Case-6-9 Heart Failure With Resulting Cardiac Cachexia – Medical Nutrition Therapy: A Case-Study Approach : Book Guide

This Document Contains Cases 6 to 9 Case 6 – Heart Failure with Resulting Cardiac Cachexia I. Understanding the Disease and Pathophysiology 1. Outline the typical pathophysiology of heart failure. Onset of heart failure usually can be traced to damage from an MI and atherosclerosis. Is this consistent with Mrs. Maney's history? • Many different events can lead to the development of congestive heart failure. • Previous myocardial infarction, valve defect, or increased work demand on the heart from other conditions such as hypertension all can damage the heart. • This damage results in a decreased ability of the heart to pump adequately. • When there is reduced blood flow to tissues, the body compensates in several ways. • The kidney responds to decreased blood flow by secreting renin and aldosterone, causing vasoconstriction and an increase in blood volume. • The heart then has to work even harder to handle the increased blood volume. • Over time, the heart enlarges (cardiomegaly) with its attempt to handle the increased workload. • Cardiac output and stroke volume decrease. • Compensation mechanisms do work for a time but eventually the heart muscle weakens. • Dr. Maney’s medical history is consistent with the typical pathophysiology of heart failure. She has a long history of coronary artery disease, hypertension, and mitral valve disorder. She also experienced a myocardial infarction. Her previous medical diagnoses are all indicative of damage to the heart muscle, which is the first step in the progression of heart failure. 2. Identify specific signs and symptoms in the patient’s physical examination that are consistent with heart failure. For any three of these signs and symptoms, write a brief discussion that connects them to physiological changes that you described in question #1. • Jugular venous distention • Ascites • 2+ pedal edema • Shortness of breath • Increased pulse (110) respirations (24), lower blood pressure (90/70) • Rales • Skin - gray a) Rales Due to decreased cardiac output and the resulting low blood pressure present in HF, the RAAS is activated by the kidneys. This system attempts to raise blood pressure by increasing sodium and water retention. Fluid accumulates in the pulmonary vein and backs up into pulmonary circulation, which increases pressure in the pulmonary capillaries. This increased pressure pushes fluid into the lungs, causing pulmonary congestion/edema. The presence of fluid in the lungs can be heard through a stethoscope as rales or crackles as the air tries to move through the fluid with each breath. Because the system lacks the oncotic pressure to pull the fluid back into the capillaries, it continues to accumulate in the lungs, leading to labored breathing and dyspnea. This, in turn, leads to tachypnea, as the patient must breathe more rapidly to get enough oxygen into the lungs. b) 2+ pedal edema As the heart enters right-sided HF, it remains unable to pump blood efficiently. The right side of the heart cannot maintain cardiac output, so blood volume decreases. The decrease in renal blood flow again activates the RAAS to increase sodium and water retention, which then causes fluid to back up into the systemic circulation.5 This increased venous pressure in the systemic circulation causes fluid to leak from the capillaries into the third spaces near the ankles and feet (largely due to gravity) leading to pedal edema. Again, the heart is not strong enough and the vessels lack the oncotic pressure needed to pull the fluid back into circulation, so it continues to accumulate, increasing the severity of the edema. c) Tachycardia As the failing heart works to increase cardiac output to normal levels, it must beat harder and faster to do so. The release of hormones by the sympathetic nervous system not only cause vasoconstriction and activation of the RAAS, but also increase the heart rate and contractility. 3. Heart failure is often described as R-sided failure or L-sided failure. What is the difference? How are the clinical manifestations different? Heart failure can involve the left side, the right side, or both sides. However, it most often begins with the left ventricle. In left-sided HF, the left side of the heart experiences dysfunction and is unable to adequately maintain cardiac output. In right-sided HF, the right side of the heart cannot maintain cardiac output. Because the left and right sides of the heart have different functions, the resulting signs and symptoms caused by their failure are different. Though initial compensation by the body occurs, it cannot be maintained, and one-sided HF often expands to the entire heart, leading to decompensated HF. Left-sided HF is typically the result of end-stage CAD or MI. When the left ventricle is damaged, it becomes weakened and cannot pump blood adequately to the systemic circulation. This can be further classified as systolic or diastolic. In systolic left-sided HF, the left ventricle has diminished contractility and cannot fully empty. In diastolic left-sided HF, the left ventricle experiences impaired relaxation and is unable to fill completely. Both of these situations lead to a decreased cardiac output and a resulting activation of the RAAS system in order to restore blood volume by increasing sodium and water reabsorption by the kidneys. The increase in fluid causes a backup of blood into the pulmonary circulation. The excess fluid in the pulmonary vein causes an increase in pressure in the pulmonary