Case-13-16 Gastrointestinal Surgery With Ostomy – Medical Nutrition Therapy: A Case-Study Approach : Book Guide

This Document Contains Cases 13 to 16 Case 13 – Gastrointestinal Surgery with Ostomy I. Understanding the Disease and Pathophysiology 1. Describe the partial colectomy procedure. How does this change the function of the gastrointestinal tract? • A partial colectomy procedure consists of the surgical removal of part of the large intestine from the abdomen. In this case, a colostomy was placed. This means a stoma was created and the end of the intestine is brought through the abdominal wall. • This changes the function of the gastrointestinal tract as the colon plays a large role in water and electrolyte reabsorption. Additionally, bacteria in the colon provide fermentation and the provision short chain fatty acids. Removing part of the large intestines will lower the amount of reabsorbed water, resulting in more watery or fluid stools. 2. What is a colostomy? What kind of fecal output can Ms. Watson expect? • A colostomy is the surgical creation of an artificial opening (stoma) where the end of the intestine is brought out through the abdominal wall. • The fecal output will be semi liquid or partially formed stools. • Additionally, without the rectum/anus's function as a storage facility and regulator of bowel movements, frequency of fecal output will increase. 3. The physician has ordered a consult for Ms. Watson for teaching regarding the care of her ostomy. What is an enterostomal therapist? Describe this specialist's training and what he or she will most likely teach Ms. Watson. • An enterostomal therapist is a specialized nurse that care for patients that need stomas for disorders of the gastrointestinal, genitourinary, and integumentary systems. • This specialist will teach Ms. Watson on proper stoma care/use, dietary behaviors, tips to acclimate back into a normal lifestyle, care and prevention of sore skin (at site of stoma), and dealing with psychological factors . II. Understanding the Nutrition Therapy 4. What is the typical postoperative sequence for nutritional intake? How long will Ms. Watson be NPO? • Initially, Ms. Watson will be placed as NPO for 1-2 days and then begin oral intake with clear liquids. • Then, she will progress towards a low-residue diet with 4-6 meals/day • Over an 8 week period, oral intake should begin to resemble that of a regular diet 5. What are the nutrition therapy recommendations for someone with a colostomy? How would this be different if she had an ileostomy? • At the beginning of the postoperative phase for patients with a colostomy the gradual incorporation of fruits/vegetables/whole grains is suggested. This begins will consuming only low-fiber options, initially. • Soluble fibers (e.g. applesauce, bananas, rice) may help thicken the stools and prevent loose/watery stools • Use of yogurt, parsley, and buttermilk may decrease gas and odor • Foods that may cause gas (e.g. broccoli, eggs, asparagus), obstruction, or diarrhea should be avoided, initially • Over time the bowel will adapt and begin to form more solid stools (this may take several months). • For patients with an ileostomy, fat malabsorption, lactose intolerance and fluid balance may be problematic. With more of the ileum removed, B12 malabsorption is more likely and supplementation may be needed. III. Nutrition Assessment 6. Evaluate Ms. Watson’s %UBW and BMI. • %UBW = 163 lbs / 175 lbs x 100% = 93% • BMI = 28.0 • Ms. Watson is considered overweight and is probably moderately malnourished due to her loss of 7% of her bodyweight (though, without a time frame in which this weight was lost, one cannot adequately determine if this is considered malnutrition) 7. Calculate Ms. Watson's energy and protein requirements. Energy Requirements: Mifflin-St. Jeor: REE = 10 x W (kg) + 6.25 x H (cm) - 5 x A (yrs) - 161 REE = 10 x 74.1 kg + 6.25 x 162.56 - 5 x 61 - 161 REE = 1291 ≈ 1300 kcal/day TEE = 1582 x 1.2 (PA) x 1.3 (SF) = 2014 ≈ 2000 kcal/day or 1900-2100 kcal/day Protein Requirements: 1.2-1.5 g/kg x 74.1 = 89-111 grams 8. Identify any significant and/or abnormal laboratory measurements for Ms. Watson. Explain possible mechanisms for the abnormal labs. Lab Patient’s value Normal value Relationship to diagnosis Glucose 151 mg/dL (11/2) 163 mg/dL (11/3) 70-99 mg/dL Not related to her diagnosis. These elevated levels are due to her insulin resistance from T2DM. The 11/3 value may be higher due to hemoconcentration from dehydration. Osmolality 296 mOsm (11/3) 275-295 mOsm This elevation in blood concentration could be explained by dehydration from fecal waste (lack of reabsorption from resected colon) or blood loss from the surgery. CRP 1.3 mg/dL (11/2) 1.1 mg/dL (11/3) < 1.0 mg/dL CRP is a positive acute phase protein and elevated due to surgery. Cholesterol 235 mg/dL < 200 mg/dL Not related to diagnosis. LDL 149 mg/dL < 130 mg/dL Not related to diagnosis. HbA1C 6.5% < 5.7% Not related to diagnosis. Elevated due to T2DM and poor blood glucose control (insulin resistance). Hgb 11.5 x106/mm3 (11/2) 10.7 x106/mm3 (11/3) 12-16 x106/mm3 Low due to blood loss from surgery. Hct 36% (11/2) 34% (11/3) 37-47% Low due to blood loss from surgery. IV. Nutrition Diagnosis 9. Select two nutrition problems and complete the PES statement for each. • Altered GI function related to partial colectomy as evidenced by surgical documentation. • Predicted suboptimal nutrient intake related to postsurgical prescription of NPO and progression to a low-residue diet as evidenced by fatigue and 10 lb weight loss prior to admission. • Food nutrition knowledge deficit related dietary changes with new colostomy as evidenced by postoperative status. V. Nutrition Intervention 10. The surgeon notes Ms. Watson probably will not resume eating by mouth for at least 3-5 days. Using ASPEN guidelines, what would be your recommendation for nutrition support for Ms. Watson? • If Ms. Watson progresses easily to an oral diet she should not require the use of enteral nutrition support. Tolerance and adequacy will need to be monitored as she was admitted with an unintentional weight loss. 11. 