Carissa Schwandt HN 631 Case Study 2 Pediatric Type 1 Diabetes Mellitus

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1 Carissa Schwandt HN 631 Case Study 2 Pediatric Type 1 Diabetes Mellitus 1. What are the current thoughts regarding the etiology of type 1 mellitus (T1DM)? No one else in Rachel s family has diabetes-is this usual? Are there any other findings in her family medical history that would be important to note? T1DM is caused by several factors such a genetics, autoimmune, and/or environmental exposure to certain viruses or infections. Any of these exposures may trigger the onset of T1DM. Rachel s onset of T1DM may be related to autoimmune or environmental factors, as there is no diagnosis of DM in the family hx. However, Rachel s family does have dx. of other chronic diseases. Her father: dx of HTN, mother dx: hyperthyroidism, and sister: dx of celiac disease. The mother having a dx of hyperthyroidism may potentially cause Rachel to develop Graves disease. This disease is linked to an autoimmune response and dysfunction of organ(s). This may play a part in Rachel dx of T1DM. However, there is no documentation stating that Rachel was dx. with Graves disease. But it is an element to consider. Rachel should also be tested for hypothyroidism. Rachel s sibling has a dx of celiac-disease. This is cause for concern for Rachel and she should be screened. Celiac-disease is in the family hx. Rachel is at an even higher risk for developing this disease, as she is dx. with T1DM. T1DM increases her risk of developing celiac-disease. Celiac-disease and T1DM is linked to irregular BGL s, hypoglycemia, and decreased glycemic control. Due to her father s dx. of HTN, Rachel should be aware of the genetic factors that could lead to the future development of HTN. 2. What are the standard diagnostic criteria for T1DM? Which are found in Rachel s medical record? Symptoms of T1DM include: polyuria, polydipsia, polyphagia, hyperglycemia, wt. loss, dehydration, electrolyte disturbance, and ketoacidosis. Rachel was admitted w/ dx of acute-onset hyperglycemia. Rachel also has complaints regarding polyuria, polyphagia, and polydipsia, which are diagnostic criteria for T1DM. Rachel s neurologic status stated she was slightly confused. This may be linked to dehydration, which is a symptom of T1DM. Rachel s hx reveals recent wt loss. Pt. relates wt. loss to recent dx. of strep throat. Last known wt. was 90# taken at clinic. Parents state no change in appetite. Auto antibody testing is used to determine T1DM. An auto immune process destroys B-cells that produce insulin, in the pancreas. Whereas T2DM is distinguished by insulin resistance. Auto antibody testing can distinguish between the two types of DM. IAA, GADA, ICA, and IA-2A testing that is positive will reflect in a dx. of T1DM. Lab testing: A1C of 6.5 or greater, FPG of 126 or greater, 2 hour pp or pg greater than 200 during an OTGG (a glucose load of 70g.), random plasma glucose of 200 or greater w/ classic hyperglycemia symptoms. A1C is preferred, as it is a reflection of chronic diseases. (2-3 month reflection.)

