Aubrey Burklin
Pediatric T1DM case study
1.what are the current thoughts regarding the etiology of type 1 DM? No
one else in Rachel’s family has diabetes- is this unusual? Are there any
other findings in her family medical history that would be important to this
note? (Krause, Escott-Stump)
The primary defect in T1DM is pancreatic beta cell destruction, usually
leading to absolute insulin deficiency. There are two forms of T1DM
immune-mediated and idiopathic. Immune-mediated DM results from an
autoimmune destruction of the beta cells of the pancreas, the only cells in
the body that make the hormone insulin. The onset of immune-mediated
DM often follows viral infection. Idiopathic T1DM refers to forms of the
disease that have no known cause, found mostly in people of African or
Asian origin.
It is not unusual or unheard of for someone to develop T1DM when there is
no familial history. If someone in your direct family (siblings, parents) has
diabetes it does increase your risk. Your risk is also increased if someone
in your family has an autoimmune disease.
It would be important to note her family has a history of an autoimmune
disease, or a polyglandular condition because that increases her risk of
having T1DM. Her mother has hyperthyroidism and her sister has celiac
disease. This puts Rachel at an increased risk for having T1DM.
2.What are the standard Diagnostic criteria for T1DM? Which are found in
Rachel’s medical record? (Krause, Escott-Stump)
For diagnosis of diabetes, a fasting plasma glucose (FPG) test or an oral
glucose tolerance test can be used to identify diabetes. But four diagnostic
measures may be used to diagnose diabetes and each, in the absence of
unequivocal hyperglycemia, must be confirmed on a subsequent day by
repeat testing.
! FPG≥ 126mg/dL or
! 2-hr PG≥ 200mg/dL during an OGTT or
! HbA1C ≥ 6.5% or
! In patients with classic symptoms of hyperglycemia or
hyperglycemic crisis, a random PG≥ 200mg/dL
Rachel was admitted to the hospital after she fainted, when conscious
reported recent wt. loss, polydipsia, polyuria, polyphagia. The day she was
admitted her blood glucose level was 683mg/dL well above the normal
limit of 110. Rachel’s HbA1C on the day she was admitted was 14.6% well
above the normal limit of 5.2%. There were also ketones present in her
urine.
3. Using the information from Rachel’s medical record, identify risk factors
that would allow the physician to distinguish between T1DM and T2DM.
(Krause, Escott-Stump, Mayo clinic)
! Clinical onset of the diabetes was abrupt
! Rachel’s is young 12y.o. and affected persons with T1DM are
usually children and young adults although it can occur at any
age.
! Has tested positive for IAA , the day she was admitted. IAA
is usually the first marker to appear in children, is an
antibody that is targeted to insulin. Insulin is the only antigen
thought to be highly specific for beta cells
! She was positive for islet cell antibodies( +ICA)
! She was positive for GADA
! She has recently experienced weight loss
! Has experienced polydipsia, polyuria, polyphagia
! Fainted in the middle of soccer practice, most likely d/t
hyperglycemia
! Has ketones present in her urine indicating her cells have
been unable to utilize glucose and has had to rely on
breakdown of fat as energy source for cell, ketones are a
byproduct of this fat breakdown.
! She has a lower than average c peptide value which means
that her proinsulin (inactive) is cut into insulin (active) + c
peptide at an amount that is lower than a normal persons, d/t
the majority of her beta cells being destroyed.
4. Describe the metabolic events that led to Rachel’s symptoms and
subsequent admission to the ER (polyuria, polydipsia, polyphagia, fatigue,
weight lost), integrating the pathophysiology of T1DM into your
discussion.
(Society for Neuroscience. "How Inflammatory Disease Causes Fatigue."
http://www.sciencedaily.com/releases/2009/02/090217173034.html)
Severe and extensive pancreatic beta cell damage is mediated by the
immune system of Rachel’s body. As glucose floods the blood stream from
the gut, it passes the pancreas which monitors glucose levels. The
pancreas would normally release from the beta cells an adequate amount
of insulin to Trigger GLUT 4 receptors uptake of glucose into cells (in
peripheral tissue), but d/t the extent of the damage to the beta cells, very
little insulin is produced from the pancreas, in response to a high
carbohydrate meal. This means that the blood glucose level stays elevated,
and cells are not delivered the adequate amount of glucose to function.