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). • Inadequate oral intake related to postsurgical state as evidenced by NPO prescription. Goal: Patient will meet estimated energy and protein needs of 1900-2100 kcal/day and 89-111 g/day, respectively after diet is advanced. Intervention: Patient education on ways to increase nutrient density within her oral diet. Suggest consumption of liquid nutritional supplements (e.g. Boost, Ensure). Use EN if needs cannot be met orally. • Food nutrition knowledge deficit related dietary changes with new colostomy as evidenced by postoperative status. Goal: Patient will acknowledge understanding of foods that are recommended/not recommended for new colostomy. Patient will understand food choices that may produce gas, foods that may reduce odor, foods that may assist to thicken stool output/ Intervention: Patient education for nutrition recommendations after colostomy. VI. Nutrition Monitoring and Evaluation 12. What would be the primary nutrition concerns as Ms. Watson prepares for rehabilitation after her discharge? Identify two nutritional outcomes and outline specific measures for evaluation. • Nutritional concerns: ○ Adequate energy/protein intake ○ Preventing micronutrient deficiencies ○ Adequate fluid intake/hydration status ○ Adherence to a low-residue diet with slow progression towards a normal healthy diet ○ Avoidance of foods that may aggravate gas, diarrhea, or bowel obstruction (e.g. high fat foods, carbonated beverages, beans, peas, broccoli, prunes/prune juice, etc.) • Nutritional outcomes: ○ Postoperative healing and weight maintenance ○ Return to a normal diet (adequate in energy, protein, fiber, and micronutrients) Case 14 – Non-Alcoholic Fatty Liver Disease (NAFLD) I. Understanding the Disease and Pathophysiology 1. Define non-alcoholic fatty liver disease and non-alcoholic steatohepatitis. • Non-alcoholic fatty liver disease (NAFLD) - refers to the wide spectrum of liver disease ranging from simply fatty liver (steatosis), to non-alcoholic steatohepatitis, to cirrhosis. • Non-alcoholic steatohepatitis (NASH) - fatty liver with inflammation and scarring/damage to the hepatic tissue; similar to alcoholic fatty liver disease, but little or no alcohol is consumed in these patients; etiology is from another source (hepatotoxin) 2. What is the potential etiology(ies) of non-alcoholic fatty liver disease (NAFLD)? Does the research indicate that there are any genetic contributions to this condition? • Potential etiologies: obesity, insulin resistance (T2DM), cystic fibrosis, metabolic syndrome, parenteral nutrition, medications (e.g. amiodarone, tamoxifen, corticosteroids), pancreatic-duodenal resection, hypopituitarism, hypogonadism, hypothyroidism ,and iatrogenic contributions • Genetic contributions: cystic fibrosis, patatin-like phospholipase 3 gene (associated with inflammation) 3. In regard to the epidemiology of this condition, are individuals of specific ethnicities or of either gender at higher risk for the development of NAFLD? • Hispanic population is at a greater risk than those of European descent • African-Americans exhibit protective genetics in relation to NAFLD (this finding is independent to risk factors such as diabetes and BMI) • Males appear to have a higher risk factor for NAFLD than women 4. How is this condition typically diagnosed? Are there common presenting signs and symptoms for NAFLD? How might the markers of metabolic syndrome be related to NAFLD? • Elevated AST and ALT lab results suggests liver damage/fatty accumulation • Diagnosed after exclusion of all other causes of abnormal LFTs and results from liver ultrasound • Dyslipidemia (primarily high triglycerides) and altered glucose values are associated with NAFLD. • Dyslipidemia as a risk factor may be only associative with NAFLD when obesity and insulin resistance are present. 5. Explain the potential role of diet in the development of NAFLD. Specifically address the roles of simple sugars, fructose, refined carbohydrates, and saturated fat. • In one systematic review, fructose appears to not be related to NAFLD when substituted isocalorically into the diet. But, when providing it in excess of energy needs and very high doses, some contribution to increasing ALT levels can be observed. • Simple sugars, refined carbohydrates, and saturated fat may exacerbate the fat accumulation observed within NAFLD (thought to be related to the elevated insulin levels with elevated serum levels of these substances). • Low-carbohydrate, low-fat, and high-protein diets appear to be beneficial for NAFLD patients • Substitution of carbohydrate for MUFA incorporation into the diet may have even greater effects on NAFLD, suggesting that the Mediterranean diet has nutritional therapeutic potential. 6. What are the long-term consequences of NAFLD if the condition progresses? • NASH (non-alcoholic steatohepatitis) and eventually cirrhosis II. Understanding the Nutrition Therapy 7. Explain the rationale for prescribing a low-carbohydrate diet in the treatment of NAFLD. • High-carbohydrate diets may lead to hepatic insulin resistance by activating carbohydrate responsive element binding protein (ChREBP), inducing glycolysis and lipogenic pathways within liver tissue 8. Describe the Mediterranean diet and how this eating pattern may support the nutritional goals of treatment of NAFLD. • Mediterranean diet - high intake of fish and white meat, fruits, vegetables, legumes, and olive oil (main source of fat). Moderate wine consumption is also part of the diet. ○ Provides high MUFAs, low saturated fats, a balance of PUFAs (ω-6 vs. ω-3), and fiber. • Antioxidants from fruits, vegetables, and olive oil provide antioxidant components which have been shown to improve the hepatic tissue abnormalities of NAFLD • Complex carbohydrates and fiber will slow the absorption of carbohydrates and lower insulin response, lowering its effect on lipogenesis. • The balance of PUFAs prevents the oxidative damage associated with linoleic acid in NAFLD. • MUFAs from olive oil appears to lower liver enzyme levels and area of fibrosis • The positive effects from increased antioxidant levels, improved CVD health (lower blood pressure/reduced risk of thrombosis), reduction in blood glucose, cholesterol, triglycerides, LDL, oxidized-LDL, and elevation in HDL lowers the pathological risk factors of NAFLD 9. Is there a role for supplementation of anti-oxidants in the treatment of individuals with NAFLD? • Vitamin E supplementation has demonstrated positive treatment benefits in the short term (though, longer studies are needed) 10. Mr. Kim asks you about an article he recently read about the benefits of coffee consumption in fatty liver disease. What recommendations might you give him? • Current research and epidemiological studies suggest the daily consumption of 3 or more cups of coffee to reduce the risk of fatty liver disease development and progression to fibrosis. III. Nutrition Assessment 11. Evaluate Mr. Kim's weight status. • BMI = 31.2 • IBW = 106 lbs + (6 lbs/1"[after 5']) x 8" = 154 lbs • %IBW = 205 lbs / 154 lbs x 100% = 133% • Mr. Kim is considered obese. 