capillaries, and fluid is forced out of the vessels and into the lungs. This fluid makes it difficult to breathe, leading to dyspnea and tachypnea. Because the blood vessels lack the oncotic pressure to pull the fluid back out of the lungs, blood pressure remains low, and the system continues to stimulate the RAAS system to try to bring the body back to homeostasis. This leads to additional fluid accumulation and further pulmonary congestion. Right-sided HF is most often the result of left-sided HF.3 When the right side of the heart begins to fail, it cannot maintain cardiac output to the pulmonary trunk. Again, the RAAS system is stimulated to retain sodium and water. This causes blood to back up into the systemic circulation. The high pressure in the periphery causes fluid to leak out into the third spaces near the feet and ankles as well as the liver and abdominal organs, resulting in pedal edema and ascites as well as splenomegaly and hepatomegaly. Additionally, venous pressure remains high, which results in the distention of the jugular vein in the neck and cerebral edema, which causes headache. Both left- and right-sided HF lead to fatigue, dyspnea, and generalized weakness. Furthermore, the presence of edema in the abdominal region and dyspnea together cause a decrease in appetite/increase in satiety. This has many nutritional implications, including malnutrition and cardiac cachexia. II. Understanding the Nutrition Therapy 4. Mrs. Maney’s husband states that they have monitored their salt intake for several years. What is the role of sodium restriction in the treatment of heart failure? What level of sodium restriction is recommended for the outpatient with heart failure? What difficulties may a patient have in following a sodium restriction? • Some level of sodium restriction is necessary in the treatment of heart failure because of the complications associated with severe fluid retention. Sodium in the body attracts fluid, meaning that an excess of sodium from the diet will cause additional fluid retention. Excessive fluid retention causes peripheral edema, ascites, and pulmonary congestion in heart failure patients. The clinical manifestations of fluid overload can increase the patients' energy expenditure (increased work of breathing/respiration rate), while causing eating difficulties (dyspnea, ascites pressing against the stomach). It is essential that these patients control their intake of sodium, which in turn controls their level of fluid retention. • A 2,000 mg sodium diet is a standard initial recommendation. • Adjustments to levels of 1,000 mg or 500 mg may be prescribed depending on an individual patient’s medical condition—specifically, fluid and volume states as well as overall oral intake. • These levels of sodium restriction are a challenge to manage outside a hospitalized setting, so it is critical to evaluate the patient’s actual PO intake to determine the level of sodium the patient is consuming prior to putting any further modifications in place. However, in malnourished or cachectic patients who have anorexia, caution should be exercised. This is because the first priority in the HF patient is to ensure they are getting enough nutrients to maintain weight and support healing. • Such difficulties include: sodium's high prevalence in Western/processed foods, salt's prominent role in flavor/taste, and salt's high use in foods at restaurants 5. Why is Mrs. Maney placed on fluid restriction? How will this assist with the treatment of her heart failure? What specific foods are typically "counted" as a fluid? • On admission she was had fluid retention and had prerenal azotemia. • Physical exam reveals 2+ pedal edema that demonstrates her fluid overload • The patient’s creatinine and BUN are also elevated. • These findings are compatible with low kidney perfusion. • Fluid restriction will improve clinical symptoms and quality of life. • Foods “counted” as fluid: All beverages (including water, milk, juices, coffee, tea, soft drinks),soups, gelatins, fruit ice, Popsicles™, liquid nutritional supplements, ice cream, puddings, custard, sherbet, ice, soups, and anything liquid (or that melts) at room temperature. 6. Identify any common nutrient deficiencies found in patients with heart failure. Common nutrient deficiencies found in patients with heart failure include: potassium, magnesium, thiamin, riboflavin, pyridoxine, folate, B-12, calcium, and zinc. Many of these nutrient deficiencies are caused by drug-nutrient interactions. A common drug-nutrient interaction in heart failure patients is the loss of water-soluble nutrients when a combination of multiple diuretics is used to remove excess fluid from the body. Additional research is being done to determine the appropriate use of some supplements, such as omega-3 fatty acids and coenzyme Q10, in HF patients. While results do not suggest any strong evidence for the supplementation of either of these substances, there remains a possibility that they may help the HF patient. L-arginine and carnitine are also being investigated for potential supplementation. III. Nutrition Assessment 7. Identify factors that would affect interpretation of Mrs. Maney’s weight and body composition. Look at the I/O record. What will likely happen to Mrs. Maney's weight if this trend continues? • Ascites and peripheral edema • Mrs. Maney’s I/O record shows an overall net fluid retention of 408 mL over a 24-hour period since her admission. If this trend continues, Mrs. Maney’s measured weight will increase to reflect additional fluid retention. A negative net I/O value would correlate with a decrease in measured weight. • Mrs. Maney also has signs of muscle wasting (temporal wasting and weak handgrip) which may indicate a loss of lean body mass. These may be masked due to fluid retention. 