In recent years, BMI has received increased attention
for pediatric use. In 1994, an expert committee charged
with developing guidelines for overweight in adolescent
preventive services (ages 11-21 years) recommended
that BMI be used routinely to screen for overweight
adolescents. In addition, in 1997 an expert committee
on the assessment and treatment of childhood obesity
concluded that BMI should be used to screen for
overweight children, ages 2 years and older, using the
BMI curves from the revised growth charts.
Can be calculated on-line at various sites
The growth charts consist of a series of percentile
curves that illustrate the distribution of selected body
measurements in U.S. children. Pediatric growth charts
have been used by pediatricians, nurses, and parents to
track the growth of infants, children, and adolescents in
the United States since 1977. The 1977 growth charts
were developed by the National Center for Health
Statistics (NCHS) as a clinical tool for health
professionals to determine if the growth of a child is
adequate. The 1977 charts were also adopted by the
World Health Organization for international use.
Growth hormone deficiencies
Hypo and hyper thyroid
Diabetes type I and type II
Disorders of the Pituitary Gland
Disorders of the pituitary gland depend on the
location of the lesion or physiologic
Secretes antidiuretic hormone (ADH or
vasopressin) and oxytocin.
The anterior pituitary is made up of endocrine
glandular tissue and secretes growth hormone
(GH), adrenocorticotropic hormone (ACTH,
TSH, FSH, LH, and prolactin).
Growth Hormone Deficiency
80% are idiopathic
1 in 10,000 children
Males are referred more often
Short at birth or premie
Growth hormone produced by the pituitary
If the pituitary gland doesn’t produce enough
hormones for normal growth, growth slows
down or stops.
Underdeveloped, damaged or malfunctioning
GH stimulates the growth of all organs and
tissues in the body, particularly the long bones.
Cherub facial features, frontal bossing, large eyes, and
Males have small testes / micro-penis
Look much younger than chronological age
Delay of onset of puberty as a teenager
Emotional difficulties related to small stature are
Short child is often treated as if younger.
Teased by peers.
Child may dress as a younger child.
Body image is altered.
Renal and Liver function test
Sedimentation rate / ESR
Done to rule out other causes of delayed
Deficiency in the Growth Hormone
Bone age by x-ray: delayed bone age
Slow growth rate: as documented on standard
CDC growth chart
Goals of Therapy
The goal of therapy is to augment growth so
that at the time of epiphyseal close, a normal or
normally expected adult height is attained.
Child will attain a final adult height consistent
with their genetic potential
Growth Hormone Replacement
GH products are currently labeled for use in
“children who have growth failure due to an
inadequate secretion of normal endogenous
Hormone Replacement Therapy
Children should receive GH injections daily and
at a minimum of three times a week
Treatment costs $10,000 to 50,000 dollars
Therapy can last for 2-4 years or until the
Children should be managed by a pediatric
Social Justice Considerations
Children must meet specific criteria to be eligible
Parents must have access to health insurance
Children who receive GH therapy will obtain the
economic and social benefits of growing taller
Outcomes of Treatment
The child will verbalize positive feelings about
his or her body image.
The child will demonstrate an increase in age-
appropriate activities with peers.
Child will be able to participate in age related
activities of daily living
Long Term Effects
Long term follow up needed:
Long term risks unknown
Physiologic trauma of daily injection
Metabolic effects of the therapy: children on GH
therapy usually lean muscular
Therapy associated with increase risk of
malignancies: leukemia, lymphoma, and tumors
Hypersecretion of Growth
In children called gigantism
15% due to pituitary tumors causing increase
release of GH.
Goal of treatment is surgical removal of GH-
Anatomy & Physiology: Mosby
Development of sexual characteristics before the
usual age of onset of puberty.
Breast development before 7.5 years
Pubic hair before 8.5 years
Menses before 9.5 years
Secondary sexual characteristics before age 9
Chart growth on growth chart.
Chronological timing of pubertal events.