12. Calculate Mr. Kim’s energy and protein requirements for weight maintenance and for weight loss. Mifflin-St. Jeor (due to obesity): REE = 10 x Wt (kg) + 6.25 x Ht (cm) - 5 x A (yrs) + 5 REE = 10 x 93.18 kg + 6.25 x 172.72 cm - 5 x 38 yrs + 5 REE = 1826.3 ≈ 1800 kcal/day TEE = 1826.3 x 1.3 (PA) = 2374.2 ≈ 2400 kcal/day or 2300-2500 kcal/day For weight loss, a 500 kcal/day reduction is needed to obtain a 1 lb/week loss in body weight: 1800-2000 kcal/day Protein requirements: 0.8-1.0 g/kg (IBW) x 70 kg: = 56-70 g/day 13. What other anthropometric measurements, if any, may be helpful in fully assessing Mr. Kim's nutritional status and disease risk? • Waist circumference • WHR (Waist to hip ratio) and WHtR (Waist to height ratio) • %Bodyfat (though, not likely to be obtained in a clinical setting) 14. Identify any significant and/or abnormal laboratory measurements for Mr. Kim. Explain possible mechanisms for the abnormal labs. Lab Patient’s value Normal value Relationship to diagnosis Glucose 121 mg/dL 70-99 mg/dL Insulin resistance due to excessive body fat (adiposity) that may contribute to inflammation associated with insulin resistance. ALT 54 U/L 4-36 U/L Damaged liver cells release enzymes when lysed (may be due to inflammation associated with NAFLD). AST 42 U/L 0-35 U/L Damaged liver cells release enzymes when lysed (may be due to inflammation associated with NAFLD). Cholesterol 285 mg/dL 50 mg/dL N/A LDL 189 mg/dL < 130 mg/dL Excessive dietary saturated fat intake. Triglycerides 350 mg/dL 40-160 mg/dL Increased triglyceride production related to NAFLD. HbA1C 6.1% < 5.7% Insulin resistance and poor glycemic control related to elevated blood glucose value. 15. Assess Mr. Kim's typical diet for total energy intake and % carbohydrate, protein, and fat. How does his estimated energy intake compare to his recommended requirements for weight loss that you calculated in question 12? Identify the most important factors that may impact his NAFLD. • Mr. Kim's typical diet is about 2200 kcal, 14% protein, 57% carbohydrate, and 30% fat • This is about 200 kcal over the upper range needed for Mr. Kim to lose weight. • Important factors that may have contributed/impact his NAFLD include his low fiber (12 g), high saturated fat (~ 8%), and high sugar (116 g added/135 g total) consumption 16. How will you assess Mr. Kim's physical activity level? List three questions that you would use in your interview to support your understanding of his daily and recreational activity. • I would assess his level of physical activity by comparing it to the standards of the Dietary Guidelines (2.5 hours per week or about 30 min. of moderate physical activity on five days of the week) • Questions: ○ Do you engage in any formal or recreational physical activities? ○ How long do those activities last and how frequently do you engage in them? ○ How much time do you spend walking/standing/sitting at your job? ○ Does your job/daily life require frequent physical labor? IV. Nutrition Diagnosis 17. Select two nutrition problems and complete the PES statement for each using the nutrition diagnostic terminology. • Obesity related to excessive consumption of energy-dense foods and large meals as evidenced by BMI of 31.2, frequent consumption of hamburgers, fries, cookies, desserts, etc, and reported high frequency of snacking on desserts between meals. • Undesirable food choices related to lack of prior nutrition education and disinterest as evidenced by acknowledgement of one's own "sweet" tooth, reported liking fruit but rarely consuming them, and high consumption of foods containing high calories, saturated fats, low fiber, and added sugar.. • Inadequate fiber intake related to lack of food- and nutrition-related knowledge as evidenced by reported low consumption of fruits, vegetables, and whole-grain products. • Excessive saturated fat intake related to high-consumption of animal products and processed foods as evidenced by frequent consumption of doughnuts, cookies, soda, pastries, hamburger, and meat, elevated total cholesterol (285 mg/dL), and elevated LDL (189 mg/dL) levels. • Excessive simple sugars related to food- and nutrition-related knowledge deficit and new diagnosis of NAFLD as evidenced by lack of previous nutrition therapy, excessive snacking of sugary foods, and frequent consumption of soda, cookies, pastries, pie, and dessert. V. Nutrition Intervention 18. What culturally appropriate nutrition therapy recommendations will you make for Mr. Kim? • Weight loss/physical activity • Reduced consumption of simple sugars and refined carbohydrates • Increased omega-3 fatty acid consumption • Vitamin E supplementation - 800 IU/day • Increasing consumption of fruits, vegetables, and whole-grains to increase fiber and anti-oxidant consumption (fruits/vegetables) • Introduce considering the Mediterranean diet • Alcohol avoidance 19. Identify the nutrition education materials and tools you may use in your nutrition education. • Handouts: ○ Mediterranean diet ○ Healthy snacking options ○ Tips for incorporating fruits/vegetables into meals/snacks ○ Portion control tips • Tools: ○ Food models (demonstrate portion size) 20. What steps might you use to assess Mr. Kim's readiness for dietary and behavior change? • Motivational interviewing ○ Probe for interests and allow for self-evaluation • Transtheoretical Model (Stages of Change) ○ Identify stage of change and you appropriate counseling techniques to move to the next stage • Health Belief Model ○ Examine perceived benefits/barriers to lifestyle/behavioral changes 21. Are there Korean traditional health practices that you would want to address? Yes, some traditional Korean health practices include Hanbang (traditional Korean medicine), which combines herbal remedies, acupuncture, and moxibustion. Kimchi, a fermented vegetable dish, is also integral to Korean health for its probiotic benefits. Additionally, Bosu, or traditional Korean exercise routines, focus on physical movement and energy balance. Chakchongyo, a breathing and meditation practice, is another part of the holistic approach to maintaining health. These practices emphasize balance, natural remedies, and preventive care. 22. Does Mr. Kim meet the criteria for metabolic syndrome? Explain how the nutrition interventions for NAFLD will help with the components of this condition. • Metabolic syndrome? - Yes - fasting blood glucose ≥ 100 mg/dL (121 mg/dL), triglycerides ≥ 150 mg/dL (350 mg/dL), blood pressure ≥130/≥85 mmHg (142/86 mmHg) • Meeting 3 of the 5 criteria is diagnostic for metabolic syndrome (the other criteria is an HDL 40 in (102 cm) for men) • Nutrition intervention crossover: ○ Weight loss (lowers blood pressure and insulin resistance) ○ Alcohol cessation (lowers blood pressure) ○ Increase in antioxidants (help reduce inflammation associated with insulin resistance and prevent atherosclerotic plaques associated with oxidized LDL) ○ Increase in fiber content (reduce hyperlipidema - cholesterol and LDL levels) ○ Physical activity for weight loss (increase HDL and insulin sensitivity) ○ Overall treatment of NAFLD may reduce the elevated triglyceride production associated with NAFLD VI. Nutrition Monitoring and Evaluation 23. What topics might you want to address with Mr. Kim in follow-up nutrition appointments? • Weight/weight loss status • Adherence to dietary plans/discussed goals • Level of physical activity • Consumption of desired foods for therapy: fruits, vegetables, whole-grains • Consumption of problematic foods for NAFLD: simple/refined carbohydrates and saturated fat (processed foods, pastries, animal meat/products) • Motivation level/perceived barriers 24. What outcomes will you monitor to evaluate the