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Background
A nontoxic goiter is a diffuse or nodular enlargement of the thyroid gland that does not result
from an inflammatory or neoplastic process and is not associated with abnormal thyroid
function. Endemic goiter is defined as thyroid enlargement that occurs in more than 10% of a
population, and sporadic goiter is a result of environmental or genetic factors that do not
affect the general population.
Intrathoracic goiter causing obstruction. This patient has a visible goiter on physical
examination. In addition, he has distension of his left external jugular vein, facial erythema
(when compared with his shoulder), and cutaneous varicosities of venous blood draining
from his head into his chest because of jugular obstruction from his goiter.
Pathophysiology
The histopathology varies with etiology and age of the goiter. Initially, uniform follicular
epithelial hyperplasia (diffuse goiter) is present, with an increase in thyroid mass. As the
disorder persists, the thyroid architecture loses uniformity, with the development of areas of
involution and fibrosis interspersed with areas of focal hyperplasia. This process results in
multiple nodules (multinodular goiter). On nuclear scintigraphy, some nodules are hot, with
high isotope uptake (autonomous) or cold, with low isotope uptake, compared with the
normal thyroid tissue (as demonstrated in the images below). The development of nodules
correlates with the development of functional autonomy and reduction in thyroid-stimulating
hormone (TSH) levels. Clinically, the natural history of a nontoxic goiter is growth, nodule
production, and functional autonomy (resulting in thyrotoxicosis in a minority of patients).
The overall risk of malignancy is the same in a patient with a nodular goiter as with a solitary
nodule.
See the images below.
Technetium-99m (99mTc) thyroid scan of a large, nontoxic multinodular goiter. Multiple
cold and hot nodules are observed in the enlarged thyroid gland. The white arrow indicates
sternal notch marker. Areas of autonomy with excess thyroid hormone secretion in a large
nodular goiter. This technetium-99m (99mTc) thyroid scan shows hot and cold nodules in a
multinodular goiter. Although the patient's thyroid-stimulating hormone level had become
progressively suppressed, it was within the reference range, at 0.4 mU/mL (reference range
0.35-5.5 mU/mL).
Epidemiology
Frequency
United States
Iodine comes from ingestion of food. Iodine content of the soil determines the iodine content
of plants and animals. Iodine is washed from the soil by water and is eventually washed out
to the oceans. In general, areas with mountain ranges or heavy rainfall and flooding are
iodine deficient. Iodine deficiency occurs in populations that depend on locally grown food
and rely on vegetable protein rather than on animal or fish protein.
Studies have shown that iodine supplementation can eliminate cretinism and is highly
effective in the prevention of endemic goiter. When urinary iodide falls below 25 micrograms
per gram of creatinine, a palpable goiter occurs in 40-90% of the population, hypothyroidism
occurs in 30-50% of the population, and cretinism occurs in 1-10% of the population. The
seminal studies by David Marine, MD, in 1917 demonstrated the reduction in goiter among
adolescent girls in Ohio from 20% to 5% by iodine supplementation.
Table salt has been supplemented in the United States since the 1920s for the prevention of
cretinism and endemic goiter. The iodine intake in the United States, according to the
National Health and Nutrition Examination Survey III (NHANES III), is adequate at 145
mcg/mg of creatinine. This adequate iodine intake in the United States eliminates the most
common cause of endemic goiter in most populations.
Sporadic goiter is the most common cause of nontoxic goiter in the United States. The
incidence of sporadic nontoxic goiter has been estimated in North America at approximately
5%. Sporadic goiter does not usually occur in people before puberty, and it does not have a
peak incidence. Generally, the development of palpable thyroid nodules and goiter
progressively increases with age. The prevalence of palpable nodules is approximately 5-6%
in people aged 60 years, but on autopsy and ultrasonographic imaging findings, the incidence
of small, nonpalpable nodules approaches 50% in people aged 60 years.
International
More than 2.2 billion people worldwide have some form of iodine deficiency disorder.
