This Document Contains Cases 17 to 18 Case 17 – Type 1 Diabetes Mellitus in the Adult I. Understanding the Disease and Pathophysiology 1. What are the differences among T1DM, T2DM, and LADA? Type 1 diabetes (5%-10% of cases): • Type 1 diabetes is an autoimmune disorder that attacks the beta cells of the pancreas. • Individuals are dependent on insulin because they do not produce insulin, since their beta cells are destroyed. • Some symptoms are similar to those of type 2 diabetes: e.g., polyphagia, polydipsia, and polyuria (excessive hunger, thirst, and urination). • Diagnosis of type 1 diabetes is similar to type 2 diabetes in that casual plasma glucose is greater than 200 mg//dL, or fasting BG is greater than 126 mg/dL. However, IAA, ICA, and GADA antibodies are usually present with a type 1 diagnosis since it is an autoimmune disease, whereas with type 2 these antibodies are not present. • C-peptide can be used to distinguish type 1 from type 2 diabetes. Low amounts of c-peptide or the absence of c-peptide indicates type 1 diabetes because it confirms that insulin is not being produced by the pancreas. • Absence of insulin causes decreased levels of cellular glucose since insulin is crucial for transporting glucose into the cells. It also causes increased glycogenolysis or breakdown of glycogen because the cells think that they are starving when they cannot uptake glucose. There is also an increase in hepatic glucose production (gluconeogenesis). • Glucose-lowering medications are not effective in treating type 1 diabetes because insulin production is necessary in order for these medications to work. Type 2 diabetes (90%-95% of cases): • Group of metabolic disorders that present with high blood glucose levels, as in type 1 diabetes, along with the similar symptoms of polyuria, polydipsia, and polyphagia. • Non-insulin dependent diabetes that results from peripheral insulin resistance that varies in severity. • There is a defect in the transportation of glucose into the cells, but the pancreas still produces insulin, unlike in type 1 diabetes. • Receptors in certain cells (muscle cells and adipocytes) do not respond to insulin, so glucose cannot be transported into the cell. • Defective insulin secretory response results in excess production of glucose in the liver (GNG). • Type 2 diabetics often take glucose-lowering medications in conjunction with making dietary and physical adjustments to help in controlling blood glucose levels. Insulin is often needed in type 2 diabetics at some point, as the beta cells can become exhausted over time. • Predisposing factors include age, obesity, and lack of physical activity. • Stronger genetic predisposition than type 1 diabetes. LADA (latent autoimmune diabetes in adults): • Auto-antibodies are present as in type 1 diabetes, but the progression of beta cell destruction is much slower than in type 1 diabetes. • Does not immediately require insulin like type 1 diabetes does (about 6 or more months after diagnosis), although insulin will probably be warranted at some point once the destruction of the beta cells is complete. ○ Some consider LADA to be an intermediate form of T1DM and T2DM along the diabetic continuum. 2. What are the standard diagnostic criteria for each of these diagnoses? Type 1 diabetes: • Casual blood glucose above 200 mg/dL • Fasting blood glucose above 126 mg/dL • Oral glucose tolerance test >200 mg/dL (2-hr postprandial) • Presence of antibodies ICA, GADA, IA-2A, and IAA • Weight loss • Polydipsia, polyuria, polyphagia • C-peptide also used to help distinguish type 1 diabetes; low c-peptide indicates low or no insulin production • HbA1c >6.5% Type 2 diabetes: • Polydipsia, polyuria, polyphagia • Casual blood glucose above 200 mg/dL • Fasting blood glucose above 126 mg/dL • Oral glucose tolerance test >200 mg/dL (2-hr postprandial) • HbA1c >6.5% LADA: Generally, the most accepted diagnostic criteria for LADA includes the following: the presence of autoantibodies (e.g. ICA, GADA, and IA-2A), onset after age 30, and non-insulin dependent for at least six months past diagnosis 3. Why do you think Matias was originally diagnosed with T2DM? Why does the MD now suspect he may actually have T1DM or LADA? • He was diagnosed with type 2 diabetes one year ago due to hyperglycemia; there were probably no antibodies present at that time, meaning he met only the type 2 criteria. • Now, the presence of antibodies GADA, IAA, and ICA indicates an autoimmune attack on the beta cells of the pancreas. The presence of antibodies makes a diagnosis of type 1 diabetes or LADA more appropriate. • His c-peptide is 0.6, which is very low, indicating that very little insulin is being produced due to the auto-destruction of the beta cells, further confirming a type 1 diagnosis. 4. Describe the metabolic events that led to Matias’s symptoms and subsequent admission to the ER (polyuria, polydipsia, polyphagia, fatigue, and weight loss), integrating the pathophysiology of T1DM into your discussion. • With type 1 diabetes, insulin is not being produced because of the autoimmune destruction of beta cells within the pancreas. • Without insulin, hepatic gluconeogenesis is not suppressed properly, leading to an increase in gluconeogenesis along with glycogenolysis. This causes hyperglycemia, a hyperosmolar condition. • Without insulin, glucose cannot be transported into the cell, also resulting in hyperglycemia. Lack of nutrients results in polyphagia, or excessive hunger. • Since hyperglycemia is a hyperosmolar condition, water is drawn from the cells into the blood in an attempt to compensate for the serum hyperosmolality. The cells become dehydrated, which contributes to polydipsia, or excessive thirst. • The increase in urinary glucose excretion occurs due to a blood glucose concentration of 180 mg/dL or higher and water follows it (due to the osmotic gradient). This increases urination and manifests itself as polyuria. • Because the cells are not getting the nutrients they need due to a lack of insulin, unintentional weight loss typically occurs in type 1. 