Taryn Berry
Type 1 Diabetes Mellitus with Diabetic Ketoacidosis Case Study
1. There are precipitating factors for diabetic ketoacidosis. List at least seven
possible factors.
 Precipitating factors for diabetes ketoacidosis include infection,
discontinuation or inadequate insulin therapy, pancreatitis,
myocardial infarction, cerebrovascular accident, psychological
problems related to an eating disorder, urinary tract infection, and
pneumonia.
 American Family Physicians,
http://www.aafp.org/afp/2005/0501/p1705.html#afp20050501p17
05-t1.
 Medscape, http://www.medscape.com/viewarticle/706727_4
2. Describe the metabolic events that led to the symptoms associated with DKA.
 An insulin deficiency causes the body to metabolize triglycerides and
amino acids instead of glucose. As a result of this, glycerol and free
fatty acids (FFAs) serum levels increase, as well as, alanine because of
muscle catabolism. Glycerol and alanine are needed for hepatic
gluconeogenesis, which is stimulated by excess glucagon. Glycerol also
stimulates the conversion of FFAs into ketones by mitochondria.
Insulin normally blocks the process of turning FFAs into ketones, but
with the absence of insulin ketogenesis proceeds. The strong organic
compounds that result create metabolic acidosis. Acetone
accumulates in serum and is disposed of through respiration.
Hyperglycemia due to insulin deficiency leads to marked urinary
losses of water and electrolytes. Also, with the excretion of ketones in
the urine, sodium and potassium are also lost. Potassium levels are
also lost during treatment because they are pushed into the cells by
insulin. As a result sodium and potassium are important to monitor.
 The Merck Manual,
http://www.merckmanuals.com/professional/endocrine_and_metab
olic_disorders/diabetes_mellitus_and_disorders_of_carbohydrate_met
abolism/diabetic_ketoacidosis_dka.html
3. Assess Susan’s physical examination. What is consistent with diabetic
ketoacidosis? Give the physiological rationale for each that you identify.
 Nausea, vomiting, and abdominal pain/tenderness are symptoms
consistent with fluid imbalance. Tachycardia is a result of dehydration
and acidosis. Rapid Kussmaul breathing is to compensate for
academia. Sunken eyes, dry membranes, dry/flushed skin/poor turgot
are due to dehydration. Lethargy is a stymtpm of more sever
decompensation.
 The Merck Manual,
http://www.merckmanuals.com/professional/endocrine_and_metab
olic_disorders/diabetes_mellitus_and_disorders_of_carbohydrate_met
abolism/diabetic_ketoacidosis_dka.html#v989292
4. Examine Susan’s biochemical indices both in the chemistry section and in her
ABG report. Which are consistent with DKA? Why?
Test
Normal
Admit
Albumin
3-6.5
4.3
Potassium
3.5-5.5
5.8
Chloride
98-108
110
PO4
2.5-4.5
4.9
Osmolality
275-295
336
Total CO2
24-30
22
Glucose
70-120
475
BUN
8-26
29
Creatinine
0.6-1.3
1.8
CHOL
140-199
201
HbA1c
4.8-7.8
12.0
WBC
4.3-10
12
HGB
12-16
18
HCT
37-47
50
pH
7.35-7.45
7.31
CO2 content
23-30
22
HCO324-28
21
Creatinine, osmolality, glucose, potassium, HbA1c, pH, and HCO3- levels are
indicative of DKA.
5. If Susan’s symptoms were left untreated, what would happen?
 If these symptoms were left untreated, the prognosis could result in
mortality. The mortality rates for DKA are between 1 and 10%.
Circulatory collapse, hypokalemia, and infection are the main causes
of death so not treating these symptoms could result in worse
conditions.
 The Merck Manual,
http://www.merckmanuals.com/professional/endocrine_and_metab
olic_disorders/diabetes_mellitus_and_disorders_of_carbohydrate_met
abolism/diabetic_ketoacidosis_dka.html#v989317
6. Assuming Susan’s SMBG records are correct, what events seem to have
precipitated the development of DKA?
 During her period, volleyball tournament, and after her birthday party
her blood glucose was significantly high. This may indicate that there
was alcohol consumption for her birthday, thus elevating her blood
glucose. Stress and emotional stress during her period and volleyball
tournament could have also increase her blood glucose at these times.
7. What, if anything, could Susan have done to avoid DKA?
 So avoid DKA, she could have taken care of her blood glucose better.