Twenty-nine percent of the world's population lives in a region that has iodine deficiency
(primarily in Asia, Latin American, central Africa, and regions of Europe). Of those at risk,
655 million were known to have goiter. In the iodine-deficient regions of the world, goiter is
more common than in the United States. The prevalence of goiter can be estimated based on
the iodine intake of the population.
As reported by the World Health Organization (WHO), the United Nations Children's Fund
(UNICEF), and the International Council for the Control of Iodine Deficiency Disorders
(ICCIDD), the absence of iodine deficiency (ie, median urine iodine >100 mg/dL) is
associated with a goiter prevalence of less than 5%; mild iodine deficiency (ie, median urine
iodine 50-99 mg/dL), with a goiter prevalence of 5-20%; moderate iodine deficiency (ie,
median urine iodine 20-49 mg/dL), with a goiter prevalence of 20-30%; and severe iodine
deficiency (ie, median urine iodine 20-49 mg/dL), with a goiter prevalence of greater than
30%.
Mortality/Morbidity
Endemic goiters arising from iodine deficiency are associated with sometimes immense
thyroid hypertrophy, hypothyroidism, and cretinism. Sporadic goiters are generally
asymptomatic and found either by a clinician's physical examination or by the patient's
observation of neck enlargement. Occasionally, the goiter may produce symptoms caused by
pressure on anterior neck structures, including the trachea (wheezing, cough, globus
hystericus [anterior neck pressure]), the esophagus (dysphagia), and the recurrent laryngeal
nerve (hoarseness).
Rarely, the obstruction can be dangerous because of narrowing of the trachea and the
development of tracheitis with edema and tracheomalacia, leading to severe narrowing of the
airway with serious obstruction resulting in a respiratory emergency. (Tracheal compression
and the results of its surgical treatment are seen in the images below.)
Nontoxic goiter of the thyroid gland with tracheal compression. An axial, noncontrast
computed tomography scan through the thyroid shows significant tracheal compression.
Relief of tracheal compression after subtotal thyroidectomy of large, obstructive, nontoxic
multinodular goiter. (A) Laryngoscopy demonstrating critical tracheal narrowing before
thyroidectomy; (B) laryngoscopy showing widened patent trachea after thyroidectomy.
Race
No convincing epidemiologic studies suggest that race plays an important role in the
development of nontoxic goiter. Generally, the lower socioeconomic conditions in
nonindustrialized countries resulting in iodine deficiency have a more important role than
race does in the development of a goiter.
Sex
Diffuse and nodular goiter is more common in women than in men. According to the best
estimate, the incidence of goiter in women is 1.2-4.3 times as great as that in men.
Age
Sporadic goiter from dyshormonogenesis, a genetic error in proteins that are necessary for
thyroid hormone synthesis, occurs during childhood. Endemic goiter due to iodine deficiency
occurs during childhood, with the goiter's size increasing with age. Other causes of sporadic
goiter rarely occur before puberty and do not have a peak age of occurrence. Thyroid nodules
increase in incidence with age.
History
The thyroid gland usually grows outward because of its location anterior to the trachea (see
the image below). Occasionally, the thyroid wraps around and compresses the trachea and/or
esophagus or extends inferiorly into the anterior mediastinum.
Multinodular goiter. On visual inspection of the neck (image on left), this patient appears to
have a goiter. The computed tomography scan (image on right) shows the asymmetrical
goiter, measuring 9.3 x 7.4 cm, with tracheal deviation, although no tracheal obstruction is
present.
Growth pattern
Determining whether the goiter has been present for many years and whether a change has
occurred in the recent past is important.
Recent or accelerated growth of a discrete nodule or thyroid lobe should raise the suspicion
of malignancy.
Goiters associated with unilateral adenopathy should raise the suspicion of malignancy.[1]
Goiters rarely are painful or grow quickly unless recent hemorrhage into a nodule has
occurred.
Obstructive symptoms (see the image below)
Intrathoracic goiter causing obstruction. This patient has a visible goiter on physical
examination. In addition, he has distension of his left external jugular vein, facial erythema
(when compared with his shoulder), and cutaneous varicosities of venous blood draining
from his head into his chest because of jugular obstruction from his goiter.
Tracheal compression is generally asymptomatic until critical narrowing has occurred.
