Advances in Assessment, Diagnosis, and Treatment
of Hyperthyroidism in Children
Kim Siarkowski Amer, RN, PhD
The thyroid gland is responsible for regulating multiple complex metabolic processes that affect most organs. Physical growth
and cognitive development are dependent on proper levels of thyroid hormone. This article will review common challenges in
the diagnosis of hyperthyroidism in children, the approaches to treatment, and the nursing interventions guided toward child
and family responses to thyroid disease. A comparison of signs and symptoms of hypothyroidism and hyperthyroidism is also
included. The nursing interventions addressed in the article integrate the biological, psychological, social, and environmental
stresses and adaptations necessary to cope with hyperthyroid disease.
n 2005 Published by Elsevier Inc.
The word thyroid comes from the Greek word bto shield Q
HE THYROID GLAND is responsible for
regulating many metabolic processes including
physical growth and cognitive development. The
underfunction or overfunction of the thyroid gland
can affect all organ systems, growth, development,
and long-term functioning (Dallas & Foley, 1996).
Nurses need to be aware of the multiple complex
systems affected by thyroid status and use appropriate nursing assessments and interventions. For
example, recent studies demonstrate that cognitive
development is dependent on early and adequate
thyroid hormone replacement in congenital hypothyroidism (Selva et al., 2002). Formerly, the most
common cause of mental retardation, congenital
hypothyroidism is now part of the newborn screening protocol in every state. Although infants are
diagnosed early, their long-term health is dependent
on normal thyroid status through thyroid hormone
replacement. In contrast to hypothyroidism, hyperthyroidism is rare in young children or infants.
However, hyperthyroidism in pregnancy can affect
multiple systems in the infant. In children, 95% of
the cases of hyperthyroidism are related to Graves’
disease (Dallas & Foley, 1996).
Thyroid function is dependent on a feedback loop
system, or the hypothalamic, pituitary, thyroidal
axis. Thyroid hormone regulation is an excellent
example of the delicate balance among the brain
(hypothalamus), the pituitary gland, and the target
gland (e.g., the thyroid gland). When too much thyroid hormone is produced, the hypothalamus
T
Journal of Pediatric Nursing, Vol 20, No 2 (April), 2005
attempts to slow down production and sends a
signal, thyrotropin-releasing hormone (TRH), to the
pituitary gland, which in turn slows down synthesis
of thyroid-stimulating hormone (TSH), which
should slow production of thyroid hormone. However, if the pathology is severe, the feedback regulation is ignored and overridden, and the thyroid may
continue producing more hormone until a dangerous
hyperthyroid state, or thyrotoxicosis, is at hand.
EMBRYOLOGY OF THE THYROID
The thyroid gland is a bow tie-shaped gland that
originates in the palate in the first trimester of
pregnancy. Because the fetus at this stage does not
produce iodine, thyroid hormones T4 and T3 cannot
be produced. Because there is no iodine produced,
thyroid hormone cannot be produced and the fetus is
dependent completely on maternal thyroid hormones. Therefore, maternal thyroid status is critical
to the development of the fetus and child. If maternal
iodine ingestion is inadequate, the fetus will not
have adequate thyroid hormone.
From the Department of Nursing, DePaul University,
Chicago, IL.
Address correspondence and reprint requests to Kim
Siarkowski Amer, RN, PhD, Department of Nursing, DePaul
University, Suite 3000, 990 W. Fullerton, Chicago, IL 60614.
E-mail: [email protected]
0882-5963/$ - see front matter
n 2005 Published by Elsevier Inc.
doi:10.1016/j.pedn.2004.12.013
119
120
In the second trimester of pregnancy, the thyroid
migrates to the neck area. Two etiologies for
congenital hypothyroidism are athyrosis (absence
of thyroid at birth) or lingual thyroid. Congenital
hypothyroidism can be caused by the failure of the
thyroid to migrate normally to the proper anatomical
area, or in the case of athyrosis, by the absence of
thyroid tissue at birth (DiGuiseppi, 1994). Thyroid
hormone production begins in the fetus through the
third trimester, and with normal function, an euthyroid state should be achieved.