5. Describe the metabolic events that result in the signs and symptoms associated with DKA. Was Matias in this state when he was admitted? What precipitating factors may lead to DKA? • The symptoms associated with DKA include: polydipsia, polyuria, polyphagia, weakness, lethargy, abdominal pain, malaise, and headaches/dizziness. Additionally, common symptoms also include: Kussmaul breathing Hypothermia, hyperapnea Acetone breath Poor skin turgor Orthostatic hypotension Mental status changes • DKA is a severe form of hyperglycemia because when insulin is not being produced, certain metabolic events occur: Glucose production via gluconeogenesis in the liver is not suppressed, contributing to high blood glucose levels. Lipolysis occurs since insulin is not there to favor triglyceride storage, which alters fat metabolism. The increased rate of fatty acid metabolism results in ketosis. Glucose and ketones accumulate in the blood, which causes osmotic diuresis leading to increased urine production in an attempt to rid the body of excess ketones and glucose (polyuria). Osmotic diuresis results in dehydration and electrolyte imbalance. Dehydration results in poor skin turgor and orthostatic hypotension due to a decreased blood volume. DKA is a metabolic acidosis condition due to the high levels of serum ketones. Kussmaul breathing represents the body’s attempt to correct this acidosis. The release of ketones can be noted in the acetone breath. • Precipitating factors for DKA include: Illness/infection Inadequate insulin dosage Initial manifestation of type 1 diabetes Emotional/physical stress • Yes, Matias was most likely in a DKA state upon admission because he had several of the signs and symptoms of DKA: Altered mental changes (he was unconscious) Extremely high blood glucose level (683 mg/dL) He was recently fighting off a virus, which is a precipitating factor for DKA He is dehydrated because his osmolality is high (his daily alcohol consumption may have contributed, too) Electrolyte imbalances: sodium and phosphate are both low High levels of CO2, which is a sign of excess acid in the body Orthostatic hypotension; his blood pressure is low due to a decreased blood volume Ketones and glucose in the urine (confirms that ketones are being produced via incomplete fatty acid metabolism) 6. Matias will be started on a combination of Novolog prior to meals and snacks with glargine given in the pm. Describe the onset, peak, and duration for each of these types of insulin. • Novolog is rapid-acting insulin, or a bolus insulin that is taken to cover the glucose ingested at meals. Peak: When insulin is at full potential of covering glucose levels or when the highest level of insulin in the blood is reached. 30-90 minutes. Onset: Time it takes for insulin to begin action. 5-15 minutes (rapid-acting). It begins to cover the glucose quickly, which is why it is given with meals. Duration: How long insulin lasts in the blood. 3-5 hours. • Glargine is long-acting or basal insulin, also known as background insulin; it covers basic functions. Peak: None; since it is long acting, there is no peak. Onset: 2-4 hours. This is the period of time that it takes for the insulin to begin working. Duration: 20-24 hours. It is designed to cover the background glucose levels, which is why is it usually given at night and/or in the morning and then lasts the whole day. 7. Using his current weight of 165 lbs, determine the discharge dose of glargine as well as an appropriate ICR for Matias to start with. • Glargine is the basal insulin, so half of the total daily insulin dose (TDD) should be from glargine. He should receive 0.3-0.5 units insulin/kg of body weight. To start, I took an average and used 0.4 units/kg body weight. 165 lbs / 2.2 = 75 kg 0.4 units/kg = 30 units of insulin (TDD). 50% is glargine: 30 / 2 = 15 units from glargine (basal insulin). • Algorithm for patient that has T1DM with small amount of ketones (use 0.3-0.5 units/kg). • Insulin: carbohydrate ratio: 500 / TDD = 500 / 30 units =16.7 or ~17. This means that for every 17 g of carbohydrates ingested, Matias will need 1 unit of insulin. 8. Intensive insulin therapy requires frequent blood glucose self-monitoring. What are some of the barriers to success for patients who begin this type of therapy? Give suggestions on how you might work with Matias to support his compliance. • Intensive insulin therapy is a flexible insulin regimen compared to conventional or standard therapy. Conventional is a fixed insulin dose whereas intensive insulin therapy uses SBGM to determine how much insulin to give at meal times plus it uses a basal insulin dose based on the patient’s weight. • Intensive insulin therapy requires multiple daily injections of bolus insulin before meals in addition to basal insulin once or twice daily. • Intensive insulin therapy, when compared to standard therapy, has demonstrated better glycemic control but it requires patients to self-monitor their blood glucose levels. • Barriers to success: Compliance with giving multiple daily injections Compliance with checking blood glucose levels in the morning, preprandially and post-prandially Learning to carbohydrate count Inconvenience of carrying glucometer with normal daily living activities Learning how to accurately use glucometer and how to calculate insulin dosages needed Lack of support system Fear of hypoglycemia • Health practitioners can help the patient overcome barriers by providing education and support Educate patient on how to effectively use glucometer. Have patient practice on himself and the dietitian to make sure he understands the proper technique to monitor blood glucose. Educate patient on carb counting. Have patient develop sample meals to demonstrate that patient understands the process of carb counting. Providing the patient with the Exchange List booklet can be beneficial. Have patient practice injections. Give patient recording tools such as graphs and charts that may help the patient keep track of physical activity, blood glucose levels, and carbohydrate intake. Teach patient about signs/symptoms of hypoglycemia and the appropriate treatment. Help patient develop appropriate target blood glucose ranges using the ADA guidelines. Refer to SBGM as “monitoring” and avoid saying the word “testing.” 