Cells are literally starved for energy, this intracellular starvation causes
polyphagia. Also according to the gluco-stat theory if insulin is low then
glucose is not able to trigger the satiety center so the feeding center stays
triggered also leading to polyphagia. Intracellular starvation is occurring,
so the body mobilizes fat stores to utilize for energy. Ketones are a
byproduct of this process but when ketones begin to overload the system
(similar to glucose) they are excreted in the urine. Insulin is also used to
signal anabolic processes, and halt catabolic processes. Since there is not a
sufficient amount of insulin present to suppress glucagon, glucagon is
released and causes the liver to produce more glucose, and dump that into
the blood adding to the already elevated blood sugar level. When the blood
sugar level surpasses the renal threshold, glucose resorption from renal
tubule does not completely happen, thusly glucose begins to appear in the
urine. So now you’ve got glucose in the urine causing the osmotic pressure
to be raised, which will slow kidney resorption of water d/t the high solute
concentration of glucose in the nephron, which means polyuria (increased
urination) and fluid loss. This increased urination and fluid loss leads to
dehydration, in your mind this triggers the hypothalmic thirst center and
causes polydipsia excessive thirst. Weight loss may be due to dehydration
and fluid loss as well as from loss of fat that the body is utilizing for energy.
Fatigue may be due to frequently disrupted sleep to use the restroom, high
blood glucose slows the flow of blood and thus delivery of nutrients and
oxygen to cells, intracellular starvation leading to energy deficit, high
blood sugar may cause inflammation of blood vessels triggering monocytes
which infiltrate the brain this May cause fatigue.
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? (Krause 703)
Signs and symptoms associated with DKA: hyperglycemia can lead to DKA,
DKA is always the result of inadequate insulin for glucose use, DKA is
characterized by elevated blood glucose, the presence of ketones in the
urine and blood. Symptoms include polyuria, polydipsia, hyperventilation,
dehydration, the fruity odor of breath and fatigue.
Despite hyperglycemia, cells are in a state of intracellular starvation d/t
the fact that there is not sufficient insulin (majority of beta cells are
destroyed) to trigger GLUT 4 translocation to the cell membrane to allow
for the uptake of glucose into the cell. The body in an attempt to fuel the
starving cells, begins to mobilize TG’s. One of the byproducts of mobilizing
a large amount of TG’s is ketone bodies (acetoacetic acid and beta
hydroxybutyric acid). Large amounts of ketone bodies present in the
serum and urine can be dangerous. Ketosis and Acidosis results from
increased production and decreased utilization of ketone bodies
(essentially an accumulation of acidic products in the blood). Recap, the
blood glucose level is high, and there are a large amount of ketone bodies
present in the blood, which result in a drop in pH. The kidneys then
attempt to eliminate glucose and ketones. When the blood sugar level
surpasses the renal threshold, glucose resorption from renal tubule does
not completely happen, thusly glucose begins to appear in the urine. So
now you’ve got glucose and ketones in the urine causing the osmotic
pressure to be raised, which will slow kidney resorption of water d/t the
high solute concentration of glucose and ketones in the nephron, which
means polyuria (increased urination) and fluid loss. This increased
urination and fluid loss leads to dehydration, in your mind this triggers the
hypothalmic thirst center and causes polydipsia, excessive thirst. Weight
loss may be due to dehydration and fluid loss as well as from loss of fat that
the body is utilizing for energy. Fatigue may be due to frequently disrupted
sleep to use the restroom, high blood glucose slows the flow of blood and
thus delivery of nutrients and oxygen to cells, intracellular starvation
leading to energy deficit, high blood sugar may cause inflammation of blood
vessels triggering monocytes which infiltrate the brain this May cause
fatigue. The lungs in an attempt to balance out the acidosis will increase
ventilation rate and subsequent elimination of CO2 (hyperventilation)
resulting in raising of the pH level. Acetoacetic acid (ketone body) may
spontaneously decarboxylate to acetone, which like ketones may be
eliminated through exhalation or the urine. It is the acetone that is
responsible for the fruity smelling breath.