8. Calculate Mrs. Maney’s energy and protein requirements. Explain your rationale for the weight you have used in your calculation. • Mrs. Maney’s IBW (50 kg) is used for calculations as her current weight is masked by fluid retention. This is within 10% of her current weight. • Energy: energy needs for cardiac cachexia may be calculated using the American Chest Physician’s nomogram. 50 x 25 = 1250 kcal 50 x 35= 1750 kcal Range: 1250-1750 kcal • Protein: AND EAL recommends 1.37 g/kg for heart failure patients. 47.7 kg  1.37 = 65 g/day 9. Do you have any evidence that Mrs. Maney may be malnourished? Identify factors that may support a diagnosis of malnutrition using the latest AND/ASPEN proposed guidelines for malnutrition diagnosis. • Yes, there is evidence that Mrs. Maney is malnourished • Muscle loss at her temporal region • Fluid accumulation is present: ascites, 2+ pedal edema (though, her heart failure complicates this clinical evidence for malnutrition) and would be difficult to interpret. • Weak grip strength • < 27% energy intake (per 2 cans of Boost daily) 10. Malnutrition in heart failure is often referred to as cardiac cachexia. What is cardiac cachexia? What are the characteristic symptoms? Explain the role of the underlying heart disease in the development of malnutrition. • Cardiac cachexia is a wasting syndrome caused by heart failure that results in a metabolic imbalance favoring catabolism over anabolism. Losses in lean and fat tissue, in addition to bone mineral density, can be observed and is not always reversible upon feeding (like starvation). • Signs and symptoms: increased plasma TNF-α, decreased GI tract perfusion (slowed peristalsis, early satiety, and impaired nutrition absorption), and endothelial dysfunction (leading to a reduction in skeletal muscle nutrient supply). • Heart failure promotes the development of malnutrition through inflammatory pathways, elevated levels of B-type and atrial natriuretic peptides, aldosterone, and cortisol, and anorexia. 11. Do you feel that Mrs. Maney may benefit from enteral feeding? What guidelines would you use to make this decision? Outline a nutrition therapy regimen for her that includes formula choice, total volume, and goal rate. • Yes, Mrs. Maney would benefit from enteral feeding since she is consuming < 5% of her meals and consumed < 27% of her energy needs prior to admission • ASPEN guidelines should be used to make this decision; since she is malnourished and critically ill at admission • Formula choice: Two-Cal HN (high-protein formula that provides 2 kcal/mL) = 1800 kcal • Total volume: 900 mL • Goal rate: 38 mL/hr • Osmolality of Two-Cal NH is 725 mOsm/kg H2O; therefore, the initial rate should be 20 mL/hr for first 8 hours, then advanced 10 mL/hr every 4 hours until goal rate is reached. 12. Identify any abnormal biochemical values associated with Mrs. Maney's heart failure or CVD and assess them using the following table: Name of Laboratory Value Normal Value Patient’s Value & Date Reason for Abnormality Sodium (mEq/L) 136-145 132 (2/14) 133 (2/16) 135 (2/20) Fluid overload resulting in dilution of serum sodium BUN (mg/dL) 6-20 32 (2/14) 34 (2/16) 30 (2/20) Decreased renal perfusion; Cardiac cachexia (protein catabolism, muscle wasting) Creatinine serum (mg/dL) 0.6-1.1 1.6 (2/14) 1.7 (2/16) 1.5 (2/20) Decreased renal perfusion; Cardiac cachexia (protein catabolism, muscle wasting) Bilirubin, direct (mg/dL) <0.3 1.0 (2/14) 1.1 (2/16) 0.9 (2/20) Abnormal liver function; hepatomegaly resulting from edema in liver Protein, total (g/dL) 6-7.8 5.8 (2/14) 5.6 (2/16) 5.5 (2/20) Fluid overload resulting in dilution of serum protein Albumin (g/dL) 3.5-5.5 2.8 (2/14) 2.7 (2/16) 2.6 (2/20) Fluid overload resulting in dilution of serum albumin; increased protein catabolism due to cardiac cachexia Prealbumin (mg/dL) 18-35 15 (2/14) 11 (2/16) 10 (2/20) Fluid overload resulting in dilution of serum prealbumin; malnutrition (cardiac cachexia); possible abnormal liver function (hepatomegaly) ALT (U/L) 4-36 100 (2/14) 120 (2/16) 115 (2/20) Impaired liver function resulting from edema in liver (hepatomegaly); Damage to heart muscle; AST (U/L) 0-35 70 (2/14) 80 (2/16) 85 (2/20) Impaired liver function resulting from edema in liver (hepatomegaly) Damage to heart muscle; CPK (U/L) 30-135 180 (2/14) 200 (2/16) 205 (2/20) Damage to heart muscle; Troponin T (ng/L) <0.03 0.035 (2/14) 0.037 (2/16) 0.036 (2/20) Past cardiac injury (myocardial infarction) Troponin I (ng/L) 59 30 (2/14) 31 (2/16) 30 (2/20) History of coronary artery disease; genetic, lifestyle and diet may contribute. LDL (mg/dL) <130 180 (2/14) 160 (2/16) 152 (2/20) History of coronary artery disease; genetic, lifestyle and diet may contribute. LDL/HDL ratio <3.22 5 (2/14) 5.23 (2/16) 4.97 (2/20) History of coronary artery disease; genetic, lifestyle and diet may contribute. WBC ( 103/mm3) 4.8-11.8 12 12 10.5 Inflammation and overall disease state 13. The following drugs/supplements that were prescribed for Mrs. Maney. Give the medical rationale for the use of each. In addition, describe any nutritional concerns for Mrs. Maney while she is taking these medications. Medication Rationale for Use Nutrition Implications Lanoxin Increases myocardial contraction. Side effects of this medication include diarrhea, loss of appetite, stomach pain, nausea, and vomiting; all of these