Tanner Scale: true precocious puberty is
characterized by 2 signs of puberty
Management / Prognosis
Treatment to halt or reverse sexual
Treatment needs to be started prior to closure of
Good outcomes if treatment stared early
Failure to develop sexually at an appropriate age.
No breast development by age 13 or lack on menses
within 5 years.
Secondary sexual characteristics not started by 14 years of
Etiology and Incidence
2 to 3% of all adolescents.
Bone age moderately delayed.
History of small stature during infancy and early
Rule out any Endocrine
12% will have a pathologic reason for delayed
Congenital adrenal hyperplasia
Growth hormone deficiency
Low dose testosterone for the male.
Oral ethinyl estradiol for the girl.
Most common endocrine disorder of childhood
Hypothyroidism can be congenital, acquired, or
Results from absence or abnormal development
of the thyroid gland or abnormal synthesis of
Most common cause is incomplete development
of the thyroid gland
Importance of Thyroid
Thyroid hormones promote normal myelination
during brain development in the first two to
three years of life and normal skeletal growth
Flat nasal bridge
Thick protruding tongue
Large posterior fontanel
Positive health history
Low levels of T3 and T4
High levels of TSH
Neonatal screening is mandatory
Replacement of sodium-l-thyroxine
Monitor TSH, T3 and T4
Monitor growth and development
Frequent visits with emphasis on importance of
15% of Down Syndrome children are
Auto-immune type of thyroiditis is most often
High TSH levels as young as 2 years of age
Difficult to diagnose due to overlap of
Excessive secretion of thyroid hormone
More common in females 7:1
Genetic and immunologic components
Autoimmune disease of unknown cause
Short attention span
Can’t sit still / Hyperactive
Fatigue but unable to sleep at night
Accelerated growth / tall for age
Enlarged thyroid gland
Asymmetric or lobular
Patient may present with neck swelling
History and Physical
Levels of T3 and T4 are increased
Levels of TSH are decreased
Antithyroid drugs to block T 4 synthesis
Radioactive Iodine is given to kill off some of
the thyroid cells
Most common negative outcome is giving too much
iodine that all thyroid producing cells are killed.
Surgical removal of gland or nodule – not always
possible since often it is the entire gland
resulting in overproduction of the hormone.
Diabetes Mellitus / Type 1
Lack of insulin production in the pancreas.
Autoimmunity involved in destruction of beta
15 new cases per 100,000 children under 20
years of age.
Peak incidence between 10 and 14 years.
Diabetes Type I
Result of a genetic-environmental interaction
Seasonal variation – midwinter to spring
Illness or infection preceding the onset
Virus triggers the autoimmune response
HLA –DR4 and HLA – DR3
20 to 40 % more susceptible
Exposure of genetically predisposed individuals
to environmental triggers
Leads to inflammation of beta cells of the
pancreatic islets (islitis) and subsequent beta-cell
Beta Cell Function
80 to 90% if beta cell function must be lost
before hyperglycemia develops
Insulin deficiency causes physiologic and
metabolic changes in the body.
Glucose from dietary sources cannot be utilized
by the cells.
Renal tubules have difficulty reabsorbing the
If the blood glucose level exceeds the renal
threshold for glucose osmotic diuresis ensues.
Renal threshold: when serum glucose levels
approach 200mg/dl the renal tubules have
difficulty re-absorbing the glucose
Hyperglycemia impairs leukocyte function –
Elevated blood glucose leads to osmotic
diuresis. (polyuria and thirst)
Protein and fat breakdown lead to weight loss.
Accumulation of ketones causes a drop in pH.
(metabolic acidosis) and spilling of ketones in
Hyperglycemia / glucose in blood stream
Glucosuria / sugar in urine
Polyuria / increased urine output
Electrolyte imbalance from dehydration
Polydipsia / attempt to relieve dehydration
Polyphagia / attempt to compensate for lost
Blood glucose levels greater than 200 mg/dL
Urine sample reveals glucosuria and possible
Glucose tolerance test would reveal low insulin
levels in the face of elevated glucose levels.
Goals of Management
Short term goals:
Prevent the development of ketosis.