Patients develop a dry cough, dyspnea, and stridor, especially with exertion. In patients with
intrathoracic goiter, the dyspnea and stridor may be nocturnal or positional (ie, occurring
when the patient's arms are raised) when the thoracic outlet is narrowed.
Hemorrhage into a nodule or cyst or development of bronchitis may acutely worsen the
respiratory symptoms in a patient with tracheal narrowing.
The esophagus is more posterior in the neck, and a goiter occasionally extends posteriorly
and causes solid food and pill dysphagia.
Compression of the recurrent laryngeal nerve by a goiter or invasion by a thyroid malignancy
results in vocal cord dysfunction and may cause hoarseness. The superior laryngeal nerve
controls the pitch of the voice. An expanding goiter may cause a change in the character of
the voice, especially in individuals who use their voice extensively (eg, in certain
occupations).
Compression of the venous outflow through the thoracic inlet by a mediastinal goiter results
in facial plethora and dilated neck and upper thoracic veins.
Iodine intake
Obtain a careful diet history for iodine deficiency, iodine excess from medications (eg,
amiodarone), health food store supplements, or seaweed.
History of radiation
Record any history of head and neck radiation exposure, especially during childhood, which
significantly increases the risk of benign and malignant nodular thyroid disease and thyroid
dysfunction (hypothyroidism and hyperthyroidism).[2, 1]
Family history
Family history is very important in the evaluation of the patient with goiter. Investigate
inherited forms of dyshormonogenesis in the pediatric patient, as well as familial papillary
carcinoma of the thyroid and familial forms of medullary thyroid cancer (multiple endocrine
neoplasia and familial medullary carcinoma of the thyroid).[2, 1]
Physical
Pertinent physical findings are limited to the evaluation of the shape, asymmetry, size, and
consistency of nontoxic goiters; ultrasonographic characteristics of individual nodules within
the goiter; lymphadenopathy; and assessment of thyroid function.[2, 1]
The thyroid evaluation starts with inspection of the neck for thyroid enlargement. Often, the
thyroid enlargement can be detected only when the patient swallows.
The thyroid isthmus is usually located at or just below the level of the cricoid cartilage of the
trachea. The lobes of the thyroid extend laterally and, if enlarged, may extend posterior to the
sternocleidomastoid muscles. Up to 80% of thyroid glands may have a pyramidal lobe
extending superiorly from the isthmus.
Assess the gland for overall size; in the United States, the normal weight is 15-20 grams.
Assess the thyroid for asymmetry and determine whether a dominant nodule is present in an
overall nodular goiter or whether a solitary nodule is present in an otherwise normal gland.
Evaluate dominant nodules that are bigger than 1-1.5 cm or a solitary nodule of the same size
by a thin-needle aspiration biopsy.[3] Diffuse or nodular goiters without a dominant nodule do
not require a biopsy for evaluation.
Obstruction
Examine patients with dyspnea and cough, especially with exertion, for tracheal obstruction.
Note any tracheal deviation from midline.
The patient's voice is assessed for hoarseness.
Venous outflow obstruction of the head and neck can be elicited by the Pemberton maneuver
by raising the patient’s arms above the head until they touch the sides of the head for 1
minute. A positive finding occurs with facial plethora or engorgement of the neck veins.
Physical assessment of thyroid dysfunction
Examine patients for signs of thyroid dysfunction.
Hypothyroidism is indicated by a sallow complexion, dysarthric speech, mental slowing,
weight gain without change in appetite, cold intolerance, constipation, hypersomnia, and
delayed relaxation of deep tendon reflexes.
Hyperthyroidism is indicated by tachycardia, atrial arrhythmia (eg, atrial fibrillation),
diaphoresis, weight loss without change in appetite, heat intolerance, hyperdefecation, palmar
erythema, lid lag, tremor, and brisk reflexes.
Lymphadenopathy
Carefully examine the neck to identify any lymphadenopathy.
Causes
The most common worldwide cause of endemic nontoxic goiter is iodine deficiency.
