Ntrs 415b Case Study Paper Final

Running head: PEDIATRIC TYPE 1 DIABETES MELLITUS CASE STUDY
Pediatric Type 1 Diabetes Mellitus Case Study

Spring Quarter 2015
California State University, Los Angeles
2
PEDIATRIC TYPE 1 DIABETES MELLITUS CASE STUDY
PI:
RR is a 12 YOWM with acute-onset hyperglycemia admitted to CSULA Hospital through the ER on
May 4th, 2015.
CC:
I have just gotten over strep throat a few days ago. I felt like I was well enough to go to soccer practice
today but after playing about 15 minutes, I just felt horrible. I sat down and they tell me I fainted...I
have been really thirsty-- thirstier than I have ever been in my whole life and then I have had to use the
bathroom a lot...I even have to get up at night to go to the bathroom.
HPI:
Previously in good health. After incidence of strep throat, patient polydipsia and polyuria especially
during the night. After 15 minutes of physical activity, RR sat down and fainted and was then taken to
ER.
PMH:
No medications at home. No surgical history. April 2015- strep throat.
FH:
Father- HTN; Mother- hyperthyroidism; Sister- celiac disease.
SH:
Single 7th-grade student who participates on a soccer team. Does not use alcohol, drugs, or cigarettes.
Lives with mother, sister age 8, and brother age 4. Parents are divorced. Father lives in city and shares
custody. When at home Mom normally prepares dinner. When with her Father, she usually eats ordered
in pizza or Chinese food.
PE:
ER assessment reveals a serum glucose of 724 mg/dL (H); Neurologic: Alert but slightly confused.
Glasgow coma scale: 15; Resp. rate: 22 (H); BP: 122/77 (WNL); Pulse: 101(H); Temp: 98.6 (WNL);
Chest/Lungs: Respirations are rapid- clear to auscultation and percussion; Peripheral vascular: pulse 4+
bilaterally, no edema; Abdomen: Active bowel sounds x4; tender, non-distended; HEENT: Head: WNL;
Eyes: PERRLA; Ears: clear; Nose: clear; Throat: Dry mucous membranes without exudates or lesions;
Skin: warm and dry; Urine: Cloudy, amber appearance; Skin temperature: diaphoretic (DI); Weight: 82
lbs
Assessment
Problem list: Diagnosis of acute hyperglycemia related to diabetes mellitus
3
Patient Treatment Course

Date: 5/4/15
Diagnosis: Acute-onset hyperglycemia
Medications: Regular insulin 1 unit/mL NS 40 mEq KCl/liter @ 35 mL/hr. Begin infusion at 0.1
unit/kg/hr = 3.7 units/hr and increase to 5 units/hr. Flush new IV tubing with 50 mL of insulin drip
solution prior to connecting to patient and starting insulin infusion.
Labs: phosphate (1.9 mg/dL-low); glucose (683 mg/dL-high); Urinalysis: specific gravity (1.035-high),
pH (4.9-low), protein (100 mg/dL-high), glucose (positive), ketones (positive), Prot chk (positive); Islet
cell antibodies screen: ICA (positive), GADA (positive), IAA (positive); sodium (126 mEq/L-low); Cpeptide (0.10 ng/mL-low); Hemoglobin A1C (14.6%-high); osmolality (295.3 mmol/kg/H20 -high).
Diet or Nutrition Order: NPO except for ice chips and medications. After 12 hours, clear liquids if
stable. Then, advance to consistent carbohydrate diet order: 70-80 g breakfast and lunch, 85-95 g dinner,
and 3-15 g snacks. 1840 mL fluid requirement.
Medical treatment plan: Consult diabetes education team for self-management training for patient and
parents to begin education after stabilized.
Brief nutrition assessment: Mom and Dad state RR is kind of a picky eater. She eats only chicken and
fish--eats salad, broccoli, carrots, tomatoes, and asparagus as her only vegetables. Breakfast consists of
cereal and milk or Pop-Tart with milk. Normally packs lunch for school which includes a peanut butter
and jelly or turkey and cheese sandwich, chips, carrots, and water. RR has cereal or a granola bar before
practice and drinks water throughout practice. RRs dinner is usually prepared by her mom when she is
at her house and includes some salad, meat, and pasta, potato, or rice. When RR eats dinner with her
father she usually eats ordered in pizza or Chinese food. RRs typical snacks include cereal, ice cream,
yogurt, some fruit (apples, bananas), popcorn, chips, or cookies.
Medical Nutrition Therapy plan: Consult diabetes education team for self-management training for
patient and parents to begin education after stabilized.
Date: 5/5/15
Diagnosis: New Diagnosis Type 1 Diabetes Mellitus
Medications: Change IVF to D5.45NS with 40 MEq K @ 135 mL/hr. Begin Apidra 0.5 units (for high
blood glucose) every 2 hours until glucose is 150-200 mg/dL. Tonight begin glargine 6 units at 9 PM (to
keep blood glucose low overnight). Progress Apidra using ICR 1:15.
Labs: Sodium (131 mEq/L- low), Glucose (250 mg/dL-high), Phosphate (2.1 mg/dL -low), osmolality
(304 mmol/kg/H20 -high).
4
Diet or nutrition order: Consistent carbohydrate controlled diet