Prevent electrolyte abnormalities and volume depletion
secondary to osmotic diuresis.
Prevent impairment of leukocyte function
Prevent impairment of wound healing
Long term goal: prevention of microcirculatory and
Administration of insulin
Blood glucose levels
Initially before every meal
Every am when diabetes under control
Dietary management / refer to nutritionist
Glycosylated hemoglobin / reflects average
glucose concentration for preceding 2 to 3
Blood Glucose Levels
Toddler and preschool: 100 to 180 mg/dL
School-age: 90 to 180 mg/dL
Adolescents (13 to 19 years): 90 to 130 mg/dL
Test urine for ketones only if blood sugar
greater than 250 or during illness
Short acting – often used to cover extra
Combination of regular and intermediate-acting
Morning and evening dosing
Children on mixed insulin dosage schedules tend to
experience hypoglycemic episodes at 11:30 and 2:30
as peaking of insulin occurs.
Symptoms: Lab Values:
Rapid onset Glucose = low, below 60
Shaky feeling, hunger
Ketones = negative
Shallow respirations sugar negative
tachycardia negative ketones
Treatment of Hypoglycemia
Day time hypoglycemia:
Simple concentrated sugars such as honey by mouth,
hard candy, sugar cubes, or glucose tablets will elevate
the blood sugar immediately. Orange juice or sugar
containing soda or fruit drink. (Blood Glucose less than
Eat a snack if next meal is more than an hour away
Identify reason for hypoglycemia. In children it is often
increase in activity without increase in food intake.
Using rapid-acting or Lispro insulin
Infusion pump (8 to 10 years of age)
Night time snack
Check blood glucose before bedtime
Do not skip snacks
Eat an extra snack on days of strenuous exercise
Night time hypoglycemia
Eat 1 ½ snacks if blood glucose is less than 100
to 120 mg/dL before going to bed
Make sure the blood glucose is 100 – 120
mg/dL before going to bed
Check blood glucose at midnight and 3 am
Onset = gradual
Lethargic, confused, weak
Abdominal pain often with nausea and vomiting
Signs of dehydration
Vital signs: deep, rapid respirations, fruity acetone
breath, and weak pulses
DKA – Diabetic Ketoacidosis
Presenting symptoms may include:
Altered level of consciousness
Complete vascular collapse
Hyperglycemia and ketonuria with an ability to
take in and retain oral fluids.
Management: increased fluid intake
Diet drinks when blood glucose > / = 240 and
supplemental insulin administration
Check urine ketone levels
Hyperglycemia, ketonuria, and acidosis (ph
between 7.25 and 7.4) associated with an
impaired ability to retain oral fluids.
Need emergency care: IV fluids (normal saline),
supplementary insulin ( regular insulin IV)
Management of underlying medical condition:
Characterized by severe acidosis (ph < 7.25),
dehydration, hyperglycemia, ketosis and a variety
of other symptoms including Kussmaul
respirations, alteration in mental status, and
unconsciousness. Severe dehydration may lead
Management of severe DKA
3 phases of management
Correction of acid-base, glucose and electrolyte
Transition to daily routine
ABC’s: securing an airway, ensuring adequate
ventilation, and correcting shock with IV
volume expanders such as normal saline.
Phase 2 & 3
Intravenous fluids and insulin (regular insulin IV
Administration of bicarbonate if acidosis is severe
Slowly bring down plasma glucose levels to avoid
Restart child on regular routine with emphasis
on teaching and review of routine
Management by endocrinologist
Blood sugar monitoring
Screen for retinopathy: ophthalmologic exam
Goals of nutritional therapy
Maintaining near-normal blood glucose by balancing food
intake with insulin and activity.
Achieving optimal serum lipid levels.
Providing appropriate calories for normal growth and
Preventing and treating acute and long-term complications.
Improving overall health through optimum nutrition
Vital component to management of child with
May decrease the amount of insulin required.
Enhances insulin absorption.
Important for normal growth and development.
Management During Exercise
Eat a snack before exercising.