9. Matias tells you that he is very frightened of having his blood sugar drop too low. What is hypoglycemia? What are the symptoms? What information would you give to Matias to make sure he is well prepared to prevent or treat hypoglycemia? • Hypoglycemia is defined as a blood glucose level of less than 70 mg/dL according to the American Diabetes Association. In other words, it is low blood sugar. • Symptoms associated with hypoglycemia include: Weakness Shakiness Perspiration Hunger Rapid heartbeat Symptoms are individual and vary from person to person If severe, altered mental status may occur (may lose consciousness) • Remedy for mild hypoglycemia is the 15/15 rule: First, Matias should be able to identify signs and symptoms associated with hypoglycemia. Matias would be instructed to monitor his blood glucose level. If he has a low reading (<70 mg/dL), he should know that he is hypoglycemic and he should apply the 15/15 rule. Matias would consume a food/beverage providing 15 g of rapid-acting carbohydrates such as ½ cup fruit juice, 3-4 glucose tablets, etc. If blood sugar is below 50 mg/dL, 20-30 g of carbohydrate should be consumed. Then Matias should wait 15 minutes and re-check his blood glucose. If it is still low, he should consume 15 g more of carbohydrates and the process should be repeated. If he has exercised, if he will not eat within the next hour, or if he is going to bed, an additional snack may be needed. • Severe hypoglycemia cannot be self-treated with the 15/15 rule. Thus, having him inform his friends and family of the signs of what to look for and how to treat hypoglycemia can be life-saving. • Determine that he feels comfortable with recognizing his personal signs and symptoms of hypoglycemia before it becomes too severe to self-treat. • Determine awareness that exercise can make one prone to hypoglycemia, especially strenuous exercise lasting a longer duration. Ensure that he knows appropriate equipment to keep on hand during exercise: personal and diabetes information, carbohydrate snack. ○ Liquid, soft, or otherwise easily chewed/swallowed simple carbohydrate options will allow quick and easy administration (for himself and others if their assistance is needed). 10. Matias’s mother has T2DM. She is currently having problems with vision and burning in her feet. What is she most likely experiencing? Describe the pathophysiology of these complications. You can tell that he is worried not only about his mother but also about his own health. Explain, using results of the Diabetes Complication and Control Trial (DCCT) as well as any other pertinent research data, how he can prevent these complications. Matias’s mother is most likely experiencing retinopathy and neuropathy secondary to T2DM and chronic hyperglycemia. • Poorly controlled blood glucose levels can lead to a state of chronic hyperglycemia, which causes further complications such as retinopathy and neuropathy. • Hyperglycemia results in increased production of sorbitol, which cannot cross the cell membrane. The accumulation of sorbitol damages blood vessels of the eye, leading to macular edema, glaucoma, and possible blindness. • In general, hyperglycemia changes the structure of the blood vessels, causing endothelial damage to the vessels, whether the blood vessels are microvascular or macrovascular. • The basement membrane of the blood vessels thickens, affecting the blood flow, especially to the extremities. This increased resistance increases blood pressure and work of the heart. • Hyperglycemia results in abnormal amounts of glycated proteins that damage nerve structure and function. The DCCT determined that in T1DM patients who improve glycemic control, complications associated with damaged vessels may be delayed or even prevented. • There was a 60% reduction in microvascular neuropathy in those who used intensive insulin therapy for glycemic control compared to conventional therapy, and a 63% reduction in retinopathy. These numbers were significant. • The EDIC study was a follow-up study using the same participants as the DCCT that demonstrated further reductions in the percentage of microvascular complications over a longer period of time. • Using this information from these studies in type 1 diabetics, Matias can prevent complications, especially microvascular complications, by being compliant with intensive insulin therapy. If he can control his blood glucose levels, the risk for complications decreases. II. Understanding the Nutrition Therapy 11. Outline the basic principles for Matias’s nutrition therapy to assist in control of his DM. • Goal: Maintain optimal metabolic outcomes to prevent micro- and macrovascular complications. Glucose levels in normal ranges: • Fasting: 80-110 mg/dL • Preprandial: 80-130 mg/dL • Postprandial: <180 mg/dL • A1c: 180 mg/dL blood glucose values allow these to spill into the urine, which is abnormal. • Low c-peptide: Confirms that pancreas is not producing adequate amounts of insulin. • Antibodies ICA, IAA, GADA: Confirm autoimmune attack on beta cells consistent with T1DM. 14. Determine Matias’s energy and protein requirements. Be sure to explain what standards you used to make this estimation. Would you recommend that he either gain or lose weight in the future? • Energy: 25-30 kcal 75 kg = 1875-2250 kcal (American Chest Physician’s Equation) • Protein: protein ranges from 15-20% of daily calories. 