Medical treatment plan: Continue bedside glucose checks hourly. Notify MD if blood glucose >200
mg/dL or <80 mg/dL.
Medical Nutrition Therapy: Referral to Certified Diabetes Educator.
Prognosis: Type 1 diabetes mellitus is a lifelong disease with no cure. Tight control of blood glucose
can prevent or delay diabetes complications.
Theoretical Discussion of Disease Processes
Type 1 Diabetes Mellitus (T1DM) is an autoimmune disease that occurs when an individuals
immune system attacks its own beta cells in the pancreas that are responsible for producing insulin.
T1DM accounts for 5%-10% of all cases of diabetes and is most commonly developed in children or
adolescents like our 12 year old patient, RR (Nelms, Sucher, & Lacey, 2014, p. 481).
Although the etiology for T1DM is still unclear, polymorphisms in the human leukocyte antigen
(HLA) complex account for 40-50% of the genetic risk of developing T1DM. In looking at RRs family
medical history it is noted that her mother has hyperthyroidism and that her sister has celiac disease.
Both of these diseases are autoimmune diseases like T1DM and therefore could indicate that RR has a
genetic component for autoimmune diseases in her family. For those who are susceptible to developing
T1DM, the onset of the disease can be triggered by many environmental factors including viruses,
gluten, vitamin D levels, the length of breastfeeding, and exposure to cows milk during infant feeding
(Nelms et al., 2014, p. 481).
Individuals with T1DM suffer from many symptoms. Due to the inability of damaged pancreatic
beta cells to produce insulin, glucose is unable to enter the cells. As a result, hyperglycemia (high blood
glucose) and cellular starvation occur. The body incorrectly perceives that this starvation is due to a lack
of glucose, so polyphagia, or the promotion of hunger, occurs in order to increase the amount of glucose
available to the cells. This was evidenced in RR as she stated that she has been more hungry than
usual. However, despite an increase in food intake, cells are still unable to absorb glucose due to the
lack of insulin. Therefore, the body will respond by beginning the process of gluconeogenesis or the
making of glucose from noncarbohydrate sources.
In gluconeogenesis, the body uses fat through the process of lipolysis to break down stored
triglycerides in the blood to fatty acids that can be converted to keto acids in the liver. In a normal state,
these ketone bodies are used as energy for the brain and muscles. However, in the case of an individual
with T1DM, an overproduction of ketone bodies occurs, causing a decrease in pH. The body
compensates for this fall in pH by excreting the ketone bodies in the urine. Bicarbonate levels also fall
5
as bicarbonate is used for further pH regulation of these ketone bodies causing a form of metabolic
acidosis called diabetic ketoacidosis (DKA). In order to compensate for DKA, individuals, like our
patient during soccer practice, will undergo deep, labored breathing, referred to as Kussmaul
respirations, to exhale excess CO2 that was formed in the blood. If the body is in a state of
hyperventilation for too long, then eventually a diabetic coma will occur. This is what RR experienced
prior to being taken to the ER. Gluconeogenesis also results in the degradation of protein to amino acids
causing muscle wasting. RR also suffered from this condition as evidenced by her recent weight loss of
8 lbs (or 8.9% of her body weight) in less than 1 month (Nelms et al., 2014, p. 481-482).
As gluconeogenesis increases the amount of glucose in the blood, the body compensates for this
hyperglycemic state through glycosuria (urinating glucose). As glucose levels in the kidney tubules
increase it causes an increase in the osmotic pressure in the tubule resulting in polyuria (frequent
urination). This was true for RR as she complained of using the bathroom a lot, including during the
middle of the night. As the kidney tubules absorb more water, body fluid is also lost (called
hypovolemia) which results in a decrease in the extracellular fluid volume and arterial blood pressure.
Additionally, as water leaves the cells it is followed by ions like potassium, sodium, magnesium, and
phosphorous resulting in an increase in serum osmolality. These two factors trigger the reninangiotensin-aldosterone system that causes polydipsia (or excessive thirst) to make up for the loss of
water. RR also experienced polydipsia, as she complained of being really thirsty--thirstier than she had
ever been in her whole life. Hypovolemia is another cause of weight loss that also occurred in RR. If
hypovolemia is left untreated and results in more than of the bodys fluid being lost it can result in
hypovolemic shock which leads to death (Nelms et al., 2014, p. 481-482).
Pertinent Laboratory Findings
Pertinent laboratory findings include elevated serum chemistry levels of glycosylated hemoglobin (A1c)
and glucose. A1c values reflect the patients average blood glucose level over the last 2-3 months. The
range from 5.7% to 6.4% indicates prediabetes, and values of 6.5% or higher indicate diabetes
(American Diabetes Association [ADA], 2015b). The patients A1c level of 14.6% puts her in the
diabetic range. Plasma glucose levels can be determined via several measures, including fasting plasma
glucose (FPG), 2-hour post-prandial glucose, and random plasma glucose (RPG). FPG is measured after
at least eight hours of food and fluid restriction (except water). Normal levels fall below 100 mg/dL.
Prediabetes is diagnosed at levels of 100-125 mg/dL, and diabetes is diagnosed at levels of 126 mg/dL
or higher (ADA, 2015b). The two-hour postprandial glucose measured via an oral glucose tolerance test
(OGTT) can also be used to diagnose diabetes. Normal levels fall below 140 mg/dL, prediabetes levels
6
range from 140-199 mg/dL, and diabetes levels are 200 mg/dL or higher (ADA, 2015b). A RPG greater
than or equal to 200 mg/dL, when paired with physical symptoms of diabetes, also indicates diabetes
(U.S. Department of Health and Human Services [HHS], National Institutes of Health [NIH], National
Institute of Diabetes and Digestive and Kidney Diseases [NIDDK], National Diabetes Information
Clearinghouse [NDIC], 2014). RRs initial RPG on 5/4 was measured at 683 mg/dL, diagnosing her as
diabetic.
Additional valuable serum chemistry measurements include those of islet cell autoantibodies.
Presence of such autoantibodies indicate the self-destruction of the bodys own beta cells, which
produce and secrete insulin. Thus, they are often used as markers for T1DM. There are three forms of
these autoantibodies: glutamic acid decarboxylase autoantibodies (GADA), islet cell autoantibodies
(ICA), and insulin autoantibodies (IAA) (Nelms et al., 2014, p. 487). The patient tested positive for all
three. The apparent destruction of her beta cells inhibits the release of insulin in response to increasing
levels of blood glucose. This phenomenon helps to explain her hyperglycemia.
Another serum chemistry measurement is that of C-peptide. This peptide is linked with insulin