MATERNAL HYPERTHYROIDISM AND THE
EFFECT ON NEWBORNS
In a mother with a history of thyroid disease (Case
1), thyroid hormone levels and physical symptoms
should be monitored closely during pregnancy
(Haddow et al., 1999). Newborn thyroid levels
and signs of overactive or underactive thyroid
should also be monitored. Laboratory tests to assess
function in both mother and infant evaluate the
pituitary hormone TSH and the thyroid hormones
for thyroxine (T4) and triiodothyronine (T3).
Almost all thyroid hormones are bound to
thyroid-binding globulin (TBG). Only 0.3% of
thyroid hormone is bfreeQ or circulating. Thyrotoxicosis occurs with very high levels of unbound
circulating thyroid hormone, which is caused by
hyperfunction of thyroid follicular cells or increased
synthesis and secretion of T3 or T4. Total thyroxine,
or TT4, is elevated in hyperthyroidism; however,
there are cases of T3 thyrotoxicosis that would not
show an increase in TT4 (Williams & Brent, 1995).
Case 1. C.J. is a newborn whose mother had active
hyperthyroidism during pregnancy. The mother was
treated with Tapazole, a thyroid suppressant; however,
her symptoms persisted.
A goiter was noted on C.J.’s initial exam, and at 7 days
of life, C.J. is tachycardic at 220, sleeps 15 minutes at
a time, and has had frequent runny stools since 2 days
of life. Thyroid-stimulating antibodies were three
times the normal level, and T4 levels were elevated
with a suppressed TSH.
The inability to self-regulate thyroid levels has
many serious effects on the newborn such as those
illustrated in Case 1. When the transplacental
thyroid-stimulating immunoglobulin (TSIG) is
passed to the infant, there may be fetal hyperthyroidism with goiter. Elevated maternal thyroid
hormones may disrupt the fetal and newborn ability
to regulate TSH and T4 levels. Newborns of
mothers with hyperthyroidism can be affected in
KIM SIARKOWSKI AMER
many ways. In maternal Graves’ disease, there is a
significant risk for low birth weight, prematurity,
small for gestational age, and intrauterine death in
infants (Seng, 2000). Congenital malformations are
more common in mothers with a history of Graves’
disease that is not controlled during pregnancy
(Momotani, Ito, & Noh, Oyanagi, Ishikawa, & Ito,
1986). Elevated maternal thyroid hormones may
disrupt the fetal and newborn ability to regulate TSH
and T4 levels. In Case 1, the baby has transient
hyperthyroidism, which should be treated with hblockers and thyroid suppressants if needed. Physical signs and symptoms such as diarrhea, abnormal
sleep patterns, and hyperreflexia should be monitored by nurses and documented.
Neonatal Graves’ disease is relatively rare with
cases occurring about 1 in 25,000 pregnancies
(Russell, 1992). Infants with neonatal Graves’
disease are usually confined to offspring of mothers
with Graves’ disease, as in Case 1. Maternal
immunoglobulins that stimulate TSH receptors in
utero result in a hyperthyroid state in the fetus
(Seng, 2000). Additional effects of neonatal
Graves’ disease is rare; the physiological effects
can include growth retardation, irritability, restlessness, elevated temperature, flushed face, tachycardia, cardiomegaly, and heart failure. The infant has
increased somatic growth, in contrast to infants of
diabetic mothers; infants with neonatal Graves’
disease have decreased fat stores, tachycardia, and
hyperalertness (Russell, 1992).
Initial treatment for infants with thyrotoxicosis
includes h-blockers and antithyroid drugs. Most
infants have cleared the maternal immunoglobulins
after 2 months and no longer need treatment. The
initial symptoms of thyromegaly, thrombocytopenia, hepatomegaly, and cardiac arrhythmias can be
significant, including mortality. Hence, although
the condition is transient, it can be serious or fatal
(Russell, 1992). After resolution of symptoms, the
infant should retain normal function for life.