The day Rachel was admitted she did have ketones present in her urine,
she did complain of fatigue, polydipsia, polyuria. I don’t see a value for ABG
to indicate acidity, but her urine was acidic. Nutrition and Diagnosis
related care e7 states that “Diagnosis of DKA requires the patient’s plasma
glucose concentration to be greater than 250mg/dL, pH level to be less
than 7.30, and bicarbonate level to be less than or equal to 18mEq/L.” I
think requesting for an additional test to determine DKA would be
reasonable in attempt to confirm. I think it seems plausible that Rachel
was in this state BUT I personally wouldn’t feel comfortable treating her
for DKA if I didn’t have the lab tests to confirm the diagnosis. I suppose it
would depend on the procedures of the facility that I worked in, ultimately.
I would say that the number one precipitating factor is physiological
stress, for example acute and severe infection or illness, possibly even
sever emotional stress. When adequate insulin is no longer available
glucose production is stimulated by the counter regulatory hormones, via
lipolysis and gluconeogenesis to avoid intracellular starvation. Then
glucose and ketones build up to such a high degree (subsequent
hyperglycemia and metabolic acidosis) and achieve osmotic diuresis,
which results in dehydration and electrolyte imbalance. Then fluid is lost,
resulting in the blood becoming more concentrated which causes
hyperglycemia. Also if you’re sick it can throw off your schedule and lead
to people not taking their injections.
6.Rachel will be started on a combination of Apidra prior to meals and
snacks with glargine given in the am and pm. Describe the onset, peak, and
duration for each of these types of insulin. Her discharge dosages are as
follows: 7 u glargine with Apidra prior to each meal or snack- 1:15 insulin:
carbohydrate ratio. Rachel’s parents want to know why she cannot take
oral medications for her diabetes like some of their friends do. What would
you tell them? (Krause 696,692)
Apidra is short acting, rapid onset insulin. Has an onset of action within 15
minutes, a peak in activity 60 to 90 minutes (or two hours), and a duration
of 3 to 5 hours.
Glargine is a long acting insulin. Has a slow rate of dissolution at the
injection site, this results in a relatively constant peakless delivery over 24
hours. Must be given at a consistent time day to day if given before meals.
Onset of action is 2-4 hours, it is peakless, it’s effective duration is 20-24
hours.
T1DM may only be treated with insulin, which needs to be injected. It may
not be given orally because it is a protein and our stomach acid would
break it down before our intestines would have a chance to absorb it. I
suspect their friends are T2DM which has many oral options for drug
treatment before progressing to insulin dependency.
7. Rachel’s physician explains to Rachel and her parents that Rachel’s
insulin dose may change due to something called a honeymoon phase.
Please explain what this is and how it might affect her insulin
requirements.
The honeymoon phase is the phase where endogenous insulin secretion
recovers after correction of: hyperglycemia, metabolic acidosis, and
ketoacidosis. During this honeymoon phase exogenous insulin
requirements decrease dramatically for up to 1 year or longer, and good
metabolic control may be easily achieved. However, the need for increasing
exogenous insulin replacement is inevitable and should always be
anticipated. (Krause 678)
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? (Krause 688, 689)
Physical activity has a mechanism independent of insulin that causes
GLUT 4 translocation to the cell membrane to allow for uptake of glucose
into the cell. This leads to a drop in blood glucose levels.
