This document provides information on caring for children with endocrine or metabolic conditions. It begins with an anatomy and physiology review of the endocrine system and key differences in children. It then discusses several important pathophysiological conditions including growth hormone deficiency, precocious puberty, hypothyroidism, congenital adrenal hyperplasia, and diabetes mellitus type 1. For each condition, it identifies signs and symptoms, diagnostic criteria, and nursing considerations for treatment and management. The focus is on applying this scientific knowledge to guide nursing care of pediatric patients with endocrine disorders.

1. Caring for the Child with an
Endocrinological or Metabolic
Condition
Joyce Buck, PhD(c), MSN, RN-C, CNE
Joy Shepard, PhD, RN-C, CNE

2. 1. Describe the Anatomy and Physiology of the Endocrine
System and Pediatric Differences
2. Identify Functions of Important Hormones
3. Identify Signs and Symptoms that May Indicate an Endocrine
Disorder
4. Identify Conditions for Which Short Stature is a Sign
Learning Outcomes

3. • Distinguish between Nursing Care for
Type 1 Diabetes Mellitus and That for Type 2
• Describe Collaborative Management for the Child with Type 1
diabetes and That for Type 2
• Develop a Nursing Care Plan for the Child with an Inherited
Metabolic Disorder
Learning Outcomes (cont’d)

4. A & P Review
Organs of the Endocrine
System
• Hypothalamus
• Pineal gland
• Pituitary gland
• Thyroid gland
• Parathyroid glands
• Adrenal glands
• Pancreas
• Gonads

5. Figure 30-1 Major organs and glands of the endocrine system

6. • Hypothalamic-pituitary system produces releasing & inhibiting
hormones that regulate the function of many endocrine glands
(thyroid, adrenal, reproductive)
• Hypothalamus synthesizes many hormones
• Pituitary gland works by stimulating or inhibiting the release of
these hormones
• Pituitary gland also secretes certain hormones
Anatomy & Physiology

7. • Hormone secretion regulation occurs through a negative
feedback system
• Occurs when an endocrine gland or secretory tissue receives a
message that the target cells have received an adequate
amount of hormone
• Further secretion is inhibited
• Secretion is resumed only when the secretory tissue receives
another message indicating that levels of the hormone are low
A & P cont’d

8. • In children the endocrine system is responsible for stimulating
growth & development during childhood & adolescence
• Multiple hormones in the endocrine system are responsible for
skeletal growth & maturation (growth hormone, thyroid
hormone, adrenal & gonadal androgens & estrogen)
• Skeletal maturity can be detected by examining the child’s bone
age (x-rays of hand & wrist)
Pediatric Differences

9. • During childhood, the production of sex hormones (estrogen,
progesterone, & testosterone) is low
• Puberty (sexual maturation) occurs when gonads begin to
secrete increased amounts of the sex hormones, estrogen &
androgens
• Lasts an average of 4.5 years
• Hypothalamus produces increased amounts of gonadotropin-
releasing hormone (GnRH) at average age of 9 years in girls &
11 years in boys
Pediatric Differences cont’d

10. • Stimulates the anterior pituitary gland to secrete luteinizing
hormone (LH) & follicle-stimulating hormone (FSH)
• In boys, LH stimulates testosterone production & FSH
stimulates sperm production
• In girls, LH & FSH stimulate development & maturation of the
ova & ovulation
Gonadotropin-Releasing Hormone (GnRH)

11. • Onset of adrenal androgen production
• These adrenal hormones lead to the development of acne,
pubic hair & adult body odor
• Pubertal development usually follows a specific sequence
(breast development, pubic hair growth, & menarche in females,
& testicular enlargement, pubic hair growth, appearance of
spermatozoa in seminal fluid, facial hair, & voice change in
males)
Adrenarche

12. • Onset of menstruation in females
• Occurs at average age of 12.1 years in African American girls &
12.6 years in White girls
Menarche

