Pediatric Case Study
1. Diagnoses? Rate of occurrence?
Diabetes mellitus type1 (aka insulin-dependent or juvenile diabetes)
Prevalence: Estimated 5-10% of North Americans; rate of new cases among youth
each year is 19 per 100,000
2. Lab tests? Possible results?
 electrolytes: deceased sodium, potassium, magnesium and phosphorus
indicates dehydration
 serum osmolality: elevated results may indicate hypovolemia
 fasting blood sugar test: 100-125 mg/dL prediabetes; > 126 mg/dL (on two
separate tests) dx diabetes
 WBC: insulin-producing antibodies (e.g., auto-antibodies, human leukocyte
antigens [HLA]) suggests diabetes
 RBC (e.g., hematocrit, hemoglobin): elevated results may indicate
dehydration
 urinalysis: ketones-pos suggests diabetes
 A1-C (for 2-3 mo blood sugar level averages): >7% suggests diabetes (ADA)
 kidney function tests (e.g., creatinine, BUN)
+
test younger sibling (DM1 has strong genetic correlation)
3. Pathophysiology.
DM1 is a chronic condition in which the pancreas produces little-or-no insulin.
Although it can develop at any age, it typically appears during childhood or
adolescence.
Quick recap: Glucose is a main source of energy for muscle and tissue cells. It
comes from two major sources – food and liver. During digestion, sugar is
absorbed into the bloodstream. When you eat, the pancreas secretes the hormone
insulin into the bloodstream, too. As it circulates, it helps sugar enter cells.
Blood sugar levels drop, also decreasing the amount of insulin secretion. The
liver acts as both a glucose manufacturing and storage center.
With DM1, the immune system attacks and destroys the insulin-producing beta cells
in the pancreas, leaving the individual with little or no insulin. Thus, instead
of moving into the cells, sugar builds up in the bloodstream. Conversely,
glucagon-producing alpha cells overproduce glucagon (triggering even more blood
glucose production).
Various factors contribute to DM1, including genetics and exposure to certain
viruses (or may be idiopathic). In spite of active research, DM1 has no cure.
However, with advances in blood sugar monitoring and insulin delivery, daily
management has been greatly simplified and most individuals can expect to live
long, healthy lives.
Symptoms include: Increased thirst and frequent urination (sugar build-up in the
blood pulls fluid from tissues); extreme hunger; weight loss; fatigue; blurred
vision; slow-healing sores; dry, itchy skin; and paresthesias in feet.
Hypoglycemia: Shakiness; sweating; palpitations; hunger; difficulty
concentrating/reading; frank mental confusion; disorientation; slurred speech;
extreme fatigue and lethargy; seizures; and unconsciousness.
Hyperglycemia: Diabetic ketoacidosis (blood glucose >250 mg/dL); polyuria;
polydipsia; dehydration; fruity odor to breath; fatigue; ketone-pos urine.
Long-term consequences: HTN; dyslipidemia; macrovascular diseases (e.g.,
peripheral vascular disease, cerebrovascular disease, coronary heart disease);
and microvascular diseases (e.g., diabetic neuropathy, retinopathy, neuropathy,
gastroparesis).