effectiveness of your nutrition intervention? • LFTs (ALT and AST levels) • Weight/weight loss status • Consumption level of saturated fat, fiber, simple sugars, and omega-3 fatty acids • Alcohol consumption (ideally abstinence) Case 15 – Acute Pancreatitis I. Understanding the Disease and Pathophysiology 1. Describe the normal exocrine and endocrine functions of the pancreas. Exocrine: • Drains into proximal duodenum through dorsal and ventral ducts • Secretes digestive enzymes • Secretes bicarbonate and electrolytes • Produces 1,000-2,500 mL of secretions/day (bicarbonate, electrolytes, and digestive enzymes) Endocrine: • Secretes insulin, glucagon, and somatostatin • Pivotal in metabolism of glucose, fats, and amino acids 2. Determine the potential etiology of both acute and chronic pancreatitis. What information provided in the physical assessment supports the diagnosis of acute pancreatitis? Alcohol plays a significant role in the pathogenesis of pancreatitis. Chronic, heavy alcohol ingestion diminishes the concentration of lithostathine, a secretory protein that helps solubilize calcium carbonate within the pancreatic ducts. As a result, there is a build-up in ductile pressure that damages acinar cells and releases pancreatic enzymes into the periacinar space. Another theory is that prolonged alcohol intake leads to the fusion of zymogen granules (which contain inactive pancreatic enzymes) with lysozomes that contain hydrolytic enzymes and results in activation of the pancreatic enzymes, leading to autodigestion of the pancreas. The exact mechanisms that lead to pancreatic injury are not fully understood, but a common characteristic appears to be a premature activation of trypsin within the pancreas, resulting in autodigestion of pancreatic cells. Enzymes released by destroyed pancreatic cells eventually reach the bloodstream, causing elevated serum amylase and lipase levels. Other conditions associated with acute pancreatitis include hypercalcemia, hypertriglyceridemia, drugs, trauma, cystic fibrosis, renal failure and other, infectious causes. Factors in the history and physical that are consistent with acute pancreatitis include: chief complaint; fever; increased pulse and blood pressure; hyperactive bowel sounds x4; extreme tenderness, rebound, and guarding; nausea and vomiting; and history of alcohol use. 3. What laboratory values or other tests support this diagnosis? List all abnormal values and explain the likely cause for each abnormal value. Serum lipase (patient’s is 980 U/L) and serum amylase (patient’s is 543 U/L). Amylase rises acutely and usually returns to normal levels within 48-72 hours in acute pancreatitis. In acute pancreatitis, especially that associated with alcohol, serum amylase has a low specificity and sensitivity. In those with chronic pancreatitis, levels may continue to be elevated. Levels over 500 U/L help to rule out other diagnoses such as cholecystitis or appendicitis. Serum lipase rises more slowly than amylase but remains elevated for much longer. Other labs consistent with (but not specific for) pancreatitis include: • Alkaline phosphatase (U/L) • ALT (U/L) • AST (U/L) • CPK (U/L) • Lactate dehydrogenase (U/L) • CRP (mg/dL) Lab Patient’s value Normal value Relationship to diagnosis BUN 30 mg/dL 6-20 mg/dL Elevated due to reduced renal function/damage. Creatinine serum 1.6 mg/dL 0.9-1.3 mg/dL Elevated due to reduced renal function/damage Glucose 142 mg/dL 70-99 mg/dL Altered insulin release/control of glycemia (damage to pancreas). Cortisol increasing gluconeogenesis. Bilirubin total 1.9 mg/dL ≤ 1.2 mg/dL Probable biliary obstruction reducing the body's excretion of bile and bilirubin. Bilirubin, direct 0.9 mg/dL < 0.3 mg/dL Probable biliary obstruction reducing the body's excretion of bile and bilirubin. Albumin 3.3 g/dL 6-7.8 g/dL Negative acute phase protein due to systemic inflammation. Alkaline phosphatatse 256 U/L 30-120 U/L Released due to liver tissue damage. ALT 42 U/L 4-36 U/L Released due to liver tissue damage. AST 56 U/L 0-35 U/L Released due to liver tissue damage. CPK 219 U/L 55-170 U/L Systemic inflammation is leading to muscular tissue damage. Lactate dehydrogenase 402 U/L 208-378 U/L Released due to liver tissue damage. Lipase 980 U/L 0-110 U/L Released due to pancreatic tissue damage. Amylase 543 U/L 25-125 U/L Released due to pancreatic tissue damage. Cholesterol 210 mg/dL < 200 mg/dL Most likely historical and not related to current diagnosis Triglycerides 585 mg/dL 40-160 mg/dL Due to alcoholism and pancreatic damage. Neutrophil 90% 40-70% Systemic inflammation/immune response. Segs 74% 0-60% Systemic inflammation/immune response. Protein (urine) + neg Hypermetabolism/catabolism; kidney dysfunction. Ketones (urine) + neg NPO status and reliance on fat stores for fuel Urobilinogen 1.2 EU/dL 55 yr, WBC > 66,000/mL, LDH > 350 IU/L, AST > 250 IU/L, and glucose > 200 mg/dL. The 48-hour criteria include: Hct decrease > 10%, BUN increase > 5 mg/dL, Ca < 8 mg/dL, PaO2 6 L. The Atlanta Criteria consists of three classifications of acute pancreatitis: mild, moderately severe, and severe. The mild classification is considered to be the absence of organ failure and local complications. The moderately severe category include local complications (such as necrosis or fluid accumulation) and/or transient organ failure (90 mm Hg). The patient’s clinical status and diagnosis of severe acute pancreatitis absolutely indicate the initiation of nutrition support. According to current ASPEN guidelines, in severe forms of pancreatitis, it is recommended that enteral nutrition is initiated within the first 24-48 hours of admission. EN will prevent bacterial translocation and the risk of sepsis. Nutritional support is also important due to the increased energy and protein needs associated with this condition. Providing adequate kcal, protein, and nutrients will help to minimize losses and optimize recovery. EN is recommended rather than PN for several reasons. Early initiation of EN has been shown to reduce the rate of mortality and infection, and to decrease the likelihood of future surgeries. In addition, EN will help to stimulate the gut, maintaining the villi and overall gut integrity. PN is only reserved for EN failure or when nutritional needs are higher than what can be met via EN and oral intake. 