13. Pathophysiological
Conditions of the
Endocrine System
Conditions of the Anterior Pituitary

14. • The release of growth hormone from the anterior pituitary gland
is controlled by the hypothalamus, which secretes releasing &
inhibitory factors
• Growth hormone (GH) stimulates linear growth & bone mineral
density, as well as growth of all body tissues
• GH also stimulates synthesis of proteins in the liver, including
somatomedins or insulin-like growth factors (IGF’s) which
promote glucose utilization by the cells
Etiology

15. • Anything that interferes with the production or release of growth
hormone (GH)
• Infarction of pituitary (SCD)
• Infection (CNS)
• Tumors (pituitary or hypothalamus)
• Cranial radiation of chemotherapy
• Psychosocial deprivation (psychosocial dwarfism)
Pituitary Hypofunction (Hypopituitarism)
Growth Hormone Deficiency (Causes)

16. • Familial
• Hypothyroidism
• Turner Syndrome
• Late Pubertal Growth Spurt
• Chronic Renal Failure
• Down’s Syndrome
• Other
Other Causes of Short Stature

17. Pituitary Hypofunction
Growth Hormone Deficiency
• Signs and symptoms
• Growth of <2 inches or 4-5 centimeters
in a year (< 3rd % by one year of age)
• Delayed closure of the anterior fontanel,
delayed dental eruption, decreased muscle
mass, delayed puberty & hypoglycemia, micropenis,
undescended testes, “cherubic” appearance

18. • Deficiency of growth hormone
• MRI (pituitary gland)
• Radiographs (bone age)
Diagnosis of Hypopituitarism

19. • Nursing care
• Administer human recombinant growth
hormone (GH) SQ
• Plot growth measurements on a growth chart
• Provide supportive resources
• Treat child appropriate to age
• Teach parents about condition & treatment ($$$)
• Adequate nutrition
Pituitary Hypofunction
Growth Hormone Deficiency

20. • Subcutaneous injections 6-7 times per week
• Continues for several years until growth is complete
• Increase growth velocity occurs for the first year, followed by a
gradual decrease in growth for subsequent months or years
• Treatment is continued until an acceptable height occurs or
growth velocity decreases to < 2 cm (1 in.) per year
• In addition, bone age of > 14 years (girls) or > 16 years (boys)
is reached
Growth Hormone Replacement

21. • Central precocious puberty occurs when the hypothalamus is
activated to secrete gonadotropin-releasing hormone (GnRH)
• Other causes: tumors of the ovary, adrenal gland, & pituitary
gland
Precocious Puberty

22. • Definition: Any secondary sex characteristics before age 8
(girls); breast & pubic hair
• Any secondary sex characteristics before age 9 (boys), pubic
hair or genital development
• May be unusually tall for age
• However, growth ceases prematurely because the hormones
stimulate closure of the epiphyseal plates, resulting in short
stature
• Behavioral changes, such as mood swings & emotional lability
may occur
Precocious Puberty

23. • Diagnostic tests:
• Luteinizing hormone (LH) & Follicle-Stimulating Hormone (FSH)
• Testosterone or Estradial
• X-ray (advanced bone age)
• Treatment:
• CNS tumors: surgery, radiation, or chemotherapy
• Medications (Lupron)
Precocious Puberty

24. • Conditions of the Thyroid
• Hypothyroidism
Other Endocrine Disorders

25. • Congenital or acquired
• Congenital occurs ~ 1 in 4,000 births
• Twice as common in females
Hypothyroidism

26. • Thyroid hormones are important for growth & development & for
metabolizing nutrients & energy
• When unavailable to stimulate other hormones or specific target
cells, growth is delayed & intellectual disability develops
Pathophysiology of Hypothyroidism

27. • Signs & Symptoms
• Few in 1st few weeks of life
• *Metabolic screening of newborn
• Cretinoid features
• Thick protuberant tongue
• Thick lips
• Dull appearance
Hypothyroidism

28. • Difficulty feeding
• Constipation
• Hoarse cry
• Intellectual disability
(cretinism)
• *Irreversible if not treated early
• Hypotonia
• Cool extremities
• Umbilical hernia
• Lethargy
Hypothyroidism