when first produced by the pancreas, and thus, there are usually about equal amounts of the two in the
blood. Measuring C-peptide is used to determine the amount of insulin within the blood. Normal levels
range from 0.5 to 2.0 ng/mL (U.S. National Library of Medicine [NLM], 2014). Patients with T1DM
produce little to no insulin, so their C-peptide levels are generally below normal. On the other hand,
T2DM patients generally have normal or high levels of C-peptide. The patients C-peptide is very low
(0.10 ng/mL), which is indicative of T1DM.
Due to polyuria, ions are lost in the urine. As a result, decreased plasma levels of potassium,
sodium, magnesium, and phosphorus can be seen. Normal serum levels of potassium are 3.5-5.5 mEq/L.
Normal levels of sodium are 136-145 mEq/L. Normal levels of magnesium are 1.8-3 mg/dL. Normal
levels of phosphorus are 2.3-4.7 mg/dL (Nelms et al., 2014, p. 131). Laboratory results show the patient
has normal levels of potassium (4.3 mEq/L) and magnesium (1.9 mg/dL). Sodium and phosphorus are
below normal at 126 mEq/L and 1.9 mg/dL. Normal serum osmolality is 285-295 mmol/kg/H20. Water
loss due to frequent urination and high blood sugar both increase osmolality (NLM, 2013a). For these
reasons, laboratory results show a high osmolality of 295.3 mmol/kg/H20 for the patient.
Pertinent urinalysis laboratory values are as follows. In response to hyperglycemia, the body
excretes the excess glucose in the urine (glycosuria) (Nelms et al., 2014, p. 481). Non-diabetic
individuals will test negative for urinary glucose, while our patient tested positive. Additionally, the
formation of keto acids from the breakdown of fat for energy usage occurs due to T1DM insulin
7
deficiency. Increased levels of keto acids cause ketone bodies to be excreted in the urine (Nelms et al.,
2014, p. 481). Non-diabetic individuals test negative for urinary ketones. The patients positive urinary
ketone test is indicative of her T1DM. The presence of these ketone bodies decreases pH. Normal pH
falls between 5 and 7, and the patients pH is below normal (4.9). Protein may be present in the urine as
a result of overworking of the kidney filtration system from high blood glucose. Overworking can cause
the kidneys to lose their filtering ability and may lead to kidney disease (ADA, 2015c). Protein is not
present in the urine of healthy individuals and its presence can be an indicator of diabetes. The patients
urine tested positive for a high level of protein, as indicated by a positive protein check and urinary
protein concentration of 100 mg/dL. The presence of glucose, ketones, and protein in the urine increases
specific gravity. The normal ranges for specific gravity is 1.003-1.030, and the patients laboratory value
is above normal at 1.035 (NLM, 2013b).
Medical/Dietary Treatment, Prescribed Drugs, Drug Classifications, Indications for Use
There is no cure for type 1 diabetes mellitus. Only through medication, correct planning of
meals, and proper exercise can this disease be managed. Injectable insulin is the only medical treatment
that assists in bringing a T1DM patients blood glucose down to an acceptable range (ADA, 2015a).
Unlike patients with T2DM, T1DM patients are not able to take oral medication because these
medications act on the pancreas to secrete more insulin or make the cells more sensitive to any insulin
being secreted (ADA, 2015a). Due to the lack of insulin being produced, none of these oral medications
would prove useful in treating T1DM.
There are four different types of insulin used to treat T1DM, including regular or short-acting
insulin, rapid-acting insulin, intermediate-acting insulin, and long-acting insulin (ADA, 2015d). Regular
or short-acting insulin begins to work 30 minutes after injection, peaks from 2-3 hours, and is effective
for about 3-6 hours. Examples include Humulin R and Novolin R. Upon admittance to the hospital, RR
was given regular insulin at 1 unit/mL with NS (normal saline) with 40 mEq KCl/liter @ 135 mL/hr.
Infusion began at 0.1 unit/kg/hr to equal 3.7 units/hr and increase to 5 units/hr. While daily insulin
dosage is estimated by dividing the patients weight in pounds by 4, RR was given a much larger dose in
order to combat her very high blood glucose of 683 mg/dL.
During RRs second day at the hospital, the MD ordered a rapid-acting insulin (Apidra) at 0.5
units every 2 hours until her blood glucose fell between the range of 150-200 mg/dL. Rapid-acting
insulin begins 15 minutes after injection, peaks in about 1 hour, and will continue to work for 2-4 hours
(Diabetes Education Services [DES], 2015). Examples of rapid-acting insulin include glulisine (Apidra),
lispro (Humalog), and aspart (NovoLog). In addition to the Apidra, a long-acting insulin was instructed
8
to be given at 6 units at 9 PM. Long-acting insulin takes effect several hours after injection and lowers
blood glucose levels evenly across a 24-hour period (DES, 2015). Detemir (Levemir) and glargine
(Lantus) are examples of long-acting insulin. The combination of multiple daily injections (MDIs) of
rapid-acting insulin in addition to once a day bolus long-lasting insulin is a more common practice of
diabetes management called intensive insulin therapy (Nelms et al., 2014, p. 490). While this method of
treatment is more common, many other combinations of insulin regimes can be recommended
depending on lifestyle factors, age, body type, and insulin sensitivity.
Insulin can be injected via insulin pens, syringes, or through the use of an automated pump.
Determining factors such as an individuals insulin-to-carbohydrate ratio (ICR) and meal time
preferences are crucial to designating appropriate insulin dosage (Nelms et al., 2014, p. 490). An insulinto-carbohydrate ratio tells you how much one unit of rapid acting insulin will cover for the
carbohydrates eaten (Fraser Health, 2009). Using this ratio, total carbohydrates eaten daily is divided by
the factor to get an estimated insulin dosage (King & Armstrong, 2007). For RR, an ICR of 1:15 was
determined by her healthcare team prescribed with the fast-acting insulin, Apidra. This ratio is
appropriate per the Merck Manual recommendations for 6-12 year olds with T1DM (Calabria, 2014).
The consistent-carbohydrate diet was additionally ordered during her hospitalization, with 70-80 g
carbohydrates for breakfast and lunch with 85-95 g for dinner. The consistent-carbohydrate diet focuses
on the amount of carbohydrates in the diet and motivates those with diabetes to read food labels, count
carbohydrates, and better manage their blood glucose level (Fraser Health, 2009). RR was given a total
of 225-255 g of carbohydrates per day, which is an appropriate amount per her height, weight, and age.
Final Nutrition Care Plan
Sex: Female
Age: 12 YO
Height: 5
Weight actual: 82#
Weight usual: 90#
Weight ideal: 100#
Weight adjusted: 95#
%IBW: 82%
%UBW: 91%
Recent weight changes & causes: Recent 8 pound weight loss, due to T1DM (unintentional weight
loss)
9
% weight lost/gained: lost 8.9%