However, in patients with sporadic goiter, the cause is usually unknown. Nontoxic goiters
have many etiologies, including the following:
Iodine deficiency - Goiter formation occurs with moderately deficient iodine intake of
less than 50 mcg/d. Severe iodine deficiency associated with intake of less than 25
mcg/d is associated with hypothyroidism and cretinism.
Iodine excess - Goiter formation due to iodine excess is rare and usually occurs in the
setting of preexisting autoimmune thyroid disease.
Goitrogens
o Drugs - Propylthiouracil, lithium, phenylbutazone, aminoglutethimide, iodine-
containing expectorants
o Environmental agents - Phenolic and phthalate ester derivatives and resorcinol
found downstream of coal and shale mines
o Foods - Vegetables of the genus Brassica (eg, cabbage, turnips, brussels
sprouts, rutabagas), seaweed, millet, cassava, and goitrin in grass and weeds
Dyshormonogenesis - A defect in the thyroid hormone biosynthetic pathway is
inherited.
Childhood head and neck radiation - Radiation exposure during childhood results in
benign and malignant nodules.
Laboratory Studies
Assess all patients with goiter for thyroid dysfunction with a serum thyrotropin (TSH)
assay. Second-generation or better TSH assays can detect clinically inapparent
(subclinical) hyperthyroidism and hypothyroidism.
o If the TSH is high, consider chronic autoimmune thyroiditis (Hashimoto
thyroiditis) or ingestion of a goitrogen, such as lithium or amiodarone, as well
as dyshormonogenesis in a child. Correction of the hypothyroid status by
withdrawal of the goitrogen or institution of thyroid hormone replacement
therapy may greatly reduce the size of the goiter.
o If the TSH is low, measurement of serum free thyroxine (free T4) or free T4
index and total triiodothyronine (T3) is used to confirm the diagnosis of
thyrotoxicosis. After many years, a nontoxic goiter may develop areas of
functional autonomy (as seen in the image below) and thyrotoxicosis.
Treatment of thyrotoxicosis includes stabilization of the hyperthyroid state
with antithyroid medications and then surgical removal of the goiter or the
administration of radioactive iodine ablative therapy.
Imaging Studies
Assessment of size and extent of the goiter is necessary to determine if progressive growth of
the thyroid is occurring. Clinical assessment by an experienced clinician is often accurate
until the thyroid increases to 4-5 times the normal size.
Measurement of neck circumference is a crude measure of thyroid size. Ultrasonography is
good for estimating the number, size, and sonographic characteristics of nodules but is
inaccurate in the clinical setting for measuring the volume of large goiters. Suspicious
ultrasound characteristics, including hypoechogenicity, microcalcifications,
macrocalcifications, intranodular vascularity, taller-than-wide dimensions, and blurred
margins, guide the clinician as to which nodule requires biopsy for malignancy. [2, 1] Computed
tomography (CT) scanning and magnetic resonance imaging (MRI), although expensive, are
excellent for assessing tracheal compression and intrathoracic extension of the goiter.
A barium swallow may be used to document esophageal obstruction in patients with
significant symptoms of dysphagia.
Thyroid scintigraphy is not routinely indicated in the assessment of goiter size unless a
concern of thyroid hemiagenesis exists or the TSH is suppressed consistent with
hyperthyroidism. A nodule with equivocal findings on thin-needle aspiration may be further
evaluated using thyroid scintigraphy. A hot area supports the presence of a benign lesion.
Examples of technetium-99m (99m Tc) thyroid scans are shown below.[2, 1]
Technetium-99m (99mTc) thyroid scan of a large, nontoxic multinodular goiter. Multiple
cold and hot nodules are observed in the enlarged thyroid gland. The white arrow indicates
sternal notch marker. Areas of autonomy with excess thyroid hormone secretion in a large
nodular goiter. This technetium-99m (99mTc) thyroid scan shows hot and cold nodules in a
multinodular goiter. Although the patient's thyroid-stimulating hormone level had become
progressively suppressed, it was within the reference range, at 0.4 mU/mL (reference range
0.35-5.5 mU/mL).