GENETICS AND THYROID DISEASE
Recent advances in elucidating the genetic
mechanisms underlying thyroid metabolism include identifying the location of the gene for the
thyrotropin h-subunit on chromosome 1 and
advances in the genetics of autoimmune thyroid
disease and the complex mechanisms of signal
transduction. The regulation of synthesis of TSH
involves a complex process of signaling receptors
that sense whether thyroid hormone levels are
121
ADVANCES IN THYROID
(T4-binding globulin), TTR (transthyretin), prealbumin, and albumin. Only 0.3% of thyroid
hormone circulates unbound. However, this unbound hormone is metabolically active at the
cellular level. Inherited or acquired deficiencies
in the carrier proteins may change the serum
thyroid levels significantly, which may be related
to thyrotoxicosis. Such changes do not always
result in clinical thyroid disease because the
concentration of the free thyroid hormone does
not change. If a patient has normal TSH, low
thyroid hormone values, and proportionately low
TBG, then thyroid function should be normal
(Sarlis & Hirshberg, 2002).
Figure 1. Thyroid activity: hypothalamic thyrotropinreleasing hormone.
THYROID ANTIBODIES
adequate. If thyroid hormone levels are low, TSH
increases to try to increase production of thyroid
hormone. If thyroid hormone levels are high, TSH
decreases in an attempt to slow thyroid hormone
production. TSH is a glycoprotein hormone that
has common alpha and unique h-subunits. The
TSHh is expressed uniquely in the anterior
pituitary just as other regulatory hormones such
as lutenizing hormone (LH) and follicle-stimulating hormone (FSH) (Williams & Brent, 1995).
Regulatory factors in TSH transcription include
TRH, somatostatin, dopamine, vasoactive intestinal peptide, and arginine vasopressin (Vacca,
Moro, Caraccio, Guerrieri, Marra & Greco,
2003). The action is initiated by TRH, which binds
to the plasma membrane receptors, which initiate a
cascade of signal transduction events that activate
phospholipase C kinases, which eventually cause
regulation of thyroid hormone activity (Figure 1).
In an animal model, thyroid hormone activity has
been disrupted by exposure of fetal and suckling
newborn rats to dioxin (2,3,7,8-tetrachlorodibenzop-dioxin), which is commonly found in the
environment. Nishimura, Yonemoto, Miyabara,
Sato, and Tohyama (2003) found that thyroid
hormone homeostasis was disrupted by the exposure to dioxins due to sustained excessive secretion
of TSH followed by hyperplasia of the follicular
cells of the thyroid. Future research on humans may
show a link between environmental toxins and
thyroid function.
THYROID-BINDING PROTEINS
Thyroid hormones T4 and T3 are bound to the
carrier proteins, most commonly identified as TBG
The most common cause of acquired hypothyroidism is Hashimoto’s thyroiditis. The name came
from the Japanese physician who first described
the inflammation of the thyroid tissue that he
examined through a microscope in 1912. The
thyroid becomes enlarged because of the infiltration with lymphocytes (white blood cells) that
cause an autoimmune reaction. The lymphocytes
gradually destroy the thyroid tissues, and the result
is underactive thyroid function with an enlarged
thyroid gland. Eighty percent of people with
Hashimoto’s thyroiditis have elevations in antimicrosomal and antithyroglobulin antibodies
(Williams & Brent, 1995).
In contrast to the hypothyroidism in Hashimoto’s
thyroiditis, Grave’s disease, or hyperthyroidism, is
caused by a different autoimmune antibody process.
In this case, the thyroid works against itself because
of the abundance of thyroid-stimulating antibodies
that cause an excessive amount of thyroid hormone
to be produced. TSIG and TSI were the antibodies
tested to determine if Graves’ disease is present
(Webster, Taback, Sellers, & Dean, 2003). The
diagnosis of Graves’ disease is confirmed by
additional laboratory data, including elevated T4,
suppressed TSH, and elevated TSI. The clinical
symptoms are similar to those for neonatal Graves’
disease and are listed in Table 1.
The symptoms consistent with Graves’ disease
are because of the hyperactivity of the sympathetic
nervous system and hyperthyroidism (see Table 1).