2 3. Using the information form Rachel s medical record, identify the factors that would allow the physician to distinguish between T1DM and T2DM. The on-set of T1DM is usually at childhood, while T2DM on-set is more prominent in adulthood. T1DM is not associated with being over wt. or obesity. While T2DM is often associated with obesity. T2DM does not display the classic symptom of T1DM. Hyperglycemia may develop over time, with T2DM w/out any of the other symptoms. T1DM is associated with genetic, autoimmune, and environmental risk factors. T2DM is r/t inactivity, ethnicity, and hx. of HTN and/or vascular disease. T1DM requires insulin dependency, while T2DM may not also require insulin. Lab testing: A1C of 6.5 or greater, FPG of 126 or greater, 2 hour pp or pg greater than 200 during an OTGG (a glucose load of 70g.), random plasma glucose of 200 or greater w/ classic hyperglycemia symptoms. A1C is preferred, as it is a reflection of chronic diseases. (2-3 month reflection.) A positive lab value of IAA will indicate a dx. of T1DM. Rachel s IAA value was positive. Rachel s GADA value was positive, and her ICA value was also positive. Rachel s IA-2A was not reflective of change. These lab values are a determinate for dx. Rachel w/ T1DM. C-peptide testing may be ordered once a person is newly dx. w/ DM. C-peptide testing, in correspondence with an insulin level, is used as a determinant to establish how much insulin is still being produced by the pancreas. Rachel s C-peptide value was 0.10, which is below the range Meaning Rachel has a low level of insulin being produced by the pancreas. 4. Describe the metabolic events that lead to Rachel s symptoms and subsequent admission to the ER (polyuria, polydipsia, polyphagia, fatigue, and weight loss), integrating the pathophysiology of T1DM into your discussion. Polyuria is caused by excessive glucose that cannot be reabsorbed and is excreted, from the body by urine. Polyuria can also be caused by excessive intake of fluids. This can be from polydipsia, or extreme thirst/ excessive intake of fluids. Polydipsia is caused from hyperglycemia. Polyphagia is increased appetite, which can signal T1DM. Wt. loss is attributed the bodies inability to reabsorb glucose into cells for energy. This is r/t insufficient insulin evident in T1DM. As a result the body responds by using muscle and fat, as sources for energy. The result is decreased body wt. T1DM is the result of the body attacking its own beta cells, found in the pancreas. As the mass of the beta cells decrease, so does the insulin secretion. This results in insufficient insulin and inability to control blood glucose levels. Hyperglycemia will develop, after 80-90% of the beta cells have been damaged/destroyed. Autoimmunity is a main factor in the pathophysiology of T1DM. Viral infections, such as strep throat, can arouse production of antibodies in contradiction to viral proteins, which trigger an autoimmune response against similar beta cells. 5. Describe the metabolic events the 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? DKA can be caused by DM. This is due to insulin insufficiency and increased production of hormones such a glucagon. DKA can be caused by hyperglycemia, dehydration, electrolyte imbalance i.e. K+ and Na+, and acidosis. DKA is associated with polydipsia, polyuria, and wt. loss.

3 These can all be s/s of DKA. Rachel showed signs of slight confusion, her throat showed dry mucus membranes, her skin color was pale. These observations can be used for diagnosing DKA. I would say that Rachel was admitted, with this state. Infection and insufficient insulin or no insulin therapy would be precipitating factors. Rachel s undiagnosed T1DM played a role in her development of DKA. Onset of DKA occurs when minimal or no insulin to transport glucose into cells. This can raise BGL s 250mg/dL or higher. DKA can occur within a 24 hour period. 6. 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, 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 her friends do. What would you tell them? Apidra: insulin glulisine antidiabetic, hypoglycemic. Short acting, rapid onset insulin. Medication can be taken 15 minutes prior to meal or 20 minutes after meal has begun. Timing of injection is taken in relation to food/meals. Medication onset is w/in 15 minutes of injection and peaks after one hour. Medication will continue to be active for 2-4 hours for coverage r/t meals. Per reference. Glargine: Lantus: antidiabetic, hypoglycemic. Long acting form. Onset is 1.1 hours, with duration being 24 hours or continuous coverage, and peaks within 5 hours. Per reference. Rachel is to receive 1 unit of insulin for every 15 grams of carbohydrates. The 7u of glargine will correlate, with her meals. The Lanus or glargine is used to give her continuous coverage, to aide in controlling her BGL s. Rachel has T1DM, which means her body is not producing insulin. Medications are used for T2DM. Oral medications act as aides for insulin resistance and help the body in its ability to process insulin. If there is insufficient insulin secession and the body is attacking the beta cells, the oral medications will not provide any type of aide. The body needs insulin injections to aid in controlling BGL s, as the pancreas is not producing any insulin. 7. 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. The honeymoon phase is the period of time, after a person is diagnosed, with T1DM. The pancreas is still able to produce some insulin, which reduces insulin needs and helps with blood glucose control. The pancreas has a reduced requirement to produce insulin, when a pt. begins insulin injections. Due to the injections, the pancreas is stimulated to produce insulin from the beta cells that have not been destroyed. Through the next few weeks or months the remaining beta cells will be destroyed. Once all of the beta cells have been depleted the honeymoon phase will end. The pancreas will discontinue producing insulin to help, with controlling BGLs. During the honeymoon phase, the body has the ability to aide in the control of BGLs. These levels may return to a normal level. Insulin levels need to be adjusted after this period, as BGLs will change. A balanced needs to be accomplished with insulin injections in order to reduce the risk of developing hyperglycemia and/or hypoglycemia.