0.15 1875 = 281 kcal / 4 kcal/g = 70 g protein, 0.20 1875 kcal = 375 kcal / 4 kcal/g = 94 g protein. Used the lower kcalorie range to maintain weight, since BMI is normal but on the upper end of the normal range. Therefore, protein needs range from 70-94 g/day. • Standards for this estimation were from the ADA guidelines that indicate that protein, carbs, total fat, sat. fat, cholesterol, fiber, vitamins, and minerals for diabetics are the same as for the rest of the population. If nephropathy is an issue, then protein needs are potentially decreased by10%. • I would recommend that the patient maintain his current weight. His BMI of 23 is within the normal range. At this point, he should try to normalize his blood glucose values. IV. Nutrition Diagnosis 15. Prioritize two nutrition problems and complete the PES statement for each. Altered nutrition-related laboratory values related to lack of insulin production as evidenced by serum glucose of 550 mg/dL, HbA1C of 10.2%, osmolality of 304.4 mOsm, +4 presence of urinary ketones, serum pH of 7.31, and C-peptide of 0.09 ng/mL. Impaired nutrient utilization (NC-2.1) related to lack of insulin production as evidenced by serum glucose of 550 mg/dL, HbA1C of 10.2%, C-peptide of 0.09 ng/mL, +4 presence of urinary ketones, and symptoms of lethargy and low consciousness. Nutrition knowledge deficit related to new need for carbohydrate counting as evidenced by patient history of no previous education. V. Nutrition Intervention 16. Determine Matias’s initial CHO prescription using his usual intake at home as a guideline, as well as your assessment of his energy requirements. What nutrition education material would you use to teach Matias CHO counting? • Matias’s estimated energy needs are 25-30 kcal/kg or 1865-2250 kcal/day, and it is estimated that carbohydrates should provide 50-60% of kcalories, depending on the individual and his or her personal lipid profile. • 0.50 1875-2250 kcal = 938-1125 kcal from carbohydrates / 4 kcal/g = 234-281g of carbohydrates. To determine the number of carbohydrate choices per day: 234-281 g / 15 g carbs = 15-18 choices/day. • For Matias, the ICR was determined to be 17 g of carbs to 1 unit of insulin. Therefore, it could be determined that 234-281 g / 17 g carbs = 14-17 carb choices • Provide Matias written materials for carbohydrate counting along with sample meal plans or a food diary to assist in tracking his diet and blood glucose readings. Provide resources for CHO counting including label reading, eating out in restaurants, computer or Smart Phone applications. 17. Matias’s usual breakfast consists of 2 slices of toast, butter, 2 tbsp jelly, 2 scrambled eggs, and orange juice (~1 cup). Using the ICR that you calculated in question #7, how much Novolog should he take to cover the carbohydrate in this meal? 2 slices of toast: 30 g carbs 1 cup OJ: 30 g carbs 2 T jelly: 28 g carbs 2 scrambled eggs: 0 g carbs Total: 88 g carbs / 17 g carbs from ICR = 5.2 units of insulin or 5 units of Novolog rapid-acting insulin. 18. Using the ADA guidelines, what would be appropriate fasting and post-prandial target glucose levels for Matias? Using the ADA guidelines, for diabetics the following ranges are used: • Fasting: 80-120 mg/dL • Pre-prandial: 80-130 mg/dL • Post-prandial: <180 mg/dL VI. Nutrition Monitoring and Evaluation 19. Write an ADIME note for your initial nutrition assessment. Date, Time A: 32 YO Hispanic male PMH: previous type 2 diabetes diagnosis Family Hx: MI—father, type 2 diabetes—mother, ovarian cancer—mother Medications: None, discontinued use of metformin Dx: Type 1 diabetes – with DKA Cardiac: tachycardia Abdomen: non-distended, bowel sounds 4 quadrants Labs: glucose: 550 mg/dL, HbA1c: 10.2%; CO2 31; osmolality 304.4; phosphate 2.1; Na 130; TG 175; cholesterol 210; LDL 137; HDL 38. Antibodies present at diagnosis: ICA, IAA, GADA, c-peptide 0.09 – consistent with T1DM/LADA. D: Altered nutrition-related laboratory values related to lack of insulin production as evidenced by serum glucose of 550 mg/dL, HbA1C of 10.2%, osmolality of 304.4 mOsm, +4 presence of urinary ketones, serum pH of 7.31, and C-peptide of 0.09 ng/mL I: Goal: maintain optimal metabolic outcomes to prevent micro and macrovascular complications Normalize glucose levels • Fasting: 80-110 mg/dL • Preprandial: 80-130 mg/dL • Postprandial: <180 mg/dL • A1c: 200 mg/dL) at time of diagnosis ○ HbA1c is 11.5% (significantly exceeds 6.5%) 2. Mitch was previously diagnosed with T2DM. He admits that he often does not take his medications. What types of medications are metformin and glyburide? Describe their mechanisms as well as their potential side effects/drug-nutrient interactions. Metformin is a biguanide and is also referred to as Glucophage. It decreases hepatic glucose production or gluconeogenesis and improves insulin resistance by increasing insulin uptake in the muscles. There are very few side effects with metformin, which is why it is commonly used as the initial drug of choice for type 2 diabetes. Hypoglycemia is not a side effect with metformin like it is with the other glucose-lowering medications. Potential side effects: • Diarrhea • Nausea • Bloating • Anorexia • Flatulence • Lactic acidosis (although this is very rare) Drug-nutrient interactions: • Decreases folate and vitamin B12 absorption (may need supplementation of these vitamins) • Avoid alcohol • Needs to be taken with meals to help avoid GI distress or symptoms of nausea, diarrhea, flatulence, etc. Glyburide is a second-generation sulfonylurea agent. Sulfonylurea drugs work by stimulating insulin secretion from the beta cells of the pancreas. It can only be used in individuals with type 2 diabetes because