Additional symptoms include irritability, emotional
lability, heat intolerance, and proximal muscle
weakness (Webster et al., 2003). Physical findings
on assessment include goiter, persistent tachycardia, systolic hypertension with widened pulse
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KIM SIARKOWSKI AMER
Table 1. Comparison of Thyroid Abnormalities, Hypothyroidism, Hyperthyroidism,
Their Symptoms, Treatment, and Follow-Up Recommendation
Thyroid Dysfunction
Clinical Symptoms
Laboratory Findings
Treatment
Follow-Up
Congenital hypothyroidism
Sleeping more
than normal, hypotonia,
poor feeding, dry skin,
hoarse cry, in infants
very few symptoms
Elevated TSH
(unless caused by
pituitary dysfunction),
low T4
10–15 Ag/kg/day
of thyroid replacement
(l-thyroxine)
(Selva et al., 2002)
Acquired hypothyroidism
Dry skin, weight gain,
constipation, sleeping
more than normal
Clinically euthyroid
(normal without
symptoms)
Low T4 and high TSH
Thyroid replacement
Low T4, T3, low TBG,
normal TSH
No treatment
Make sure patient
understands that
thyroid screening tests
may be abnormal (if TBG
is not measured)
Malaise, weight gain,
constipation, delayed
relaxation phase in
deep tendon reflexes,
dry skin and hair
Sweating, tachycardia,
shakiness, a more
hearty appetite than
usual, mood changes/
feeling or acting more
nervous, muscles aches,
especially when climbing
stairs, protruding eyes,
difficulty in swallowing
(because of a large thyroid),
difficulty in concentration,
diarrhea, weight loss
Tachycardia, hyperkinesis,
restlessness, diarrhea, poor
weight gain, premature
craniosynostenosis, and
advanced bone age
Elevated TSH, low T4
and T3, elevated
antimicrosomal and
antithyroglobulin
antibodies
Elevated T4 and T3,
suppressed TSH
(b1 Ag/L),
elevated TSI
Thyroid replacement
Monitor several times
a year to ensure adequate
replacement
Treatment for hypothyroidism
may cause hyperthyroidism
Treatment may cause
hypothyroidism
High free T4 and
suppressed TSH,
elevated TSI
will persist for
3–5 months
Lasts weeks to
6 months; if symptomatic,
treat with
medications
TBG deficiency (can be
inherited, such as
X-linked deficiency or
carbohydrate-deficient
glycoprotein syndrome,
which is autosomal
recessive, or acquired,
such as hyperthyroidism,
nephrotic syndrome,
renal failure,
or malnutrition
Hashimoto’s thyroiditis
(acquired hypothyroidism)
(autoimmune process)
Graves’ disease
hypertyroidism
(autoimmune process)
Neonatal thyrotoxicosis
(neonatal Graves’
disease)
pressure, brisk reflexes, exophthalmus (protruding
eyes), eyelid retraction, hand tremor, hyperreactive
deep tendon reflexes, and smooth, moist, and warm
skin (Siarkowski Amer, 1993). At the time of
diagnosis of Graves’ disease, there may be a
history of declining school performance over
several months. The reported average duration of
symptoms in the pediatric population prior to
diagnosis is 1 year (Cooper, 1983; Safa, Schumacher, & Rodriguez-Antunez, 1975; Webster
Thyroid suppressant
drugs such as
propylthiouracil or
Tapazole, ablation
therapy, or surgery
also may need
h -blocker for elevated
heart rate
Frequent blood tests
to ensure adequate
replacement (higher
thyroid hormone values
show better cognitive
development in the first
2 years of life)
Follow-up at least
twice a year
Presence of maternal
antibodies (TSI) may
occur even after mother
is euthyroid; can cause
hyper- or hypothyroidism
in infant
et al., 2003) A thorough history, physical assessment, and thyroid function testing usually makes
the diagnosis straightforward.
Unfortunately, there is no cure for the autoimmune process that occurs during Graves’ disease.