8. Does this patient’s case indicate the use of an immune-modulating formula? The most current evidence regarding EN and immune-modulating formulas in patients with pancreatitis suggests that these formulas should not be used in this situation. However, this decision will vary amongst different institutions and should ultimately be decided on an individual basis. A small-peptide-based, medium-chain triglyceride formula would be appropriate for Mr. Mahon. III. Nutrition Assessment 9. Assess Mr. Mahon’s height and weight. Calculate his BMI and % usual body weight. Ht: 71” Wt: 245# BMI: 34 (obese) UBW: 195# (based off pt. reports of 50# wt. gain over 5 years) %UBW: 126% IBW: 172# +/-10% %IBW: 142% 10. Evaluate Mr. Mahon’s initial nursing assessment. What important factors noted in his nutrition assessment will affect your nutrition recommendations? • Has not eaten over past 3 days (d/t pain) • Alcohol intake • Frequent consumption of fast food • 50# wt. gain  5 years • Attempting to stop antidepressant meds (may affect appetite or may use food as a replacement) Mr. Mahon’s initial nursing assessment shows signs of dehydration (cloudy, amber urine; tenting of skin; poor skin integrity—dry, tears; dry mucous membranes), which will affect calculations for fluid requirements. Mr. Mahon has a fever and his skin is clammy and diaphoretic. Presence of fever may increase energy needs. 11. Determine Mr. Mahon’s energy and protein requirements. Explain the rationale for the method you used to calculate these requirements. Provide 30-35 kcal/kg of IBW. Used his IBW for this calculation because he is obese and it is recommended to base calories on IBW for obese individuals. This caloric value is still enough to account for the hyper-metabolic state caused by pancreatitis (it is known that caloric needs increase by about 20%). EER: 2345-2736 kcal/d 30-35 kcal/kg IBW/per ASPEN guidelines EPR: 94-117 g pro/d (1.2-1.5 g/kg IBW) 12. Determine Mr. Mahon’s fluid requirements. Compare this with the information on the intake/output record. Fluid requirements: around 2400-2700mL/d (1 mL/kcal; rounded) Or 35-40 mL/kg: 2736-3127 mL/d (or 2700-3100 mL/day) Currently receiving: 4500 mL (total intake) – 4879 mL (total output), indicating adequate renal function at this time to handle the fluid load. 13. From the nutrition history, assess Mr. Mahon’s alcohol intake. What is his average caloric intake from alcohol each day using the information that he provided to you? 6 pack beer: 150 kcal/beer  6 = 900 kcal 4-5 shots bourbon: 100 kcal/shot  5 = 500 kcal Total: 1400 kcal/d on weekdays or about 70% of daily calories from alcoholic beverages alone. Alcohol caloric contribution: Beer (assuming 4.2%) = 6 beers x 360 mL/beer x 0.042 g/L x 7 kcal/g = 635 kcal Shots (assuming 80 proof) = 5 shots x 45 mL/shot x 0.4 g/L x 7 kcal/g = 630 kcal Total: 1265 kcal from alcohol (ethanol) 14. List all medications that Mr. Mahon is receiving. Determine the action of each medication and identify any drug-nutrient interactions that you should monitor. Medication Action Drug-nutrient interaction or nutrition-related side effects Imipenem Antibiotic N/V, cramps, diarrhea Pepcid Antiulcer, anti-GERD Decreases Fe and vitamin B12 absorption; Mg or AI/Mg antacids decrease drug absorption ; avoid alcohol; limit caffeine Meperidine Narcotic (often used to prevent acute infusion reactions to IV amphotericin B) Dry mouth, N/V, GI pain, constipation; avoid alcohol Ondansetron Antiemetic Dry mouth, GI pain, constipation Colace (docusate) Stool softener Alters intestinal absorption of water and electrolytes Milk of Magnesia (MOM) Laxative, antacid 15-30% of Mg is absorbed; nausea, cramping, diarrhea Ativan Antianxiety, skeletal muscle relaxant Caution w/ grapefruit; anorexia (decreased wt.) or increased appetite w/ alprazolam or chlordiazepoxide (increased wt.); avoid alcohol and excessive caffeine; take with food IV. Nutrition Diagnosis 15. Identify the pertinent nutrition problems and the corresponding nutrition diagnoses. • Inadequate protein-energy intake or inadequate oral food/beverage intake • Altered GI function • Increased nutrient needs 16. Write your PES statement for each nutrition problem. • Inadequate oral intake related to acute pancreatitis as evidenced by N/V, abdominal pain, dry skin and mucous membranes, poor skin turgor, patient self-report of limited oral intake 3 days PTA, and NPO status since admission. • Altered GI function related to compromised exocrine function of pancreas as evidenced by recent diagnosis of acute pancreatitis and current NPO status. • Increased nutrient needs related to compromised pancreatic function as evidenced by C-reactive protein of 141 mg/dL and diminished albumin level of 3.3 g/dL consistent with increased stress and metabolic requirements. V. Nutrition Intervention 17. Determine your enteral feeding recommendations for Mr. Mahon. Provide a formula choice, goal rate, and instructions for initiation and advancement. It is recommended that feedings be initiated in the jejunum (past the ligament of Treitz) and that either a chemically defined/fat-free formula or a small-peptide formula w/ MCT be delivered. One option is to use Perative, as it has MCT and consists of small peptides. The MCT will be better absorbed and the small peptides better tolerated in the jejunum. Estimated energy requirements: 2345-2736 kcal/d 30-35 kcal/kg IBW/per ASPEN guidelines Estimated protein requirements: 94-117 g pro/d (1.2-1.5 g/kg IBW) Estimated fluid requirements: 2400-2700 mL Perative: 1.3 kcal/mL 0.667 g protein/mL 79% water 2400/1.3= 1846 for total volume 1846 mL (total volume) / 24 hrs = 77 mL/ hr is goal rate 1846 mL  0.0667 g pro/mL = 123 g pro 1846  1.3 kcal/mL = 2399 kcal 1458 mL water (Perative is 79% water) 1950 - 1327 = 623 mL free water Initiate at 25 mL/hr, advancing 20-40 mL/hr every 6-8 hours until goal of 77 mL/hr is reached. This will provide 2399 kcal and 123 g protein. 18. What recommendations can you make to the patient’s critical care team to help improve tolerance to the enteral feeding? • Initiate EN early after admission to downregulate stress response and prevent bacterial translocation. • Infuse EN distally in the GI tract (recommended NJ route) • Choose an enteral formula that contains small peptides and MCT or a nearly fat-free elemental formula VI. Nutrition Monitoring and Evaluation 19. List factors that you would monitor to assess tolerance and adequacy of nutrition support. • Physical Exam: abdominal distention, presence of N/V, bowel sounds • Amount of formula delivered vs. amount recommended: calculate % of kcal received from prescription; check water flushes • Body weight: calculate changes, interpret in the context of intake/output information • Input/output/fluid status (stool output) • Labs: serum electrolytes, BUN, Creatinine, glucose, nitrogen balance, hepatic proteins (CRP, albumin, prealbumin) • Nausea/vomiting (and potentially abdominal pain) • Progression of pancreatitis recovery—i.e., lipase and amylase improvements 20. If this patient’s acute pancreatitis resolves, what will be the recommendations for him regarding nutrition and his alcohol intake when he is discharged? • Abstention from alcohol • Adequate calories and protein for recovery. • Low-fat diet initially until long term pancreatic function is determined and/or tolerance is assessed. • Pancreatic enzyme replacement—30,000 units of lipase activity per meal and 20,000 units with snacks if long-term pancreatitis function is compromised • Fat-soluble vitamin supplementation • Water-soluble vitamins (especially thiamin, riboflavin, niacin) 21. Write an ADIME note that provides your initial nutrition assessment and enteral feeding recommendations. A: 29 yo M Dx: Acute pancreatitis PMH: Depression Ht: 71” Admission Wt: 245# BMI:34 (obese) IBW: 172# +/-10% % IBW: 142% Meds: Imipenem, Pepcid, Meperidine, Ondansetron, Colace (docusate), Milk of Magnesia (MOM), Ativan Labs: BUN (mg/dL) 8-18 30 !