PT: Underweight
Serum albumin: 3.7 g/dL (WNL)
Total lymphocyte count: 18% (WNL)
Nutritional Diagnoses
1. Impaired nutrient utilization (NC 2.1) RT compromised endocrine function of the pancreas AEB
hyperglycemic blood glucose lab values of 683 mg/dL on admission.
2. Unintended weight loss (NC 3.2) RT malabsorption of glucose AEB severe weight loss of 8.9%
of her body weight in less than one month.
3. Food and nutrition related knowledge deficit (NB-1.1) RT lack of exposure to information AEB
new diagnosis of diabetes and hyperglycemic blood glucose level of 683 mg/dL.
Diet History
Changes in dietary habits due to medical problems: Consistent-carbohydrate controlled diet
along with newly instituted insulin regimen.
Chewing/swallowing abilities: Normal
Loss of teeth: No
Changes in taste/smell: None
Change in appetite: Normal
Presence of nausea/vomiting: No
Presence of constipation/diarrhea: None
Food allergies/intolerances: None
Previous instruction on therapeutic diet/comprehension/compliance: None, until recently
diagnosed with T1DM.
Voluntary attempts at dietary changes: None
Use of dietary supplements: None
Routine exercise: Plays soccer and participates during P.E classes.
Physical handicaps/assistance feeding: No
Evaluation of Laboratory Findings
According to the ADA (2015b), formal diagnosis of diabetes is determined by the following lab values:
A1c, FPG, 2-hour postprandial glucose, and/or RPG levels. The patients above normal A1c (14.6%) and
serum glucose (636 mg/dl) are used to diagnose her diabetes. Patient RRs positive ICA, GADA, and
IAA values imply that she is a type 1 diabetic, due to her destructive autoimmune-like disease,
10
previously mentioned. The low measurement of C-peptide (0.10 ng/mL) correlates with low insulin
secretion, as these two particles are secreted together by the pancreas.
Insulin infusion appears to be improving serum chemistry levels based on two days laboratory
results. Plasma glucose is trending downward, as seen in a decrease from 683 mg/dL to 250 mg/dL.
Though this change indicates improvement, plasma glucose remains at hyperglycemic levels.
Additionally, serum sodium increased from 126 mEq/L to 131 mEq/L, and phosphate increased from 1.9
mg/dL to 2.1 mg/dL. The patient has a net positive (+900) intake/output since admission. Her fluid
retention accounts for her increasing serum sodium and phosphate levels. Potassium and magnesium
levels were within normal limits upon admission and have remained within appropriate range. The
initial magnesium level of 1.9 mg/dL was near the lower limit of 1.8 mg/dL, but results show an
increase to 2.1 mg/dL after 24 hours. Serum osmolality was 295.3 mmol/kg/H20 upon admission and
increased to 304 mmol/kg/H20. Both of these values are higher than the normal range. Although RRs
plasma glucose levels have decreased, her serum osmolality is trending upward due net fluid loss on 5/5.
Resultant hypovolemia, along with the increase in ions, such as sodium, phosphate, and magnesium, has
led to increased blood osmolality.
Urinalysis values were also indicative of T1DM. To compensate for hyperglycemia, excess
glucose is lost in the urine. This explains the patients positive result for urinary glucose. RRs urine also
tested positive for ketones. The patients low insulin levels inhibit the uptake and usage of glucose for
energy. Her body relies on fat for energy and the breakdown of fat results in the formation of keto acids.
Increased levels of keto acids cause the excretion of excess ketone bodies in the urine (Nelms et al.,
2014, p. 481). The presence of these ketones acidifies the urine to a pH of 4.9, which is outside the
normal range of 5 to 7. Additionally, protein is present in the urine at a high value of 100 mg/dL. Protein
loss in the urine, also known as proteinuria, can be a sign of kidney damage. High blood glucose, such
as that seen in the patient, results in the overworking of the kidney filtration system and subsequent
leakage (ADA, 2015c). Reduction of plasma glucose is pertinent for the prevention of further kidney
damage and kidney disease. Furthermore, RRs specific gravity of 1.035 is above normal. This high
value is due to the presence of glucose, proteins, and ketones in the urine.
Review of Medications and Food/Nutrient Interactions
Upon admittance to the hospital, RR was given regular insulin 1 unit/mL NS (normal saline) 40
MEq KCl/liter @ 135 mL/hr. The beginning infusion was at 0.1 unit/kg/hr to equal 3.7 units/hr and to
increase to 5 units/hr. RR was classified as NPO, then progressed to clear liquids and then finally a
consistent carbohydrate-controlled diet order. Regular insulin (R), is a short-acting insulin that can cause
11
side effects such as hypoglycemia (low blood glucose level <70 mg/dL) (Nelms et al., 2014, p. 491). In
order to prevent this complication, adjusting the amount of medication and/or type in coordination with
timing of foods and activity is a recommended strategy (Nelms et al., 2014, p. 488). After RRs blood
glucose levels declined from the regular insulin, RR was transitioned onto a consistent carbohydrate diet
with IVF (intravenous fluids) changed to D5.45NS (dextrose 5% with normal saline) with 40 MEq K at
135 mL/hr. Apidra 0.5 units was given every 2 hours until RRs blood glucose normalized to an
acceptable range of 150-200 mg/dL. Glargine was then administered at 6 units at 9:00 p.m.
Apidra (insulin glulisine [rDNA origin] injection) solution for injection, is a fast-acting insulin
that is taken 15 - 20 minutes before a meal or within 20 minutes after starting a meal (Sanofi-Aventis,
2015). Important medication/food interactions include monitoring blood glucose levels for
hypoglycemia. Severe hypoglycemia may lead to unconsciousness and/or convulsions and may result in
temporary or permanent impairment of brain function or death (Sanofi-Aventis, 2015). Correction of
hypoglycemia include consumption of 15 grams carbohydrate and re-testing of blood glucose until
normalization occurs. Patients should not use Apidra if they are under hypoglycemic conditions.
Additional concerns when using Apidra include hypokalemia (low potassium serum levels) due to the
shift in potassium from the extracellular to intracellular space (Sanofi-Aventis, 2015). Glargine (Lantus),
a long-acting insulin, acts on the body for 24 hours and has similar nutrient precautions as Apidra,
including hypoglycemia and hypokalemia. Following the prescribed consistent-carbohydrate diet,
medication guidelines, and using appropriate insulin correction factors will assist in preventing possible
side-effects.
Evaluation of Physical or Clinical Findings
No significant physical findings. Clinical findings are diagnosis of Type 1 Diabetes Mellitus. The patient
is currently on D5.45NS with 40 MEqK @ 135 ml/hr. Patient is NPO, but receiving 550 calories (135
mL/hr of D5). After 12 hours begin clear liquids if patient is stable and monitor with hourly bedside
glucose checks to make sure blood glucose is not >200 mg/dL or <80 mg/dL.
Energy Requirements
EER: 1650 kcal/day [based on Schofield equation, using 1.3 out of bed activity factor and adjusted body
weight (ABW) of 95.5 lbs]
Protein Requirements
15% of total kcal from protein/day
1650 x .15 = 248 kcal/ 4 kcals/ g = 62 g protein/day
Diet Order
12
NPO except for ice chips and medications. While on TPN, RR received 550 calories of
carbohydrates from D5.45NS and 40 MEq of potassium every 8 hours. RR had a net positive I/O,
trending upward from +480 mL/kg to +600 mL/kg. RRs serum glucose is decreasing toward normal
levels. Initial findings of glucose in urine are expected to decrease. On second day of admission, clear
liquids (320 mL) were added to the patient's diet. Once stable RR will advance to consistent
carbohydrate diet order: 70-80 g breakfast and lunch, 85-95 g dinner, and 3-15 gram snacks.
D5.45NS with 40 MEqK @ 135 ml/hr:
135 mL/hr x 24 hr = 3240 mL or 3.24 L
Total gram dextrose: D5= 50 g/L X 3.24 L= 162 g X 3.4 kcal/g = 550.8 kcal
Diet Therapy
The goals of dietary treatment are as follows. Initial reduction of blood glucose to <200 mg/mL.
Glycemic control, as indicated by a preprandial blood glucose of 70-130 mg/dL, 1-hour and 2- hour
postprandial glucose of <180 mg/dL, and A1c <7%, will follow. This normalization of blood glucose will
decrease the symptoms of glucosuria, polyuria, polydipsia, and polyphagia. As a result, serum sodium
and phosphate levels will increase, serum osmolality will decrease, and urine will be free of protein,
glucose, and ketones. Additionally, dietary treatment will prevent further weight loss and promote
weight gain. Furthermore, educating the patient and her family about basic nutrition, carbohydrate
counting, and self-monitoring of blood glucose will decrease risk for future hospitalization and prevent
further complications of T1DM. With this set of skills and knowledge, the patient will be able to
maintain a healthy, active lifestyle, despite her T1DM diagnosis.
The patient is NPO and receiving 500 calories/day from dextrose along with Apidra and glargine
in order to reduce her serum glucose to 150-200 mg/dL. After 12 hours, RR will consume clear liquids
and will progress to a consistent-carbohydrate diet. Based on the dietary goals, the calculated energy and
protein requirements, diet order and the patients medical condition, the consistent carbohydrate diet
within the initial diet order is modified slightly. Using the Schofield equation, an activity factor of 1.3,
and the patients ABW, a 1650 calorie diet is recommended. Contributing 60% of the total kcal to
carbohydrates results in a diet order of approximately 250 grams carbohydrate less than the initial
order of 270-300 grams carbohydrate. Also, the distribution of carbohydrates throughout day has been
altered. The three 1-carbohydrate serving (15 g) snacks within the initial diet order have been increased
to three 1-2 carbohydrate servings (15-30 g) due to the patients active lifestyle. Patient RRs prolonged
and vigorous exercise during soccer practice requires that she consume more carbohydrates to prevent
13
hypoglycemia. To allow for this increase in snack size, the total carbohydrates within each of the three
daily meals has been reduced to 60 grams. Calculations shown below.
Carbohydrates based on 60% of total kcal:
1650 x .60 = 990 kcal / 4 kcal/g = 250 g / 15 g = 17 serving CHO per day
Per meal 3x day = 4 servings of 15 g CHO (60 g)
Per snack 3x day = 1-2 servings of 15 g CHO (15-30 g)
Protein based on 15% of total kcal:
1650 x .15 = 248 kcal / 4 kcal/g = 62 g protein per day
Fat based on 25% of total kcal:
1650 x .25 = 412 kcal / 9 kcal/g = 45 g fat/day
Nutritional Goals
Short-Term Goals
1. Improved glycemic control. Preprandial glucose at 70-130 mg/dL, 1-hour postprandial glucose
<180 mg/dL, and 2-hour postprandial glucose <180 mg/dL.
a. Administration of insulin via intensive insulin therapy. RR and family will be educated
about effects and importance of insulin.
b. Follow carbohydrate controlled diet with carbs coming from fruits, vegetables, legumes,
low-fat dairy products, and whole grains.
2. Prevent further weight loss and promote weight gain.
a. Determine food preferences of RR and incorporate these foods into meal plan. This will
help increase energy intake to adequate levels.
b. Distribute meals and snacks around RRs school, physical activity, and other daily
events. Planning ahead will ensure that no meals or snacks are skipped.
c. Administration of insulin prior to eating.
3. Normalization of laboratory values.
a. Lab values will normalize with improved glycemic control. (see goal #1)
i.
Subsequent decrease in polyuria will lead to normalization of serum sodium,