Future research may use TSI for treatment as well as
diagnosis. The goal is to find a physiological way to
block the production of immunoglobulins. The
direct effect of this immune component on the
hyperthyroidism is not fully understood; however,
123
ADVANCES IN THYROID
current research suggests that there is a defect in
immune surveillance.
The exact prevalence of Graves’ disease is not
known; however, it is estimated to be approximately 0.4% of the population of the United States
(Williams & Brent, 1995). It is much less common
in children than in adults and is five to six times
more common in girls than in boys. Graves’
disease may appear at any time; however, it is rare
in infancy, unless the mother has hyperthyroidism,
and shows a peak incidence during preadolescence
and adolescence (Dallas & Foley, 1996).
Case 2. Lucy is a 15-year-old who was diagnosed
with Graves’ disease at 11. She was initially
treated with thyroid-suppressive drugs and
then received radioactive iodine (RAI). Her
thyroid replacement has been adequate for the
past 3 years; however, lately, she has been
very tired, sleeping 12 hours a day. She also
has had some weeks where she only has two
to three stools. Her constipation is making her
bloated and she is frustrated. Lucy’s deep
tendon reflexes are slow to react. Is this
adolescent malaise or hypothryoidism caused
by the treatment of her Graves’ disease?
As in Case 2, after initial diagnosis and initiation
of treatment for Graves’ disease, thyroid function
tests should be followed regularly every month for
the first 2 months, then at least three times a year
until they normalize with treatment. If thyroid
values are borderline, more specific tests can be
done. These include T3 resin uptake, free T4,
thyroid antibody titer, or RAI uptake (Williams &
Brent, 1995). If there is an elevation in T4 without
suppression of TSH, it is unlikely the patient will
require treatment. After treatment for Graves’
disease or a remission, the patient may need to
be treated for hypothyroidism, as in Case 2. During
active Graves’ disease, the state of such extreme
hyperfunctioning can sometimes lead to bburnout
Graves’ disease,Q which is a state of hypothyroidism. In addition, suppressant drugs and other
treatments may leave the thyroid underfunctioning
or with very minimal function. Such is the case of
Lucy (Case 2), who needs thyroid replacement
after treatment of Graves’ disease.
Nurses must be aware of the divergent symptoms of hypothyroidism and hyperthyroidism and
the potential for shifts between diagnosis. For
example, if a patient has a diagnosis of Graves’
disease, they have hyperfunction initially, but may
become hypothyroid from treatment.
MEDICAL MANAGEMENT
Treatment of Grave’s disease consists of three
options: medical therapy with thioamides (antithyroid drugs), surgical resection of all or a major
portion of the thyroid gland, or ablation of the
thyroid with RAI. Because the specific cause of the
gland hyperactivity is not known, these are the
most effective therapies at this time. The two most
commonly used thioamides are propylthiouracil
and methimazole (Tapazole). Both block the
formation of T4 and T3. Agranulocytosis is a very
serious side effect of both drugs (Cooper, 1983).
Families should be educated about the importance
of reporting any fever and/or sore throat to the
physician immediately, as these symptoms may
signify the onset of agranulocytosis. Scheduled
periodic white blood cell counts have not been
useful to monitor patients because the agranulocytosis can occur over a short period, over 2 weeks
(Siarkowski Amer, 1993). Mild leukopenia can be
a result of the hyperthyroidism itself, and if it
remains mild, it poses no threat. Other side effects
of the medications include rash, fever, nausea, and
arthralgia. Side effects occur in less than 5% of
patients on thioamides.
Medical management with thioamides is the
least invasive approach, and many patients achieve
a remission of the disease with thioamide treatment. About 20–25% of patients achieve remission
in 2 years and up to 50% by 5 years of therapy.
Compliance is an concern with thioamides, especially with adolescents who self-administer, since
an every-6-hour or an every-8-hour schedule can
be difficult in some patients. Patients may skip
their afternoon dose while at work or at school,
which is against the advice of health-care providers. Reminders, such as watches with alarms,
cell phones, or personal digital assistants (PDAs),
can be invaluable for busy teens.
