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16 Thyroiditis
Michel Adamina and Daniel Oertli
Contents
16.1
16.2
16.2.1
16.2.1.1
16.2.1.2
16.2.2
16.2.3
16.2.4
16.2.5
16.2.6
16.3
16.3.1
16.3.2
16.4
16.4.1
16.4.2
16.4.3
16.5
Introduction . . . 207
Autoimmune Thyroiditis . . . 208
Hashimoto’s Thyroiditis . . . 208
Fibrotic Hashimoto’s Thyroiditis . . . 208
Atrophic Autoimmune Thyroiditis . . . 208
Focal Lymphocytic Thyroiditis . . . 209
Postpartum Thyroiditis . . . 209
Subacute de Quervain’s Thyroiditis . . . 209
Painless Thyroiditis . . . 209
Riedel’s Fibrosing Thyroiditis . . . 210
Acute Infectious Thyroiditis . . . 210
Etiologies of Infectious Thyroiditis . . . 211
Surgical Treatment . . . 211
Non-autoimmune Thyroiditis . . . 211
Drug-induced Thyroiditis . . . 212
Postoperative Necrotizing Thyroiditis . . . 213
Radiation Thyroiditis . . . 213
Indications for Surgery . . . 214
References . . . 214
autoantibodies). An association of autoimmune thyroiditis with defined HLA haplotypes implies a genetic
predisposition [5]. Iodine therapy, viral infections,
pregnancy and menopause, stress [6], and immunomodulating drugs (interferon-α, interleukin-2) have
also been linked to autoimmune thyroiditis. Except
for Graves’ disease, most autoimmune thyroiditides
initially present with a limited hyperthyroid state, and
thereafter return to euthyroidism or definitively fall
to permanent (subclinical or overt) hypothyroidism.
Thus, over 90% of cases of clinical hypothyroidism
are caused by an autoimmune thyroiditis. Conversely,
about 1–10% of cases of hyperthyroidism are related
to a thyroiditis. Clinically, patients may present either
with an acute illness with severe thyroid pain (e.g.,
subacute de Quervain’s thyroiditis, acute suppurative
thyroiditis, radiation thyroiditis, traumatic thyroiditis) or without evident inflammation but with thyroid dysfunction or a goiter (e.g., silent thyroiditis,
Hashimoto’s or Riedel’s thyroiditis).
Table 16.1 Etiologies of thyroiditis
16.1
Introduction
Thyroiditides make up approximately 20% of all thyroid diseases [1] and are caused by multiple factors
(Table 16.1). Autoimmune diseases represent the
most common etiologies. According to the clinical
course, thyroiditides have been subdivided into acute,
subacute, and chronic forms. Once a suppurative inflammation has been ruled out, most other types of
thyroiditis have either a definitive autoimmune etiology or are possibly autoimmune in nature [2].
In life, one out of 100 individuals will develop an
overt autoimmune thyroiditis. Thyroid autoantibodies may be found in up to 10% of the general population [3,4]. These autoantibodies are mainly directed
against thyroid peroxidase or thyroglobulin. They are
not the cause of the disease, but the consequence of a
lost immune tolerance to the thyroid gland. Autoantibodies may promote thyroid hormone dysfunctions
(stimulating thyroid autoantibodies, blocking thyroid
Autoimmune
thyroiditis
Chronic lymphocytic thyroiditis
(Hashimoto’s)
Fibrotic variant of Hashimoto’s thyroiditis
Atrophic thyroiditis (primary myxedema)
Variants of
autoimmune
thyroiditis
Postpartum thyroiditis
Silent or painless thyroiditis
Subacute de Quervain’s thyroiditis
Fibrotic Riedel’s thyroiditis
Non-immune
thyroiditis
Acute infectious thyroiditis
Radiation thyroiditis
Palpation/trauma-induced thyroiditis
Sarcoidosis
Vasculitis
Postoperative necrotizing thyroiditis
Drug-induced thyroiditis
Carcinoma-associated thyroiditis
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Michel Adamina and Daniel Oertli
16.2
Autoimmune Thyroiditis
The largest community study published so far on autoimmune thyroiditis revealed elevated thyroid autoantibodies against thyroid peroxidase and thyroglobulin
in more than 10% of a British community (Whickham study) [3]. On the one hand, in 7.5% of this
community, elevated TSH together with a euthyroid
state indicated a subclinical hypothyroidism, which
became overt hypothyroidism in 1.9% of the study’s
population. On the other hand, subclinical or overt
hyperthyroidism was shown in 2% of people in the
Whickham community. Women showed a 10 times
higher prevalence of autoimmune thyroiditis, but this
gender difference declined with age so that, for people
over 75 years of age, 16% of the men and 20% of the
women showed subclinical hypothyroidism.