Other Tests
Pulmonary function tests may be used as a functional assessment of tracheal
compression. Characteristic changes of external tracheal compression can be detected
in flow-volume loop tracings in asymptomatic patients with goiter. Direct
laryngoscopy can, as indicated in the image below, also demonstrate tracheal
compression. Relief of tracheal compression after subtotal thyroidectomy of large,
obstructive, nontoxic multinodular goiter. (A) Laryngoscopy demonstrating critical
tracheal narrowing before thyroidectomy; (B) laryngoscopy showing widened patent
trachea after thyroidectomy.
Procedures
A subset of patients presenting with goiter who do not have hyperthyroidism or has a cold
nodule on nuclear thyroid scan with hyperthyroidism should have a fine-needle aspiration
biopsy as the first diagnostic procedure. Clinical indication for biopsy includes suspicious
sonographic characteristics listed above,asymmetrical and/or rapid growth of a nodule or lobe
of a thyroid gland or unilateral adenopathy. Generally, in patients with the usual nonnodular
nontoxic goiter that is long-standing with slow growth, fine-needle biopsy is not necessary
unless sonographically suspicious nodules are present.[2, 1]
Histologic Findings
A variety of features may be observed with fine-needle aspiration cytology of a multinodular
goiter.[3] This variation is mostly explained by different stages of nodule formation. A
proliferative phase exists in which the sample may contain many follicular cells. This can
sometimes be difficult to distinguish from a follicular adenoma versus a follicular carcinoma.
Colloid is another prominent feature. It represents the stored thyroid hormone within the
follicle. Its absence suggests a more worrisome diagnosis.
After proliferation of follicular cells, a hemorrhage may occur inside the nodule. Erythrocytes
and foamy macrophages that have ingested colloid material may be observed. Another
potential area of concern is an aspiration that only returns cyst contents, ie, erythrocytes and
macrophages without follicular cells. This cannot be used to definitively rule out the presence
of thyroid cancer, and a reaspiration should be performed.
Medical Care
Nontoxic goiters usually grow very slowly over decades without causing symptoms. Without
evidence of rapid growth, obstructive symptoms (eg, dysphagia, stridor, cough, shortness of
breath), or thyrotoxicosis, no treatment is necessary. Therapy is considered if growth of the
entire goiter or a specific nodule is present, especially if intrathoracic extension of the goiter,
compressive symptoms, or thyrotoxicosis exists. The intrathoracic extension of the goiter
cannot be assessed by palpation or biopsy. The goiter, if significant in size, should be
removed surgically.[4] The currently available therapies include thyroidectomy, radioactive
iodine therapy, and levothyroxine (L-thyroxine, or T4) therapy.
Radioactive iodine therapy - Radioiodine therapy of nontoxic goiters is often performed in
Europe. It is a reasonable therapeutic option, particularly in patients who are older or have a
contraindication to surgery.[5, 6, 7]
Radioactive iodine therapy for nontoxic goiters was reintroduced in the 1990s. Careful
studies have shown a reduction in thyroid volume in nearly all patients after a single dose of
therapy.[1]
Of patients with nontoxic diffuse goiter, 90% have an average of 50-60% reduction in goiter
volume after 12-18 months, with a reduction in compressive symptoms. The decrease in
goiter size has positively correlated with the dose of iodine-131 (131 I). Reduction in goiter
size is greater in younger patients and in individuals who have only a short history of goiter
or who have a small goiter. Baseline TSH is not a predictor of response to radioactive iodine.
Obstructive symptoms improved in most patients who received radioactive iodine.
Adverse effects, including thyroiditis, occurred, but no patient reported worsening of
compressive symptoms requiring treatment. No long-term follow-up reports on patients
treated with radioactive iodine exist. Patients should always be monitored clinically after131 I
therapy, for evidence of goiter regrowth.
Transient hyperthyroidism is rare and typically occurs in the first 2 weeks after treatment.
Unlike patients with hyperthyroidism who are treated with radioactive iodine, only a small
percentage of patients with nontoxic goiter develop hypothyroidism after radioactive iodine
treatment
Recombinant human TSH (rhTSH) may have a role in radioactive iodine treatment for
nontoxic goiter. Pretreatment with rhTSH 24 hours prior to therapy can reduce the amount of
radioiodine needed to shrink the goiter (up to a 50% reduction).[8, 9, 10, 11]
Thyroid hormone suppressive therapy - The use of T4 in a euthyroid individual to shrink a
nontoxic goiter is controversial.