If achievement of remission fails, the other
options are surgery or RAI. Both have potential
side effects and possible morbidity. The hesitancy
to use radioiodine in children because of the
oncogenic potential has not been validated in the
small number of studies reported (Moll & Paatel,
1997). Moll and Paatel (1997) compared outcomes
from three different treatment groups: one used
radioiodine as the second choice after antithyroid
medication failure, one had thyroidectomy after
medication failed, and the third group received
initial radioiodine treatment. Of the three groups,
the group receiving immediate radioiodine had the
highest first year remission (88%). The other two
groups had a remission rate of 65% within 5 years.
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KIM SIARKOWSKI AMER
Hence, from this pilot study, it appears that RAI may
be the first choice for a timely remission with
minimal medical therapy or surgical intervention.
This approach was also confirmed by Webster et al.
(2003), who state that in many Canadian centers,
radioiodine is used as a first course treatment with
adolescents who may have trouble with compliance.
Surgical removal of most of the thyroid gland is
an acceptable treatment especially if there is an
experienced pediatric thyroid surgeon in the institution. The risks associated with surgery include
thyroid storm if the child is hyperthyroid before
surgery or if thyroid hormone is released during
surgery (Ball & Bindler, 2003). Other risks include
potential loss of part or all of the parathyroid
glands, vocal cord paralysis, and bleeding, in
addition to all the risks associated with any surgery
and anesthesia (Siarkowski Amer, 1993). Calcium
and phosphorous should be monitored closely after
thyroidectomy (Maier et al., 1984).
In the United States, the trend is to attempt
medical management, and if this is unsuccessful,
then either surgery or RAI is used. RAI is considered
a safe and effective means of treating pediatric
Graves’ disease (Chapman, 1983). Many clinicians
remain cautious with its use because of the possible,
although not proven, risk of infertility or cancer. The
RAI treatment dose of radiation to the gonads is
equal to an upper gastrointestinal series or intravenous pyelography. Both thyroidectomy and RAI
treatments may leave patients hypothyroid because
of the removal or ablation of the thyroid gland
(Siarkowski Amer, 1993). This may occur some
time after treatment. Thus, these therapies can
commit the patient to lifelong thyroid replacement.
Patients who achieve a remission within the first
year of treatment have a much better long-term
prognosis (Siarkowski Amer, 1993). If medical
therapy fails, ablation or thyroidectomy should be
discussed (Ball & Bindler, 2003).
THYROID STORM
The most emergent risk for a patient with
Graves’ disease is thyroid storm in uncontrolled
hyperthyroidism or during times of stress or
infection. Thyroid storm is not common in neonatal
Graves’ disease. Thyroid storm can be caused by
noncompliance with medication or overdosage of
l-thyroxine replacement. The symptoms include
more pronounced symptoms of hyperthyroidism.
The patient may complain of palpitations, eyelid
lag, fever, muscle weakness, excessive sweating,
voracious appetite, diarrhea, or tremor, mostly due
to sympathetic nervous system hyperactivity (Ball
& Bindler, 2003). In late stages, there may be stupor
or coma, cardiac failure, or circulatory collapse
(Dallas & Foley, 1996).
Thyroid storm is a medical emergency, and
treatment is the same as the treatment for hyperthyroidism but with higher dosages of thioamides
and possibly a h-blocker such as propranolol
(Inderal) to control the cardiovascular hyperactivity
and to decrease the risk of heart failure (Ball &
Bindler, 2003). The patient must be hospitalized for
management and stabilization. In some cases, it is
necessary to do monitoring in the intensive care unit
(Dallas & Foley, 1996).
NURSING ASSESSMENT, INTERVENTION,
AND ONGOING EVALUATION
The family aspects of managing the care of a
child with thyroid disease are related to the health
perception and health management of the patient
and family. Common concerns include difficulties
adhering to the medical regime, the child being
perceived as fragile or different from other
children, missing school, or poor school performance due to illness. Before the diagnosis and
during treatment, the child may be irritable and
hyperactive, and such hyperthyroid child may be
misdiagnosed as having attention deficit/hyperactivity disorder, or a child who is lethargic and
always sleeping when hypothyroid can strain even
the strongest family relationships (Ball & Bindler,
2003). Some families become overly concerned
about the disease because of the language that is
used. Words such as grave represent an ominous or
dismal outcome, and when remission is mentioned,
people often associate it with cancer. Because of
this, it is important to state clearly to parents and
patients that this is not a life-threatening disease if
well managed (Siarkowski Amer, 1993).