insulin production is necessary in order for the mechanism of this drug to be effective. Hypoglycemia can be a potential side effect when using sulfonylurea drugs, especially glyburide. Hypoglycemia is the main side effect associated with this medication (weight gain and contraindicated with renal insufficient patients, too). Since glyburide increases insulin secretion, more than enough insulin may be released into the blood, which can lead to hypoglycemia. Drug-nutrient interactions: Avoid alcohol; take once before breakfast (30-60 min. prior) 3. What other medications does Mitch take? List their mechanisms and potential side effects/drug-nutrient interactions. Dyazide is also known as hydrochlorothiazide (thiazide diuretic) combined with triamterene (potassium-sparing diuretic). It works by decreasing the blood volume, which ultimately lowers blood pressure. Dyazide also increases urinary output and inhibits sodium and water reabsorption to help with edema or fluid retention in the extremities. Side effects: • Hypokalemia, • Hyperlipidemia • Hypertriglyceridemia • Hypercholesterolemia • Glucose intolerance • N/V • Anorexia • Dehydration/Dry mouth • Diarrhea • Weakness • Potentially hypotension • Constipation Drug-nutrient interactions: • Increases potassium excretion, so may need a potassium supplement • Cannot take with NSAIDSs • Avoid licorice • Take with food • Do not take with Ca, Al, Mg, or Fe supplements within 2 hours of medication Lipitor (trade name for atorvastatin) is a statin drug in the HMG-CoA reductase inhibitor class. Therefore, it works on the rate-limiting step of cholesterol production to decrease cholesterol, LDL, and triglycerides. It also raises HDL levels 7-30%. Side effects: • Myopathy: muscle pain • Increased liver enzymes Drug-nutrient interactions: • Cannot be prescribed if patient has liver disease • Cannot take with certain antibiotics, various anti-fungal agents, and P 450 inhibitors (e.g. grapefruit) • Fibrates and niacin should be used with caution He is also beginning insulin. • Lispro: rapid-acting insulin. Taken with meals to help control high blood glucose levels. • Glargine: basal insulin to help control high blood glucose levels. • Potential side effects: Hypoglycemia 4. Describe the metabolic events that led to Mitch’s symptoms and subsequent admission to the ER with the diagnosis of uncontrolled T2DM with HHS (be sure to include the information in Mitch's chart that supports his diagnosis). Compare and contrast HHS with the other common clinical emergency condition of diabetes - diabetic ketoacidosis (DKA). • Patient was previously diagnosed with diabetes, and by his own admission has not been taking his medications. This led to a state of hyperglycemia. • Patient reports vomiting persistently, which probably led to severe dehydration. In fact, patient has many signs that are consistent with dehydration: ○ Poor skin turgor ○ Tachycardia • Low blood pressure (90/70 mmHg) ○ High BUN ○ Urinalysis reveals high specific gravity (1.045, dehydration) ○ High hematocrit (% RBC increases when blood volume is concentrated) ○ High osmolality • HHS (hyperosmolar hyperglycemic state) results from severe dehydration—as may occur with type 2 diabetes in conjunction with a co-existing illness. In this case, Mitch was vomiting, which led to dehydration and a decrease in fluid intake; this, along with diabetes, allowed Mitch’s blood glucose levels to reach very high levels (1524 mg/dL), indicating HHS. • With type 2 diabetes, the transport of glucose into the cell is hindered because of insulin resistance. There is a decrease in circulating insulin when there is an acute illness such as vomiting. There is a simultaneous increase in counter-regulatory hormones that stimulate gluconeogenesis, causing more glucose production. This allows blood glucose to rise to very high levels. High blood glucose levels and little circulating insulin further contribute to insulin resistance, keeping glucose levels high. Osmotic diuresis occurs as the hyperosmolality of the blood draws water from the cells. Glucose of >180 mg/dL is over the renal threshold (leading to glucosuria). This also explains the low sodium levels, as sodium is excreted via urine along with excess water and glucose. • HHS is often indistinguishable from the illness that is co-existing with diabetes. In this case, the persistent vomiting from being ill allowed blood glucose levels to spike uncontrollably. • HHS symptoms: ○ Osmolality is high (322.6 mmol/kg/H2O) ○ Glucose levels are severely high (1524 mg/dL) ○ Severe dehydration (specific gravity of 1.045, which is significantly high) ○ Non-ketosis, which differentiates HHS from DKA. Although Mitch has some ketones present in the urine, it is not a significant amount. In addition, DKA is more common in type 1 diabetics. • HHS is defined as: ○ Plasma blood glucose levels >600 mg/dL, whereas severe DKA is >250 mg/dL (pt. blood glucose is 1524 mg/dL, or >600 mg/dL) ○ Quantity of ketones in urine is small – consistent with pt. diagnosis ○ Arterial pH >7.30 – N/A ○ Serum osmolality is greater than 320 mmol/kg (pt. osmolality is 322.6 mmol/kg upon diagnosis) ○ Altered mental capability (stupor/coma) – consistent with pt. diagnosis 5. HHS is often associated with dehydration. After reading Mitch’s chart, list the data that are consistent with dehydration. What factors in Mitch’s history may have contributed to his dehydration? • High BUN • High osmolality • Poor skin turgor/dry skin • Elevated heart rate • Low blood pressure (90/70 mmHg) • High hematocrit • High specific gravity • Net I/O of +2140 mL • Mitch’s precipitating illness that is causing vomiting along with his uncontrolled diabetes (since Mitch is not taking his glucose-lowering medications) are probably the biggest contributors to HHS. ○ Vomiting contributes to fluid loss and a decrease in fluid intake, which contribute to dehydration. • Osmotic diuresis from HHS also contributed to dehydration, as electrolytes are lost via urine, as indicated by a low serum sodium level. 