↑ Creatinine serum (mg/dL) 0.6-1.2 1.6 !↑ Alkaline phosphatase (U/L) 30-120 256 !↑ ALT (U/L) 4-36 42 !↑ AST (U/L) 0-35 56 !↑ CPK (U/L) 30-135 F 55-170 M 219 !↑ Lactate dehydrogenase (U/L) 208-378 402 !↑ Lipase (U/L) 0-110 980 !↑ Amylase (U/L) 25-125 543 !↑ CRP (mg/dL) 200 mg/dL with sx. of polydipsia, polyuria, polyphagia, and unexplained wt. loss (casual is defined as any time of day without regard to time since last meal) • Fasting (no caloric intake for > 8 hrs.) glucose of >126 mg/dL on at least 2 occasions • Oral glucose tolerance test (OGTT) 2-hour sample >200 mg/dL • Islet cell antibodies The following were found in Rachel’s medical record: serum glucose of 724 mg/dL; Symptoms of polydipsia, polyuria, polyphagia, and unexplained wt. loss; and + ICA, GADA, IAA, and IA-2A autoantibodies consistent with type 1 DM. 3. Dr. Cho requested these labs be drawn: Islet cell autoantibodies screen; TSH; thyroglobulin antibodies; C-peptide; immunoglobulin A level; hemoglobin A1C; and anti-tissue transglutaminase antibodies. Described how each is related to the diagnosis of type 1 diabetes. • Islet cell autoantibodies: serve as an indicator of the body's self-destructive attack against its pancreatic β-cells. • TSH: diabetic patients are more likely to be affected by thyroid dysfunction and an elevated TSH level may suggest an autoimmune attack against the thyroid gland; 17% to 30% of children with T1DM develop autoimmune thyroid disorders. • Thyroglobulin antibodies: as discussed above, due to the similarity in the autoimmune etiology of type 1 diabetes and thyroid dysfunction, presence of these antibodies can help diagnose hypothyroidism early. • C-peptide: C-peptide is cleaved from proinsulin to produce insulin and its presence in the bloodstream is an indirect measure of insulin production/beta cell function. • Immunoglobulin A: increased levels can be observed during beta-cell destruction seen in type 1 diabetes • Hemoglobin A1C: is an indicator of average blood glucose level over the previous 2-3 months (RBCs life span is 120 days) as Hgb will have a higher level of glycation with greater blood glucose levels. • Tissue transglutaminase: This value can allow the physician evaluate the patient for celiac disease as it too is a disease of improper autoimmune assaults and more common in type 1 diabetics; 1%-16% with T1DM develop celiac disease. 4. Using the information from Rachel’s medical record, identify the factors that would allow the physician to distinguish between T1DM and T2DM. Diabetes-related antibodies are often measured to distinguish between type 1 and type 2 DM. It is these antibodies that cause self-destruction of the β-cells of the pancreas and lead to inability of the β-cells to synthesize and secrete adequate insulin. The antibodies that are tested for include: islet cell cytoplasmic autoantibodies (ICA), insulin autoantibodies (IAA), insulinoma-associated-2 autoantibodies (IA-2A), and glutamic acid decarboxylase autoantibodies (GADA). The presence of antibodies can be used to distinguish between type 1 and type to diabetes because it is only type 1 that is auto-immune in origin. Type 2 is not auto-immune in origin, and therefore will not demonstrate antibodies in antibody testing. C-peptide is also used as a marker for determining if the individual is producing insulin. If C-peptide is present, insulin is being produced and the patient most likely has T2DM. Due to the presence of the autoantibodies and the lower levels of C-peptide, the self-destruction of Rachel's beta cells is currently taking place. This allows the physician to clearly diagnose her with T1DM over T2DM. 5. Describe the metabolic events that led to Rachel’s symptoms and subsequent admission to the ED (polyuria, polydipsia, polyphagia, fatigue, and weight loss), integrating the pathophysiology of T1DM into your discussion. With inadequate insulin levels present in her system, glucose is unable to get into her cells that require insulin for the translocation of GLUT-4 transporters. As a result, her body has been attempting to filter the excess glucose from the blood via the kidneys, which has resulted in glycosuria and polyuria. The fluid loss from excess urination then triggered her thirst mechanism, causing polydipsia. Without fuel, her cells are releasing signals that they’re starving, which stimulate gluconeogenesis in the liver (which further exacerbates her hyperglycemia) and leads to excessive hunger, or polyphagia. Other effects of the absence of insulin include the lack of signals to the body to increase storage of nutrients and an increase in catabolic hormones, leading to lipolysis and production of ketones as fuel. This contributes to her weight loss as fat stores are utilized, muscle is catabolized, and fluid weight is lost. Fatigue is a factor for several reasons, including the lack of fuel the cells can access, decreased energy stores, the stress placed on the body to try to clear the excess glucose from the blood, dehydration from fluid loss, electrolyte imbalances, and metabolic acidosis from elevated levels of ketones in her system. 6. Describe the metabolic events that result in the signs and symptoms associated with DKA. Was Rachel in this state when she was admitted? What precipitating factors may lead to DKA? Precipitating factors that may lead to the complication of diabetic ketoacidosis are illness or infection, an inadequate insulin dose, initial manifestation of the disease, or emotional and physical stress. Diabetic ketoacidosis is a severe form of hyperglycemia, resulting from physiological responses to hyperglycemia and insulin deficiency. When sufficient insulin is not available to regulate blood glucose levels, hepatic gluconeogenesis and lipolysis are stimulated by counter-regulatory hormones in an attempt to provide a fuel source for cells and, ultimately, prevent starvation. This production of excessive glucose further increases blood sugar levels. Also stimulated by the presence of counter-regulatory hormones is the production of ketones in the liver. Ketones are produced as a byproduct of increased lipolysis that occurs from insulin deficiency and reliance on fat metabolism. Several symptoms occur with DKA, each relating back to an abnormal physiological process. For example, hyperglycemia causes polydipsia, polyuria, and polyphagia. Also associated with DKA is dehydration—these signs and symptoms often are present as well: poor skin turgor, and orthostatic hypotension from excessive fluid losses associated with hyperglycemia and ketonemia. When Rachel was admitted, she had s/s of dehydration, polydipsia, polyuria, polyphagia, weakness, and lethargy (fainted at soccer) as well as ketones present in her urine. Thus, it can be concluded that she was in diabetic ketoacidotic state. 