Families learning about thyroid disease may
have a great deal of anxiety related to managing a
chronic illness. There may be concerns about
cognitive and perceptual functioning and sleep
and rest patterns with this disease. Nurses should
be actively involved in the patient and family by
teaching things related to thyroid disease (Ball &
Bindler, 2003). The alterations in cognitive, perceptual, and sleep and rest patterns should be
temporary, lasting only until the patient is euthyroid. The patient and family need to be supported
during the difficult time of adjusting dosage or
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ADVANCES IN THYROID
evaluating other treatment modalities (Wong,
Wilson, Hockenberry-Eaton, Winklestein, &
Schwartz, 2003). The goal of the family should
be normalization, which includes acknowledging
the disease, integrating the management into the
family routine, and getting back to normal routines
(Deatrick, Knafl, & Murphy-Moore, 1999).
Self-perception and self-concept may be altered
in patients with thyroid disease if they have outward
signs such as exophthalmos or tremor (Ball &
Bindler, 2003). Nursing interventions should be
aimed at identification of positive aspects of the
child. It should also be stressed that with a variety
of treatment options, the likelihood of controlling
the disease is good. Siarkowski Amer (1993)
emphasizes that anticipatory dietary counseling is
essential as treatment of the hyperthyroidism is
initiated. As the metabolic rate normalizes with
treatment, parents, children, and adolescents must
learn to reregulate food intake to avoid extreme
weight fluctuations (Siarkowski Amer, 1993).
Nurses may need to communicate with the
child’s teacher or principal to explain the difficulties the child may be experiencing because of the
disease. It is important to stress the fact that these
problems are temporary and should abate after the
thyroid levels normalize. Several weeks to months
may elapse before the child is back to normal.
Potential side effects of antithyroid medications
should be taught to patients and their caregivers.
The most important of these is monitoring the
patient for fever during illness. The potential
agranulocytosis coupled with a fever can constitute
a great risk (Ball & Bindler, 2003).
The nurse should assess the family to evaluate if
compliance with medication will be a problem.
Frequently, when patients are not well controlled on
antithyroid drugs, it can be traced back to a
misunderstanding of dosage or noncompliance.
For this reason, the medical regime should be
reviewed in detail at each visit. The patient and
caregiver should repeat the medication name,
dosage, and times administered and the nurse should
document the interchange. The family should also
verbalize knowledge that the medication takes many
days to weeks to correct the hyperthyroidism
(Wong et al., 2003).
Nursing management of thyroid storm includes
educating patients about the phenomenon at initial
diagnosis of Graves’ disease and monitoring the
patient’s vital signs, laboratory data, and response
to treatment in the hospital. If propranolol (Inderal)
is ordered immediately for thyroid storm, it can
be given intravenously (Ball & Bindler, 2003).
The nurse needs to monitor heart rate and blood
pressure every 30 minutes for 2 hours after administration. Although thyroid storm is rare in
the pediatric population, it is important to recognize it because of the risk of significant mortality
if not treated properly. In the past, it was a common
problem postsurgically in both elective and unplanned surgeries and was the main cause
of morbidity and mortality in thyrotoxicosis
(Webster et al., 2003). Now that good treatment
options are available, there is less concern about
this phenomenon.
With educated counseling from well-educated
and prepared nurses, patients and parents managing
thyroid disease should feel confident that their lives
will be normal. Long-term health of patients with
thyroid disease can be ensured with excellent
comprehensive care managed by nursing.
REFERENCES
Ball, J. W., & Bindler, R. C. (2003). Pediatric nursing caring
for children. New Jersey: Prentice-Hall.
Chapman, E. M. (1983). History of the discovery and early
use of radioactive iodine. Journal of the American Medical
Association, 250, 2042 - 2044.