4. Medical interventions? Include medication options and side effects.
 PO fluids
 insulin inj – will probably begin 4 shot/day regimen (rapid-/short-acting
insulin) before qmeal and an additional one (e.g., Lente) qHS

tx options include
Name
Use
Side Effects
Miscellaneous
INSULIN, rapidacting (e.g.,
lispro, Humalog,
Novolog)
onset 15 min;
peak 1 hr;
duration 3-5 hr;
used just before
meals
skin rxn (e.g., hives,
wheal, induration,
hypertrophy); hypoglycemia;
allegic rxn (e.g., local
itching, erythema, burning
around inj site)
hypoglycemia occurs
if lag time is too
long or pt
exercises w/in 1 hr
of administration;
dose should be
decreased w/ highfat meals
INSULIN, shortacting (e.g.,
Humulin R, Novolin
R)
onset 30-45 min;
peak 2-3 hr;
duration 5-8 hr;
used before
meals
skin rxn (e.g., hives,
wheal, induration,
hypertrophy); hypoglycemia;
allegic rxn (e.g., local
itching, erythema, burning
around inj site)
lag time not used
appropriately
(should be given
20-30 min before
eating)
INSULIN,
intermediate/basal
(e.g., NPH,
Humulin N, Lente,
Humulin L)
takes long to
work and works
longer (than
rapid-acting
insulin), onset
2/3-4 hr; peak
4-10/12 hr;
duration 10/1216/18 hr; taken
in PM to keep
insulin in body
overnight
skin rxn (e.g., hives,
wheal, induration,
hypertrophy); hypoglycemia;
allegic rxn (e.g., local
itching, erythema, burning
around inj site)
AM inj may not last
until PM; qHS inj
may not last until
AM (“dawn
phenomena”); zinc
susp binds w/ Lente
(lessening it’s
effect)
INSULIN, longacting (e.g.,
Ultralente,
Humulin U,
Glargine)
onset 6-10 hr;
peak 16-20 hr;
duration 18-20
hr; take in AM
or qHS
INSULIN, premixed
insulin
onset 5-15 min;
peak varies
INSULIN, pump
therapy
pralintide
(Symlin)
low-dose aspirin
therapy
lipodystrophy
provides rapid/short-/basalinsulin; boluses
given before
meals
inj form; slows
mvmt of food
through stomach
to curb sharp
increase in
blood sugars
after meals
prevent heart
and blood vessel
disease
skin rxn (e.g., hives,
wheal, induration,
hypertrophy); hypoglycemia;
allegic rxn (e.g., local
itching, erythema, burning
around inj site)
skin rxn (e.g., hives,
wheal, induration,
hypertrophy); hypoglycemia;
allegic rxn (e.g., local
itching, erythema, burning
around inj site)
allergic rxn (e.g., local
itching, erythema, burning
around inj site)
constipation
N; V; rash; Reye’s syndrome
atrophy or hypertrophy of
subcutaneous tissue
(especially if same inj
zinc susp binds w/
Lente; peak time
may vary w/ pts
allergic rxn may
improve after 1-3
mo or w/
antihistamine
TRANSPLANT,
pancrease
TRANSPLANT, islet
cell
TRANSPLANT, stem
cell
site is used often)
may no longer need insulin,
but aren’t always
successful and have serious
risks; in addition, will
have lifelong potent
immune-suppressing drugs
that may increase risk of
infection and cause organ
injury (thus this tx is
often reserved only for
those who can’t control
their diabetes or already
have serious complications)
experimental
experimental; risky surgery
5. Nursing interventions.
 Monitor blood glucose, and for sx of hypo-/hyper- glycemia closely
 Tchg: Insulin types, action and goals
 Tchg: Sx and causes of diabetes, and hypo-/hyper- glycemia
 Tchg: Nutrition and wt mgmt
 Assess patient education needs
 Encourage pt and family to express feelings/concerns
 Identify psychosocial barriers to diabetes and family-process management
 Give information about education programs and support groups
6. Discharge education. Include at least one developmental theorist to support the
method of education.
Discharge education should be completed with both Sally and her parents.
According to Erikson’s psychosocial stage, Sally is in stage 4 (Industry vs
Inferiority). At this Sally develops a sense of pride in her accomplishments and
abilities through her social interactions (e.g., encouragement, commendation from
parents and teachers). Developing a feeling of competence and belief in her own
skills is important. Thus, at this stage, Sally should be allowed to a part of
her own cares (e.g., finger stick), and praised when performing them accurately.
Piaget would recommend that at this third stage (Concrete Operational Stage)
inductive logic (e.g., specific to general reasoning) and concrete examples
(e.g., let Sally see a blood glucose monitor) work best.
Topics include: Diabetes management (especially sx of hypo-/hyper- glycemia);
glucose testing; insulin use; nutrition; extra needs for activities (especially
since Sally is active); foot care; “sick day” management; oral/skin care; regular
physical and eye exams
7. Recommended informational websites?
 Juvenile Diabetes Research Foundation Internation (JDRF):
http://www.jdrf.org/
o “Life with Diabetes eNewsletter”
 JDRF Kids Online: http://kids.jdrf.org/
 Medline Plus: http://www.nlm.nih.gov/medlineplus/diabetestype1.html
o links to NIH, JAMA, JDRF-I and FDA
o many languages
 American Diabetes Association: http://www.diabetes.org/home.jsp
 Mayo Clinic Diabetes Center:
http://www.mayoclinic.com/health/diabetes/DA99999
 Kid’s Health Diabetes Center:
http://kidshealth.org/kid/centers/diabetes_center.html