phosphorous, and osmolality.
ii.
Subsequent decrease in glucosuria will decrease glucose concentration in urine.
b. Administration of insulin.
i.
Subsequent decrease in lipolysis and thus, fewer ketone bodies and proteins in the
urine.
14
4. Improved nutrition-knowledge and skills for controlling T1DM.

a. Educate RR and her family about carbohydrate counting and how to read food labels.
b. Demonstrate to RR and her family proper technique for self-monitoring of blood glucose
(SMBG).
c. Educate RR and her family about effects of physical activity on blood glucose levels.
Explain how to properly alter food intake and/or insulin dosage to prevent hypoglycemia.
d. Refer patient to CDE.
Long-Term Goals
1. Continued glycemic control, as demonstrated by A1c< 7%.
a. Routine administration of insulin via intensive insulin therapy.
b. Mastery of carbohydrate counting, label reading, and SMBG by patient. RR will be able
to correctly identify carbohydrate content of regularly consumed foods.
c. RR will continue to follow a carbohydrate controlled diet with carbs coming from fruits,
vegetables, legumes, low-fat dairy products, and whole grains.
2. Achieve and maintain normal body weight as determined by anthropometric scales/growth
charts.
a. Continue to follow carbohydrate controlled meal plan. Diet will be modified according to
RRs growth rate, age, and physical activity.
b. Adequate administration of insulin prior to meals. Doses will change as energy
requirements change.
3. Prevent further complications of diabetes.
a. Schedule at least 1 follow-up appointment annually to reinforce lifestyle changes and to
evaluate and monitor outcomes that indicate the need for changes in medical nutrition
therapy (MNT) or medications. As energy requirements change with age, physical
activity, and growth rate, an evaluation of height, weight, BMI, and nutrition plan is
recommended at least once every year.
b. Education is not a one-time event that occurs at diagnosis. Families and children will
receive ongoing education and support as RR grows and takes on more elements of selfcare. Knowledge and skills should be evaluated regularly by the CDE.
15
ADIME Note
5/20/15, 10:00 a.m.
Assessment:
Pt recently recovered from strep throat a few days ago. Pt complains of feeling very thirsty and
constantly having to go to the bathroom including in the middle of the night. Pt fainted after 15
minutes of physical activity.
12 yo; Female; Dx: New Diagnosis Type I Diabetes Mellitus; PMH: Strep throat; FH: FatherHTN,
Mother-hyperthyroidism, Sister- celiac disease.
CC: Admitted with new diagnosis of acute hyperglycemia.
Ht. 5; Wt. 82#; UBW: 90#; %UBW: 91% (severe weight loss of 8.9% of body weight in less
than 1 month); IBW: 100#; %IBW: 82%; ABW: 95.5#; BMI: 16. BMI-for-age percentile:
17.5 (unhealthy).
Labs: HbA1C: 14.6% (H); FBG: 683 mg/dL (H); urine glucose: + (H); sodium: 126 mEq/L (L);
K: 4.3 mEq/L (WNL); calcium: 10 mg/dL (WNL); Mg: 1.9 mg/dL (WNL); phosphate,
inorganic: 1.9 mg/dL (L); C-peptide: 0.10 ng/mL (L); ICA: + (H); GADA: + (H); IAA: + (H);
UA: specific gravity: 1.035 (H), pH: 4.9 (H), protein: 100 mg/dL (H), glucose: + (H), ketones: + (H).
Meds: None
GI: Active bowel sounds x 4; tender, non distended. Cloudy amber urine, protein & ketones
present.
I/O: 3560/2660: +900 Input net I/O for stay at hospital
Physical Assessment: Respirations are rapid, clear to auscultation and percussion. Pt is alert but
slightly confused. Glasgow Coma Scale: 15.
Skin: Braden score: 21 (no risk). Skin color: pale
EER: 1650 calories (based of of Schofield equation, activity factor of 1.3, and ABW); EPR: 62 g
protein/day (based on 15% of total calories); Fluid: 2 L/day (based on 1700 mL plus
30 mL/kg over 3 kg child fluid requirement).
Current Diet: Mother and father report that RR is a picky eater. RR only consumes chicken and fish for
meat and salad, broccoli, carrots, tomatoes, and asparagus for vegetables. RR usually eats cereal
with milk or a Pop-Tart with milk for breakfast. RR brings a sack lunch to school that includes
either a peanut butter and jelly or a turkey and cheese sandwich, chips, carrots, and water. RR
consumes a granola bar before soccer practice and drinks water throughout practice. When with
her mom, dinner is usually prepared at home and always includes some salad, meat, and pasta,
potato, or rice. RRs father does not cook very often and dinner usually consists of ordering pizza
or Chinese food. Typical snacks for RR include cereal, ice cream, yogurt, some fruits (apples or
bananas), popcorn, chips, or cookies.
Diagnosis:
2. Unintended weight loss (NC 3.2) RT malabsorption of glucose AEB severe weight loss of 8.9% of
her body weight in less than 1 month.
3. Food and nutrition related knowledge deficit (NB-1.1) R/T lack of exposure to information AEB
Intervention:
Nutrition Prescription: Recommend 1650 kcal per day (based off of Schofield equation, activity factor
of 1.3, and ABW), consisting of 60% of total calories from carbohydrates (248 g), 25% of total calories
16
from fat (45 g), and 15% of total calories from protein (62 g). Carbohydrate counting meal plan
including 4 carbohydrate servings (60g) at 3 meals, along with three 1-2 carbohydrate (15-30 g) snacks,
for a total of 16.5 carbohydrate servings per day. Recommend less than 10% of total calories from
simple sugars (40 g), less than 7% of total calories from saturated fat (12 g), less than 200 mg per day of
cholesterol. Maximum intake of 2 g sodium. Fluid requirement of 2 L.
1. Treatment of Rachels condition will consist of modifying her normal intake to a carbohydrate
controlled diet. A goal of 4 servings of CHO with each meal 3x a day with one snack of 1-2 serving
of CHO. Emphasis on choosing healthy fats over saturated and trans-fats, as well as including fiberrich whole grains for refined products.
2. Education will be provided on identifying carbohydrate sources, reading nutrition fact labels, basic
facts about average portion sizes, and scheduling meals appropriately around medications. Education
will be provided to the family on identifying signs and symptoms of hypoglycemia and
hyperglycemia, as well as the importance of preventing meal-skipping.
3. Nutrition counseling will be achieved through motivational interviewing, assessment of readiness to
change, and facilitating changes in existing food and nutrition related behaviors. Counseling will
mostly rely on patients family to monitor Rachels blood glucose levels and provide appropriate
meals per her diet order.
Monitoring and Evaluation:
1. Monitor blood glucose levels (self-monitoring of blood glucose), on second and third follow-up.
2. Evaluate adherence to controlled carbohydrate diet order through diet records.
3. Patient will be able to correctly identify carbohydrate content of regularly consumed foods.
4. Patient will be able to state carbohydrate goals with appropriate insulin coverage.
5. Set up with outpatient CDE for follow up appointment.
Signatures:
A. Galvan
N. Leffler
K. Martin
K. Matsuura
17
References
American Diabetes Association. (2015a). Can diabetes pills help me. Retrieved from
http://www.diabetes.org/living-with-diabetes/treatment-and-care/medication/oral-medications/candiabetes-pills-help-me.html
American Diabetes Association. (2015b). Diagnosing diabetes and learning about prediabetes.
Retrieved from http://www.diabetes.org/diabetes-basics/diagnosis/
American Diabetes Association. (2015c). Kidney disease (nephropathy). Retrieved from
http://www.diabetes.org/living-with-diabetes/complications/kidney-disease-nephropathy.html
American Diabetes Association. (2015d). Living with type 1 diabetes. Retrieved from
http://www.diabetes.org/living-with-diabetes/recently-diagnosed/living-with-type-1diabetes.html?loc=lwd-slabnav
Calabria, A. (2014). Diabetes in Children and Adolescents. Retrieved from
http://www.merckmanuals.com/professional/pediatrics/endocrine-disorders-in-children/diabetesin-children-and-adolescents
Diabetes Education Services. (2015). Insulin pocket card. Retrieved from
http://www.diabetesed.net/page/_files/Insulin-PC-3-2015.pdf
Fraser Health. (2009). Advanced carbohydrate counting. Retrieved from
https://www.fraserhealth.ca/media/Advanced%20Carb%20Counting%20Colour.pdf
King, A. B., & Armstrong, D. U. (2007). A Prospective Evaluation of Insulin Dosing Recommendations
in Patients with Type 1 Diabetes at Near Normal Glucose Control: Bolus Dosing. Journal of
Diabetes Science and Technology (Online), 1(1), 4246.
Nelms, M., Sucher, K., & Lacey K. (2014). Nutrition therapy and pathophysiology. Boston, MA:
Cengage Learning.
Sanofi-Aventis. (2015). Apidra (insulin glulisine [rDNA origin] injection) solution for injection
prescribing information. Retrieved from http://products.sanofi.us/apidra/apidra.html
U.S. Department of Health and Human Services, National Institutes of Health, National Institute of
Diabetes and Digestive and Kidney Diseases, National Diabetes Information Clearinghouse. (2014).
Diagnosis of diabetes and prediabetes (NIH Publication No. 144642). Retrieved from
http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/#3
U.S. National Library of Medicine. (2014). Insulin C-peptide test. Retrieved from
http://www.nlm.nih.gov/medlineplus/ency/article/003701.htm
18
U.S. National Library of Medicine. (2013a). Osmolality - blood test. Retrieved from
U.S. National Library of Medicine. (2013b). Urine specific gravity test. Retrieved from
19
Case Study Questions