16.2.1
Hashimoto’s Thyroiditis
Synonyms: chronic lymphocytic thyroiditis, struma
lymphomatosa
Hashimoto’s thyroiditis is the most frequent autoimmune thyroiditis and is the archetypic example of organ-specific autoimmune disease. With a
prevalence of about 3% it represents the most common cause of hypothyroidism in the general population [1]. In regions where iodine intake is adequate,
Hashimoto’s thyroiditis also represents the most common cause of goiter. The peak incidence culminates
in the fifth decade of life and the prevalence increases
with age. Women are 10–20 times more affected than
men. A genetic association with the haplotypes HLADR3, -DR4, and -DR5 is found. Many other autoimmune diseases are associated with Hashimoto’s thyroiditis: Graves’ disease, juvenile diabetes, Addison’s
disease, pernicious anemia, rheumatoid arthritis,
Sjögren’s syndrome, and systemic lupus erythematosus. Hashimoto’s thyroiditis mostly presents with an
oligosymptomatic clinical course, a painless homogeneous goiter, and with signs of hypothyroidism. Low
concentrations of thyroid hormones with high TSH
and circulating thyroid autoantibodies (against peroxidase in 70–90% of cases and against thyroglobulin
in 40–70% of cases) confirm the diagnosis [1]. Occasionally, a transient hyperthyroidism state may be
noted, up to a marked hyperthyroidism or hashitoxicosis, associated with the presence of anti-TSH receptor antibodies. Like all autoimmune diseases, the
clinical picture is one of relapsing episodes, with up
to one quarter of the patients showing a spontaneous
recovery. Hashimoto’s thyroiditis is probably related
to an acquired defect of the thyroid’s specific T suppressor lymphocytes, resulting in the emergence of
helper T lymphocytes directed against the gland,
and the production of autoantibodies against various
components of the thyroid. The binding of these autoantibodies to the thyrocytes accounts for complement
and T lymphocyte-mediated lysis of the thyrocytes
and non-regulated release of thyroxine and triiodothyronine, resulting in the transient hyperthyroidism
occasionally noted. Later, the destruction of thyroid
parenchyma may lead to permanent hypothyroidism.
A causal treatment is unknown and substitutive
thyroid hormone therapy is indicated when overt
hypothyroidism (i.e., in about 20% of patients) is
identified. Most patients require lifelong replacement
therapy.
On fine-needle biopsy, Hürthle cells or oncocytes
are frequently seen. Hashimoto’s thyroiditis may at
times be difficult to distinguish on a fine-needle aspiration biopsy from a follicular neoplasm, papillary
carcinoma, or low-grade MALT lymphoma. Immunohistochemistry studies may help to clear the differential diagnosis.
16.2.1.1 Fibrotic Hashimoto’s Thyroiditis
A fibrotic variant of Hashimoto’s thyroiditis accounts
for up to 10% of the clinical presentations, predominantly in elderly patients with preexisting goiter. The
disease is characterized by a rapid increase of goiter
size, which may lead to the suspicion of malignancy
and to subsequent surgery. Nevertheless, the extensive
fibrotic changes and metaplasia noted on specimen or
biopsies are always limited to the gland, in contrast to
the invasive Riedel’s fibrosing thyroiditis.