side effects can make eating difficult and unpleasant, resulting in suboptimal oral food and nutrient intakes. Avoid avocado, high fiber foods within 2 hours of taking medication, limit sodium, avoid milk, Ca supplements, iron, antacids or aluminum salts 2 hours before or 6 hours after taking medication. Avoid K containing salt substitutes, limit garlic, ginger, gingko, and horse chestnut Lasix Diuretic used in edematous states to improve fluid balance; sometimes used to lower blood pressure. Hypokalemia, hypomagnesemia, thiamin deficiency, calcium deficiency; supplementation may be necessary depending of severity of electrolyte or nutrient deficiency. Dopamine Increases myocardial contraction and has a pressor effect to help support blood pressure when low. Side effects include potential decrease in serum potassium, proteinuria, nausea, and vomiting; may require potassium supplementation or high-potassium diet choices; nausea and vomiting may inhibit adequate caloric intake. Thiamin Diuretic use can lead to thiamin deficiency. NA IV. Nutrition Diagnosis 14. Select two nutrition problems and complete a PES statement for each. • Inadequate oral food/beverage intake related to poor appetite as evidenced by few sips of liquids, soft foods, and “trying to take Ensure.” • Inadequate intake from enteral nutrition related to intolerance secondary to uncontrolled diarrhea as evidenced by ___ (more data would be needed regarding the specific amount that was either provided or withheld during this period of time, e.g. “only X mL of formula compared to goal rate”). • Malnutrition related to anorexia and SOB as evidenced by consumption of <75% of estimated energy needs, moderate temporal wasting and reduced handgrip strength. V. Nutrition Intervention 15. Mrs. Maney was not able to tolerate the enteral feeding because of nursing report for diarrhea. What recommendations could be made to improve tolerance to the tube feeding? • The formula could be changed to one with added fiber (such as Jevity) or fiber could be added to Mrs. Maney's medications. • It is important to remember that fiber supplements should not be added separately to the enteral formula or placed down the feeding tube. It may cause interactions with the formula and could result in a tube blockage. • Additionally, an antidiarrheal agent such as loperamide could be used. • Depending the osmolality of the formula, it may be advisable to have a lower initiation rate to lower the "water-pulling" effect that the higher osmolar formula may have in the intestinal tract. 16. The tube feeding was discontinued because of continued intolerance. Parenteral nutrition was not initiated. What recommendations could you make to optimize Mrs. Maney's oral intake? • If she is able to eat, provide her with foods that she likes with increased nutrient density. • Small, frequent feedings work well to minimize the volume of food consumed and stress on both the cardiac and respiratory systems. • Within her fluid allowance, use of a nutrient-dense liquid supplement may be easier than attempting to consume solid food. • Consume fluids between meals to prevent their contribution to fullness during mealtime 17. Outline steps you would take to assist Mrs. Maney as she prepares for discharge. Include the specific nutrition education that you would include. • Assess readiness/motivation for change • Educate the importance of sodium and fluid restriction and their implications on the clinical manifestations and exacerbations of her cachexic state (increased work of breathing due to pulmonary congestion, anorexia, etc.) • Educate Mrs. Maney on nutrient density – steps to add both kcal and protein to her diet. Suggest that Mrs, Maney have assistance with meal preparation and grocery shopping. Attempt to get at least 1/3 of her kcal at the meal where she is hungriest. Could also suggest spreading meals over 5-6 small feedings rather than only three. Discuss the use of high calore and high protein supplements. Every bite of food should provide both kcal and protein –discourage consumption of empty calorie foods. • Educate Mrs. Maney on fluids: ○ See question 5. for examples ○ How to optimize/reduce intake (e.g. avoid salty foods, drink only when thirsty, etc.) • Educate on low-sodium and avoidance of high-sodium options: ○ Low sodium: fresh or frozen vegetables, fruits, unprocessed meats, noodles, rice, English muffins, etc. ○ High-sodium: processed foods, salty snack foods, soups, sauces, fast foods, pickles, etc. Case 7 – Gastroesophageal Reflux Disease I. Understanding the Disease and Pathophysiology 1. How and where is acid produced and controlled within the gastrointestinal tract? • Parietal cells within the stomach are primarily responsible for synthesis of hydrochloric acid (HCl). • Acid secretion is released in three phases: the cephalic phase, gastric phase, and intestinal phase. • There is also a basal secretion that occurs without any environmental or gastrointestinal stimulation and is controlled by circadian rhythms. • Numerous substances affect parietal cell secretion, including signals to the brain stimulated by our sensory perception of food; presence of food within the stomach; and the substances pepsinogen, acetylcholine, histamine, and gastrin. • Histamine, gastrin, and acetylcholine all mediate the final step in the secretion of HCl. 2. What role does lower esophageal sphincter (LES) pressure play in the etiology of gastroesophageal reflux disease? What factors affect LES pressure? • Normally the lower esophageal sphincter prevents reflux of gastric contents into the esophagus. • This is accomplished by the competence of the sphincter muscle and relative pressures on either side of the sphincter. • If LES competence is compromised or if gastric pressure is greater than esophageal pressure, then gastric contents will flow into the esophagus. • Factors that potentially affect LES pressure include the hormones gastrin, estrogen, and progesterone; presence of hiatal hernia; presence of scleroderma, smoking, or some medications including dopamine, morphine, and theophylline; and nutritional factors. • Foods high in fat, chocolate, spearmint, peppermint, alcohol, and caffeine have been noted to decrease LES pressure. 