Understanding the Diagnosis and Pathophysiology
1.What are the current thoughts regarding the etiology of type 1 diabetes mellitus (T1DM)? No
one else in Rachels family has diabetes--is this unusual? Are there any other findings in her
family medical history that would be important to note?
Type 1 diabetes mellitus (T1DM) is an autoimmune disease that is caused by the immune system
attacking the beta cells in the pancreas that produce insulin. An individual can have a 50-60% genetic
risk of developing T1DM if they have a polymorphism in the HLA complex of chromosome 6.
Additionally, several environmental factors including viruses, gluten, vitamin D levels, length of
breastfeeding, and exposure to cows milk proteins as an infant can interact with these genes to also
cause the onset of T1DM. It is not unusual for RR to have T1DM while no one else in her family does
because many people may have the genes that predispose them to T1DM, but never develop the disease,
as they are not exposed to environmental factors that trigger the development of T1DM. Hence, in RRs
case, her parents could be carriers for T1DM, but not diagnosed with the disease. RRs family medical
history is also important to note as her mom has hyperthyroidism and her sister has celiac disease which
are both autoimmune diseases like T1DM. Hence, RR could very well have a genetic component of
autoimmune diseases that runs in her family.
2. What are standard diagnostic criteria for T1DM? Which are found in Rachels med record?
Test
Range for Diagnosing

Diabetes
Rachels Laboratory
Results
Fasting plasma blood glucose
above 126 mg/dL
683 mg/dL
Hemoglobin A1C
greater than or equal to 6.5%
14.6%
Symptoms
polyuria, polydipsia,
polyphagia, and unexplained
weight loss
polyuria, polydipsia,
polyphagia, and unexplained
weight loss
Random plasma glucose

concentration during an oral
glucose tolerance test
greater than or equal to 200

mg/dL
Not administered
Ketone levels
positive
positive
Islet cell antibodies
elevated ICA, GADA, IA-2A, elevated ICA, GADA, and

and/or IAA
IAA
20
3. Using the information from Rachels medical record, identify the factors that would allow the
physician to distinguish between T1DM and T2DM?
RRs sudden onset of the symptoms of diabetes in only a few days is one indicator that she has
developed T1DM as Type 2 Diabetes Mellitus (T2DM) develops over a longer span of time.
Additionally, in looking at RRs labs her glucose levels are 6 times above the reference range which is
typical in a patient diagnosed with T1DM, the most significant indicator that RR has T1DM is her
pancreatic islet cell antibodies results. Rachels ICA, GADA, and IAA markers were all above normal
limits indicating that her pancreatic beta cells were being destroyed by these antibodies.
4. Describe the metabolic events that led to Rachels symptoms and subsequent admission to the
ER (polyuria, polydipsia, polyphagia, fatigue, and weight loss), integrating the pathophysiology of
T1DM into your discussion.
Because RR has T1DM, her pancreatic beta cells were destroyed and not able to secrete insulin
into the blood. Without insulin, glucose was not able to be absorbed into the cell resulting in
hyperglycemia and cellular starvation. In response to the hyperglycemia, RR excreted excess glucose in
the urine (glycosuria). As this occurred, the osmotic pressure inside her kidney tubules also increased,
resulting in osmotic diuresis as water left the cells and was urinated out with glucose. With water
leaving the cells to be excreted in the urine, RR suffered from polyuria or excessive urination.
Additionally, with less fluid in the blood, RR experienced an increase in serum osmolality which
triggered her RAAS thirst mechanism. This mechanism caused RR to develop polydipsia, or excessive
thirst.
In addition, RR also developed polyphagia, or excessive hunger, in response to the cellular
starvation of glucose. However, as glucose was still not able to be absorbed into her cells, RRs body
responded through gluconeogenesis, or the making of glucose from non-carbohydrate sources. For
instance, RRs protein stores were used to make glucose for body. This was evident as an increase in
protein degradation and therefore muscle wasting resulted in an 8.9% weight loss in less than 1 month
for RR. Lipolysis, or the breakdown of fat into ketone bodies, also occurred. For a normal individual,
these ketone bodies can be used as energy for the muscles and brain. However, in RR an excessive
amount of ketone bodies are produced resulting in an decreased pH in the blood. This condition is
known as diabetic ketoacidosis (DKA). As excess ketone acids in her bloodstream were neutralized by
bicarbonate and formed into carbon dioxide, RR developed Kussmaul respirations, or deep labored
21
breathing, in order to get CO2 out of her system. These Kussmaul respirations in combination with the
fatigue due to a lack of energy being utilized by her cells furthermore caused RR to pass out and be
taken to the ER.
5. 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?
Without insulin, lipolysis occurs in the cells releasing ketone bodies into the blood. Ketones are
acids that the body uses to provide energy to the cells. However as ketone production increases it causes
a lower serum pH. This results in metabolic acidosis as bicarbonate levels are reduced in order to
neutralize the acids in the bloodstream. In order to counteract metabolic acidosis both the respiratory
and renal systems respond. The respiratory system will promote hyperventilation and Kussmaul
respirations, or deep labored breathing, in order to get CO2 out of the body. The renal system will
compensate by conserving bicarbonate and excreting positively charged cations like (Na+, K+, and
NH4+) resulting in polyuria. Upon admittance into the hospital, RR was in the beginning stages of
DKA as she had passed out during soccer practice and was still slightly disoriented upon admittance into
the hospital. Additionally, RRs urinalysis showed an elevation of ketones and a decrease in pH.
Precipitating factors that may lead to DKA include: infection, myocardial infarction, cerebrovascular
accidents, pancreatitis, inadequate insulin therapy, and the new onset of T1DM (as was the case for RR).
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, 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. Rachels parents want to know why she cannot take oral medications
for her diabetes like some of their friends do. What would you tell them?
Glargine is a long-acting insulin with a 2-4 hour onset, no peak of action, and a 20-24 hour
duration. Glargine must be taken with a rapid-acting insulin, such as Apidra. Apidra has a 5-15 minute
onset, 30-90 minute peak of action, and 3-5 hour duration.
Oral medication only helps to treat individuals with T2DM. These pills help the body to better
use the insulin it produces thus reversing insulin resistance in T2DM patients. Individuals with T1DM,
however, cannot produce insulin, so this medication would be ineffective. Insulin must be injected.
22
7. Rachels physician explains to Rachel and her parents that Rachels 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 a period in which the beta cells of the pancreas still secrete some
insulin. When insulin injections begin upon diagnosis of T1DM, the remaining pancreatic beta cells are
given a time of rest. This rest actually stimulates the cells to produce insulin, and secretion may last
weeks, months, or even years. During this phase, RR will require smaller doses of insulin, but doses
must eventually increase as secretion stops.
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 lowers blood glucose levels. RR should check her blood glucose before and
after exercise to determine how her body specifically reacts to physical activity. If her glucose levels fall
below 100 mg/dL, she should immediately consume at least 15-20 grams of fast-acting carbohydrate,
such as a sports drink. Blood glucose levels should be rechecked 15 minutes later, before returning to
practice. As a general rule, RR should consume an extra 15 grams of carbohydrate for each hour of
moderate activity. Up to 30 grams of carbohydrate may be required for more strenuous practices or
games.
9. Rachels 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 human body produces cortisol and growth hormone, two hormones controlling circadian
rhythms, at about 4:00am daily. These hormones stimulate gluconeogenesis and cause hyperglycemia
between 5:00am and 9:00am. This increase in morning blood glucose levels is known as the dawn
phenomenon. RRs body cannot produce insulin as a normal response to this increase in glucose, so her
fasting glucose levels are increased. To help prevent this, RR should decrease her blood glucose prior to
going to sleep. Recommendations include eating dinner earlier at night or participating in light physical
activity after dinner.
23
Understanding the Nutrition Therapy