One study showed that T4 therapy for nontoxic goiter reduced thyroid volume in 58% of
patients, compared with 4% of patients treated with a placebo. However, these results have
not yet proven to be reproducible, and the benefit of using T4 needs to be weighed against the
risk of the resultant subclinical hyperthyroidism associated with an increased risk of
decreased bone mineral density and increased atrial fibrillation.
Goiter growth typically resumes after cessation of T4 therapy.
The American Thyroid Association and American Association of Clinical Endocrinologists
have released guidelines for the management of hyperthyroid and other causes of
thyrotoxicosis, including the use of radioactive iodine or surgery to treat toxic multinodular
goiter.[12]
Surgical Care
Thyroidectomy or surgical decompression causes rapid relief for obstructive symptoms.[4, 13, 1]
Most intrathoracic goiters may be removed from a cervical incision without
sternotomy. Performing bilateral subtotal thyroidectomy has been recommended to
reduce the risk of continued goiter growth. The rate of goiter recurrence depends on
the extent of surgery but should not be higher than 10% in 10 years.
After bilateral subtotal thyroidectomy, all patients require thyroid hormone
replacement therapy. The full replacement therapy should start immediately after
surgery, with TSH levels checked 3-4 weeks postoperatively. Adjust thyroid hormone
therapy, such as T4, to maintain a TSH level in the reference range. Some evidence
exists that thyroid hormone replacement therapy prevents recurrence of nontoxic
goiter after surgical removal.[14]
The use of total thyroidectomy to treat benign multinodular goiter has met with some
concern, owing to the risk of parathyroid function damage and laryngeal nerve injury
posed by the procedure. Nonetheless, total thyroidectomy is also seen as a means of
avoiding the pitfalls of subtotal thyroidectomy, specifically, the recurrence of goiter
and the inadequate treatment of thyroid cancers, which can occur in apparently benign
goiters. Results from a 2008 literature review indicated that the rate of permanent
complications is the same for subtotal and total thyroidectomy; consequently, the
report's authors concluded that total thyroidectomy should be the procedure of choice
for the surgical treatment of benign multinodular goiters.[4]
The same conclusion was reached in a study of 600 patients with nontoxic
multinodular goiter. Barczynski et al compared outcomes from total thyroidectomy
(200 patients), the Dunhill procedure (unilateral total lobectomy plus contralateral
subtotal lobectomy; 200 patients), and bilateral subtotal thyroidectomy (200 patients).
The authors found that over a 5-year follow-up period the incidence of recurrent
goiter after total thyroidectomy was 0.52%, while that following the Dunhill operation
was 4.71%, and recurrence after bilateral subtotal thyroidectomy was 11.58%. The
frequency of completion thyroidectomies was also lower in total thyroidectomy than
in the other operations.
The incidence of transient hypoparathyroidism in the above study, as well as that of
transient and permanent laryngeal nerve injuries, was greater in total thyroidectomy
than in the other types of surgery. Nonetheless, the authors concluded that, owing to
the fact that following total thyroidectomy there was a reduced incidence of goiter
recurrence requiring repeat thyroidectomy, total thyroidectomy should be considered
the procedure of choice for patients with nontoxic multinodular goiter.[15]
Results from a Swiss study of 72 patients indicated that a single dose of steroid prior
to thyroidectomy for benign disease can, within 48 hours postsurgery, significantly
reduce pain, nausea, vomiting, and voice alteration related to the procedure.[16]
Consultations
Consult an endocrinologist in the complicated nontoxic goiter with nodule formation
or obstructive symptoms.
If a high index of suspicion for malignancy exists in a patient with hoarseness,
lymphadenopathy, and previous radiation exposure as a child, consult a thyroid
surgeon.
Diet
Diets low in iodine need supplementation, especially in developing countries where
government-supported iodine supplementation is not available. Patients taking iodine
supplements may need a reduction to avoid iodine-induced thyroid disease in predisposed
individuals.