3. What are the complications of gastroesophageal reflux disease? • Consistent reflux of gastric contents can severely erode the mucosa of the esophagus, resulting in an esophageal ulcer. • Scar tissue development may also occur, resulting in esophageal stricture and dysphagia. • An additional complication associated with GERD is development of Barrett’s esophagus. Barrett’s esophagus is characterized by metaplastic changes in esophageal cells, and for a small percentage of individuals may result in esophageal adenocarcinoma. 4. The physician biopsied for H. pylori. What is this? • Helicobacter pylori is a microorganism whose only natural host is the human. • It is found primarily on the surface of the antrum of the stomach. • This microorganism has been established to be the most common cause of gastritis and it is estimated that 92% of duodenal ulcers and 70% of gastric ulcers are caused by H. pylori. • By-products produced by the organism result in damage to the epithelium and impairment of the mucus barrier within the stomach. 5. Identify the patient’s signs and symptoms that could suggest the diagnosis of gastroesophageal reflux disease. • The patient’s complaints of indigestion and chest pain are symptoms. • The physician’s assessment of epigastric tenderness and heme positive stool also suggest GERD as well as possibly other complications of GERD such as peptic ulcer disease. • Fried foods worsening the indigestion that he is experiencing is suggestive of compromised LES pressure contributing to GERD 6. Describe the diagnostic tests performed for this patient. (1) 48-hour pH monitoring with intraesophageal pH electrode and recorder: • This test involves placing a pH probe into the distal esophagus for a 12- to 24-hour period in order to generate a graph depicting continuous pH readings. • Information is obtained regarding quantity and pattern of gastroesophageal (GE) reflux events, the correlation with symptoms, and the efficiency of esophageal acid clearance. (2) Barium esophagram: • A radiologist attempts to demonstrate reflux using abdominal pressure and positional changes. • In these procedures; the patient is given a contrast medium to drink. The most common medium is barium sulfate, which is a chalky, white, radiopaque substance the patient drinks like a milkshake. • The barium can be visualized by fluoroscopy or by x-ray. • This study allows the physician to monitor swallowing and the movement through the stomach into the duodenum. It also can distinguish many other abnormalities such as ulcers, tumors, or inflammation. (3) Endoscopy with biopsy to r/o H. pylori infection: • After sedation, a fiberoptic endoscope is passed through the oral pharynx, through the esophagus, and into the stomach. • This allows the physician to visualize the anatomy of the upper gastrointestinal tract. • A needle biopsy can be passed through the endoscope, allowing for determination of the presence of microorganisms within the collected tissue. 7. What risk factors does the patient present with that might contribute to his diagnosis? (Be sure to consider lifestyle, medical, and nutritional factors.) • Weight gain (promotes abdominal pressure upon the stomach) • High-fat diet • High caffeine intake • Alcohol intake • Lack of physical activity (related to weight gain) 8. The MD has decreased the patient’s dose of daily aspirin and recommended discontinuing his ibuprofen. Why? How might aspirin and other NSAIDs affect gastroesophageal disease? • Both of these medications can result in gastritis. • Aspirin and NSAIDs cause gastrointestinal disease by 2 independent mechanisms: • topical injury to the mucosa and • systemic depletion of cytoprotective prostaglandins. • Decreasing the aspirin dosage can allow it to provide cardiovascular protection while minimizing its toxic effect on the gastric mucosa 9. The MD has prescribed omeprazole. What class of medication is this? What is the basic mechanism of the drug? What other drugs are available in this class? What other groups of medications are used to treat GERD? • Omeprazole is an acid pump or proton pump inhibitor. • These drugs interrupt the action of the H+/K+-ATPase enzyme, which moves hydronium ions across parietal cell membranes in exchange for potassium ions, resulting in an inhibition of the secretion of HCl. • Other proton pump inhibitors include lansoprazole, esomeprazole, and pantoprazole. • Other drugs used to treat GERD include antacids, histamine-2 receptor antagonists, foaming agents, and prokinetic medications that increase gastric motility. II. Understanding the Nutrition Therapy 10. Summarize the current recommendations for nutrition therapy for GERD. • Goals of the nutrition therapy are consistent with goals of medical care discussed earlier. • These goals include reducing gastric acidity, restricting foods that lower LES pressure, and protecting the esophageal mucosa. • To reduce gastric acidity, black and red