29. • Older Children (Acquired)
• Decreased appetite
• Cool skin
• Hair loss or thinning
• Decreased DTR’s
• Bradycardia
• Constipation
• Goiter (nontender enlarged thyroid)
Hypothyroidism

31. • Diagnosis:
• Newborn screening of Thyroxine (T4) & Thyroid-Stimulating Hormone
(TSH)
• ↓ T4, normal T3 & ↑TSH
• Treatment:
• Levothyroxine (Synthroid)
Hypothyroidism

32. Conditions of the Adrenals
• Congenital Adrenal Hyperplasia (CAH)
Other Endocrine Disorders

33. • Autosomal recessive
• Enzyme deficiency for synthesis of cortisol & aldosterone
• Occurrence~ 1 in 10,000-15,000 births
Congenital Adrenal Hyperplasia

34. • 2 Forms:
• Salt-Losing (75%) caused by aldosterone deficiency & overproduction
of androgen
• Non-Salt-Losing (25%) with virilization (production of mascular
secondary sexual characteristics in females)
• Both forms: increased secretion of adrenocorticotropic hormone (ACTH
) occurs in response to decreased cortisol levels
Congenital Adrenal Hyperplasia, cont’d

35. • During fetal development the lack of cortisol triggers the
pituitary to continue secretion of ACTH
• This stimulates overproduction of the adrenal androgens
• Virilization of the female external genitalia begins in week 10 of
gestation
• If untreated, overproduction of androgens results in accelerated
height, early closure of epiphyseal plates, & premature sexual
development with pubic & axillary hair
Congenital Adrenal Hyperplasia, cont’d

36. • Most common cause of pseudohermaphroditism in newborn
girls
• AKA ambiguous genitalia
• S/S
•
Enlarged clitoris & partial or complete labial fusions
• Vagina usually has a common opening with urethra
• May be mistaken for males with cryptorchidism, hypospadias or
micropenis
• Uterus, ovaries & fallopian tubes normal
Congenital Adrenal Hyperplasia

38. • Male infants may look normal at birth or may have slightly
enlarged penis & hyperpigmented scrotum
• Boys may have be tall with an adult-sized penis by school-age
Congenital Adrenal Hyperplasia, cont’d

39. • As child grows precocious puberty may develop in males &
females:
• Other S/S
• Tall stature
• Acne
• Excessive muscle development
• Shorter adult stature (due to early epiphyseal fusion)
Congenital Adrenal Hyperplasia

40. • Recurrent vomiting
• Dehydration
• Weakness
• Metabolic acidosis
• Hypotension
• Hypoglycemia
• Hyponatremia
• Hyperkalemia
S & S (Salt-wasting form)

41. • Diagnosis
• Newborn screening for Congenital Adrenal Hyperplasia*
• With ambiguous genitalia, a karotype (microscopic chromosome study)
determines gender
• U/S (pelvic structures)
Congenital Adrenal Hyperplasia

42. • Treatment:
• Dexamethosone ↓ genital masculinization in females
• Lifelong use of glucocorticoids
• Dexamethasone, prednisone or hydrocortisone
• Adrenalectomy if medical treatment ineffective
• Salt-wasting form: salt added to formula & Florinef (mineralocorticoid)
Congenital Adrenal Hyperplasia

43. • Reconstruction surgery of enlarged clitoris (females) in 1st year
• Several surgeries may be required prior to age 2
• Surgery may also be required during adolescence to dilate the vagina
• Optional: delay tx til adolescence & allow pt. to decide
• Genetic counseling for child during adolescence
Treatment cont’d

44. • During acute illness, may become dehydrated quickly & need
IVF’s & electrolyte replacement
• Higher doses of hydrocortisone
• Teach parents to administer hydrocortisone IM
Treatment (salt-wasting)

45. • Always follow prescribed schedule
• Never abruptly discontinue
• Medical alert bracelet
• Have emergency kits available
• Check expiration dates frequently
• Administer injections if unable to take PO
Hydrocortisone Administration

46. 46
• Sit down if you have pre-diabetes, any kind of diabetes, or a first
degree relative with any kind of diabetes.
• Sit down if you have any relative with diabetes.
• Sit down if you have a close or not-so-close friend with diabetes.
• Sit down if you personally know anybody with diabetes.
• Sit down if, as a nurse or student, you have ever cared for anyone
with diabetes or a blood glucose issue.
Anybody left standing?
Everybody stand up!