Medication Summary
No specific treatment for nontoxic goiter exists. Childhood or adult goiter that is established
because of iodine deficiency does not shrink after supplementation with iodine. Goiters due
to a defect in thyroid hormone synthesis, dyshormonogenesis, are often reduced in size by
thyroid hormone therapy. Attempting to shrink nontoxic goiters with T4 has been standard
practice, but this therapy has generally fallen out of favor because of the risks of
hyperthyroidism, with its detrimental effects on bone and cardiac function.
Thyroid hormones (L-thyroxine)
Class Summary
T4 has been used to reduce the size or suppress the further growth of goiters.
View full drug information
Levothyroxine (Synthroid, Levoxyl, Unithroid, Levothroid)
Minimal excess doses of T4 suppress thyrotropin (TSH) secretion from the pituitary. TSH is
the primary stimulator of thyroid gland growth and thyroid hormone synthesis. For many
years, the standard therapy of nontoxic goiter has been suppression of thyroid function by
exogenous T4 therapy. This practice has been largely abandoned because of data showing
cortical bone loss with chronic excess of thyroid hormone therapy and lack of benefit in
suppressing growth of large nodular goiters. Studies have shown that T4 therapy is most
effective in decreasing the size of small diffuse goiters in patients with a basal TSH within
the reference range.
Antithyroid agents
Class Summary
Reduce goiter size.
Sodium iodide, or131 I (Iodotope)
Ultrasonographic studies have shown a decrease in thyroid volume after131 I therapy in the
majority of patients with nontoxic goiter. When administered at a dose of 100 µCi per g of
goiter (corrected for percent uptake of131 I at 24 h), thyroid volume decreases an average of
50-60% in 12-18 mo. In most patients, radioactive iodine therapy reduces compressive
symptoms. Commonly used in Europe and Latin America but is not standard therapy in the
United States unless the patient has contraindication for surgery. Theoretical concerns of
radiation-induced swelling and worsening of compressive symptoms have not been supported
in European studies. Often, low-iodine diets are recommended for 5 d up to several wk before
therapy.
Further Outpatient Care
The patient with a large goiter and no obstructive symptoms can be monitored in an
outpatient setting. Conduct a physical examination every 6 months to determine if
obstructive symptoms have developed or worsened and to perform thyroid function
tests (ie, TSH, free T4).
Depending on iodine intake in the diet, some of these patients develop thyroid
autonomy and thyrotoxicosis.
Often, thyroid imaging is not necessary when the patient is examined by an
endocrinologist experienced in thyroid examinations. The method of choice is
ultrasonography unless the goiter extends into the thoracic inlet.
Routine nuclear scintigraphy is not necessary.
Transfer
Transfer may be required in patients with significant tracheomalacia who require
surgery. Long-term compression of the trachea by a nontoxic goiter causes tracheal
cartilage to lose its strength. This can be life threatening, and tracheal intubation or
tracheotomy may be required.
Additionally, if a goiter extends significantly into the thorax, a thoracic surgeon may
be needed to open the chest wall to fully excise the goiter.
Deterrence/Prevention
Prevention of endemic goiter may be accomplished by iodine supplementation, using
iodine supplements in drinking water sources or iodized oil on bread (strategies that
can be applied to a whole country).
Complications
Complications of a nontoxic goiter occur because of growth and compression of neck
structures or the development of areas of autonomy and thyrotoxicosis.[17]
Prognosis
Prognosis is good.
Usually, nontoxic goiters grow very slowly over many years. Any rapid growth
behavior must be evaluated for either degeneration or hemorrhage of a nodule or for
growth of a neoplasm.
Often, in patients who present with progressive goiter growth, those with significant
dysphagia or dyspnea must be evaluated for subtotal thyroidectomy.
In some patients, radioactive iodine therapy can be considered, especially if the
patient is older.
Patient Education
Thyroid self-examination may be taught to patients, allowing them to monitor their
own body for early changes in gland size.
For excellent patient education resources, visit eMedicine's Endocrine System Center.
Also, see eMedicine's patient education article Thyroid Problems.