4 8. 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 does aide in improving the body s insulin sensitivity, increased utilization of glucose, and also reduces the production of glucose in the liver. Due to physical activities improving insulin sensitivity there is risk of hypoglycemia. This may develop from a few minutes to a few hours after the activity has concluded. Another risk is developing hyperglycemia. This is due to a large amount of counterrregulatory hormones, when high intensity activities are taking place. This causes glucose levels to become elevated and may last for several hours. This may mean a double dose of insulin to aide in controlling the high BGL. Rachel needs to track her BGLs. She needs to monitor her levels prior, during, and post physical activities. If her levels are above 250mg/dL, Rachel should be checked for ketones, due to hyperglycemia. If levels are high, Rachel should discontinue exercise until levels can be maintained/improved. The ketone level should be negative. Rachel may need to bring a carbohydrate snack in relation to decreased BGLs caused by physical activity. Rachel does play soccer, which would be considered moderate to high intensity. For moderate activities of minutes, 15g of CHO should be consumed, for every hour of activity. Also, for high intensity activities of 60minutes Rachel should consume 30-50g, of CHO per hour of activity. CHO that is consumed during long bouts of exercise can improve performance. Rachel also needs to remain hydrated, throughout the day. Rachel s short acting insulin may need to be decreased by 1-2 units, when she participates in moderate activities, that last minutes in length. If Rachel participates in high intensity activities, her daily insulin dosage may need to be decreased by 15%-20%. 9. 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? It is the abnormal effect of increased or high BGL s in early mornings, for pt. diagnosed with DM. The elevated BGLs may be related to the secretion of growth hormones, glucagon, cortisol, and epinephrine. These rises by contribute to insulin resistance, which may cause an elevation in BGLs. Another cause may be a lack of insulin prior to sleep. This may cause increased levels, in the am. Insufficient insulin medications or a CHO snack at bedtime may cause an increase in BGLs. Rebound or the Somogyi effect: It is the rebound of high BGLs levels, as a response to low BGLs. This by be caused by injections of insulin from the prior night. There is excess insulin resulting in elevated BGLs in the am. Hypoglycemia may happen in the evening and in response hyperglycemia may occur, in am. Rachel has had consistent high BGLs in the am. This could be an indicator that she is experiencing the dawn effect. However, she has not had prolonged problems with untreated hypoglycemia. I would decline Rachel is experiencing the Somogyi effect. Rachel can prevent the dawn effect by not consuming a CHO snack prior to sleep. She may also need to adjust her insulin dosage or time of dosage, to avoid the dawn effect. If problems continue to persist, Rachel may need to consider a change in insulin or starting an insulin pump to offer more coverage of insulin in the am.

5 10. The MD ordered a consistent carbohydrate-controlled diet when Rachel begins to eat. Explain the rationale for monitoring carbohydrate in diabetes nutrition therapy. The methodology is to base her rapid acting insulin dosing, with her snacks or meals. Consistent CHO counting allows for more flexibility, when snacks or meals are consumed. There is also an improved match of insulin bolus, with her CHO intakes. This may reduce post-prandial hyperglycemia and hypoglycemia. Constant CHO counting is used to determine the needed insulin per the amount of CHO consumed. Rachel may need to follow the 1700 rule, as a correction factor. The primary focus is for Rachel to achieve normal BGLs. 11. Outline the basic principles for Rachel s nutrition therapy to assist in control of her T1DM. Maintain BGLs within normal ranges or remain at a safe range. Maintain a lipid profile that reduces risk of developing vascular disease. Maintain normal blood pressure levels or at a safe range. Prevent the development or onset of chronic complications, by modification of lifestyle and nutrient changes. Integrate pt. nutritional needs, with pt. preferences and adaptability to the recommended changes. Provide adequate Kcals for the maintaining of body wt, growth and development. Create a constant CHO diet that allows flexibility and meets the pts nutritional needs. Provide education for safely participating in physical activities, with the inclusion of preventing and treating hypoglycemia, when using insulin injections. Provide education for treatment during sick days. Insulin to CHO ratio- 1:15 (1 unit of insulin per 15 grams of CHO) Educate on correction factor of the 1700 rule. Education in reference to reading food labels. Education and comprehension of relationship between physical activity, food, and medications. How these factors contribute to BGLs. Initial base of 3-4 CHO per meals and 1-2 per snack. Monitor for adjustments. Minimum of 130g/day of CHO. >5g/serving of fiber. (fruits and vegetables, and whole grains. Protein intake of 15-20% of diet. Reduce intake of saturated fatty acids as they may delay gastric emptying. Fat intake of 25-35% (total fat) Monitor BGLs prior meals and 2 hrs. after first bit of meal. 12. Assess Rachel s ht/age; wt/age; ht/wt; and BMI. What is her desirable weight? Ht/age % of ht: 50 th -75 th percentile (54 th ht percentile) Wt/age % of wt: 25 th -50 th percentile (27 th wt percentile) BMI: 16 % of BMI: 17 th percentile Healthy Wt. Desirable wt: Healthy wt. BMI percentile range for healthy 12yrs. girl is 5 th %tile to the 85 th %tile. Rachel does fall into the ranges for a healthy wt. However, I would monitor her wt. as she is at the lower end of the spectrum. Any further wt. loss may lead to her becoming under wt. If Rachel was to gain wt, until she reaches a wt. of 93# to 95#. This would put her in the 50 th percentile range.