pepper, coffee (both caffeinated and decaffeinated), and alcohol should be avoided because all have been identified as stimulants for gastric acid production. • Likewise, meals of larger quantity that are high in fat delay gastric emptying and increase the risk of reflux. • Thus, smaller, more frequent meals may be indicated. • Foods that lower LES pressure should also be restricted. These include • Chocolate • Mint • Foods with a high fat content • Any food the client identifies as irritating should be avoided. • If the patient is obese, weight reduction should be a component of the plan for nutrition therapy. • Remaining upright after eating and the avoidance of eating within three hours prior to bedtime can help utilize gravity in order to prevent acid reflux. III. Nutrition Assessment 11. Calculate the patient’s %UBW and BMI. What does this assessment of weight tell you? In what ways may this contribute to his diagnosis? • %UBW = 215/185 = 116% • BMI = 31.8 = Class I obesity • Obesity has been correlated with GERD and is thought to increase intra-abdominal pressure. 12. Calculate energy and protein requirements for Mr. Gupta. How would this recommendation be modified to support a gradual weight loss? • Mifflin-St. Jeor = 10W + 6.25H – 5A + 5 10(97.73) + 6.25(175.26) - 5(48) + 5 = 977.3 + 1095.375 - 240 + 5 = 1837.7 or 1,800 kcal 1837.7  1.3 (AF)  1.1 (SF) = 2628 or 2,600 kcal • EPR = 0.8  97.73 = 78-80 g protein. • Gradual weight loss could be addressed in a couple of different ways: ○ 500 kcal could be subtracted from 2,600 kcal to promote a 1#/wk weight loss (2,100 kcal). ○ A 500-kcal deficit could be provided by subtracting 250 kcal from his kcal needs and increasing his activity level by 250 kcal. ○ Mr. Gupta’s activity level could be increased by 500 kcal/day to provide the 1#/wk weight loss, although this is probably unlikely due to possible limitations from past knee surgery. 13. Mr. Gupta and his wife are originally from India. Are there components of their traditional diet that may aggravate his symptoms of GERD? • High use of pepper may increase gastric acidity • Tea may aggravate symptoms 14. What considerations related to Hinduism should you keep in mind when assessing Mr. Gupta's diet? • Fasting • Ayurveda (form of Complementary and Alternative Medicine [CAM]) -- foods and herbs may be used for healing powers/abilities • May be vegetarian (quite individualized though and type may vary) 15. Estimate his caloric intake from his 24-hour recall. How does this compare to your calculated energy requirements? • Nutrient analysis for his 24-hour recall indicates that he consumed approximately 2880 kcal and 99 grams of protein. • This is 111% of his estimated energy and 127% of his estimated protein requirements. 16. Are there any other abnormal labs that should be addressed to improve Mr. Gupta’s overall cardiac health? Explain. • Mr. Gupta has elevated total cholesterol, high LDL, and high triglycerides. • These values indicate that he is at high risk for heart disease, atherosclerosis, and their subsequent complications. 17. Mr. Gupta's history includes the use of fenugreek and turmeric as alternative treatments for his symptoms of GERD. Examine the evidence regarding these supplements. What could you tell Mr. Gupta? Are there any concerns with the ingestion of these supplements? • Turmeric: It has the potential to relieve dyspepsia, but side effects can include dyspepsia, GERD, and vomiting, to name a few. Turmeric's efficacy for GERD is not well established and it appears that it is primarily known for its anticoagulant/antiplatelet effects and thus may increase the risk of bleeding. It should be recommended that Mr. Gupta discusses this supplementation with his physician/pharmacist. • Fenugreek: Fenugreek has shown in some research to improve heartburn symptoms if taken before the two largest meals of the day. That being said, it may cause diarrhea, dyspepsia, flatulence, and hypoglycemia (with large doses). It can also result in allergic reactions and have anticoagulant/antiplatelet effects, increasing one's risk of bleeding. Considering the possible additive/synergistic effects of turmeric and fenugreek, it is advised he stops supplementation until given permission to continue their use by his physician. 18. What other components of lifestyle modification would you address in order to help in treating his disorder? • The client should remain upright during and immediately after meals. • He should avoid eating or drinking anything for up to 3 hours prior to retiring in the evening. • Mr. Gupta may also benefit from smaller meals prior to bedtime. • The head of his bed may also be elevated at night to assist with nighttime reflux. • Possibly consume smaller, more frequent meals • Avoid tight-fitting clothing IV. Nutrition Diagnosis 19. Identify pertinent nutrition problems and corresponding nutrition diagnoses and write at least two PES statements for them. • Excessive energy intake related to frequent consumption of fast foods as evidenced by typical daily intake of approximately 2900 kcal compared to recommended intake of 2600 kcal, BMI of 31.8, and frequent consumption of burgers, pizza, and ice-cream. • Undesirable food choices related to knowledge deficit and family’s busy schedule prompting frequent fast food consumption as evidenced by fried foods, night snack of ice cream, and 1-2 beers daily followed by symptoms of indigestion; requiring TUMS. • Excessive fat intake and excessive saturated fat intake. (Students may identify that these two problems have an etiology very similar to that of “excessive