10. The MD ordered a consistent carbohydrate-controlled diet when Rachel begins to eat. Explain
the rationale for monitoring carbohydrate in diabetes nutrition therapy.
All carbohydrate are converted into glucose and in people without diabetes their bodies can
produce insulin automatically to deal with the glucose that enters the blood from the carbohydratecontaining foods that they ate or drank. With Type 1 diabetes the same principle applies, but because
your body does not produce any insulin, you have to take synthetic insulin either by injections or via a
pump. This will help to lower the glucose in the blood after eating carbohydrate-containing foods. Most
people can follow this with either twice daily or basal bolus insulin regimens. With twice daily insulin it
might be easier to have consistent amounts of carbohydrates on a daily basis and even eating about the
same amount at similar times each day. If a person were to eat more carbohydrates than they usually do,
it can cause the blood glucose to get too high and the same thing can happen if I person does not eat
enough carbohydrates, because it can cause low blood sugar. However, with basal bolus insulin, you can
be flexible with how much insulin you take and when you take it. Carbohydrate-counting is what most
people with diabetes end up following because it allows them to calculate how much insulin they need
to take depending on how much they have eaten.
11. Outline the basic principles for Rachels nutrition therapy to assist in control of her T1DM.
- Maintain optimal glucose levels to the normal range of 70-110 mg/dL (130-140, list recommended by
who ADA) list if these ranges is fasting or post-prandial?
- Maintain blood pressure levels
- Improve nutrition through healthy food choices and regular physical activity
- Modify both nutrient intakes and lifestyle to an appropriate level for the prevention and treatment of
obesity, dyslipidemia, cardiovascular disease, hypertension, and nephropathy.
- Provide the adequate energy to ensure normal growth and development and integrating insulin
regimens into usual eating and physical activity habit
- macronutrient ranges: CHO (60-70%...learn control amounts), Protein (12-20%)-look at DRI, Sat Fat
(less than 7%), cholesterol (less than 200 mg/dL)
- control and manage lipids
24
Nutrition Assessment
12. Assess Rachels ht/age; wt/age; ht/wt; and BMI. What is her desirable weight?
- Ht/age: 5 ft/12 years old:Normal range at 50-75th percentile
- Wt/age: 82 lbs/12 years old Normal range at just above the 25th percentile
- Ht/Wt: 5 feet / 82 lbs Normal range
- BMI: 16.01 which is at 17th percentile which is within a unhealthy range
- Desirable weight: 100lbs
5 feet = 100 lbs
13. Identify any abnormal laboratory values measured upon her admission. Explain how they
may be related to her newly diagnosed T1DM
Low Sodium levels may be explained by her polydipsia and drinking large quantities of water in
response. A low sodium level in the blood may result from excess water or fluid in the body, which
dilutes the normal amount of sodium so that the concentration appears low.
High Glucose levels might be due to her being recently diagnosed with type 1 diabetes and not having
enough insulin to clear the blood of glucose.
Low phosphate levels could be due to her lungs compensating for blood pH and attempting to raise it
via increased ventilation rate and eliminating CO2 (respiratory alkalosis). A decrease in blood CO2 will
increases intracellular pH. The increase in pH will stimulate phosphofructokinase which will enhance
glycolysis, causing phosphate to move into cells to supply the enhanced resulting phosphorylation. This
could be due to her insulin administration or could be due to increased renal loss.
High Osmolality is due to the high blood glucose level, because she didnt realize she was an
uncontrolled T1DM until she was recently diagnosed.
High HbA1C HbA1C is a long-term measure of glycosylated hemoglobin it is high because she has had
uncontrolled T1DM, and subsequent high levels of blood glucose.
Low C-peptide is due to a large amount of beta cell destruction. Proinsulin (inactive) is chopped into cpeptide+ insulin (active) in lower than usual amounts. Low insulin secretions parallel low c-peptide
levels.
ICA, GADA, IAA is present which indicates that there has been an autoimmune destruction of
pancreatic beta cells, these antibodies are identified as contributing to the destruction of beta cells.
High specific gravity concentrated urine has a high specific gravity value. Probably due to the
concentration of glucose and ketones.
25
Low urine pH is due to the concentration of acidic ketone bodies

protein in urine is due to the damaged glomeruli that have an impaired ability to filter the blood and
prevent protein from leaking into blood.
High glucose in urine is due to a high blood glucose levels that surpasses the renal thresh hold
Ketones in urine indicate that the level of ketones in the body is so high (because it is utilizing fat as an
energy source) that they are being excreted in the urine.
Prot chk indicates that there is protein in her urine.
14. Determine Rachels energy and protein requirements. Be sure to explain what standards you
used to make this estimation.
The Schofield equation for women ages 10 - 18 years old was used to estimate RRs energy
needs because it takes into account her age. Adjusted body weight of 95.5 lbs was used in the equation
and a 1.3 out of bed factor. Normal protein requirements of 15% of total kcal was used to determine her
protein needs.
Schofield for women 10-18
13. 384 x W + 692.6
13.384 x 43.4 kg + 692.6
= 1,273 x 1.3
= 1,655 kcal/day
Nutrition Diagnosis
15. Prioritize two nutrition problems and complete the PES statement for each.
1.
Impaired nutrient utilization (NC 2.1) RT compromised endocrine function of the pancreas AEB

2.
Unintended weight loss (NC 3.2) RT malabsorption of glucose AEB severe weight loss of 8.9% of

Nutrition Intervention
16. Determine Rachels initial nutrition prescription using her diet record from home as a
guideline, as well as your assessment of her energy requirements.
26
Recommend 1650 kcal per day (based off of Schofield equation, activity factor of 1.3, and
ABW), consisting of 60% of total calories from carbohydrates (248 g), 25% of total calories from fat (45
g), and 15% of total calories from protein (62 g). Carbohydrate counting meal plan including 4
carbohydrate servings (60g) at 3 meals, along with three 1-2 carbohydrate (15-30 g) snacks, for a total of
16.5 carbohydrate servings per day. Recommend less than 10% of total calories from simple sugars (40
g), less than 7% of total calories from saturated fat (12 g), less than 200 mg per day of cholesterol.
Maximum intake of 2 g sodium. Fluid requirement of 2 L.
Carbohydrates based on 60% of total kcal:
1650 x .60 = 990 kcal / 4 kcal/g = 250 g / 15 g = 17 serving CHO per day
Fat based on 25% of total kcal
1650 x .25 = 400 kcal/9 = 45.8 g fat/day
17. What is an insulin: CHO ratio (ICR)? Rachels 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?
Insulin to CHO ratio is the number of grams of carbohydrate covered by one unit of insulin. A
physicians order of 1:15 ICR (insulin to carbohydrate ratio) would mean for every 15 g of CHO
consumed, one unit of insulin would need to be delivered in order to help the body process or
metabolize the glucose. If Rachel consumed her usual breakfast of 2 Pop-Tarts and 8 oz skim milk, she
will need to take 6 units of Apidra.
Skim milk 8 oz = 12g CHO
2 Pop Tarts = 76 g CHO
TOTAL breakfast: 88 g CHO
88/15 = 5.86 = 6 units of Apidra
18. Dr. Cho set Rachels 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 corrected dose be?
In order to correct Rachels total daily insulin dose of 33 units, she would have to take 1 unit
more of Apidra in order to reach a fasting blood glucose goal of 180 mg/dL.
-
1 unit of apidra will lower blood glucose by 54 mg/dL
27
1800 GRAMS/33 UNITS = 54
240 (current blood glucose) - 180 (fasting goal)

-
is 60 mg/dL over.
Adjusted total daily insulin dose of 34 units Apidra.