I would recommend that Rachel ask her doctors permission before
returning to soccer and that her blood glucose be under control. I want her
and her parents to talk with the doctor about the fact that she is returning
to exercise and may need to adjust insulin level accordingly I would also
like for her to be aware of the symptoms of hypoglycemia and
hyperglycemia in case either of these situations happen during or after
exercise. I want her to understand that heat intolerance will affect her
easily as a diabetic and that maintaining proper hydration is important.
Before exercise I would like for Rachel to check her blood glucose level, if it
is below 100mg/dL then I would like for her to follow the 15:15 rule. Ingest
at least 15g of carbohydrates and wait 15minutes and then test her blood
again. There is a general recommendation to add 15g of carbohydrate for
every 30-60minutes of activity (variable by intensity of activity). Since
exercise causes a general decline in blood glucose level gradually, ingesting
carbohydrates during prolonged exercise can improve performance by
maintaining availability and oxidation of blood glucose. So ingest
carbohydrates after 40-60minutes of exercise is important and may also
assist in preventing hypoglycemia. Drinks that contain 6% or less of
carbohydrates are a quick way to deliver these carbs and stay hydrated
during exercise. Eating carbohydrates immediately after exercise
optimizes repletion of muscle and liver glycogen stores, this is important
for diabetics because they have an increased risk for late onset
hypoglycemia post exercise.
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? (Krause 703)
Fasting hyperglycemia is common in people with diabetes. The amount of
insulin required to normalize blood glucose levels at night during the
predawn period (1am-3am) is less than at dawn (4-8am). The increased
need for insulin at dawn causes a rise in fasting blood glucose levels this is
the dawn phenomenon. The dawn phenomenon results in insulin levels
decline between predawn and dawn or if overnight hepatic glucose output
becomes excessive.
To identify the dawn phenomenon, blood glucose levels need to be taken at
bedtime and at 2-3am. With the dawn phenomenon, predawn blood glucose
levels will be in the low range of normal but not in the hypoglycemic range.
It looks like Rachel is experiencing this but to be sure I would like for levels
to be checked before going to bed, at 2-3am, and when she wakes up (this
would be easier if she was still in the hospital but to confirm the dawn
phenomenon This should be done)
Since Rachel is T1DM administering an insulin that does not peak at 1-3am
should be considered, such as a long-acting insulin (obviously something
she needs to discuss with her doctor before altering), but I believe that she
is already on the longer duration of the long acting insulin’s (considering
the information available in the charts of the Krause book).
Also by looking at question 20 I am curious if she is even checking her
blood glucose before going to bed. It is not indicated on her chart. That does
not necessarily mean she is not checking it but it is something I would
want to address with Rachel and her parents.
10. The MD ordered a consistent carbohydrate-controlled diet when Rachel
begins to eat. Explain the rationale for monitoring carbohydrate in
diabetes nutrition therapy. ( krause702,697,685)
Blood glucose levels after eating are primarily determined by the rate of
appearance of glucose from carbohydrate digestion and absorption into the
bloodstream and the ability of insulin to clear glucose from the circulation.
The total amount of carbohydrate eaten at a meal is the primary
determinate of postprandial glucose levels. Although numerous factors
influence glycemic response to foods, monitoring total grams of
carbohydrates remains a key strategy in achieving glycemic control. Dayto-day consistency in the amount of carbohydrate eaten at meals and
snacks is reported to improve glycemic control, especially in persons on
fixed insulin regimens. Insulin doses are (or should be) adjusted to match
carbohydrate intake. If Rachel is monitored for how many carbohydrates
she has eaten and her glycemic response, it will allow for an accurate
dosing of insulin.
11. Outline the basic principles for Rachel’s nutrition therapy to assist in
control of her T1DM. (Krause 683)
Maintenance of normal growth and development, maintaining a healthy
weight is the main overarching goal. Integrate an insulin regimen into
Rachel’s usual eating habits and physical activity. Stress the importance of
SMBG when wake up & before bed, before & after exercise. Would get her
parents in with her during the nutrition education to talk about successful
meal plan approaches, insulin dosing, SMBG, and carbohydrate counting
vs. meal plan. Most of all I want to make sure whatever intervention
choice we go with fits the family and their lifestyle the best of all options,
and I want to ensure we discuss any possible barriers, and answer any
questions Rachel or her parents may have.