16.2.1.2 Atrophic Autoimmune Thyroiditis
Synonyms: primary myxedema, idiopathic myxedema, atrophic Hashimoto’s thyroiditis
The atrophic autoimmune thyroiditis is the cause
of primary myxedema and should not be confused
with endstage fibrotic Hashimoto’s thyroiditis. Most
of the cases proceed over years without overt signs or
symptoms. The related hypothyroidism then becomes
clinically obvious around the fourth to sixth decade
of life. Women are 5 times more affected than men.
On histologic specimen, the thyroid gland weighs
less than 5 g, whereas in some milder asymptomatic
cases, the thyroid gland weighs around 10 g (reference weights: male 20 g, female 17 g [7]).
16 Thyroiditis
A postpartum thyroiditis occurs in 2–16% of women
4–6 months following delivery (by definition within
one year after parturition or abortion) [8,9]. The disease represents an exacerbation of a preceding (undiagnosed) autoimmune thyroiditis and is classically
linked to the haplotypes HLA-DR3, -DR4, and -DR5.
It may be interpreted as rebound autoimmunity after the pregnancy-associated immunosuppression.
Eighty-five percent of these patients develop autoantibodies against thyroid peroxidase and thyroglobulin, which may vanish over time. Clinically, women
may show a transient hyperthyroidism state, which
rapidly converts to hypothyroidism, and then to euthyroidism within 12 months. Treatment consists of
thyroid hormone substitution when required. Thyreostatic medication, occasionally β-blockers, may be
needed in the presence of exacerbated hyperthyroidism. Neither prophylaxis nor predicting marker have
been identified so far and women affected once have
a higher probability of relapse following further pregnancies.
Women with a known autoimmune thyroiditis
prior to pregnancy and an elevated titer of autoantibodies against thyroglobulin during pregnancy nearly
always suffer from a postpartum exacerbation of their
autoimmune thyroiditis.
lassitude, and a feeling of illness. The thyroid is exquisitely tender and enlarged to palpation. The erythrocyte sedimentation rate is markedly elevated. Initially,
the local inflammation process leads to a destruction
of thyroid follicles with a transient hyperthyroidism,
due to the breakdown of stored thyroglobulin. Later
on, hypothyroidism emerges as the thyroid is not able
to cope with the body’s demand for thyroid hormones.
Finally, as the subacute thyroiditis heals, euthyroidism returns. Subacute de Quervain’s thyroiditis tends
to recur, although at a low rate of 4% [11]. Permanent
hypothyroidism requiring substitutive therapy is then
noted in 15% of the patients [11].
The etiology of subacute de Quervain’s thyroiditis
remains uncertain, but evidence implicates viral infection. A postviral cytokine-mediated inflammation of
the thyroid is suspected because a seasonal frequency
and an association with upper respiratory tract infection is noted. In half of the patients antibodies against
mumps, measles, influenza, adenovirus, coxsackievirus, or echovirus are found. Furthermore, a genetic
predisposition exists with the haplotype HLA-Bw35.
The differential diagnosis encompasses acute suppurative thyroiditis. In contrast to acute suppurative
thyroiditis, the gland sonographically reveals irregular hypoperfused areas instead of hyperperfused tissue. On fine-needle biopsy, the differential diagnosis
further includes palpation thyroiditis, as well as other
granulomatous diseases such as sarcoidosis, tuberculosis, and rheumatoid diseases.
Treatment is supportive with non-steroidal antiinflammatory agents (NSAR) and β-blockers in severe
cases with hyperthyroidism. Corticosteroids are useful (about 40 mg hydrocortisone equivalents daily)
when the NSAR medication is not successful. Symptoms usually improve within 2–3 days after the initiation of corticosteroid treatment. However, it may take
about 4 weeks for the disappearance of the thyroid
mass.