6 13. Identify any abnormal laboratory values measured upon her admission. Explain how they may be related to her newly diagnosed T1DM. Sodium Ref. 136 to /4 126 decreased 5/5 131 decreased May be a sign of DKA. Glucose Ref /4 683 increased 5/5 250 increased Elevated levels are used with (+) urine test of glucose to dx. T1DM. Phosphate Ref /4 1.9 decreased 5/5 2.1 decreased Reflective of possible DKA and/or hyperglycemia. Osmolality Ref / increased 5/5 304 increased Sugars may spill into urine and take Na and K+ with them to be excreted. This lead to polyuria, dehydration and polydipsia. HbA1c Ref / increased Indicator of diabetic nephropathy. Shows long term glucose exposure. May be used as a guide for management. C-peptide Ref / decreased Correspondence with an insulin level is used as a determinant to establish how much insulin is still being produced by the pancreas. ICA 5/4 (+) Reflective (+) for dx of T1DM. GADA 5/4 (+) Reflective (+) for dx of T1DM. IAA 5/4 (+) Reflective (+) for dx of T1DM. Specific gravity Ref / increased ph Ref /4 4.9 decreased Reflective of possible DKA. Protein Ref. Neg 5/4 100 increased Reflective or hyperglycemia and kidney function Glucose Ref. Neg 5/4 (+) A (+) result is used with elevated levels of glucose to dx T1DM. Ketones Ref. Neg 5/4 (+) Dx. of hyperglycemia can be used as a marker for DKA and insulin resistance. Prot chk Ref. Neg 5/4 (+) Reflective hyperglycemia and kidney function 14. Determine Rachel s energy and protein requirements. Be sure to explain what standards you used to make the estimation. Used Bayler website to determine energy and protein needs. Energy needs based on high activity: 2593 kcal per day. Discretionary: 410 kcal per day. Protein needs based on high activity: 7g per day.

7 15. Prioritize two nutrition problems and complete the PES statement for each. Altered nutrition-related laboratory values: Glucose 683, HbA1c 14.6, C-peptide.10, ICA +, GADA +, IAA +, Glucose urinalysis +, ketones + (NC 2.2) RT new dx of T1DM AEB polyuria, polydipsia, and polyphagia, and wt. loss. Food-and nutrition-related knowledge deficit (NB 1.1) RT acute on-set of hyperglycemia AEB abnormal laboratory values Glucose 683, HbA1c 14.6, Glucose urinalysis +, ketones Determine Rachel s initial nutrition prescription using her diet record from home as a guideline, as well as your assessment of her energy requirements. Energy Requirements: 2593 Kcal per day (very active factor included) Pt. to consume 5-6 meals/snacks daily. 2-4 CHO choices per meal grams of CHO 2 CHO choices per snack. 30 grams of CHO Minimum of 130 grams of CHO per day. Diet consists of % of CHO Diet consists of 10-20% of Protein Diet consists of <30% of Fats and <7% of SFA 6-8 8oz glasses of fluids/water daily Current diet Breakfast: 2-4 CHO choices example: 1 small banana 15 grams, 8 oz milk 15 grams, 1 Pop Tart 30 grams Total CHO: 60 grams Lunch: 2-4 CHO choices: 1/2 peanut butter and jelly Sandwich (1 slice bread 15 grams) Whole Grain Bread, jelly 1 Tbsp 15 grams Raw carrots 1 cup 5 grams of CHO Potato Chips: chips 15 grams Protein/Fat: 1 tablespoon peanut butter Fluid: 8oz of water Total CHO: 50 grams Snack 1: 2 CHO: Granola Bar 30 grams Fluid: 8oz of water Total CHO: 30 grams Practice: 2 8oz fluids during practice (water and Gatorade) Supper: 2-4 CHO choices example: 2/3 cup brown rice 30 grams, 1 cup lettuce 5 grams Protein: 3oz chicken breast Fluid: 8oz fluid with meal Total CHO: 35 grams Snack 2: 2 CHO: 3 cups popcorn 15 grams, 1 Fresh Fruit example apple 15 grams