Nutrition Monitoring and Evaluation
ADIME Note
5/20/15, 10:00 a.m.
Assessment:
Pt recently recovered from strep throat a few days ago. Pt complains of feeling very thirsty and
constantly having to go to the bathroom including in the middle of the night. Pt fainted after 15
minutes of physical activity.
12 yo; Female; Dx: New Diagnosis Type I Diabetes Mellitus; PMH: Strep throat; FH: FatherHTN,
Mother-hyperthyroidism, Sister- celiac disease.
CC: Admitted with new diagnosis of acute hyperglycemia.
Ht. 5; Wt. 82#; UBW: 90#; %UBW: 91% (severe weight loss of 8.9% of body weight in less
than 1 month); IBW: 100#; %IBW: 82%; ABW: 95.5#; BMI: 16. BMI-for-age percentile:
17.5 (unhealthy).
Labs: HbA1C: 14.6% (H); FBG: 683 mg/dL (H); urine glucose: + (H); sodium: 126 mEq/L (L);
K: 4.3 mEq/L (WNL); calcium: 10 mg/dL (WNL); Mg: 1.9 mg/dL (WNL); phosphate,
inorganic: 1.9 mg/dL (L); C-peptide: 0.10 ng/mL (L); ICA: + (H); GADA: + (H); IAA: + (H);
UA: specific gravity: 1.035 (H), pH: 4.9 (H), protein: 100 mg/dL (H), glucose: + (H), ketones: + (H).
Meds: None
GI: Active bowel sounds x 4; tender, non distended. Cloudy amber urine, protein & ketones
present.
I/O: 3560/2660: +900 Input net I/O for stay at hospital
Physical Assessment: Respirations are rapid, clear to auscultation and percussion. Pt is alert but
slightly confused. Glasgow Coma Scale: 15.
Skin: Braden score: 21 (no risk). Skin color: pale
EER: 1650 calories (based of of Schofield equation, activity factor of 1.3, and ABW); EPR: 62 g
protein/day (based on 15% of total calories); Fluid: 2 L/day (based on 1700 mL plus
30 mL/kg over 3 kg child fluid requirement).
Current Diet: Mother and father report that RR is a picky eater. RR only consumes chicken and fish for
meat and salad, broccoli, carrots, tomatoes, and asparagus for vegetables. RR usually eats cereal
with milk or a Pop-Tart with milk for breakfast. RR brings a sack lunch to school that includes
either a peanut butter and jelly or a turkey and cheese sandwich, chips, carrots, and water. RR
consumes a granola bar before soccer practice and drinks water throughout practice. When with
her mom, dinner is usually prepared at home and always includes some salad, meat, and pasta,
potato, or rice. RRs father does not cook very often and dinner usually consists of ordering pizza
or Chinese food. Typical snacks for RR include cereal, ice cream, yogurt, some fruits (apples or
bananas), popcorn, chips, or cookies.
Diagnosis:
28
2. Unintended weight loss (NC 3.2) RT malabsorption of glucose AEB severe weight loss of 8.9% of
3. Food and nutrition related knowledge deficit (NB-1.1) R/T lack of exposure to information AEB
Intervention:
Nutrition Prescription: Recommend 1650 kcal per day (based off of Schofield equation, activity factor
of 1.3, and ABW), consisting of 60% of total calories from carbohydrates (248 g), 25% of total calories
from fat (45 g), and 15% of total calories from protein (62 g). Carbohydrate counting meal plan
including 4 carbohydrate servings (60g) at 3 meals, along with three 1-2 carbohydrate (15-30 g) snacks,
for a total of 16.5 carbohydrate servings per day. Recommend less than 10% of total calories from
simple sugars (40 g), less than 7% of total calories from saturated fat (12 g), less than 200 mg per day of
cholesterol. Maximum intake of 2 g sodium. Fluid requirement of 2 L.
1. Treatment of Rachels condition will consist of modifying her normal intake to a carbohydrate
controlled diet. A goal of 4 servings of CHO with each meal 3x a day with one snack of 1-2 serving
of CHO. Emphasis on choosing healthy fats over saturated and trans-fats, as well as including fiberrich whole grains for refined products.
2. Education will be provided on identifying carbohydrate sources, reading nutrition fact labels, basic
facts about average portion sizes, and scheduling meals appropriately around medications. Education
will be provided to the family on identifying signs and symptoms of hypoglycemia and
hyperglycemia, as well as the importance of preventing meal-skipping.
3. Nutrition counseling will be achieved through motivational interviewing, assessment of readiness to
change, and facilitating changes in existing food and nutrition related behaviors. Counseling will
mostly rely on patients family to monitor Rachels blood glucose levels and provide appropriate
meals per her diet order.
Monitoring and Evaluation:
1. Monitor blood glucose levels (self-monitoring of blood glucose), on second and third follow-up.
2. Evaluate adherence to controlled carbohydrate diet order through diet records.
3. Patient will be able to correctly identify carbohydrate content of regularly consumed foods.
4. Patient will be able to state carbohydrate goals with appropriate insulin coverage.
5. Set up with outpatient CDE for follow up appointment.
Signatures:
A. Galvan
N. Leffler
K. Martin
K. Matsuura
29
20. When Rachel comes back to the clinic, she brings the following food and blood glucose record
with her.
Time
Diet
7:30 a.m. 2 Pop-Tarts

1 banana
16 oz skim
milk with
Ovaltine (2
tbsp)
Grams of
CHO
Exercise
76 g
27 g
24 g
10 g
BG
(mg/dL)
What
patient
took
What you
would
recommend
(Pre) 150
5 u Apidra
9 u Apidra
(pre) 180
6 u Apidra
5 u Apidra
Total: 137g
10:30
a.m.
12 noon
2 p.m.
2 slices of
pepperoni
pizza
2 chocolate
chip cookies
water
50 g
22 g
Granola bar
17 g
Total: 72 g
PE class 30 minutes

Ntrs 415b Case Study Paper Final

Uploaded by

Document Information

Original Description:

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Ntrs 415b Case Study Paper Final

Uploaded by

Copyright:

Available Formats

Running head: PEDIATRIC TYPE 1 DIABETES MELLITUS CASE STUDY

Pediatric Type 1 Diabetes Mellitus Case Study

Patient Treatment Course

Diet or nutrition order: Consistent carbohydrate controlled diet

% weight lost/gained: lost 8.9%

Subsequent decrease in polyuria will lead to normalization of serum sodium,

Subsequent decrease in glucosuria will decrease glucose concentration in urine.

4. Improved nutrition-knowledge and skills for controlling T1DM.

Case Study Questions

Range for Diagnosing

Fasting plasma blood glucose

above 126 mg/dL

greater than or equal to 6.5%

Random plasma glucose

greater than or equal to 200

Islet cell antibodies

elevated ICA, GADA, IA-2A, elevated ICA, GADA, and

Understanding the Nutrition Therapy

Low urine pH is due to the concentration of acidic ketone bodies

hyperglycemic blood glucose lab values of 683 mg/dL on admission.

her body weight in less than 1 month.

1 unit of apidra will lower blood glucose by 54 mg/dL

1800 GRAMS/33 UNITS = 54

240 (current blood glucose) - 180 (fasting goal)

Adjusted total daily insulin dose of 34 units Apidra.

7:30 a.m. 2 Pop-Tarts

You might also like