Carb distribution across the day, appropriate portion of carbohydrates in
the meal, insulin dose to match carbohydrates,
12. Assess Rachel’s ht./age, wt./age, ht./wt., and BMI. What is her desirable
weight? Used the CDC calculator for children
(http://apps.nccd.cdc.gov/dnpabmi/Result.aspx?&dob=1/1/2002&dom=2/12/2014&age=145&ht=6
0&wt=82&gender=2&method=0&inchtext=0&wttext=0)
For ht./age she is between the 50-75%
For wt./age she is just above the 25%
For ht./wt. she is
For BMI she is at 16 which is at the 17th percentile within healthy weight
range
Desirable weight, go to the 50% percentile, that would put her at about
93lbs.
13. Identify and abnormal lab 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, diluting the normal amount of
sodium so that the concentration appears low.
High Glucose levels d/t her being T1DM and not having enough insulin to
clear the blood of glucose.
Low phosphate levels could be d/t her lungs compensating for blood pH and
attempting to raise it via increased ventilation rate and elimination of CO2
(respiratory alkalosis). Decrease in blood CO2 which increases
intracellular pH. The increase in pH stimulates phosphofructokinase which
enhances glycolysis, causing phosphate to move into cells to supply the
enhanced phosphorylation that results. Could be d/t her insulin
administration. Could be d/t increased renal loss.
High Osmolality d/t the high blood glucose level, because she didn’t realize
she was an uncontrolled T1DM
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 d/t large amount of beta cell destruction. So proinsulin
(inactive) is chopped into c-peptide+ insulin (active) in lower than usual
amounts. Low insulin secretion parallels low c-peptide levels.
ICA, GADA, IAA is present indicating that there has been an autoimmune
destruction of pancreatic beta cells, these three antibodies are identified as
contributing to the destruction of beta cells.
High specific gravity concentrated urine has a high specific gravity value.
Probably d/t the concentration of glucose and ketones
Low urine pH d/t the concentration of acidic ketone bodies
protein in urine d/t damaged glomeruli, that have an impaired ability to
filter the blood and prevent protein from leaking into blood
High glucose in urine d/t high blood glucose levels that surpass the renal
thresh hold
Ketones in urine indicate that the level of ketones in the body is so high
(d/t utilizing fat as energy source) that they are being excreted in the
urine
Prot chk indicates that there is protein in her urine
14. Determine Rachel’s protein and energy requirements. Be sure to
explain what standards you used to make this estimation.
In persons with type 1 or type 2 diabetes with normal renal function, the
RD should advise that usual protein intake of approximately 15 to 20% of
daily energy intake does not need to be changed. Although protein has an
acute effect on insulin secretion, usual protein intake in long-term studies
has minimal effects on glucose, lipids, and insulin concentrations, if there
is nephropathy damage though a protein intake of one gram or less per kg
body weight per day is recommended.
I found a paper by the ADA that says to use DRI for healthy kids
http://care.diabetesjournals.org/content/28/1/186.full#ref-86
So I used the DRI formula from Krause and then multiplied it by a low
active PAL (PAL Krause p26, formula p 27)
82/2.2= 37 rounded down
60x2.54=152.4 age=12
EER= 135.3-30.8 x age +PA x (10 x Wt.kg + 934 x ht m) +25
EER= [135.5- 30.8 x 12 + 1.4 x (10x 37 + 934 x 1.524) + 25
EER=
135.5 - 369.6 + 1.4 x ( 370 + 1,423.416) +25
EER= 2301.1824
Protein needs are 15-20% of daily needs (Nutrition and diagnosis related care e7)
2300x.15 = 345cal
2300x.20=460cal
345/4=86.25
460/4=115
range 86-115g protein daily
15. Prioritize two nutrition problems and complete the PES statement for
each. (used IDNT book)
Food and nutrition related knowledge deficit related to lack of exposure to
information as evidenced by new diagnosis of diabetes, hyperglycemia
blood glucose level of 683 mg/dL , HbA1C of 14.6%
Impaired nutrient utilization related to polydipsia, polyuria, polyphagia,
weight loss and fatigue as evidenced by lab results of 295.3 mmol/kg/H2O
osmolality level, 683mg/dL glucose level, HbA1C 14.6%, weight loss of 9%
in past month.
