nontoxic goiter is an enlargement of the thyroid gland in a euthyroid patient, not associated with any
neoplastic or inflammatory process
Etiology
worldwide, the most common cause of goiter is iodine deficiency
goitrogens may be found in many foods (sweet potatoes, bamboo shoots, maize)
certain drugs are goitrogens (lithium)
hypersecretion of TSH in response to a defect in hormone synthesis may result goiter formation
Clinical Manifestations
some patients are asymptomatic
most common symptom is a pressure sensation in the neck
in large goiters, patients may complain of dysphagia or dyspnea
may have a large substernal component
Evaluation
TSH and free T4 levels to assess thyroid function
US with FNA of any suspicious nodule
CT scan to look for substernal extension or airway compression
Substernal Goiter with Tracheal Compression
Treatment
correct the underlying cause if possible and eliminate the stimulus for thyroid hyperplasia
TSH suppression therapy does not reduce the size of a goiter
radioactive iodine can reduce goiter size, but it takes several years to show an effect
surgery is indicated for tracheal or esophageal compression, suspicious or malignant nodules,
or cosmetic considerations
Hyperthyroidism
Thyrotoxicosis
clinical state produced by excess circulating thyroid hormone
the most common causes are Graves’ disease, toxic multinodular goiter, or a toxic thyroid nodule
Diagnosis
hyperthyroidism may be obvious or subclinical
patients with overt disease with have a low TSH and high T4, T3
patients with subclinical disease will have a low TSH and normal T4, T3
TSH receptor antibodies should be measured for Graves’ disease
radioactive iodine scanning or US can be used to diagnose multinodular goiter or a toxic nodule
Initial Management
symptomatic patients should be started on β-blockers, unless contraindicated
(asthma, congestive heart failure, bradycardia)
Thyroid Storm
severe, life-threatening exacerbation of thyrotoxicosis
may be precipitated by anesthesia, surgery, or radioiodine therapy in an unblocked patient,
infection, labor, administration of iodine (amiodarone)
patients usually present with high fever, tachycardia, congestive heart failure,
abdominal pain, nausea and vomiting, and central nervous system symptoms ranging from confusion to coma
best management is prophylaxis: patients should be euthyroid before operation
acute management includes fluid resuscitation, antithyroid drugs at high doses,
beta blockers, IV or oral iodine, hydrocortisone, cooling blanket
in extreme cases, dialysis may be necessary to lower serum T4 and T3 levels
Graves’ Disease
Epidemiology
6 times more common in women
most prevalent in young adults (ages 20 to 40)
identical twins have a 50% chance of developing the disease if the twin has it; 30% chance in
fraternal twins
Pathogenesis
autoimmune disorder
pathogenic thyroid-stimulating antibodies are directed against the TSH receptor on thyroid follicular cells
binding of the antibodies stimulates the receptor and leads to excess hormone secretion,
thyroid enlargement, and increased thyroid vascularity
what initiates the pathogenic antibody production is unclear: one theory is that altered antigens on the
follicular cells stimulate the immune attack
Clinical Features
characterized by the classic triad of goiter, thyrotoxicosis, and exophthalmos
exophthalmos is believed to result from overstimulation of TSH receptors in the retro-orbital tissue
pretibial myxedema is present in 3 to 5%
other associated conditions include dermopathy and vitiligo
Exophthalmos ('Bug Eyes')
Diagnosis
thyrotoxicosis
autonomous thyroid function with ↓ TSH and ↑ T4
increased levels of serum TSH receptor antibodies are diagnostic
several different treatment approaches are possible, each with their specific risks and benefits
Antithyroid Medications
the main antithyroid drugs are propylthiouracil (PTU) and methimazole
both drugs act by inhibiting thyroid hormone production
these medications have no effect on the underlying cause of the disease
antithyroid drugs cross the placenta, inhibiting fetal thyroid function, and are excreted in breast milk
serious side effects of both drugs include granulocytopenia, agranulocytosis, and, rarely, aplastic anemia
methimazole is associated with birth defects and should be avoided in pregnancy
PTU is associated with severe hepatotoxicity
most patients become euthyroid in 6 – 8 weeks
treatment course is 12 – 18 months
relapse rate is 20% - 30%
for patients who relapse, definitive therapy with radioactive iodine or surgery will be necessary
Radioactive Iodine (RAI)
most common therapy chosen in the U.S.