16.2.4
16.2.5
16.2.2
Focal Lymphocytic Thyroiditis
Synonyms: focal autoimmune thyroiditis, chronic unspecific thyroiditis
Focal lymphocytic thyroiditis is a coincidental
finding in 50% of women’s and 25% of men’s autopsies, without clinical relevance. This low-grade autoimmune thyroiditis is characterized by focal lymphocytic infiltrates of less than 5% of the thyroid gland.
16.2.3
Postpartum Thyroiditis
Subacute de Quervain’s Thyroiditis
Synonyms: granulomatous thyroiditis, pseudotuberculous thyroiditis, giant cell thyroiditis
Subacute de Quervain’s thyroiditis is a self-limiting
disease accounting for 0.5–3% of all thyroid pathologies and lasts a few weeks to 2 months [10]. Women
are 3–6 times more affected than men. The peak incidence is between the second and fifth decade of life.
Patients complain of moderate to severe pain in the
neck of sudden onset that irradiates to the jaw, ear,
face, and down to the thorax; they present with fever,
Painless Thyroiditis
Synonym: subacute lymphocytic thyroiditis
Patients present with a diffuse but modest enlargement of the thyroid and function tests reveal a
transient hyperthyroidism, followed by hypothyroidism. The painless thyroiditis is self-limited and rarely
necessitates thyroid hormone substitution therapy.
Women are again more often affected than men with
a peak of incidence in middle life and in the postpartum period. Autoantibodies against thyroid peroxidase and thyroglobulin are found, as well as an
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association with HLA-DR3 and -DR5 haplotypes.
Histologic examination of a specimen reveals a lymphocytic infiltration with destruction of follicles; this
is in contrast to Hashimoto’s thyroiditis. Neither giant
cell granulomas (typical for a subacute thyroiditis)
nor an association with a viral infection are present.
16.2.6
Riedel’s Fibrosing Thyroiditis
Riedel’s thyroiditis is a rare chronic thyroiditis in
which the thyroid gland is replaced by fibrous tissue.
The underlying etiologic mechanisms are unclear. An
autoimmune component is suspected, due to elevated
titers of thyroid autoantibodies. The prevailing view
is that Riedel’s thyroiditis is part of a multifocal fibroinflammatory process also involving other tissues
(mediastinum, liver, lung, retroperitoneum, orbital).
Women in middle to advanced ages are more affected
than men. The clinical manifestations of Riedel’s thyroiditis are protean, often resembling malignancy due
to a goiter of remarkably hard consistency. Patients
complain of a rapid indolent enlargement of the thyroid that becomes very hard on palpation and difficult to delineate. Neck discomfort and dysphagia are
frequently reported. Thirty to 40% of these patients
develop overt hypothyroidism. Hoarseness and hypoparathyroidism may also appear due to involvement
of the recurrent laryngeal nerve and/or the parathyroid glands. Physical examination, laboratory analysis, cytology, and imaging features are not useful for
differentiating between Riedel’s thyroiditis and neoplastic diseases or the fibrotic variant of Hashimoto’s
thyroiditis [12]. Histologic examination is necessary
to establish the final diagnosis and surgical biopsy
is mandatory. The differential diagnosis further encompasses anaplastic carcinoma and sarcoma of the
thyroid. In contrast to the fibrotic variant of Hashimoto’s thyroiditis where fibrosis is strictly limited to
the gland, Riedel’s thyroiditis displays a dense fibrotic
replacement of thyroid parenchyma that penetrates
the capsule and extends into contiguous neck structures. Once the diagnosis is confirmed, treatment is
supportive with thyroid hormone substitution, when
required.
16.3
Acute Infectious Thyroiditis
Synonym: acute suppurative thyroiditis
Infectious thyroiditis is a rare disease of the thyroid. A bacterial or a fungal infection is the main
cause, though only a few hundred cases are reported
worldwide. Mycobacterial, parasitic, and viral forms
of thyroiditis have also been described, predominantly in immunodepressed hosts. The thyroid gland
appears to be relatively resistant to infection. A rich
vascular supply and an extended lymphatic drainage,
as well as a fibrous capsule and an anatomic separation from the other structures of the neck by fascial
planes, represent protective mechanisms. The high
iodine content of the gland may account for some
bactericidal effect. Infection of the gland occurs either
through hematogenous spread from a primary focus
or by direct extension from adjacent neck structures
such as infected tonsil, pharynx, thyroglossal duct
cyst, or through a pyriform sinus fistula, especially in
children [13].