16. Determine Rachel’s initial nutrition prescription using her diet record
from her home as a guideline, as well as your assessment of her energy
requirements.
Basic Nutrition Prescription
(Krause 700)
Food
group
Break
fast
Snack
Lunch
Snack
Soccer
pract
Snack
Dinner
Total
daily
servings
CHO
Pro
Fat
cal
starch
2
1
2-3
1
1
1
2-3
12
15
180
3
36
1
12
80
fruit
1
1
0-1
1
4
15
60
milk
1
1
1
3
12
36
8
24
veg
2-3
2-3
5
5
25
2
10
meat
2-3
3-4
6
60
7
42
1
3
100
25
5
30
75(55)
fats
1
0-1
1-2
0-1
0
0-1
1-2
6
5
30
CHO
choices
3-4
1
4-5
1
1
1
4-5
Total
grams
301
112
75
Cal/
gram
X4
1,204
X4
448
X9
675
Percent
calories
52%
19%
29%
45
Total
calories
2327
Basic meal plan was developed that can be tailored with the patient and
parents. Discuss feasibility of meal plan, timing of meals and snacks with
insulin, appropriate sizes of meals and snacks. Distribution of meals with
snacks must be assessed along with the types of medication prescribed.
Developed a plan that includes 11 starches, 4 fruits, 3 milks, 5 veggies, 6
meats/subs., 6 fats that calorically comes close to the Kcal average of
2300.
Basic carbohydrate counting emphasizes the following topics: basic facts
about carbohydrates, primary food sources of carbohydrates, average
portion sizes, the importance of consistency and accurate portions,
amount of carbohydrates that should be eaten, and label reading. An
important goal of nutrition counseling is to facilitate changes in existing
food and nutrition related behaviors and the adoption of new ones, through
motivational interviewing, assessment of readiness to change, adapt the
nutrition intervention plan to the clients lifestyle as much as possible, and
agree upon set goals. For Rachel a lot of this would involve her parents
since they are the caregivers and are most likely packing her lunches and
preparing her dinners, they will also probably be helping with glucose
monitoring and insulin administrations.
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- poptarts and 8oz of skim milk,
how much Apidra should she take to cover the carbohydrate in this meal?
Insulin carbohydrate ratio is the number of grams of carbohydrate covered
by one unit of insulin. For example, if your insulin-to-carbohydrate ratio is
1:15, then you need to deliver one unit of insulin to cover every fifteen
grams of carbohydrates you eat. ICR can be established for an individual
by physician and will guide decisions on the amount of mealtime insulin to
inject.
www.supertracker.usda.gov/foodapedia used to find carbohydrates grams:
76g (2 poptarts)
+ 12g (8oz skim milk)
so, 88gCHO /15=5.86 ≈6u
88g CHO
18. Dr. Cho set Rachel’s fasting blood glucose goal at 90-180mg/dL. If her
total daily insulin does is 33u and her fasting a.m. blood glucose is
240mg/dL, what would her correction dose be? (Krause p. 693)
CD= 1700/33= 51.5
about 52mm/dL.
1 unit of insulin should lower blood glucose level by
Using a dose of 2 units of insulin should be enough to lower blood glucose to
around 140mg/dL which is within her target range. Of 90-180mg/dL
19. Write an ADIME note for your initial nutrition assessment.
Assessment
Rachel Roberts
Anthropometric Measurements:
Age:12 Y.O. Sex: female Height: 5ft Weight: 82lbs.