energy intake”; therefore, it may not be necessary to develop complete PES statements. If the students do write either of these as a PES statement, the amount of total fat and/or saturated fat in terms of grams or % should be reflected in the evidence.) • Excessive sodium intake related to frequent consumption of fast foods and processed foods as evidenced by typical daily sodium intake at least 200% above recommended intake. • Obesity related to excessive energy intake and physical inactivity as evidenced by BMI of 31.8, consumption of an excess of about 300 kilocalories per day, and reported minimal physical activity. • Altered nutrition-related laboratory value. This could be written as a separate PES statement or used as further evidence (signs and symptoms) for the excessive fat intake and/or physical inactivity. • Food and nutrition-related knowledge deficit related to lack of previous nutrition education as evidenced by undesirable food choices. • Physical inactivity related to inability to find consistent replacement to previous physical activity of running following knee arthroplasty as evidenced by patient stating that he engages in little to no exercise. (This PES statement may also provide some evidence of a lack of motivation to exercise and reflect a possible “not ready for diet/ lifestyle changes” problem.) V. Nutrition Intervention 20. Determine the appropriate intervention for each nutritional diagnosis. • Excessive energy intake related to frequent consumption of fast foods as evidenced by typical daily intake of approximately 2900 kcal compared to recommended intake of 2600 kcal, BMI of 31.8, and frequent consumption of burgers, pizza, and ice-cream. ○ Ideal Goals: Average daily caloric intake of 2600 kcal and /or weight loss (about 2100 kcal/day) to reach a more desirable BMI between 25 and 30 ○ Intervention: Modify meals and snacks to include more nutrient-dense and lower-fat foods • Undesirable food choices related to knowledge deficit and family’s busy schedule prompting frequent fast food consumption as evidenced by fried foods, night snack of ice cream, and 1-2 beers daily followed by symptoms of indigestion requiring TUMS. ○ Ideal Goals: Food and behavior choices that include lower-fat foods, less alcohol, and not eating prior to bedtime to decrease symptoms of GERD ○ Intervention: • Comprehensive nutrition education that includes the purpose of and instruction on selecting foods that decrease the symptoms of GERD (refer to question #11 above) and/or: • Nutrition counseling that includes strategies of self-monitoring and social support ○ Nutrition/lifestyle behavior counseling that involves planning of meals and preparing larger batches of healthy meals to be consumed later throughout the week. 21. Does the long-term use of proton pump inhibitors have nutritional effects? Are there specific interventions that you might implement to address these effects? • Chronic use of proton pump inhibitors (PPIs) can decrease the absorption of calcium, vitamin B12 and iron • Additionally, hypergastrinemia may occur resulting in a hypersecretion of gastric acid upon discontinuation of PPIs • Interventions for these concerns could be iron, calcium vitamin B12 supplementation, adequate consumption of foods with high iron, calcium and vitamin B12 content. Case 8 – Gastroparesis I. Understanding the Disease and Pathophysiology 1. Identify the major physiological controls for gastric emptying. • Meal content/size: large meals with high fat, protein, and fiber content decreases the rate of gastric emptying by their stimulatory effects on hormonal secretions • Hormones/Neuropeptides: ○ Gastrin: protein, peptides, amino acids, coffee, alcohol, gastric distention and vagal stimulation will stimulate its release, which will cause an increase in gastric acid secretion and gastric motility, while decreasing gastric emptying. ○ Secretin: acid in the duodenum will result in its secretion and its inhibitory effects on gastric emptying ○ Cholecystokinin: fat in the duodenum (and protein to a lesser extent) will result in its secretion and cause its inhibitory effects on gastric emptying. ○ Glucose-dependent insulinotropic peptide will inhibit gastric emptying and motility during interdigestive states and is stimulated by serum glucose, amino acids, and fatty acids • Vagal Stimulation/Enteric Nervous System: Parasympathetic activity indirectly effects gastric motility via the enteric nervous system. This will result in the tonic contractions needed to propel and break up food particles to move towards the pyloric sphincter in sizes no larger than 2 mm. 2. List and discuss the primary factors that may lead to the diagnosis of gastroparesis. • Gastric emptying involves complex communication (as discussed in question #1) among hormones, muscles and the nervous system. An abnormality in any one of these systems can contribute to gastroparesis. Gastroparesis is commonly seen with autonomic nerve damage related to diabetes or as a post-surgical complication. Other cases of gastroparesis are designated as idiopathic. 