Her HbA1c is very high, at a 12, indicating that in the past two to three
months, her blood glucose concentration was high. Also, being more
aware of her carbohydrate intake, increasing fluid consumption, and
appropriate amounts of insulin to be taken.
8. While Susan is being stabilized, Tagamet is being given IV piggyback. What
does “IV piggyback” mean? What is Tagamet, and why has it been
prescribed?
 IV piggyback is a way to administer medication through an IV into the
vein. It can be medication or antibiotic that needs to be diluted and
administered slowly. This is either administered by a gravity drip or
IV pump. Tagament is a drug used to treat ulcers, gastroesophageal
reflux disease (GERD), heartburn, injury to the esophagus, and acidity
in stomach. This was most likely prescribed to help Susan with the
nausea, vomiting, and stomach pains she is currently having.
 Nutrition Therapy and Pathophysiology 2e
 Medline Plus,
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682256.html
9. The diabetes Control and Complications Trial was a landmark multicenter
trial designed to test proposition that complications of diabetes mellitus are
related to elevation of plasma glucose. It is the longest and largest
prospective study showing that lowering blood glucose concentration slows
or prevents development of complications common to individuals with
diabetes. The trial compared “intensive” insulin therapy (“tight control”)
with “conventional” insulin therapy. Define “intensive” insulin therapy.
Define “conventional” insulin therapy.
 Conventional insulin therapy consists of a constant dose of basal
insulin combined with short or rapid acting insulin. Insulin may be
mixed or premixed formulas. Intensive insulin therapy requires
multiple daily injections of bolus insulin before meals in addition to
basal insulin once or twice daily.
 Nutrition Therapy and Pathophysiology 2e, 487-488.
10. List the microvascular and neurologic complications associated with type 1
diabetes.
 Microvascular complications include nephropathy and retinopathy.
Neurologic complications include peripheral neuropathy and
autonomic neuropathy, which can include cardiovascular,
genitourinary, and gastroparesis.
 Nutrition Therapy and Pathophysiology 2e, 487.
11. What are the advantages of intensive insulin therapy?
 The advantages of intensive insulin treatment is that insulin can be
adjusted based on food intake, thus replicating insulin secretion like a
person without diabetes. Another advantage is that it delays onset and
slows progression of complications such as retinopathy, nephropathy,
and neuropathy.
 Nutrition Therapy and Pathophysiology 2e, 488.
12. What are the risks of intensive insulin therapy (tight control)?

The risks involved with intensive insulin therapy are that the insulin
regimen must be in sync with the individuals lifestyle, so they must be
aware of the needed doses at all times. Stress, illness, unpredicted
insulin absorption, or changes in exercise must also be address with
the patients because these can affect the amount on insulin the patient
needs to take. Being aware of these are important and could pose a
risk if not taken care of properly.
 Nutrition Therapy and Pathophysiology 2e, 489.
13. Dr. Green consults with you, and the two of you decide that Susan would
benefit from insulin pump therapy combined with CHO counting for
intensive insulin therapy. This will give Susan better glycemic control and
more flexibility. What are some of the key characteristics of candidates for
intensive insulin therapy?
 Key characteristic of candidates for intensive insulin therapy are
patients that need flexibility, eat meals at different times of the day,
are active, and are willing to learn about their own insulin tendencies.
 Nutrition Therapy and Pathophysiology 2e, 489.
14. Explain how an insulin pump works. Is Susan a candidate for an insulin
pump?
 An insulin pump is a form of intensive therapy in which insulin is
pumped continuously in small amounts through a subcutaneous
catheter 24 hours a day. Boluses of short or long acting insulin are
given before meals. I believe that Susan is a candidate for an insulin
pump, especially considering her age, activity level, and involvement
with school and friends. An insulin pump is often easier then deal with
shots ever day.
 Nutrition Therapy and Pathophysiology 2e, 489.
15. How would you describe CHO counting to Susan and her family?
 CHO counting can be explained by first going over serving sizes and
sources of carbohydrates. Sources of carbohydrates include, starches,
fruits, milk/dairy, and sweets. CHO counting is based on the amount,
not the type of carbohydrate. There are two ways to actually count the
carbohydrates. The first is that 15 grams of carbohydrate counts as
one choice or the total grams of carbohydrates can be counted using
the food label.