BMI: 16=17th % healthy
Usual weight: 90lbs
Admitted: w/ acute-onset hyperglycemia after fainting in soccer practice.
Caucasian, catholic, student, English only
Nutrition Focus Physical Findings:
General appearance: Slim, healthy-appearing
Skin: pale, diaphoretic
Urine: Cloudy and Amber
Vitals: Temp:98.6 Pulse:101 BP:122/77 Resp. rate:22
Pt. chief complaint: polyphagia, polydipsia, polyuria, wt. loss indicated by
looser clothing
MHX: None-recently had strep throat
Meds: none at home
SHX: nonsmoker, no alcohol use
FHX: Father- HTN, Mother-Hypothyroidism, sister-celiac disease. Single
7th grade, Parents divorced, siblings sister 8, brother 4.
Neurologic: alert but slightly confused
Biochemical Data:
Increased: Glucose, osmolality, HbA1C, +ICA, +GADA, +IAA, Specific
gravity in urine, +protein in urine, +glucose in urine, +ketones in urine,
+prot chk. In urine
Decreased: sodium, phosphate, c-peptide, decreased pH in urine
Food and Nutrition Related History:
Usual Intake:
Mom and Dad state that Rachel is kind of a picky eater. She eats only
chicken and fish- eats salad, broccoli, carrots, tomatoes, and asparagus as
her only vegetables. Breakfast-cereal and milk or pop-tart with milk; packs
lunch for school- peanut butter and jelly or turkey and cheese sandwich,
chips, carrots, and usually drinks water. Has cereal or granola bar before
soccer practice- drinks water throughout practice. Dinner is usually
prepared by Mom when she is at her house-always some salad, meat, and
pasta, potato, or rice. Dad states that when the kids a re with him he
doesn’t cook very often and they usually order pizza or Chinese food.
Snacks include cereal, ice cream, yogurt, some fruits (apple, bananas),
popcorn, chips, or cookies.
Estimated needs: 2,300 Kcal
Nutrition Diagnosis
Food and nutrition related knowledge deficit related to lack of exposure to
information as evidenced by new diagnosis of diabetes, hyperglycemia
blood glucose level of 683 mg/dL , HbA1C of 14.6%
Nutrition Intervention
Basic Nutrition Prescription
(Krause 700)
Food
group
Break
fast
Snack
Lunch
Snack
Soccer
pract
Snack
Dinner
Total
daily
servings
CHO
Pro
Fat
cal
starch
2
1
2-3
1
1
1
2-3
12
15
180
3
36
1
12
80
fruit
1
0-1
1
4
15
60
1
60
milk
1
1
1
3
12
36
8
24
veg
2-3
2-3
5
5
25
2
10
meat
2-3
3-4
6
7
42
1
3
100
25
5
30
75(55)
5
30
45
fats
1
0-1
1-2
0-1
0
0-1
1-2
6
CHO
choices
3-4
1
4-5
1
1
1
4-5
Total
grams
301
112
75
Cal/
gram
X4
1,204
X4
448
X9
675
Percent
calories
52%
19%
29%
Total
calories
2327
Basic meal plan was developed that can be tailored with the patient and
parents. Discuss feasibility of meal plan with , timing of meals and snacks
with insulin, appropriate sizes of meals and snacks with Rachel and her
parents. Distribution of meals with snacks must be assessed along with the
types of medication prescribed. Developed a plan that includes 12
starches, 4 fruits, 3 milks, 5 veggies, 6 meats/subs., 6 fats that calorically
comes close to the Kcal average of 2300.
Basic carbohydrate counting emphasizes the following topics: basic facts
about carbohydrates, primary food sources of carbohydrates, average
portion sizes, the importance of consistency and accurate portions,
amount of carbohydrates that should be eaten, and label reading. An
important goal of nutrition counseling is to facilitate changes in existing
food and nutrition related behaviors and the adoption of new ones, through
motivational interviewing, assessment of readiness to change, adapt the
nutrition intervention plan to the clients lifestyle as much as possible, and
agree upon set goals. For Rachel a lot of this would involve her parents
since they are the caregivers and are most likely packing her lunches and
preparing her dinners, they will also probably be helping with glucose
monitoring and insulin administrations.
