needs ○ Provides rationale for the nutrition prescription that determines the goal rate for nutrition support and regaining of lost weight; however, based on the risk for refeeding syndrome, parenteral nutrition should be provided at a slower rate and gradually advanced to meet increased nutrient needs. ○ Ideal Goal: Provide adequate nutriture for an expedited recovery without experiencing refeeding syndrome. ○ Intervention: Slowly introduce PN. • Inadequate oral food/beverage intake ○ Provides rationale for the initiation of nutrition support; also identifies a contributing etiology of malnutrition. • Increased energy expenditure ○ Ideal Goal: Weight stabilization and reduction in CRP. ○ Intervention: Initiate enteral/parenteral nutrition. •• Involuntary weight loss ○ Ideal Goal: Similar to that of protein-energy malnutrition ○ Intervention: Provide adequate energy and protein via nutrition support and then advance to oral foods and beverages. VI. Nutrition Monitoring and Evaluation 21. Would you make any changes to his prescribed nutrition support? What should be monitored to ensure adequacy of his nutrition support? Explain. What recommendations would you make to transition to enteral feeding? It would be best to continue with the current regimen as it meets his measured energy requirements. Assess actual intake from intake/output records to ensure the prescription meets estimated nutrient needs. Obtaining nitrogen balance will help support current rationale for nutrition prescription. When able, wean Mr. Page from the parenteral nutrition support to enteral nutrition support or an oral diet.. 22. What should the nutrition support team monitor daily while on PN? What should be monitored weekly? Explain your answers. • Daily: electrolytes, serum glucose, vital signs, weight, intake and output (hydration status) • Weekly: CBC, PT, PTT, prealbumin, triglycerides, TG, ALT, AST, ALP, total bilirubin, nitrogen balance • It is essential to monitor electrolytes and glucose daily to ensure tolerance to the feeding regimen. • This also provides the framework from which serum electrolytes can be managed through changes in the parenteral solution. Refeeding status is a serious concern and requires monitoring of Mg, Phos., and K levels. • Monitoring weight and intake/output records allows the team to monitor hydration status and to ensure tolerance to the fluid load that the parenteral solution provides. • Weekly laboratory values provide data needed to monitor changes in nutritional status. ○ These would include the prealbumin and the nitrogen balance. • Other labs allow the team to evaluate organ function and any potential intolerance to the nutrition support. 23. Mr. Page’s serum glucose increased to 172 mg/dL. Why do you think this level is now abnormal? What should be done about it? • It is not unusual for serum glucose to be elevated as a result of stress, surgery, and his nutrition support. • Research indicates serum glucose should be managed aggressively as those patients with hyperglycemia have more complications during the hospitalization. • Insulin can be added to his parenteral nutrition, or the hyperglycemia can be managed by use of short-acting insulin within a sliding-scale regimen. 24. Evaluate the following 24-hour urine data: 24-hour urinary nitrogen for 12/20: 18.4 grams. By using the daily input/output record for 12/20 that records the amount of PN received, calculate Mr. Page’s nitrogen balance on 12/20. How would you interpret this information? Should you be concerned? Are there problems with the accuracy of nitrogen balance studies? Explain. Nitrogen balance = N intake (g/24 hr) – (urinary N [g/24 hr] + 3 g/24 hr) N intake: 1600 mL TPN  0.0425 g protein/cc = 68 g protein 68 ÷ 6.25 = 10.88 g nitrogen intake 10.88 – (18.4 + 3) = -10.5 g • Mr. Page is in negative nitrogen balance, indicating he continues to be catabolic. • He has only been on nutritional support for 4 days and it will likely take much longer to reverse his catabolic state. • It would be wise to repeat the nitrogen balance to ensure the amount of catabolism is decreasing. • Any test that relies on the collection of urine over a 24-hour period is at risk for inaccuracies. • Nitrogen balance studies in this situation, however, are much easier because the amount of nitrogen in the parenteral nutrition is known and his urine is being collected via a catheter, which decreases the risk of losses. 25. On post-op day 7 (12/22), Mr. Page’s team notes he has had bowel sounds for the previous 48 hours and had his first bowel movement. The nutrition support team recommends consideration of an oral diet. What should Mr. Page be allowed to try first? What would you monitor for tolerance? If successful, when can the parenteral nutrition be weaned? • Mr. Page can be advanced to a diet consisting of the following: 5-6 small meals. 50% complex carbohydrates with avoidance of simple sugars and FODMAPS such as fructose, high fructose corn syrup and sugar alcohols. Fat should be restricted to <30% of total calories. Protein should be 20-30% of total calories with an emphasis on high biological food choices. Soluble fiber should be emphasized with approximately 5-10 g/day. Limit high oxalate foods. • The hyperosmolality of clear liquids, which might be typically ordered, may actually increase stool output. • Any food that causes an increase in diarrhea or pain should be avoided and tried at a later date. • The use of a lactose-free liquid supplement would be a good choice to increase his overall intake. • When Mr. Page can consume 60% of his requirements by mouth, the parenteral nutrition can be weaned. 26. What would be the primary nutrition concerns as Mr. Page prepares for rehabilitation after his discharge? Be sure to address his need for supplementation of any vitamins and minerals. Identify two nutritional outcomes with specific measures for evaluation. Malabsorption: Short bowel syndrome is probably the biggest concern. It is generally felt that if more than 50% of the small bowel remains then there is the hope that the remaining small bowel will make the appropriate adaptations. Also, Mr. Page has his ileocecal valve, which controls transit time through the small intestine which may reduce his risk of malabsorption. Malnutrition: The major concern for Mr. Page is the effect of Crohn’s disease on the remaining small bowel, stool output, and his state of malnutrition preoperatively. Micronutrient Deficiency: Mr. Page will need a general chewable or liquid multivitamin but he may also experience deficiencies of specific nutrients such as folate or B12. Nutrients that are specifically absorbed in the jejunum and ileum include: magnesium, amino acids, carbohydrates, vitamin B12, and bile salts. Mr. Page appears to be deficient in vitamins A, C, and D preoperatively. Specific supplementation will need to be considered for these three micronutrients. Risk of oxalate kidney stones: If a patient experiences fat malabsorption, calcium binds to fat in the small bowel instead of oxalate. Since Mr. Page has his colon in continuity, free oxalate can be absorbed and then is excreted by the kidney. To prevent the development of oxalate kidney stones, Mr. Page needs to stay hydrated and have adequate urine production. Dietary sources of high oxalate foods may need to be avoided: beets, spinach, rhubarb, strawberries, nuts, chocolate, tea, wheat bran, and all fresh, canned, or cooked dry beans. Outcomes: 1. Mr. Page will gain weight at the rate of approximately 1 lb. per month post-operatively. 2. Mr. Page will tolerate solid food with appropriate GI tolerance. 3. Mr. Page will consume a minimum of 2400-2700 kcal/day postoperatively. 4. Mr. Page will maintain adequate hydration by consuming a minimum of 3L fluid/day. Solution Manual for Medical Nutrition Therapy: A Case-Study Approach Marcia Nahikian Nelms 9781305628663, 9780534524104, 9781133593157