6. Assess Mitch’s intake/output record for the first 24 hours of his admission. What does this tell you? Assuming that Mitch tells you that his usual weight is 228 lbs., can you estimate the volume of his dehydration? • According to his I/O record since admission, Mitch has a positive balance, meaning he consumed more fluid than there was fluid loss. His net input was 2140 mL. This means that he was dehydrated; i.e., greater input than output confirms that his body is being replenished with fluid. Otherwise, his net I/O would be more balanced. • Usual weight = 228 lbs., current weight = 214 lbs. Weight loss = 228 – 214 = 14 lbs. lost. 14 lbs. / 228 lbs 100% = 6% weight loss. 14 lbs / 2.2 = 6.4 kg or ~6 liters of fluid loss (1 L = 1 kg). OR 14 lbs / 2.2. lbs/kg / 999.97 kg/m3 x (100 cm/m)3 / 1000 cm3/L ≈ 6.4 L 7. Mitch was started on normal saline with potassium as well as an insulin drip. Why are these fluids a component of his rehydration and correction of the HHS? • Normal saline delivered via an IV will restore the electrolyte imbalance that occurred due to HHS (more specifically, that occurred from osmotic diuresis). Sodium was lost during this process, which is why saline is administered. This will correct the severe state of dehydration more rapidly than drinking water. • Potassium is another electrolyte that will be out of balance with dehydration. In addition, the patient is taking Dyazide, which is not a potassium-sparing diuretic. Therefore, potassium is commonly lost when using this medication. Although patient is not taking his diabetes medications, he claims to still be taking Dyazide to help with his blood pressure. Potassium is commonly lost in the urine with osmotic diuresis. This occurred because of the serious hyperosmolar state of the blood. • The infusion of the potassium in the saline is due to the low levels of intracellular potassium. This potassium deficit is not apparent in Mitch's labs (3.9 and 4.0 mEq/L), but that is a measure of his serum levels which are typically normal or high in HHS patients. That is because the hypertonic and insulin-deficient bloodstream supports retention of potassium in the extracellular space. If potassium is not supplemented during rehydration and insulin infusion, hypokalemia will result as potassium rushes into the cells. • Insulin is used to help correct the extremely high blood glucose levels. Since the patient has low levels of circulating insulin, which is associated with HHS, insulin is needed to help insulin-dependent tissues uptake glucose. 8. Describe the insulin therapy that was started for Mitch. What is Lispro? What is glargine? How likely is it that Mitch will need to continue insulin therapy? • Mitch was started on Lispro 0.5 u every 2 hours until glucose is 150-200 mg/dL. In addition, Mitch was ordered to begin glargine that night at 19 u (9 pm).His established carb-to-insulin ratio was 15:1. • Lispro is a rapid-acting insulin that is taken just prior to meals. It has a peak of action at 30-90 minutes. This is when the insulin is at its full potential to lower blood glucose levels. The onset is 5-15 minutes, meaning at that time, the action of insulin should begin working to lower blood glucose levels. Lastly, it has a duration of 3-5 hours, meaning that is how long these rapid-acting insulin lasts when used with the correct carb-to-insulin ratio, which in this case is 15 g of carbs per unit. • Glargine is a basal insulin, which is why it is taken at night. It covers the baseline blood glucose levels but it is not enough to cover the carbs that are consumed with meals and snacks. There is no peak for basal insulin and the duration is much longer than that of rapid-acting insulin: 20-24 hours. The onset is 2-4 hours. • Since Mitch is non-compliant with taking his medications, it seems unlikely that he will want to stay on insulin because it requires consistent carbohydrate intake throughout the day, carbohydrate counting, and adjusting insulin doses depending on exercise, food consumption, etc. This all takes work and requires much more effort than oral glucose-lowering medications. • However, Mitch needs insulin because his type 2 diabetes is very out of control at the moment. His glucose level at admission was very high, and his HbA1c, or his average blood glucose level, was 11.5%. This is considerably over 6.5%. According to the American Diabetes Association, when HbA1c is over 9%, insulin is recommended immediately or at least will be needed in the future. Glucose-lowering medications only lower HbA1c by a few percentage points. Therefore, insulin is required for Mitch. II. Understanding the Nutrition Therapy 9. Mitch was NPO when admitted to the hospital. What does this mean? What are the signs that will alert the RD and physician that Mitch may be ready to eat? • NPO translates to “nothing by mouth.” Mitch was not allowed to consume liquids or foods by mouth. The only source of hydration that Mitch was receiving was the saline solution that was being administered intravenously. • Since Mitch was vomiting, he was made NPO. After 8 hours of not vomiting, Mitch will probably be ready to eat solid foods. He will then probably be initiated on a low-residue, low-fat diet with foods such as bananas, rice, applesauce, and toast. Small meals may be better tolerated, as well as foods at room temperature and smooth consistency (due to potential soreness from vomiting). • He will be more inclined to eat when his blood glucose levels go down and when he does not feel so drowsy and disoriented. 