47. Diabetes

48. • Incidence ~ 1 in every 400-600 children (Type 1)
• Peak age 7-15 years
• But Type 1 can present @ any age
• Caucasions ↑ Type 1
Diabetes

49. • Pathophysiology:
• Autoimmune (Type 1)
• Destruction of pancreatic islet beta cells→ fail to secrete insulin*
• Familial (child inherits susceptibility not disease)
• Believed that event (virus or toxin) triggers inflammatory
process→ development of islet cell serum antibodies
Diabetes

50. • Insulin helps transfer glucose into cells so body can use it
• As destruction cont’s, insulin secretion ↓
• As insulin ↓ blood glucose level ↑ and glucose in cells ↓
• As serum glucose reaches 180 mg/dL, renal tubules cannot
reabsorb all glucose, so spilled in urine
• Lg. amts electrolytes (Na, K, Ca, Ph, & Mg) excreted too
(polyuria & dehydration)
• Polydipsia- attempt to relieve dehydration
Pathophysiology of Diabetes cont’d

51. • Polyphagia- attempt to compensate for calories lost during
polyuria
• Insulin deficiency ↑catabolism of protein results in ↑ production
of amino acids
• Liver converts triglycerides to fatty acids (lipolysis)→ketone
bodies
• Ketone bodies accumulate & excreted via kidneys (ketonuria)
• Ketones produce ↑ free H+ → metabolic acidosis (↓ serum pH)
Pathophysiology of Diabetes cont’d

52. Diabetes Mellitus Type I
• Signs and symptoms
• Polyuria, polydipsia, polyphagia, and unintended weight loss
• High glucose levels (blood and urine)
• Nausea, vomiting, abdominal pain, excessive fatigue, susceptibility to
infection, dehydration, blurred vision, and irritability

54. Diabetes Mellitus Type I
• Diagnosis
• Elevated blood glucose levels (usually in excess of 200 mg/dL)
• Elevated hemoglobin A1C level (greater than 6.5%)
• Increase sugar and ketones in urine
• Diabetic ketoacidosis (DKA)

55. • Insulin dose too low for food eaten
• Illness, injury, or stress
• Too many CHO’s eaten
• Meals/ snacks too close together
• Insulin injected just under the skin or injected into hypertrophied
areas
• Decreased activity
Hyperglycemia Causes

56. • Weakness, fatigue
• Headache, abdominal pain,
nausea & vomiting
• Blurred vision
• Shock
• Gradual onset
• Lethargy, sleepiness, slowed
responses or confusion
• Deep rapid breathing
• Flushed, dry skin
• Dry mucous membranes,
thirst, hunger, dehydration
Hyperglycemia

57. • Give additional insulin at usual injection time
• Give correction scale insulin doses for specific blood glucose
levels when ill or injured
• Give extra injections if hyperglycemia & moderate to large
ketones
• Increase fluids
Treatment of Hyperglycemia

58. Diabetes Mellitus Type I
• Nursing care
• Major components of management and care include family education on:
• Insulin types (dose and frequency)
• Diet and nutrition
• Exercise
• Stress management
• Blood glucose and ketone monitoring
• Long-term treatment
• Patient/family teaching that optimize outcomes

59. 59
• Many children use insulin pumps.
• Pros:
• Convenience
• Better quality of life and control
• Mimics insulin dosage of a pancreas with bolus and basal
rates
• Cons:
• VERY Expensive!
• DKA may occur due to pump or user error
• Overall, more insulin is required and wasted due to priming
Insulin Pump Therapy

60. 60
Early Insulin Pumps

61. 61
PDM
Omnipod Pod

62. 62
Medtronic
Insulin Pump
Infusion Site
& Set
CGM

64. Insulin Types

65. 65
ROTATE THOSE SITES!
Or it WILL look
like this!