Other less common sources of infection include
neck trauma or lymphatic spread; surgical site infections are extremely rare [14]. The most common predisposing factor for suppurative thyroiditis is immunodepression in association with HIV, tuberculosis,
old age, or debilitation. Other predisposing factors
include preexisting thyroid diseases, such as multinodular goiter, autoimmune thyroiditis, and thyroid
cancers [14–16].
Patients are febrile with a sudden onset of disease, a
painful, mostly unilateral enlargement of the thyroid,
and local inflammatory signs (Fig. 16.1). The thyroid
hormone tests are usually normal, but a slight hyperor hypothyroidism may appear. The erythrocyte sedimentation rate and acute phase proteins are elevated,
and leucocytosis is present. Neck sonography reveals
patchy hyperperfused areas in the thyroid with liquid
content when an abscess is present. A fine-needle biopsy and cultures allow for pathogen identification
and guide the antibiotic treatment. Depending on the
clinical context, dedicated stainings and/or immunohistochemistry or in situ hybridization techniques
may be necessary to identify the causative pathogen.
Immunodepressed patients tend to present with more
chronic thyroid infections, bilateral disease, and less
prominent signs and symptoms: a high index of suspicion and aspiration biopsy are invaluable to pose
the correct diagnosis and initiate correct treatment.
The differential diagnosis of a painful anterior
neck mass with febrile status encompasses subacute
de Quervain’s thyroiditis, hemorrhage into a thyroid
nodule, an infected thyroglossal or branchial cleft
cyst, an infected cystic hygroma, and cervical adenitis. In addition to fine-needle biopsy, sonography
helps to establish the correct diagnosis: acute suppurative thyroiditis usually shows hyperperfused areas
(Fig. 16.2). In contrast, sonography in de Quervain’s
thyroiditis depicts only microabscesses and no hyperperfused areas. Computed tomography (CT) and/or
contrast oesography may further refine the diagnosis
16 Thyroiditis
Fig. 16.1 Clinical picture of a
31-year-old female with acute
infectious thyroiditis. Steroid
therapy was initiated for a subacute
de Quervain’s thyroiditis. Six weeks
later, the patient developed a unilateral painful neck mass, dysphagia,
and fever. Surgical incision and
drainage was necessary to cure this
condition
or parasitic infections occur preferentially in immunodepressed patients. Dedicated stainings and a high
index of suspicion may be necessary to identify atypical pathogens, such as Pneumocystis carinii and mycobacteria. Table 16.2 lists the pathogens commonly
involved in acute thyroiditis. In children, an acute
suppurative thyroiditis is caused in up to 90% of the
cases by a pyriform sinus fistula [17].
16.3.2
Surgical Treatment
(Fig. 16.3) and help to delineate the extent of surgical
treatment, particularly in the case of an infected pyriform sinus fistula.
When an abscess is identified, surgical drainage is
mandatory. Surgical incision and drainage of the abscess are curative only in patients whose acute thyroiditis is unrelated to a pyriform sinus fistula or thyroglossal duct fistula. Sometimes an affected thyroid
lobe needs complete resection (Fig. 16.4a–c). In patients with recurrent acute thyroiditis, an undetected
fistula must be postulated. Complete removal of the
infected fistula is therefore required to prevent recurrence. Injection of 0.5% methylene blue solution
through a Nélaton’s catheter into the fistula usually
enables the complete resection of the fistula tract.
When the origin of the fistula is difficult to identify,
transection of the inferior pharyngeal constrictor
muscle makes intervention easier.