Exercise lasting less than 1 hour usually requires a small
snack / complex carbohydrate or protein.
Longer exercising may require more frequent snacks /
complex carbohydrates or a protein.
Insulin adjustment may be needed if hypoglycemia
occurs during the activity.
Check blood glucose after activity and before bedtime
to prevent night time hypoglycemia
Diabetes Type 2
Between 8 and 45 percent of newly diagnoses
cases of childhood diabetes are type 2
Type 2 diabetes is caused by resistance to insulin
as well as the inability of the pancreas to keep up
with the increase demand of insulin.
Insulin resistance + chronic hyperglycemia
Type 2 diabetes
85% of children are obese
Age of onset is middle to late puberty
Minority populations have an especially high rate
of type 2 diabetes
Native American, Alaska Native, African
American and Mexican American
Who is at risk?
Obesity: BMI greater than 30 (normal range is 15 to 17
in the pediatric population)
Waist to hip ratio: apple shape
Acanthosis nigricans: hyper-pigmentation and
thickening of the skin into velvety irregular folds in the
neck and flexural areas – reflects hyperinsulinemia
+ family history of type 2 diabetes
Often diagnosed during routine physical
Girls often present with vaginal monilial
Severe infections: pharyngitis or osteomyelitis:
Plasma insulin and C peptide are high reflecting
Autoantibodies to the islet cell are negative in
Comprehensive education on importance of
regular exercise and how to self-monitor for
blood glucose levels.
Glucose-lowering agent: drugs that improve
insulin sensitivity such as Glucophage
A few may need Insulin to initiate control
Disorder of the posterior pituitary
It results in deficiency in the secretion of ADH
ADH concentrates urine
Deficiency result in massive renal loss of fluid
¼ occur after craniotomy
Idiopathic or familial
Antidiuretic hormone works directly on the
renal collection ducts and distal tubules to
increase membrane permeability for water and
A deficiency in ADH will cause failure of
kidneys to reabsorb water.
This leads to massive water loss
Polyuria (excessive urination)
Polydipsia (excessive thirst)
Onset on symptoms abrupt
In the older child nocturia and enuresis are
The first symptoms of diabetes insipidus seen in
children, especially in infants, are irritability and
incessant crying that can only be alleviated with
feedings of water and not formula or breast
Very low specific gravity: 1.005
NO glucose or ketones
Desmopressin (DDAVP): synthetic analogue of
Administered by nasal insufflation once or twice
Aqueous pitressin may be given IV, IM or sub-q
Administration of the medication
Signs and symptoms of fluid imbalance:
dehydration and over-hydration
Sign of hypernatremia
Wear medi-alert tag
Fluid volume deficit
Desmopressin: medication used to treat
DI…over use may result in Fluid volume excess
Activity intolerance: due to dehydration,
excessive thirst and frequent urination
First discovered in 1934
PKU is an autosomal recessive genetic defect found on
Child must receive the defective gene from both parents
1 in 60 people is an asymptomatic carrier
Symptoms 1 in 10,000 births
In turkey 23 in 10,000
Phenylalanine is an essential amino acid found in all
The accumulation of phenylalanine leads to severe
With early identification of the defective gene
intervention can prevent retardation.
Heel stick done 24 to 48 hours after birth.
Infant must have an adequate intake of breast milk or
The drop of blood must be large enough to fill the
imprinted space on the filter paper.
Squeezing out more blood onto the paper creates a
layered effect that can produce a false-positive test
Focuses on preventing
of phenylalanine by
restricting protein intake.
Maintain levels below 0.9
mmol/L but maintain
at0.2 to allow for normal
growth and tissue repair.
NutraSweet need to be
avoided in diet.
Teaching that reinforces the dietary regimen is critical to the
successful management of PKU
Family cohesion and adherence to the restricted diet positively
correlates with higher IQ levels.
Children at high risk for learning difficulties.
Diet generally discontinued around 10 years with full brain
Pregnant women with PKU deficiency at high risk for having a
fetus with mental retardation.