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Endocrine Disorders in Pediatric Nursing

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Endocrine Disorders in Pediatric Nursing Powered By Docstoc
					Endocrine Disorders
     Pediatric Nursing
                          BMI

   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.
               BMI Calculation
   Can be calculated on-line at various sites
    including www.cdc.gov
                  Growth Charts
   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.
          Endocrine Disorders
   Growth hormone deficiencies
   Hypo and hyper thyroid
   Diabetes type I and type II
   Diabetes Insipidus
   PKU
    Disorders of the Pituitary Gland
   Disorders of the pituitary gland depend on the
    location of the lesion or physiologic
    abnormality.
             Posterior Pituitary

   Secretes antidiuretic hormone (ADH or
    vasopressin) and oxytocin.
              Anterior Pituitary
   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

   Hypopituitarism
   80% are idiopathic
   Familial patterns
   1 in 10,000 children
   Males are referred more often
   Short at birth or premie
                     Causes
   Growth hormone produced by the pituitary
    gland
   If the pituitary gland doesn’t produce enough
    hormones for normal growth, growth slows
    down or stops.
   Underdeveloped, damaged or malfunctioning
    pituitary gland.
              Growth Hormone
   GH stimulates the growth of all organs and
    tissues in the body, particularly the long bones.
              Clinical Manifestations

   Cherub facial features, frontal bossing, large eyes, and
    button nose
   Males have small testes / micro-penis
   Look much younger than chronological age
   Delay of onset of puberty as a teenager
           Emotional Difficulties
   Emotional difficulties related to small stature are
    common.
   Short child is often treated as if younger.
   Teased by peers.
   Child may dress as a younger child.
   Body image is altered.
Hypopituitarism
                Diagnostic Tests

   Renal and Liver function test
   Thyroid function
   Sedimentation rate / ESR

Done to rule out other causes of delayed
 growth
           Definitive Diagnosis
   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
    growth hormone”
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
    annually
   Therapy can last for 2-4 years or until the
    epiphyses close
                Management
   Children should be managed by a pediatric
    endocrinologist
                  Ethical Issues
   Social Justice Considerations
      Children must meet specific criteria to be eligible
      for treatment
     Parents must have access to health insurance
      coverage
     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
              Hormone
   In children called gigantism
   Uncommon disease
   15% due to pituitary tumors causing increase
    release of GH.
   Goal of treatment is surgical removal of GH-
    secreting adenoma.
                       Gigantism




                                   Acromegaly
Anatomy & Physiology: Mosby
                  Precocious Puberty
   Development of sexual characteristics before the
    usual age of onset of puberty.
       Girls
          Breast development before 7.5 years
          Pubic hair before 8.5 years

          Menses before 9.5 years

       Boys
            Secondary sexual characteristics before age 9
                     Assessment
   Chart growth on growth chart.
   Chronological timing of pubertal events.
       Tanner Scale: true precocious puberty is
        characterized by 2 signs of puberty
   Family history
        Management / Prognosis
   Treatment to halt or reverse sexual
    development.
   Treatment needs to be started prior to closure of
    epiphysis.
   Good outcomes if treatment stared early
                    Delayed Puberty
   Failure to develop sexually at an appropriate age.
       Girls
            No breast development by age 13 or lack on menses
             within 5 years.
       Boys
            Secondary sexual characteristics not started by 14 years of
             age.
         Etiology and Incidence
   2 to 3% of all adolescents.
   Bone age moderately delayed.
   History of small stature during infancy and early
    childhood.
   Familial history
         Rule out any Endocrine
             Abnormalities
   12% will have a pathologic reason for delayed
    puberty
     Congenital adrenal hyperplasia
     Hypothyroidism

     Growth hormone deficiency
                  Management
   Low dose testosterone for the male.