8 Fluid: 8oz of water Total CHO: 30 grams 17. 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 8oz skim milk, how much Apidra should she take to cover the carbohydrate in this meal? Insulin: CHO ratio is a basis, which for every 15 grams of CHO 1 unit of rapid-acting insulin needs to be injected, in order to match the amount of CHO consumed. 2 Pop-tarts is 60 grams (30 grams per pop-tart) 8oz milk 15 grams Total CHO: 75 grams 5 units of Apidra are needed to cover the 5 CHO or 75 grams of CHO. 18. Dr. Cho set Rachel s fasting blood glucose goal at mg/dl. If her total daily insulin dose is 33u and her fasting a.m. blood glucose is 240 mg/dl, what would her correction does be? 1700/33=51.5 or 52 One unit of insulin will lower blood glucose by 52 mg/dl. Rachel would need to 2 doses to lower her blood glucose level between the mg/dl = mg/dl. 19. Write an ADIME note for your initial nutrition assessment. See on following page. 20. When Rachel comes back to the clinic, she brings the following food and blood glucose record with her. See Chart Below for answers for A, B, C. A. Determine the amount of carbohydrate she is consuming at each meal. B. Determine whether she is taking adequate amounts of Apidra for each meal according to her record. C. Calculate a correction dose for her to use. Time Diet Grams CHO 7:30 am 2 pop-tart 1 banana 16 oz skim milk Ovaltine 2oz 10:30am 12 noon 2 slices peperoni pizza 2 choc. Chip cookies water Total Total 100 Exercise BG (mg/dl) (Pre) 150 No correction Insulin Dosages What What you Pt. Took recommend 5 u Apidra 8.6 or /15=8.6 (Pre) u Apidra 7 or 8 100/15= unit =7 or8

9 2pm Granola Bar 20 PE class 30 minutes 4:30pm 5-6:30pm 6:30pm 8:30pm 10:30pm Apple (med) 6 saltines 2tsp peanut butter 16oz Gatorade Chicken with Broccoli stir-fry (1 cup fried rice, 2 oz chicken, ½ cup broccoli) Egg Roll-1 2 cups skim milk 2 cups ice cream 2 tbsp peanuts Bed Total Total Soccer Practice 1.5 hours None Due to exercise (Pre) 110 No correction (Pre) 140 (Pre) =60 (Pre) 150 No correction 40/15=2.66 Soccer practice in 30 minutes 5 u Apidra 5 or 6 99/15= unit 5 or 6 4 u Aprida 4.3 o 4 65/15=4.3 References Type 1 Diabetes. (n.d.). Retrieved March 21, 2015, from google&utm_medium=cpc&utm_term=type 1 diabetes&utm_campaign=m_general Diabetes&utm_content Mayo Clinic Staff. (n.d.). Type 1 diabetes. Retrieved March 21, 2015, from Graves Disease.(2014, May 30). Retrieved March 21, 2015, from Diabetes Care. JANET SILVERSTEIN, MD1GEORGEANNA KLINGENSMITH, MD2KENNETH COPELAND, MD3LESLIE PLOTNICK, MD4FRANCINE KAUFMAN, MD5LORI LAFFEL, MD, MPH6LARRY DEEB, MD7MARGARET GREY, DRPH, CPNP8BARBARA ANDERSON, PHD9LEA ANN HOLZMEISTER, RD, CDE10NATHANIEL CLARK, MD, MS, RD.(n.d.). Retrieved March 22, 2015, from Diabetes-related Autoantibodies. (2015, January 1). Retrieved March 22, 2015, from