goal is to make the patient hypothyroid
80% - 90% effective
major advantage is avoidance of a surgical procedure and its risks
disadvantages include a slower correction of hyperthyroidism, higher relapse rate after initial therapy,
worsening of ophthalmopathy
Indications
small to moderate size goiters
relapses after medical or surgical therapy
any contraindication to surgery or antithyroid drugs
Contraindications
pregnant or breast-feeding women
children or adolescents (concerns for long-term cancer risks and fertility)
exophthalmos is a relative contraindication (may see progression of eye signs)
compressive or unsightly goiter
require rapid correction of hyperthyroidism
Surgical Treatment
Indications
radioiodine treatment is contraindicated
young patients
pregnant women
ophthalmopathy
suspicious nodule
large goiters with severe thyrotoxicosis
Pre-op Preparation
patient should be euthyroid on antithyroid drugs
antithyroid drugs should be continued up to the day of surgery
propranolol reduces the risk of thyroid storm
Lugol’s iodine solution reduces the vascularity of the gland
Surgical Procedures
total thyroidectomy is the procedure of choice
subtotal thyroidectomy has a lower complication rate, but a higher rate of
recurrent hyperthyroidism
Complications
hematoma resulting in airway obstruction: emergency management requires opening the
wound at bedside
hypocalcemia is the most common complication, and may be permanent in up to 15% of patients
injury to the superior laryngeal nerve reduces dynamic pitch range (high-note nerve)
unilateral recurrent nerve injury results in hoarseness; dyspnea and aspiration are also
occasional complications
bilateral recurrent nerve injury may result in acute airway obstruction that requires
reintubation or an emergency tracheostomy
Toxic Multinodular Goiter
Pathogenesis
thyrotoxicosis is usually a late manifestation of multinodular goiter
pathogenesis of multinodular goiter is the result of chronic stimuli causing thyroid hyperplasia
these stimuli may include iodine deficiency, dietary goitrogens, inherited defects in T4 synthesis
with time, one or more nodules become autonomous and secrete T4 or T3 in excess
Clinical Presentation
most common in females over 60
symptoms are often mild
atrial fibrillation may be the only clinical finding other than the goiter
dysphagia and dyspnea may be present
no extrathyroidal manifestations such as ophthalmopathy or pretibial myxedema
on exam, an enlarged thyroid with at least several palpable nodules is present
Diagnosis
suggested by the history and physical exam
documented by a low TSH and elevated T4
antithyroid antibodies are not present
thyroid scan will usually show several hot nodules
thyroid US is mandatory, and FNA should be done on any suspicious nodule
RAI - TMN Goiter
Treatment
patients should be made euthyroid with PTU or methimazole
antithyroid medicines will not reverse the underlying process and would require life-long treatment
RAI or total thyroidectomy is the treatment of choice
radioactive iodine is not effective in shrinking the goiter
Toxic Thyroid Nodule
Pathogenesis
solitary nodule that functions autonomously
almost always benign
Diagnosis
RAI scan will show a single hyperfunctioning nodule
thyroid US is mandatory
RAI - Toxic Adenoma
Treatment
patient should be euthyroid before definitive treatment RAI or surgery
thyroid lobectomy is recommended for young patients, large lesions, or suspicion of malignancy
RAI is also very effective because the isotope preferentially accumulates in the hyperfunctioning nodule
Hashimoto's Thyroiditis
Thyroiditis
Etiology
autoimmune disorder
most patients have elevated antimicrosomal and antiperoxidase antibodies; less commonly, antibodies
against thyroglobulin and the TSH receptor are elevated
7 times more common in women
most prevalent between ages 30 to 50
may be familial
associated with primary B cell lymphoma of the thyroid
may be associated with other autoimmune diseases: lupus, rheumatoid arthritis, myasthenia gravis
Pathology
thyroid is firm and mildly enlarged
histologically, there is lymphocytic and plasma cell infiltration and formation of lymphatic follicles
over time, the thyroid tissue degenerates and is replaced by fibrous tissue
Clinical Manifestations
20% present with hypothyroidism
a small number present with transient hyperthyroidism
most patients are euthyroid at the time of diagnosis
most common presenting symptom is a tightness in the throat,
often associated with a painless, nontender enlargement of the thyroid
compression of the trachea or recurrent laryngeal nerve is rare
palpation reveals an enlarged, firm thyroid
US demonstrates a diffusely enlarged thyroid with heterogenous echogenicity
Diagnosis
as the disease progresses, TSH rises and serum T4 and T3 fall
diagnosis confirmed by the presence of antithyroid antibodies
a rapidly enlarging goiter should undergo an FNA to rule out lymphoma
Treatment
patients with goiter, with or without hypothyroidism, are treated with thyroid hormone
surgery is reserved for patients with obstructive symptoms, cosmetically unacceptable goiters,
or enlarging goiter despite being on thyroid hormone suppression
Subacute Thyroiditis (De Quervain’s Thyroiditis)
Etiology
granulomatous or giant cell thyroiditis
acute, self-limited inflammatory disease of the thyroid
believed to be secondary to a viral infection of the thyroid and often follows an
upper respiratory infection
occurs mostly in women between 30 - 40
Clinical Manifestations
patients present with fever, malaise, thyroid pain
thyroid gland is moderately enlarged and exquisitely tender, but without evidence of abscess formation
some patients present with thyrotoxicosis, which is caused by the release of thyroid hormones
from disrupted follicles
transient hypothyroidism may follow thyrotoxicosis
15% of patients develop permanent hypothyroidism
Diagnosis
thyroid function studies usually show elevated levels of T4 and T3 with suppression of TSH
erythrocyte sedimentation rate is elevated in 100% of cases
radioactive iodine uptake is low or negligible, which rules out other causes of thyrotoxicosis
Treatment
NSAIDs for pain relief
beta blockers may be necessary to treat thyrotoxic symptoms
steroids may be necessary in more severe cases
surgery is only necessary for the very rare patient that has a prolonged course that doesn’t respond
to medical management
Acute Suppurative Thyroiditis
Etiology
acute bacterial infection, with staph and strep species being the most common isolates
usually associated with an acute upper respiratory tract infection
peak incidence is in childhood or adolescence, but it may also occur in elderly
and immunocompromised patients