   Oral ethinyl estradiol for the girl.
              Hypothyroidism
   Most common endocrine disorder of childhood
   Hypothyroidism can be congenital, acquired, or
    secondary
      Congenital Hypothyroidism

   Results from absence or abnormal development
    of the thyroid gland or abnormal synthesis of
    thyroid hormone.
   Most common cause is incomplete development
    of the thyroid gland
         Importance of Thyroid
              Hormones
   Thyroid hormones promote normal myelination
    during brain development in the first two to
    three years of life and normal skeletal growth
   Regulates metabolism
            Clinical Manifestations
   Dull appearance
   Feeding difficulties
   Inactivity
   Constipation
   Characteristic faces
       Flat nasal bridge
       Puffy eyelids
       Thick protruding tongue
       Low hairline
       Large posterior fontanel
                    Diagnosis
   Diagnosis
     Positive health history
     Physical findings

     Low levels of T3 and T4

     High levels of TSH

     Neonatal screening is mandatory
                Management
   Replacement of sodium-l-thyroxine
   Monitor TSH, T3 and T4
   Monitor growth and development
   Frequent visits with emphasis on importance of
    therapy
       Acquired Hypothyroidism
   15% of Down Syndrome children are
    hypothyroid
   Auto-immune type of thyroiditis is most often
    the cause
   High TSH levels as young as 2 years of age
   Difficult to diagnose due to overlap of
    symptoms
              Hyperthyroidism
   Excessive secretion of thyroid hormone
   More common in females 7:1
   Genetic and immunologic components
   HLA-B8
   Autoimmune disease of unknown cause
           Clinical Manifestations
   Cry easily
   Emotionally labile
   Nervous
   Short attention span
   Can’t sit still / Hyperactive
   Fatigue but unable to sleep at night
   Accelerated growth / tall for age
               Physical Exam
   Enlarged thyroid gland
   Asymmetric or lobular
   Patient may present with neck swelling
Exophthalmos
                 Diagnosis
History and Physical
Levels of T3 and T4 are increased
Levels of TSH are decreased
                       Treatment

   Antithyroid drugs to block T 4 synthesis
       Prophylthiouracil
       Methimazole (Tapaxole)
            Permanent Treatment
   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
    cells.
   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
   Family history
   Illness or infection preceding the onset
   Virus triggers the autoimmune response
               Genetic Marker

   Genetic Markers:
     HLA –DR4 and HLA – DR3
     20 to 40 % more susceptible
                Natural History
   Exposure of genetically predisposed individuals
    to environmental triggers
   Leads to inflammation of beta cells of the
    pancreatic islets (islitis) and subsequent beta-cell
    injury.
             Beta Cell Function

   Hyperglycemia
     80 to 90% if beta cell function must be lost
      before hyperglycemia develops
              Pathophysiology
   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
    glucose.
              Pathophysiology
   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 –
    yeast infection
         Clinical Manifestations
   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
    the urine
          Presenting Symptoms
   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
    calories
              Diagnostic Tests
   Blood glucose levels greater than 200 mg/dL
   Urine sample reveals glucosuria and possible
    ketonuria.
   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
    neuropathic changes
                 Interventions
   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
    months.
           Blood Glucose Levels
   Target 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
                       Urine
   Test urine for ketones only if blood sugar
    greater than 250 or during illness
                            Insulin
   Insulin
     Short acting – often used to cover extra
      carbohydrate consumption
     Combination of regular and intermediate-acting
      insulin
            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.
                      Hypoglycemia
Symptoms:                      Lab Values:
 Rapid onset                     Glucose = low, below 60
 Shaky feeling, hunger
                                  Ketones = negative
 Headache
                                  Urine output
 Dizziness

 Vital signs
                                    Normal

       Shallow respirations        sugar negative
       tachycardia                 negative ketones
   Tremors
      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
      70 mg/dL)
     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.
       Hypoglycemia Prevention
   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
              Hyperglycemia
Symptoms:
Onset = gradual
Lethargic, confused, weak
Thirsty
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
     Dehydration