10. Outline the basic principles for Mitch’s nutrition therapy to assist in control of his DM. • Consistent carbohydrates throughout the day: ○ Carbohydrate counting: 1 serving of carbohydrates is 15 g ○ Educate patient on label reading to determine carbohydrate content ○ Teach patient to recognize foods that are low in carbs and foods high in carbs • Insulin therapy: his HbA1c is greater than 9%, which warrants insulin therapy to help with blood glucose control and to prevent another episode of HHS. ○ ICR: 15 g : 1 unit insulin • Glucose-lowering medications if pt. is willing to comply. • Choose snacks low in sugar such as vegetables. Sugar-free substitutes should be used as alternatives to sugary snacks. • Healthy carbohydrate options include vegetables, fruits, whole grains, legumes, and dairy products. • Limit amount of saturated fat, total fat, and trans fatty acids in the diet to help improve cholesterol profile and reduce risk of CVD. • Weight reduction/increased exercise may improve insulin-resistance. III. Nutrition Assessment 11. Assess Mitch’s weight and BMI. What would be a healthy weight range for Mitch? • UBW was used since patient’s current weight is after fluid loss. This will probably be re-gained once patient is re-hydrated. UBW: 228 lbs. / 2.2 = 103.6 kg. Ht.: 5’ 9” (69 in.). BMI: 228 lbs. 703 / 69 in. / 69 in.= 33.7. Using current weight of 214 lbs., BMI = 214 703 / 69 / 69 = 31.7. Either way, Mitch is considered obese based on his BMI assessment since his BMI is greater than 30. • A healthy weight range would be achieved if Mitch lost approximately 10% of his body weight. 0.90 214 = 193 lbs. An initial goal would be to reduce Mitch’s BMI below 30. Mitch should aim to lose about 20 lbs. to meet this goal. • His ideal body weight per the Hamwi equation is: 106 lbs + 6 lbs/1" (after 5') = 106 + 6 x 9 = 160 lbs. Allowing some flexibility of +/- 10%, gives a range of 144-176 lbs. This goal is 52 lbs from his UBW or a loss of 33% of his bodyweight. This is not a realistic goal at this point. • Weight reduction should be gradual, not exceeding more than 2 lbs. per week, which promotes fat loss and minimizes risk of lean body mass loss. 12. Identify and discuss any abnormal laboratory values measured upon his admission. How did they change after hydration and initial treatment of his HHS? Initial lab values: • Glucose: 1524 mg/dL (high) – due to HHS with dehydration. • Creatinine: 1.9 mg/dL (high) – elevated due to admitting dehydration. • Sodium: 132 meq/L (low) – osmotic diuresis. Loss of sodium in urine. • Phosphate: 1.8 (low) – osmotic diuresis; loss of phosphate in urine; kidney function may be impaired due to very high level of hyperglycemia. • Cholesterol: 205 mg/dL (high) – related to cardiovascular risk factors and diagnosis of hyperlipidemia • HbA1c: 11.5% (high) – average blood glucose levels are very high as patient has uncontrolled type 2 diabetes and is not taking his medications as prescribed. • C-peptide: 1.10 – means that patient is producing insulin, but insulin resistance is a problem. • Osmolality: 322.6 mmol/kg (high) – because HHS is a hyperosmolar condition triggered by an illness and severe dehydration. • Specific gravity (1.045) high – due to dehydration. • BUN: 31 (high) – due to dehydration and HHS, which is a hyperosmolar condition. • Glucose in urine: present due to diabetes. High blood glucose levels >180 mg/dL allow glucose to spill over into the urine due to impaired kidney filtration. • Protein in urine: presence of protein in urine is indicative of impaired kidney function secondary to his diabetes. • Triglycerides: 185 mg/dL (high) - due to diagnosis of hyperlipidemia Changed values: • Glucose: 475 mg/dL, lowered with insulin therapy but still high as glucose is above 200 mg/dL and patient has been NPO. • Osmolality decreased to 303.5 mmol/kg but is still considered high. • Sodium is still low, but is improving as pt. is receiving hydration via saline solution. • Phosphate: still low but levels are improving as pt. is receiving electrolytes and is rehydrated. 13. Determine Mitch’s energy and protein requirements for weight maintenance. What energy and protein intakes would you recommend to assist with weight loss? • Energy: Mifflin-St. Jeor using his UBW since he should rapidly regain his lost water weight. REE = 10 x W(kg) + 6.25 x Ht(cm) - 5 x A(yrs) +5 REE = 10 x 103.6 kg + 6.25 x 175.26 cm - 5 x 53 yrs + 5 = 1872 kcal/day TEE = 1872 kcal/day x 1.3 = 2433 kcal/day or 2300-2500 kcal/day For weight loss (1 lb/wk): 2300-2500 kcal/day - 500 kcal = 1800-2000 kcal/day • Protein: 0.8-1.0 g/kg. IBW: 72.7 kg 0.8-1.0 = 58-73 g protein/day. Pt. range for protein would be 15-20% of daily calories. For weight maintenance, if pt. consumes 2400 kcal per day, 2400 kcal 0.20 = 480 kcal / 4 kcal/g = 120 g protein. 2400 kcal 0.15 = 360 kcal / 4 kcal/g = 90 g. 90-120 g/day. For weight loss, if pt. consumes 1900 kcal per day, 1900 kcal 0.20 = 380 kcal / 4 kcal/g = 95 g protein. 1900 kcal 0.15 = 285 kcal / 4 kcal/g = 71 g. 71-95 g protein/day. IV. Nutrition Diagnosis 14. Prioritize two nutrition problems and complete the PES statement for each. • Altered nutrition-related lab values related to severe dehydration and HHS as evidenced by glucose >200 mg/dL (855 mg/dL) and osmolality of 322.6 mOsm. • Nutrition-related knowledge deficit related to carbohydrate counting as evidenced by patient’s inability to identify any current diet modifications. • Obesity related to excessive energy intake related to BMI > 30 (33.7 or 31.7), large portion meals at lunch and dinner, and consumption of energy-dense foods. • Inconsistent carbohydrate intake related to type 2 diabetes and food- and nutrition-related knowledge deficit as evidenced by self-report of limited diabetes education, inconsistency of daily carbohydrate intake due to restaurant frequency, and carbohydrate intake variability for meals. V. Nutrition Intervention 15. Determine Mitch’s initial CHO prescription using his diet history as well as your assessment of his