Cooper, D. S. (1983). Antithyroid drugs. The New England
Journal of Medicine, 31, 1353 - 1362.
Dallas, J., & Foley, T. (1996). Hyperthyroidism. In F. Lifshitz
(Ed.) Pediatric endocrinology. 3rd ed. New York, NY: Marcel
Dekker.
Deatrick, J., Knafl, K., & Murphy-Moore, C. (1999).
Clarifying the concept of normalization. Image: The Journal
of Nursing Scholarship, 31, 209 - 214.
DiGuiseppi, C. (1994). Screening for thyroid disease. US
Preventive Service Task Force. Retrieved from www.angelfire.
com/md/danil/thyroidpysiology6/04.
Haddow, J. E., Palomaki, G. E., Allan, W. C., Williams, J. R.,
Knight, G. J., Gagnon, J., et al. (1999). Maternal thyroid
deficiency during pregnancy and subsequent neuropsychological development of the child. The New England Journal of
Medicine, 341, 549 - 555.
Maier, W. P., Derrick, B. M., Marks, A. D., Channick, B. J.,
Au, F. C., & Caswell, H. T. (1984). Long-term follow-up of
patients with Graves’ disease treated by subtotal thyroidectomy.
American Journal of Surgery, 147, 266 - 268.
Moll, G. W., & Paatel, B. R. (1997). Pediatric Graves’
disease: Therapeutic options and experience with radioiodine at
the University of Mississippi Medical Center. Southern Medical
Journal, 90, 1017 - 1022.
Nishimura, N., Yonemoto, J., Miyabara, Y., Sato, M., &
Tohyama, C. (2003). Rat thyroid hyperplasia induced by
gestational and lactational exposure to 2,3,7,8,-tetrachlorodibenzo-p-dioxin. Endocrinology, 144, 2075 - 2081.
Russell, W. E. (1992). Endocrine and other factors affecting
growth. In R. A. Polin, W. W. Fox (Eds.) Fetal and neonatal
physiology (pp. 295 - 305). Philadelphia: WB Saunders.
126
Safa, A. M., Schumacher, O. P., & Rodriguez-Antunez, A.
(1975). Long-term follow-up results in children and adolescents
treated with radioactive iodine (I131) for hyperthyroidism. The
New England Journal of Medicine, 292, 167 - 171.
Sarlis, N. J., & Hirshberg, B. (2002). Thyroxine binding
globulin deficiency. Retrieved from www.emedicine.com5/04.
Selva, K. A., Mandel, S. H., Rien, L., Sesser, D., Miyahira, R.,
Skeels, M., et al. (2002). Initial treatment dose of l-thyroxine in
congenital hypothyroidism. The Journal of Pediatrics, 141,
786 - 792.
Seng, L. Y. (2000). Maternal graves’ disease: Effects on the
newborn. Retrieved from www.med.nus.edu.sg/paed/medical_
education/postgraduate/endocrine_metabolism/maternal_
graves.htm5/04.
Siarkowski Amer, K. (1993). Nursing care of children with
Graves’ disease. Pediatric Endocrinology Nursing Society
KIM SIARKOWSKI AMER
resource manual. Pediatric Endocrinology Nursing Society,
Gaithersburg, MD.
Vacca, R., Moro, L., Caraccio, G., Guerrieri, F., Marra, E., &
Greco, M. (2003). Thyroid hormone administration to hypothyroid rats restores the mitochondrial membrane permeability
properties. Endocrinology, 144, 3783 - 3788.
Webster, J., Taback, S. P., Sellers, E., & Dean, H. (2003).
Graves disease in children. Canadian Medical Association
Journal, 169, 104 - 105.
Williams, G. R., & Brent, G. A. (1995). Thyroid hormone
response elements. In B. D. Weintraub (Ed.) Molecular
endocrinology: Basic concepts and clinical correlations. Raven
Press.
Wong, D., Wilson, D., Hockenberry-Eaton, M., Winkelstein,
M., & Schwartz, P. (2003). Nursing care of infants and children.
St Louis, MO: Mosby.