66. • FSBS AC
• Provide meal
• Calculate CHO’s consumed
• Administer insulin (rapid-acting) based on:
• CHO count
• +
• FSBS (sliding scale)
• ______________
• Total insulin
Pediatric Protocol for Insulin Administration

67. Diet & Nutrition
• Goal for a dietary plan: balance various foods and include the
caloric intake from
• Carbohydrates (50 – 60%)
• Fats (20 – 30%)
• Proteins (10 – 20%)
• Goal is to maintain normal glucose levels. AIC levels are indicative of
the average blood glucose over the past 2 to 3 months

68. Exercise & Stress Management
• Exercise and extracurricular activities should not be restricted
• Stressful life events can worsen diabetes (consult with mental
health professionals)

69. Blood Glucose &
Ketone Monitoring
• Monitor blood glucose levels 3 – 6 times per day
• Monitor urine ketones whenever blood glucose readings exceed
240 mg/dL, when the child experiences unexplained weight
loss, or if the child is ill

70. • Blood glucose < 70 mg/dL
• Caused by:
• Insulin dose too high for food eaten
• Insulin injection into muscle
• Too much exercise for insulin dose
• Too long between meals/snacks
• Too few CHO’s eaten
• Illness or stress
Hypoglycemia

71. • Headache, dizziness, blurred
vision, double vision,
photophobia
• Numb lips or mouth
• Moist mucous membranes,
hunger
• Unconsciousness, seizure
• Rapid onset
• Irritability, nervousness,
tremors, shaky feeling,
difficulty concentrating or
speaking, behavior change,
confusion
• Shallow breathing,
tachycardia
• Pallor, sweating
Hypoglycemia S & S

72. • Children are at high risk for hypoglycemia due to their rapid
growth rates and unpredictable eating habits & physical activity
• Severe hypoglyemic episodes may occur at night in children
who receive 2 or more injections of insulin per day
Hypoglycemia cont’d

73. • If signs of hypoglycemia (pallor, sweating, tremors, dizziness,
numb lips or mouth, confusion, irritability or altered MS) check
BG
• If BG < 70 mg/dL give glucose rapidly
• Wait 15 minutes and recheck BG
• Repeat 15 gms CHO if still < 70mg/dL
• Recheck BG in 15 minutes
• Once BG is at least 80 mg/dL give snack with a protein such as
cheese & crackers or peanut butter and crackers
Treating Hypoglycemic Episodes

74. • If conscious:
• Give 15 gms CHO’s
• Wait 15 minutes and recheck BS
• Give another 15 gms CHO’s if 70mg/dL or below
• If unconscious:
• Give glucagon by injection IM or SC or rub glucose paste on
gums
• Call 911
15.15.15 Rule

75. • Half cup juice or non-diet soda
• 3-4 glucose tablets or hard candy
• Small box of raisons
15 grams of CHO’s

76. Long-term Treatments
• The focus is on reducing symptoms and preventing
complications
• The emphasis is placed on teaching the child and family about
the chronic illness and its management
• The nurse assesses the family’s readiness to learn

77. Patient/Family Teaching that
Optimizes Outcomes
• Education is the route by which a family achieves the best glucose
control for the child
• Education focus on insulin administration and schedule, meal
planning, physical exercise, blood glucose monitoring, and
extremity care
• Alternative therapies

78. Diabetic Ketoacidosis (DKA)
• DKA is an acute life threatening condition characterized by
hyperglycemia. It results in the breakdown of body fat for
energy leading to ketosis and acidosis.
• DKA is the presenting complaint in almost ¼ of all newly
diagnosed pediatric patients with D.M.
• DKA is the leading cause of death in these children.