3. According to the American College of Gastroenterology, scintigraphy is the gold standard for diagnosis of gastroparesis. This test was performed on Mrs. Williams. Explain this test and discuss how her results confirm her diagnosis. Are there other diagnostic tests that could be used? • The gold standard for diagnosis is the scintigraphic gastric emptying test. It involved the ingestion of a standardized meal of 4 oz. of liquid egg white, two slices of white bread, strawberry jam, water, and technetium-99m sulfur colloid (0.5-1 mCi). • Since Mrs. Williams' test results show higher gastric retention of her meal at 1 hour (95%) and 2 hours (85%) compared to the normal ranges (30-90% and 20% (24% loss in 11 months), oral intake <50% of estimated needs. IV. Nutrition Diagnosis 23. Select two nutrition problems and complete the PES statement for each. Intake Domain: • Inadequate intake from enteral nutrition related to (students may recognize that more information is needed to accurately identify the reason for this problem such as intolerance, increased residuals, error in administration or charting, and/or interruption of infusion secondary to other types of patient care) as evidenced by patient receiving only 450 mL/24 hours compared to prescribed 600 mL. OR: • Inadequate intake of enteral nutrition as evidenced by nutrition prescription of 25 mL/hour providing only 900 kcal and 56 g protein compared to goal rate of 54 mL/hour providing 1944 kcal and 122 g protein. • Increased nutrient needs related to impaired nutrient utilization of vitamin B12 post gastrectomy (in this case, evidence may not be necessary to develop appropriate nutrition care). • Malnutrition related to prolonged inadequate oral/food beverage intake as evidenced by 24% weight loss in 11 months and oral intake <50% of estimated needs. Clinical Domain: Even though these are concerns initially, students can utilize this knowledge as part of etiology and evidence of intake and behavioral-environmental problems. • Altered GI function (it may not be necessary to develop this as a PES as it can be incorporated as part of the etiology for increased nutrient needs above) • Impaired nutrient utilization (this actually is the etiology for increased nutrient needs) • Involuntary weight loss or underweight (this is reflected in the signs and symptoms of protein-energy malnutrition) Behavioral-Environmental Domain: • Food and nutrition-related knowledge deficit related to altered GI function as evidenced by patient requesting nutrition education and concern for “special diet forever.” V. Nutrition Intervention 24. 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). • Inadequate intake of enteral nutrition as evidenced by nutrition prescription of 25 mL/hour providing only 900 kcal and 56 g protein compared to goal rate of 54 mL/hour providing 1944 kcal and 122 g protein. ○ Ideal Goal: Provide enteral nutrition to meet kcal needs of 1900 kcal and 60 g protein. ○ Intervention: Modify rate of enteral feeding by increasing goal rate to 54 mL/hour. • Increased nutrient needs related to impaired nutrient utilization of vitamin B12 post gastrectomy (in this case evidence may not be necessary to develop appropriate nutrition care). ○ Intervention: Vitamin supplementation; may require order for injection of vitamin. • Evident protein-energy malnutrition related to prolonged inadequate oral/food beverage intake as evidenced by BMI of 20, involuntary weight loss, and pre-albumin of 14 mg/dL. ○ Ideal Goal: Weight maintenance and slow, steady weight gain of 1-2 pounds/week and improved pre-albumin to within normal of 18-35 mg/dL. • Food and nutrition-related knowledge deficit related to altered GI function as evidenced by patient requesting nutrition education and concern for “special diet forever.” ○ Ideal Goal: Patient will understand the rationale for advancing oral food from liquid to soft diet as tolerated without adverse symptoms from dumping syndrome. ○ Intervention: Nutrition education to include purpose of modification for simple carbohydrates and liquids. Additionally, initially avoiding lactose will be beneficial. Nutrition counseling that provides tools for self-monitoring and social support may also be helpful. (Refer to question 25 below.) 25. Mrs. Rodriguez asks to speak with you because she is concerned about having to follow a special diet forever. What might you tell her? What nutrition education should this patient receive prior to discharge? The ability to liberalize the diet is highly individualized. You could tell her that she will be able to try small amounts of simple carbohydrate when she has had no symptoms of dumping. Small amounts can continue to be added as long as she tolerates them. After simple carbohydrates such as sweetened fruit juice or canned fruits are tolerated, then other carbohydrates can be added. Very hot or very cold foods may also be tried at this time. The patient can then progress to fresh fruits and vegetables. Lactose-containing foods may also be added slowly to determine tolerance. It is important to only add one new food at a time so that if intolerance occurs, the food can be eliminated and tried again later. Informing Mrs. Rodriguez that the remaining parts of her GI tract will adapt and take on some of the responsibilities of the removed (duodenum) portion. The villi height and crypt depth will increase to provide more surface area, due to the obvious loss from her gastrojejunostomy (Billroth II) procedure Goals for nutritional rehabilitation should be set with the patient, specifically identifying her energy and protein needs. Discussion of meal timing with food choices to prevent dumping syndrome. Prescribing multivitamin and B12 supplementation should be discussed. 26. Do any lifestyle issues need to be addressed with this patient? Explain. The role of smoking in ulcer disease should be addressed. Referrals to assist with smoking cessation can be made within the health care team. Solution Manual for Medical Nutrition Therapy: A Case-Study Approach Marcia Nahikian Nelms 9781305628663, 9780534524104, 9781133593157