 Nutrition Therapy and Pathophysiology 2e, 492.
16. How is CHO counting used with intensive insulin therapy?
 CHO counting is used in intensive insulin therapy because based on
the amount of carbohydrate choices eaten or total amount of grams
eaten, the amount of insulin will need to be given. The amount of
insulin cannot be determined without knowing how many
carbohydrates were eaten.
17. Estimate Susan’s daily energy needs using the Harris- Benedict equation.
 110 lbs/ 2.2 kg=50kg
 63 in x 2.54 cm=160 cm

655 + (9.56 x 50 kg) + (1.85 x 160 cm) – (4.68 x 16)= 1354 x 2.0
(PAL)=2708 or 2700 kcal.
 Harris Benedict Equation
18. Using the 1-week food diary from Susan (next page), calculate the average
the amount of CHO usually consumed each meal and snack.
138 gm CHO breakfast
68 gm CHO lunch
30 gm CHO snack
70 gm CHO dinner
14 gm CHO HS
19. After you have calculated Susan’s usual CHO intake from her food record
(Question 18), develop a CHO—counting meal plan that she could use.
Include menu ideas.
 Carb: 2700 x .5=1350 kcal/ 4=340 g
 PRO: 2700 x .2=540 kcal/ 4=135 g
 Fat: 2700 x .3=810/9=90 g
Daily Total: CHO 340 g
Protein 135 g
Fat 90 g
Total kcal 2700
 Carb: 340g – 30 g (snack)=310 g/3 meals=103 g
 Breakfast: 1 c cereal, 1 c 2% milk, 1 banana, ½ c OJ=102 g CHO
 Snack: 5 saltines, 1 tbs peanut butter=15 g CHO
 Lunch: Cheeseburger-1 bun, 1 slice of cheese, 2 oz beef, 1 apple, 1 c
French fries, ½ c carrots=97 g CHO
 Dinner: Fish sandwich, raw broccoli and cauliflower, ranch dressing, 1
c mashed potatoes, 1 c strawberries=100 g CHO
 Snack: 3 cups popped popcorn, water=15 g CHO
 Total CHO: 329 g CHO.
20. Just before Susan is discharged, her mother asks you, “My friend who owns a
health food store told me that Susan should use stevia instead of artificial
sweeteners or sugar. What do you think?” What will you tell Susan and her
mother?
 Stevia is considered an artificial sweetener. This means that it can be
used to sweeten food without the extra calories. Stevia is also referred
to as Rebaudioside A, or Reb-A. It is a purified product from the stevia
plant and is several hundred times sweeter then sugar. Stevia is
recognized as a safe (GRAS) food additive and tabletop sweetener by
the FDA. In regards to diabetic use, although stevia is lower in calories,
it is not carbohydrate free. As a result, if Susan used stevia, she would
still need to be cognizant to the amount she had consumed and take
the correct amount of insulin.

American Diabetes Association, http://www.diabetes.org/food-andfitness/food/what-can-i-eat/understanding-carbohydrates/artificialsweeteners/
Resources
American Diabetes Association. “Low-Calorie Sweeteners.” 16 Dec 2014. Referenced
from http://www.diabetes.org/food-and-fitness/food/what-can-ieat/understanding-carbohydrates/artificial-sweeteners/
Kishore, Preeti. “Diabetic Ketoacidosis (DKA).” The Merck Manual. June 2014.
Referenced from http://www.merckmanuals.com/professional/
endocrine_and_metabolic_disorders/diabetes_mellitus_and_disorders_of_car
bohydrate_metabolism/diabetic_ketoacidosis_dka.html#v989317
Kitabchi, A.E., Umpierrez, G.E., Miles, J.M., Fisher, J.N. “Hyperglycemic Crises in Adult
Patients With Diabetes.” Medscape. 2009. Referenced from
http://www.medscape.com/viewarticle/706727_3
Medline Plus. “Cimetidine.” 1 Sept 2010. Referenced from
http://www.nlm.nih.gov/medlineplus/druginfo/meds/a682256.html
Nelms, Sucher, Lacey, Roth. (2012). Nutrition Therapy & Pathophysiology (II ed.):
Belmont, CA: Wadsworth.
Trachetenbarg, David E. “Diabetic Ketoacidosis.” American Family Physician. May
2005. Referenced from http://www.aafp.org/afp/2005/0501/p1705.html
#afp20050501p1705-t1.