     Electrolyte disturbances

     Dysrhythmias

     Shock

     Complete vascular collapse
         Diabetic Ketoacidosis
   Mild
   Moderate
   Severe
                   Mild DKA
   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
               Moderate DKA
   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:
    infections, trauma
                  Severe DKA
   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
    to shock.
        Management of severe DKA
   3 phases of management
     Resuscitation
     Correction of acid-base, glucose and electrolyte
      abnormalities
     Transition to daily routine
                Resuscitation
   ABC’s: securing an airway, ensuring adequate
    ventilation, and correcting shock with IV
    volume expanders such as normal saline.
                    Phase 2 & 3
   Correct acid-base:
     Intravenous fluids and insulin (regular insulin IV
      drip)
     Administration of bicarbonate if acidosis is severe

     Slowly bring down plasma glucose levels to avoid
      cerebral edema
   Restart child on regular routine with emphasis
    on teaching and review of routine
             Life Management
   Management by endocrinologist
   Insulin
   Blood sugar monitoring
   Diet
   Exercise
   Screen for retinopathy: ophthalmologic exam
    annually
          Nutritional Management
   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
        development.
       Preventing and treating acute and long-term complications.
       Improving overall health through optimum nutrition
                   Exercise
   Vital component to management of child with
    diabetes.
   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
   Hypertension
   + family history of type 2 diabetes
   Ethnicity
           Presenting Symptoms
   Chronic hyperglycemia
   Often diagnosed during routine physical
   Girls often present with vaginal monilial
    infection
   Severe infections: pharyngitis or osteomyelitis:
               Diagnostic tests
   Plasma insulin and C peptide are high reflecting
    insulin resistance
   Autoantibodies to the islet cell are negative in
    type 2
                 Management
   Comprehensive education on importance of
    regular exercise and how to self-monitor for
    blood glucose levels.
   Dietary management
   Glucose-lowering agent: drugs that improve
    insulin sensitivity such as Glucophage
    (Metformin)
   A few may need Insulin to initiate control
             Diabetes Insipidus
   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
                    Causes
   Hypothalamic lesion
   ¼ occur after craniotomy
   Idiopathic or familial
              Pathophysiology
   Antidiuretic hormone works directly on the
    renal collection ducts and distal tubules to
    increase membrane permeability for water and
    urea.
   A deficiency in ADH will cause failure of
    kidneys to reabsorb water.
   This leads to massive water loss
                  Assessment
   Polyuria (excessive urination)
   Polydipsia (excessive thirst)
   Onset on symptoms abrupt
   In the older child nocturia and enuresis are
    common
                   CaReminder
   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
    milk.
                       Urine
   Very low specific gravity: 1.005
   Dilute
   Colorless
   NO glucose or ketones
                 Management
   Desmopressin (DDAVP): synthetic analogue of
    ADH
   Administered by nasal insufflation once or twice
    a day
   Aqueous pitressin may be given IV, IM or sub-q
              Parent education
   Administration of the medication
   Signs and symptoms of fluid imbalance:
    dehydration and over-hydration
   Sign of hypernatremia
   Wear medi-alert tag
            Nursing Diagnosis
   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
                     Phenylketonuria

   PKU
   First discovered in 1934
   PKU is an autosomal recessive genetic defect found on
    chromosome 12
   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
                   Pathophysiology

   Phenylalanine is an essential amino acid found in all
    protein food.
   The accumulation of phenylalanine leads to severe
    retardation.
   With early identification of the defective gene
    intervention can prevent retardation.
                     Diagnosis
   Heel stick done 24 to 48 hours after birth.
   Infant must have an adequate intake of breast milk or
    formula. (protein)
   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
    result.
                        Treatment

   Focuses on preventing
    excessive accumulation
    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.
   Aspartame or
    NutraSweet need to be
    avoided in diet.
                         Prognosis
   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
    development
   Pregnant women with PKU deficiency at high risk for having a
    fetus with mental retardation.

				
DOCUMENT INFO
Description: Endocrine disorders like hyperthyroidism and diabetes and nursing interventions or nursing management