79. • Signs and symptoms
• Toddlers: classic manifestations often absent
• Altered mental status, tachycardia, tachypnea, Kussmaul respirations,
normal or low blood pressure, poor perfusion, lethargy and weakness,
fever, and acetone or “fruity" breath.
• C/O nausea, vomiting, abdominal pain
• S/S dehydration
Diabetic Ketoacidosis (DKA)

80. Diabetic Ketoacidosis (DKA)
• Diagnosis
• Blood glucose of >200mg/dL
• Ketonuria
• Ketonemia with a serum bicarbonate level of <15 mEq/L
• pH of the blood (acidosis)</= 7.3

81. Diabetic Ketoacidosis (DKA)
• Nursing care
• Four essential physiologic principles
• Restore fluid volume
• Return child to a glucose utilization state by inhibiting lipolysis
• Replace body electrolytes
• Correct acidosis and restore acid-base balance

82. • Signs of DKA:
• Change in mental status
• BG > 250 mg/dL
• Moderate to large ketones in
urine
• Fruity breath odor
• Evidence of a bacterial infection
(eg. UTI)
• Difficulty breathing
• Decrease urine output
• When to monitor for DKA:
• Abdominal pain
• Nausea & vomiting that persists
for > 6 hours
• > 5 diarrhea episodes per day
• 1-2 day history of polyuria &
polydipsia
• Has illness (eg. virus) and
unable to eat
Prevention of DKA

83. 83
•Remember, we are human and we make
mistakes! 
•Puberty is a very crazy time for teenagers and
blood sugar control.
•Treat us as a person, not a disease.
Advice from a Type 1 Diabetic …

84. Type 2 Diabetes

85. 85
• Type 2 Diabetes is growing at an alarming rate for children.
• You must approach them differently than a Type 1 patient.
•Education and prevention is KEY!
Children with Type 2

86. • Characterized by insulin resistance
• In response to increased body weight, the visceral fat produces
a cytokine hormone (tumor necrosis factor) that desensitizes
cellular insulin receptors to insulin
• The pancreatic cells produce more insulin to try to overcome
insulin resistance & facilitate glucose transfer
• This results in hyperinsulinemia
• The child maintains a balance between hyperinsulinemia &
insulin resistance and a normal glycemic state
Pathophysiology of Type 2 Diabetes

87. • As insulin resistance worsens, the islets of Langerhans beta
cells fail in their ability to hypersecrete insulin
• This leads to glucose tolerance and overt diabetes develops
• The onset of puberty and increased secretion of growth
hormone are believed to be contributing factors in the
development of insulin resistance
Pathophysiology of Type 2 Diabetes
cont’d

88. Diabetes Mellitus Type 2
• Signs and symptoms
• High blood glucose levels
• Sometimes symptoms may mimic type 1 diabetes
• Diagnosis
• Criteria for type 2 diabetes in children
• BMI >85 percentile for age, sex, and weight
• Two of the following risk factors
• Family history of type 2 diabetes
• Race/ethnicity
• Insulin resistance
• Maternal history or gestational diabetes
• Diagnosis is confirmed with 2 fasting glucose results that exceed 125
mg/d: or 2 random readings >200 mg/dL

90. • Hyperpigmentation and thickening of the skin
• Occurs on the back of the neck, medial aspects of thighs and
axillae
• Associated with insulin resistance
• Present in up to 90% of children with Type 2 Diabetes
Acanthosis Nigrans

91. • Metformin is used when diet and exercise is inadequate
• Improves the sensitivity of target cells to insulin, slows the GI
absorption of glucose & reduces hepatic and renal glucose
production
• Sulfonylureas may be used if metformin is no adequate or
contraindicated
• Insulin may be needed for periods of increased stress or illness
and may ultimately be requires for glycemic control
Medical Management of Type 2 Diabetes

92. Diabetes Mellitus Type 2
• Nursing care
• Provide nutrition teaching (decreasing calories)
• Encourage behavioral changes: increasing activity
• Lifestyle modification to the entire family to ensure compliance
• Teach family about oral hypoglycemic agent
• Monitor for complications

94. Questions?