7. Rachel will be started on a combination of Apidra prior to meals and snacks, with glargine given in the a.m. and p.m. Describe the onset, peak, and duration for each of these types of insulin. Her discharge dosages are as follows: 7 u glargine with Apidra prior to each meal or snack—1:15 insulin: carbohydrate ratio. Rachel’s parents want to know why she cannot take oral medications for her diabetes like some of their friends do. What would you tell them? Because individuals with type 1 DM are lacking insulin, an exogenous source of insulin is required on a daily basis in order to manage blood glucose levels. When answering her parent’s question regarding her insulin and the reason she cannot take oral medication alone, describe the pathophysiology of both type 1 and type 2 diabetes, emphasizing that an oral medication can only be used for someone who is able to produce insulin. This is because oral medications typically target insulin resistance and in type 1 diabetes, insulin is not produced. Additionally, with insulin being a protein, the stomach acid and GI proteolytic enzymes will digest it if it is given orally. That is why insulin injections are a necessary route of administration. Insulin Type Onset of Action Peak of action Duration of Action Apidra (glulisine) 5-15 minutes 30-90 minutes 3-5 hours Glargine 2-4 hours None 20-24 hours Apidra's rapid onset of action, peak, and shorter duration make it an excellent form of insulin to mimic normal physiological postprandial levels after a meal. On the other hand, glargine's long duration of steady action allows it to mimic the constant insulin levels produced throughout the day needed to feed her cells. 8. Rachel’s physician explains to Rachel and her parents that Rachel’s insulin dose may change due to something called a honeymoon phase. Explain what this is and how it might affect her insulin requirements. A “honeymoon phase” is a term used often with newly diagnosed type 1 DM patients and refers to an unexpected production of endogenous insulin by the β-cells of the pancreas. This endogenous insulin production is from the remaining, active β-cells that have not yet been destroyed. If this phase does occur, insulin needs will not be as high and the dosage may decrease temporarily. 9. How does physical activity affect blood glucose levels? Rachel is a soccer player and usually plays daily. What recommendations will you make to Rachel to assist with managing her glucose during exercise and athletic events? Physical activity can greatly affect blood glucose levels. The benefits of exercise far exceed the risks. For example, exercise can improve Hgb A1c percentages, improve blood lipid levels and blood pressure, reduce the risk of developing cardiovascular disease, and improve one's ability to cope with stress. However, both hypoglycemia and hyperglycemia are acute risks of exercise. Exercise naturally lowers blood glucose levels, especially during unusually strenuous, sporadic, or prolonged exercise (greater than 1 hour). If the diabetic poorly controls her/his blood sugar, exercise can actually cause hyperglycemia and the production of ketones. When insulin is not available, counter-regulatory hormones that increase during exercise cause an increase in hepatic glucose production and free fatty acids from fat metabolism. Because of this, blood glucose should be monitored before, during, and after the exercise to identify how blood sugar levels change. For moderate exercise lasting less than 30 minutes, additional carbohydrate or insulin adjustment is not needed. In some cases, carbohydrate could be administered without insulin coverage. A small snack (15 grams of carbohydrates) can be eaten if the exercise will last longer than 30 minutes. This should be adequate for each hour of moderate physical activity. For each hour of strenuous exercise, a 30-gram snack of carbohydrate is needed. Also, insulin adjustments might be needed. For most, a 20% or greater decrease in insulin during the period of exercise is necessary. 10. At a follow-up visit, Rachel’s blood glucose records indicate that her levels have been consistently high when she wakes in the morning before breakfast. Describe the dawn phenomenon. Is Rachel experiencing this? How might it be prevented? The dawn phenomenon is the tendency for blood glucose to rise between 4 am and 8 am. This is fairly common for T1DM and over 55% of patients are likely to experience the dawn phenomenon. This occurs because of impaired insulin sensitivity in muscle and liver cells from nocturnal secretion of growth hormone due to circadian rhythms. This increases the production of glucose and hyperglycemia results. Also, poor glucose control is related to high and more frequent changes to blood glucose levels. Patients experiencing the dawn phenomenon have an increase of blood glucose >10 mg/dL or an increased insulin requirement of 20% during these hours of the night. Because Rachel’s blood glucose is dropping low and then is running high by the morning, she is not experiencing the dawn phenomenon, but rather “rebound.” Rebound also results in high fasting blood glucose, but for a different reason. Along with Rachel treating the 2 am hypoglycemia with 15 grams of carbohydrates orally, her body is naturally treating the hypoglycemia by the increased secretion of counter-regulatory hormones, such as glucagon, epinephrine, and growth hormone/cortisol. These increase gluconeogenesis from lipids and proteins, causing more glucose to be secreted into the blood, further raising Rachel’s blood glucose. To prevent this from happening, Rachel should check her blood sugar before going to bed, as well as in the middle of the night. She can also decrease her evening insulin dosage or increase the amount of carbohydrates in her bedtime snack. Either of these steps will keep hypoglycemia from occurring and avoid the promotion of glucose production by counter-regulatory hormones. II. Understanding the Nutrition Therapy 11. The MD ordered a consistent carbohydrate-controlled diet when Rachel begins to eat. Explain the rationale for monitoring carbohydrate in diabetes nutrition therapy. Carbohydrate counting is extremely important when monitoring diabetes through nutrition therapy, because it is carbohydrate sources that provide the greatest contribution to blood glucose levels. Carbohydrates are the major macronutrient in food that causes postprandial glucose variability. Consistent carbohydrate intake is generally needed when fixed dosages of insulin are prescribed for meals. Fixed insulin dosing is easier for patients to follow and is commonly prescribed. 12. Outline the basic principles for Rachel’s nutrition therapy to assist in control of her T1DM. 1. Attain optimal metabolic outcomes: → blood glucose levels in normal range → lipid profile that reduces risk of microvascular disease → blood pressure levels that reduce the risk for vascular disease 2. Prevent and treat chronic complications—modify nutrient intake and lifestyle as appropriate. 