Nutrition Monitoring and Evaluation
(Krause 702)
Food intake, medication, metabolic control, anthropometric
measurements, and physical activity should be monitored and evaluated.
Medical and clinical outcomes should be monitored after the second and
third visit to determine whether the patient is making progress toward
established goals. If no progress is evident, the individual and RD need to
reassess and perhaps revise nutrition interventions. Blood glucose
monitoring results can be used to determine whether adjustments in foods
and meals will be sufficient to achieve blood glucose goals or if medication
additions or adjustment need to be combined with MNT. Nutrition care
must be coordinated with an interdisciplinary team. Documentation in the
patients medical record serves as a communication tool for members of the
health care team, it also serves as a legal document of what was done and
not done. Food records can be compared with the meal plan which will help
to determine whether the initial meal plan needs changing and can be
integrated with the blood glucose monitoring records to determine changes
that can lead to improved glycemic control.
20. When Rachel comes to the clinic she brings her food and blood glucose
record with her.
A. Determine the amount of carbohydrates she is consuming at each meal.
To get the carbohydrate grams I again utilized:
www.supertracker.usda.gov/foodapedia
7:30 a.m.
2pop tarts (76 g) + 1 banana (27g) + 16 oz skim milk 16oz. (24g) +ovaltine
2tbsp. (9g) =136g CHO
noon
2 slices pepperoni pizza (57g)+ 2 chocolate chip cookies-I used chips a hoy
(13g) = 70g CHO
2p.m.
granola bar (19g)= 19g CHO
4:30 p.m.
Apple (19g) + 6saltines (13g) + 2tbsp. peanut butter (3g) = 35g CHO
Soccer practice
16 oz Gatorade (31g)= 31g CHO
6:30
1cup rice (35g)+ 2oz chicken (o)+ 1/2c broccoli (17g)+ egg roll (19g)+ 2c
skim milk (24g) =95g CHO
8:30p.m.
2c ice cream (63g)+ 2 tbsp peanuts (4g) = 67g CHO
B. Determine whether she is taking adequate amounts of Apidra for each
meal according to her record.
7:30a.m.
136g/15= 9.06 ≈9u
Rachel gave herself 5u
noon
70g/15=4.6≈ 5u rounded up to 5u because I am not sure if insulin is
allowed to does at ½ units
Rachel gave herself 6u
6:30p.m.
95g/15=6.3 ≈6u I rounded down again because I am not sure if insulin is
allowed to be dosed in partial increments, also her BG was 80 which is the
lowest we would ever want for it to drop because we don’t want her to slide
into hypoglycemia. So with that being said I actually think that her dosing
at 5u was appropriate considering that her BG was at the low end.
8:30p.m.
67g/15=4.46 ≈5u again I rounded d/t the fact that I am not sure that
partial doses/ increments of insulin are given or not.
(Rachel took 4u )
She did not note whether she took her blood glucose level before bed, make
sure to talk with her about the importance of doing so.
C. Calculate a correction dose for her to use.
Using information from Jennifer Morgan’s power point :
Normal weight persons with T1DM
• Dosage: 0.5-1 unit/kg body wt.
• Approx. 30-50% of the total daily insulin dose is used to provide for
basal or background insulin needs
• The remainder (bolus insulin) is divided among meals
o Insulin-to-carbohydrate ratio
o Proportionally to CHO content
o 1-1.5 units/ 10-15g CHO consumed
o Higher amount usually needed to cover breakfast
carbohydrates
Rachel is 82lbs ≈ 37kg
1unit x 37kg = 37u
37u x .4 = ≈15units basal "37-15= 21 units bolus
so assuming 37 total daily insulin dose
1700/37=45.9 (using the correction factor in Krause)
so one unit of insulin should lower the blood glucose by ≈ 45mg/dL