energy requirements. • According to his BMI, pt. should aim for weight reduction. According to calculated energy needs, pt. should follow 1900-kcal diet. ○ To start, approximately 50% of energy should come from carbohydrates ○ 1900 kcal 0.50 = 950 kcal from carbs / 4 kcal/g = 237.5 g or 238 g carbohydrates ○ Using ICR of 15 g carbs to 1 unit of insulin, 238 g carbs / 15g = 16 carb choices for the day • Using his diet history as a reference, Mitch should aim to eat consistent amounts of carbohydrates throughout the day. ○ 4-5 carbs for breakfast: 1 bagel, or small bagel with cream cheese (light), coffee w/ half-and-half (free) ○ 1-2 carbs for a snack: piece of fruit, small- to medium-sized banana or apple ○ 5-6 carbs for lunch: 12" subway sandwich, turkey with veggies, light on sauce if any (no chips) ○ 5-6 carbs for dinner: 1 cup of rice, salad, grilled chicken, and 8 oz of fruit juice 16. Identify two initial nutrition goals to assist with weight-loss. Initial weight-loss goals would be to restrict energy intake by 500 kcal a day to lose 1 lb per week. These 500 kcal a day should be subtracted from 2400 kcal, which is the approximate calculated energy requirement for Mitch for weight maintenance. Mitch should aim to lose about 1 lb a week until BMI is less than 30 or until he has lost about 10% of body weight. • Goal #1: Restrict calories by 500 kcal a day or eat close to 1900 kcal each day. ○ Limit foods high in saturated fat and trans fatty acids (education necessary on which foods these are). • Goal #2: Aim to incorporate at least 150 minutes of moderate physical activity each week. 17. Mitch also has hypertension and high cholesterol levels. Describe how your nutrition interventions for diabetes can include nutrition therapy for his other conditions. • The American Diabetes Association recommends the following lipid profile, which is the same as the general population’s recommendation. ○ LDL 40 mg/dL for men ○ Cholesterol < 200 mg/dL ○ TG < 150 mg/dL • As a part of diabetes education, an individual should be counseled on fiber and how it affects glycemic control/heart health. ○ The recommendation for fiber is 25-30 g per day ○ Patients can be instructed to subtract half of the carb grams when fiber content is greater than 5 g per carbohydrate choice/serving. ○ Increasing fiber intake by increasing fruit, vegetable, and whole grain consumption instead of refined grains or simple carbohydrates can also help reduce cholesterol by 2-3% and lower LDL levels by 7%. ○ Fiber acts as a cardioprotective agent that generally may improve one’s lipid profile. • Diabetes increases an individual’s risk for cardiovascular disease. Hypertension also increases the risk of CVD. This is why targeting cholesterol and hypertension is a part of the cardioprotective nutrition therapy that is associated with diabetes education. • Studies have shown that treatments targeting cholesterol and hypertension reduce CVD in people with diabetes. ○ Cardioprotective nutrition therapy includes: Reduction in saturated fat, trans fatty acids, and total fat. • When counseling Mitch on diabetes, one should incorporate consistent carbohydrate intake; reduction of saturated fat, trans fatty acids, and total fat; and reduction in sodium. This will decrease Mitch’s risk of cardiovascular disease, which is a complication associated with diabetes. Fiber should also be discussed. • Weight loss/increased levels of physical activity can improve insulin resistance and HDL levels. VI. Nutrition Monitoring and Evaluation 18. Write an ADIME note for your initial nutrition assessment. Date, Time Mitchell Fagan A: 53 YOWM Dx: Hyperglycemic Hyperosmolar Syndrome (HHS), type 2 diabetes PMH: type 2 diabetes Dx 1 year ago, HTN, gout, hyperlipidemia Meds: At home: glyburide 20 mg daily; 500 mg metformin twice daily; Dyazide once daily (25 mg hydrochlorothiazide and 37.5 mg triamterene); Lipitor 20 mg daily. (pt. states he does not take meds for diabetes) Tobacco use: 1 ppd 20 years – now quit. Alcohol use: 3-4 drinks/week Skin: warm, dry, poor skin turgor Throat: dry mucous membranes Abdomen: active bowel sounds 4, tender, non-distended BP:90/70 mm Hg I/O: net +2140 mL Labs: glucose 855 mg/dL, HbA1c 11.5%, C-peptide 1.10, osmolality 322.6 mOsm, sodium 132 meq/L, phosphate 1.8 mg/dL Urinalysis: presence of glucose and protein in urine, specific gravity (high), minimal amount of ketones in urine. Height: 5’ 9” (69 in.) current wt. 214 lbs., UBW: 228 lbs. IBW: 160 lbs. BMI: 32 (obese) % weight loss since admission: 6% Energy needs: 2300-2500 kcal for weight maintenance; 1800-2000 kcal for weight loss; protein: 71-95 g/day Diet Hx: pt. does not follow particular diet. Pt. states being confused about particular diet to follow and has not received diabetes education for nutr. therapy. Pt. tries to avoid foods high in cholesterol and sodium. Pt eats inconsistent carbs per day (estimated 0, 55, 80, 60 g per breakfast, snack, lunch, and dinner). No portion sizes given. D: Altered nutrition-related lab values (glucose) related to severe dehydration and HHS as evidenced by serum glucose of 855 mg/dL and osmolality of 322.6 mOsm. I: Goal: Educate patient on carb counting • Advance pt. from NPO when glucose levels are under 200 mg/dL • Initiate CHO-controlled diet: 16 carb choices each day, 4-5 for breakfast, 1-2 for a snack, and 5-6 for lunch and dinner ○ ICR 15 g : 1 unit insulin ○ Demonstrate carb counting using sample menus using pt’s diet Hx. M/E: Pt. will receive carb counting education from RD. Reviewed sx and treatment for hypoglycemia. Follow-up appointment made. RD name and number provided for additional questions. Monitor weight status, glycemic control lab values, and dietary adherence. Solution Manual for Medical Nutrition Therapy: A Case-Study Approach Marcia Nahikian Nelms 9781305628663, 9780534524104, 9781133593157
Download
Close
Close