10 C-peptide. (n.d.). Retrieved March 22, 2015, from Type 1 Diabetes Mellitus. (2015, January 1). Retrieved March 22, 2015, from Polyuria - Frequent Urination. (2015, January 1). Retrieved March 22, 2015, from Unexplained Weight Loss. (2015, January 1). Retrieved March 22, 2015, from Diabetic Ketoacidosis. (2015, January 1). Retrieved March 22, 2015, from Apidra(R)(insulin glulisine [rdna origin] injection) Dosing. (2015, January 1). Retrieved March 22, 2015, from Honeymoon Phase. (2015, January 1). Retrieved March 22, 2015, from Castro, M. (n.d.). Diabetes. Retrieved March 22, 2015, from Somogyi Phenomenon - Rebound Hyperglycemia. (2015, January 1). Retrieved March 22, 2015, from Maahs, D., Owen, D., & Bishop, F. (n.d.). Carbohydrate Counting in Youth with Type 1 Diabetes. Retrieved March 22, 2015, from hing-keystone2008/owen_maahs_bishop.ppt Diabetes Care. (2007, January 1). Retrieved March 22, 2015, from Retrieved March 22, 2015, from ender=2&method=0&inchtext=0&wttext=0 Lamb, W. (2013, September 30). Pediatric Type 1 Diabetes Mellitus Treatment & Management. Retrieved March 22, 2015, from Krause s Food and Nutrition Therapy. CHAPTER 31 ppt. Medical Nutrition Therapy. Mellitus and Hypoglycemia of Nondiabetic Origin.

11 Carissa Schwandt ADIME Note A: 12 yo. pt. arrived at ER, after fainting at soccer practice. Admitted c acute-onset hyperglycemia. Admission serum Glucose level 724 mg/dl. Reports polyuria, polydipsia, polyphagia, fatigue, and wt. loss. Pt. states wt. loss r/t recent dx. of strep throat. Pt. is highly active and participates in soccer events. Per parent statement eats balanced meals at mother s house. Father s house consists of ordering in high fat foods. Household: mother, father, sister, and brother. Family hx: Father-HTN, mother-hyperthyroidism, sister-celiac disease. 12 yo. Female Admitting dx. acute-onset hyperglycemia dx of T1DM Ht: 5 or 60 wt. 82# wt. hx 90# Ht/age % of ht: 50 th -75 th percentile (54 th ht percentile) Wt/age % of wt: 25 th -50 th percentile (27 th wt percentile) BMI: 16 % of BMI: 17 th percentile Healthy Wt. Diet Order: NPO than progress to clear liquids and then consistent carbohydrate-controlled diet. Fluid Requirement: 1840mL. EER: 2593 kcal per day. Discretionary: 410 kcal per day. Protein: 7g per day. Pertinent Meds: Regular insulin 1 unit/ml NS 40 meq 135 ml/hr. Apidra 0.5 every 2 hrs. until glucose is mg/dl, glargine 6 u. Discharge Dosage: 7 u glargine c Apidra 0.5 prior to each meal/snack. Insulin: CHO ratio 1:15. Pertinent Labs: Sodium 126, Glucose 683, Osmolality 295.3, HbA1c 14.6, C-peptide 0.10, ICA (+), GADA (+), IAA (+). Urinalysis: Specific gravity 1.035, ph 4.9, Protein 100, Glucose (+), Ketones (+), Prot chk (+). D: Altered nutrition-related laboratory values: Glucose 683, HbA1c 14.6, C-peptide.10, ICA +, GADA +, IAA +, Glucose urinalysis +, ketones + (NC 2.2) RT new dx of T1DM AEB polyuria, polydipsia, polyphagia, & wt. loss. Food-and nutrition-related knowledge deficit (NB 1.1) RT acute on-set of hyperglycemia AEB abnormal laboratory values Glucose 683, HbA1c 14.6, Glucose urinalysis +, ketones +. I: The pt. individual recommended dietary intake of energy & selected foods & nutrients based on current reference standards & dietary guidelines & the pt. health & nutrition diagnosis of T1DM. (NP 1.1) Educate pt./family on constant CHO diet. Consume 5-6 meals/snacks c 2-4 CHO per meal & 2 CHO per snacks, minimum of 130g CHO per day. Establish a diet plan, which includes pt. likes & nutritional needs/requirements 2593 Kcal & 7g protein per day. Educate on importance of hydration 1840ml fluids per day. Encourage carrying snack r/t potential of low BGLs. Initiate a food record & activity record. Education of monitoring BGL prior to meal & 2hrs post first bit. Education on correction factor, times of dosage & amount. Education r/t Dawn effect. Referral to Social Worker (RC 1.5) for potential depression r/t separation of parents and pt. status r/t potential psychological distortion of body image. M/E: Upon Discharge, schedule follow-up c RD, in 2 wks. to monitor: wt (AD 1.1.2), energy intake (FH ), Meal/snack pattern (FH ), total protein (FH ), total carbohydrate (FH ), Insulin-to-carbohydrate ratio (FH ), modified diet order (FH ), self-monitoring at agreed upon rate (FH 5.1.4), physical activity history (FH 7.3.1).