16.3.1
16.4
Fig. 16.2 Thyroid sonography in acute infectious thyroiditis
of the patient shown in Fig. 16.1. Hyperperfused areas and a
liquid collection in the left thyroid lobe are shown. Fine-needle
biopsy revealed Streptococcus constellatus, Peptostreptococcus,
and fusobacteria
Etiologies of Infectious Thyroiditis
A bacterial infection (mainly gram-positive bacteria)
contracted through hematogenous spread or neck
trauma is the most common cause of acute thyroiditis in the immunocompetent patient. Viral, fungal,
Non-autoimmune Thyroiditis
Non-immune thyroiditis consist of a heterogeneous and rare group of thyroid inflammatory diseases. Some of them are clearly iatrogenic, such as
drug-induced thyroiditis, postoperative necrotizing
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Fig. 16.3 Thyroid aspergilloma in an
immunodepressed kidney transplant
patient. CT scan of the neck reveals
a diffuse enlargement of the right
thyroid gland with abscess formation
Table 16.2 Pathogens involved in acute thyroiditis
Bacteria
Staphylococcus aureus (30%)
Staphylococcus pyogenes
Staphylococcus pneumoniae
Streptococcus
Finally, a few thyroiditides are caused by systemic
diseases, such as a vasculitis-associated thyroiditis
(phenytoin therapy may precipitate a hypersensitive
thyroid vasculitis), a sarcoidosis (the thyroid is involved in up to 6% of sarcoidoses [18]), metastatic
cancer, or a globus hystericus.
Enterobacteria
Fungi
Aspergillus
Pneumocystis carinii
Cryptococcus
Candida
Virus
EBV
CMV
Measles
Adenovirus
Echovirus
Mumps
Parasites
Echinococcus
Strongyloides
Taenia
thyroiditis, and radiation thyroiditis. Other causes
are related to a local process, such as an acute hemorrhage into a thyroid cyst or nodule.
Palpation thyroiditis refers to a mild, self-limited
thyroiditis occurring after physical examination, surgery, or trauma to the thyroid. It is not associated with
any thyroid disease.
16.4.1
Drug-induced Thyroiditis
Chronic iodine therapy may cause a drug-induced
thyroiditis with follicular hyperplasia. Likewise,
lithium therapy may cause a goiter with or without
hypothyroidism in 5–15% of patients under longterm lithium therapy [1]. Anticonvulsants (phenytoin, carbamazepine) may cause unspecific thyroiditis with subclinical or clinical hypothyroidism.
Patients with chronic hepatitis or with cancer treated
using interferon-α will develop a painless thyroiditis
in about 1–5% of cases [19]. Elevated antithyroid
antibodies are noted in a higher percentage in these
patients and permanent hypothyroidism as well as
Grave’s disease may appear [20]. Prior interferon-α
therapy in the presence of antithyroid antibodies is
associated with a higher probability of a subsequent
antibody titer elevation and thyroid dysfunction
[21]. These changes usually occur within 3 months
of interferon-α therapy and seldom thereafter. As a
practical matter, TSH should be measured prior to
initiation of interferon-α therapy and periodically
during treatment.
For immunomodulation, interleukin-2 is also used
in malignant melanoma, renal cell cancer, and leuke-
16 Thyroiditis
Fig. 16.4 a Intraoperative finding of the patient depicted in
Fig. 16.3 showing inflammatory swelling of the right thyroid
lobe with aspergilloma. b Removed lobe after right hemithyroidectomy. c Opened specimen presenting abscess with aspergilloma
mia, alone or in combination with chemotherapy. In
several studies, interleukin-2 therapy has been linked
to the development of a painless thyroiditis in about
2% of the patients treated [22].
Finally, the antiarrhythmic drug amiodarone contains 35% iodine and may cause thyroid dysfunctions
in several different ways [23]. Amiodarone may cause
a thyrotoxic crisis, due to its high iodine content
(usually in patients with preexisting nodular goiter).
