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.