3. Improve health through healthy food choices and physical activity. Macronutrient ranges should be: • CHO and monounsaturated fat: 60-70% of total energy intake • Protein: 12-20% of total energy intake • Limit saturated fat: <7% of energy • Dietary cholesterol intake: 180 mg/dL results in loss of glucose in the urine; protein and ketones are indicative of the increased rates of gluconeogenesis and lipolysis 15. Determine Rachel’s energy and protein requirements. Be sure to explain what standards you used to make this estimation. Energy using Schofield equation for females 10-18 years and PA level of 1.31 (value for active female, 3-18 years): REE = 8.365W + 4.65H + 200 = 8.365 (37 kg) + 4.65 (152 cm) + 200 = 1216  1.31 = 1593 kcal/d Estimated Energy Requirement (EER) for females 9 through 18 years developed by the Institute of Medicine: EER = 135.3 – 30.8  age + PA  (10.0  weight + 934  height) + 25 = 135.3 – 30.8  12 + 1.56  (10.0  37.27 + 934  1.524) + 25 = 2592.64 kcal/d Note: PA = 1.56 for very active DRI for females 9 through 13 years = 2071 kcal/day Energy requirement = 2100-2600 kcal/day Protein RDA for females 9 through 13 years = 0.95 g/kg/day Protein = 0.95  37.27 kg = 35.41 g or ~35 grams/day IV. Nutrition Diagnosis 16. Prioritize two nutrition problems and complete the PES statement for each. • Altered nutrition-related laboratory values (blood glucose) related to insufficient insulin administration as evidenced by hyperglycemia (68 3mg/dL admit) and HbA1c value of 14.6%. • Food- and nutrition-related knowledge deficit related to limited exposure to diabetes education as evidenced by patient’s new diagnosis of type 1 diabetes mellitus. • Inconsistent carbohydrate intake related to limited exposure to diabetes education as evidenced by patient diet history and patient’s new diagnosis of type 1 diabetes mellitus. • Impaired nutrient utilization R/T inadequate insulin AEB blood glucose serum value of 724 mg/dL and C-peptide of 0.10 ng/mL. • Underweight R/T impaired glucose utilization AEB BMI below 25th percentile. V. Nutrition Intervention 17. Determine Rachel’s initial nutrition prescription using her usual intake at home as a guideline, as well as your assessment of her energy requirements. Carbohydrate needs based on 45-65% of total kcal from CHO: 2400  0.45 = 1080 kcal/4 kcal/g = 270 grams CHO/d/15 grams/serving = 18 servings/day 2400  0.65 = 1560 kcal/4 kcal/g = 390 grams CHO/d/15 grams/serving = 26 servings/day Current meals/snacks consumed: Breakfast, lunch, dinner, and a snack before soccer practice Nutrition prescription: 90 grams CHO for breakfast, lunch, and dinner (6 CHO equivalents/meal) 30 grams CHO (2 CHO equivalents) for snacks, twice per day (one mid-morning and one before soccer practice or other physical activity) It is typical in pediatric practice to not prescribe a certain amount of CHO. It is more important for the patient to understand the insulin: CHO ratio and cover her intake accordingly. 18. What is an insulin: CHO ratio (ICR)? Rachel’s physician ordered her ICR to start at 1:15. If her usual breakfast is 2 Pop-Tarts and 8 oz. skim milk, how much Apidra should she take to cover the carbohydrate in this meal? An insulin: CHO ratio is an individualized ratio that specifies how many grams of carbohydrate one unit of insulin will cover. It can be determined by dividing 500 by the total daily insulin dose (TDD) of that person. 2 Pop-Tarts = 76 grams CHO 8 oz. skim milk = 12 g CHO Total: 88 grams CHO/15 = 5.8 or 6 units to cover this meal 19. Dr. Cho set Rachel’s fasting blood glucose goal at 90-180 mg/dL. If her total daily insulin dose is 33 u and her fasting a.m . blood glucose is 240 mg/dL, what would her correction dose be? Correction dose = 1800/TDD 1800/33 = 54.00; 1 unit of Apidra will lower her blood glucose by 54 mg/dL. 240 – 180 = 60 so her correction dose would be 1 unit of insulin in addition to her mealtime insulin. VI. Nutrition Monitoring and Evaluation 20. Write an ADIME note for your initial nutrition assessment. Roberts, Rachel 5/4/12 1600 A: 12 yo female Dx: hyperglycemia, type 1 diabetes mellitus PMH: none Family medical history: father – HTN; mother – hyperthyroidism; sister – celiac disease Meds: 7 u glargine, Apidra; ICR 1:15 Skin: warm and dry, good turgor, intact, Braden 21 Abdomen: + BS GI: soft, light brown stool; cloudy, amber urine with ketones, protein, glucose present I/O: 3,560/2,660; net I/O +900 Labs: glucose 683 mg/dL; osmolality 295.3; HgbA1C 14.6%; low C-peptide; + ICA, GADA, IA-2A, and IAA; specific gravity 1.035, pH 4.9, protein, glucose, and ketones present (urinalysis) Ht. 5’0 Wt. 82 # UBW(per Mother) 90# BMI: 16 EER: 2100-2600 EPR: 35-40 g/day Current diet: Somewhat “picky” eater. Cereal with milk or a Pop-Tart for breakfast; PBJ or turkey/cheese sandwich for lunch with chips and carrots on the side; granola bar before soccer practice; salad, meat, and pasta, potatoes, or rice for dinner; sugary snacks including ice cream, chips, cookies, yogurt, some fruit. Plays soccer and exercises daily. D: Altered nutrition-related laboratory values (blood glucose) related to insufficient insulin administration as evidenced by hyperglycemia (683 mg/dL admit) and HbA1c value of 14.6%. I: Patient will adhere to nutrition therapy for T1DM with help and support of family members: carbohydrate-controlled diet and proper insulin doses. M/E: Follow up for continued DM management – RD name and number given for assistance – will monitor adherence, diabetic/CHO knowledge, weight, and blood glucose levels through outpatient clinic appointments. Signed 21. When Rachel comes back to clinic, she brings the following food and blood glucose record with her. a. Determine the amount of carbohydrates she is consuming at each meal. Carbohydrates at each meal: Breakfast = 139 g Lunch = 105 g Snack = 23 g Snack = 30 g Snack = 30 g Dinner = 99 g Snack = 60 g Total: 486 g CHO b. Determine whether she is taking adequate amounts of Apidra for each meal according to her record. She is underestimating for most of her meals during the day, except for her bedtime snack. Also, she needs to avoid snacking as much during the middle of the day, even though it is appropriate to not give insulin because she is exercising. Overall, her blood glucose levels are within her target range of 90-180 mg/dL before each meal. A higher ICR may need to be used for her breakfast insulin dosage. If she was following the ICR of 1:15 at breakfast, she would need to take 4 more units of Apidra, which might cause her to have hypoglycemia. Otherwise, she is doing well by avoiding hypoglycemia throughout the day, even with 2 hours of exercise. More accurate carbohydrate counting with appropriate carbohydrate exchanges can be achieved at the other meal times. Solution Manual for Medical Nutrition Therapy: A Case-Study Approach Marcia Nahikian Nelms 9781305628663, 9780534524104, 9781133593157