Conversely, amiodarone may cause hypothyroidism
via the antithyroid action of iodine, especially in patients with preexisting thyroid disease. Amiodarone
decreases the conversion of T4 to the biologically active T3. It is worth noting that if the decision is taken
to cease amiodarone therapy, the drug is not eliminated for months due to a very long half-life.
16.4.2
Postoperative Necrotizing Thyroiditis
Postoperative necrotizing thyroiditis is a rare surgical
complication [24,25]. No predictive marker or factor
has been identified and the very rich vascular supply
of the thyroid usually prevents this rarest complication. On histologic examination, the specimen typically shows postoperative granulomas, as found in
other organs (bladder, prostate) following surgery.
Postoperative necrotizing thyroiditis is related to
a trauma of the thyroid, through vigorous manipulation of the gland at surgery or through repeated fineneedle aspiration [26]. Such manipulation could induce an acute thyroiditis, which in turn may lead to
thyrotoxicosis or to a necrotizing thyroiditis.
16.4.3
Radiation Thyroiditis
Radiation thyroiditis occurs in a dose-related fashion
after radioiodine or external beam radiation therapy.
Follicle destruction due to radiation injury may cause
a transient hyperthyroidism, followed eventually by
hypothyroidism. Neck pain and tenderness usually
develop 5–10 days following treatment. Symptoms
are mild and subside spontaneously in a week.
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16.5
Indications for Surgery
Surgical interventions are exceptionally indicated for
the management of a thyroiditis, accounting for less
than 1% of all thyroid procedures [27]. Patients with
autoimmune thyroiditis may pose significant technical challenges to the endocrine surgeon. The glands
are firm, rigid, and highly vascular. The tissues surrounding the thyroid are inflamed with lymphadenopathy. This makes preservation of the parathyroids
and recurrent nerves a highly demanding task. However, it is rather the exception than the rule to pose
a surgical indication for an autoimmune thyroiditis,
as most patients are effectively managed with thyroid
hormone replacement therapy.
In the rare instance where a large Hashimoto’s goiter may develop and become symptomatic, near-total
thyroidectomy is an option [2,27,28]. Moreover, as
thyroiditis patients bear a higher risk of developing
thyroid carcinoma, a cold nodule suspicious on fineneedle biopsy may indicate a thyroid lobectomy. Similarly, the rapid growth of a chronic lymphocytic thyroid gland is suggestive of non-Hodgkin’s lymphoma.
While total thyroidectomy may surgically cure a
stage I lymphoma (i.e., confined to the thyroid), most
thyroid lymphomas involve regional lymph nodes and
distant sites and require multimodal systemic therapy. Open biopsy or thyroid lobectomy is sufficient in
these cases to establish the definitive diagnosis.
A subacute de Quervain’s thyroiditis exceptionally deserves surgical consideration. This indication is
given when intractable neck pain is present in spite of
a consequent analgesic and substitution therapy with
thyroxin over 6 months. Thyroidectomy may then be
indicated for definitive cure [27].
Riedel’s fibrosing thyroiditis often requires an
open biopsy to confirm the diagnosis and rule out an
anaplastic carcinoma (or the fibrotic variant of Hashimoto’s thyroiditis). However, thyroidectomy can
be highly demanding because of the dense fibrotic
reaction extending beyond the thyroid that puts the
surrounding structures at risk for injury. Surgery
is therefore confined to diagnosis of thyroiditis and
exclusion of malignancy or to decompression of the
trachea and the esophagus by isthmectomy and/or
lobectomy.
The fibrotic variant of Hashimoto’s thyroiditis is
characterized by a rapid enlargement of a preexisting
goiter that may lead to the suspicion of a thyroid cancer and to surgical resection.
Amiodarone-induced thyrotoxicosis in the setting
of a rare patient with otherwise intractable arrhythmia is an indication for thyroidectomy.
Finally, the acute suppurative thyroiditis is a classic
indication for surgical drainage followed by antibiotic
therapy. Rarely lobectomy is necessary when the suppurative process is necrotizing. An underlying thyroglossal (pyriform) fistula should be excluded by the
time of surgical exploration.
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