Painful thyroid acute pyogenic or fungal thyroiditis subacute thyroiditis hemorrhage into a cyst Acute hemorrhagic degeneration in a
nodule, Hashimoto’s disease with painful
recurrence thyroid malignancy(lymphoma) amiodarone-induced thyroiditis or
amyloidosis
ThyroiditisThyroiditis11--Acute: Acute: Bacterial Bacterial -- FungalFungal
RadiationRadiationDrugsDrugs
22--SubacuteSubacute::Viral Viral -- MycobacterialMycobacterialSilent Silent thyroiditisthyroiditis
33--Chronic:Chronic:AutoimmuneAutoimmuneReidelReidelTraumaTrauma
Acute Thyroiditis Causes
68% Bacterial (S. aureus, S. pyogenes) 15% Fungal 9% Mycobacterial
May occur secondary to Pyriform sinus fistulae Pharyngeal space infections Persistent Thyroglossal remnants Thyroid surgery wound infections (rare)
More common in HIV
Acute Thyroiditis Symptoms
Thyroid pain and tenderness Fever Dysphagia Dysphonia Warm, tender, enlarged thyroid
Acute Thyroiditis Diagnosis
FNA to drain abscess, obtain culture RAIU normal&TFT NL (versus decreased in
DeQuervain’s) CT or US if infected TGDC suspected
Treatment High mortality without prompt treatment IV Antibiotics
• Nafcillin / Gentamycin or Rocephin for empiric therapy Search for pyriform fistulae (BA swallow, endoscopy) Recovery is usually complete
Subacute Thyroiditis
Subacute Most common cause of
painful thyroiditis
20% of thyrotoxic cases De Quervain’s thyroiditis Giant cell thyroiditis Pseudogranulomatous
thyroiditis Subacute painful
thyroiditis
characteristic features well-developed follicular
lesion that consists of a central core of colloid surrounded by the multinucleated giant cells, hence the designation giant cell thyroiditis.
Colloid may be found in the interstitium or within the giant cells.
Sub Acute ThyroiditisViral (granulomatous) Mumps, coxsackie, influenza, adeno and echoviruses
Subacute thyroiditis features 5:1 female predominance Age of onset 20-60y Prodrome (myalgias, fever, pharyngitis) Seasonal variation (correlation with enterovirus?) Fever/severe neck pain Dysphagia,odynophagia,hoaresness The pain, which is aggravated by turning thehead or swallowing, characteristically radiates to the ear,jaw, or occiput and may mimic disorders arising in these areas.
Usually low to absent titer of anti-TPO immunoglobulins Thyroid storm – case reports
Subacute thyroiditis features On palpation, at least part of the thyroid is slightly
to moderately enlarged, firm, often nodular, and usually exquisitely tender.
One lobe is frequently being more severely affected than the other, and the symptoms may
be truly unilateral. The overlying skin may be warm and
erythematous.
Subacute ThyroiditisDeQuervain’s, Granulomatous
FNA may reveal multinuleated giant cells or granulomatous change.
Course Pain and thyrotoxicosis (3-6
weeks) Asymptomatic euthyroidism Hypothyroid period (weeks to
months) Recovery (complete in 95% after 4-
6 months)
2-9% with recurrent disease 5% residual hypothyroidism
Clinical Course of Sub Acute Thyroiditis
Subacute ThyroiditisDeQuervain’s, Granulomatous Diagnosis
Elevated ESR usually>100 Elevated/NL CBC Anemia (normochromic, normocytic) Low TSH, Elevated T4 > T3, Low anti-TPO/Tgb Low RAI uptake (same as silent thyroiditis)
Treatment NSAID’s and salicylates. Oral steroids in severe cases Beta blockers for symptoms of hyperthyroidism, Iopanoic acid
for severe symptoms PTU not indicated since excess hormone results from leak
instead of hyperfunction Symptoms can recur requiring repeat treatment
Treatment: Subacute Thyroiditis large doses of aspirin (e.g., 600 mg every 4–6 h) or NSAIDs marked local or systemic symptoms, glucocorticoids usual
starting dose is 40–60 mg prednisone, depending on severity. The dose is gradually tapered over 6–8 weeks, in response to improvement in symptoms and the ESR.
If a relapse occurs during glucocorticoid withdrawal, treatment should be started again and withdrawn more gradually. In these patients, it is useful to wait until the radioactive iodine uptake normalizes before stopping treatment.
monitoring every 2–4 weeks using TSH and unbound T4 levels. Symptoms of thyrotoxicosis improve spontaneously but may be
ameliorated by -adrenergic blockers. antithyroid drugs play no role in treatment of the thyrotoxic
phase. Levothyroxine replacement may be needed if the hypothyroid phase is prolonged, but doses should be low enough (50 to 100 g daily) to allow TSH-mediated recovery.
Patient’s follow up 11.3.92
T4:5.3 T3:81 TSH:2.3 ESR:4 FBS:107
Thank You for Your Attention
Thyroid noduleRisk factors for cancer: Age <15, > 45 Male sex Hx of radiation ( up to 5% of patients develop Ca) Solitary thyroid nodule + h/o radiation = 40% will
have Ca Family Hx or h/o diseases associated with thyroid Ca:
Cowden’s and Gardner syndromes, FAP, Pheo and Hyperparathyroidism
Size > 4 cm Prior h/o thyroid Ca
Thyroid nodule
Sign of malignancy: Rapid growth Hard nodule Fixated Vocal cord paralysis Enlarged lymph nodes Family h/o thyroid Ca Symptoms of invasion All - 71% risk of malignancy
Dx of follicular neoplasm on FNA: 20% thyroid Ca
NCCN Practice Guidelines 2003J. Hamming. Arch Intern Med 1990R. Wein, Otolaryngology Clinics of NA 2005
US signs of malignancy
Microcalcifications Solid nodule / marked
hypoechogenicity Irregular margins Absence of a
hypoechoic halo around the nodule
Lymphadenopathy and local invasion of adjacent structures
High vascularity on Doppler flow
Benignnodule
Radioactive Iodine Uptake (RAIU)
• A small amount of 131I is given orally, and 4 & 24 hr dosimetry readings are taken from the thyroid
• Normal range: ~5-30%• Increased RAIU
Graves Disease Toxic Multinodular Goiter Thyroid Adenoma
• Decreased RAIU Subacute or Silent Thyroiditis Iodine-Induced Factitious
27
Ultrasonography Findings suggestive of malignancy:
No Presence of halo Irregular border Presence of cystic components Presence of calcifications Heterogeneous echo pattern Extrathyroidal extension
No findings are definitive
Silent ThyroiditisPost-partum Thyroiditis
Postpartum thyroiditis 2-21% of pregnancies Can occur up to one
year post partum Usually transient and
returns to euthyroid state
Treat • Hypothyroidism• Symptoms with
‘hyperthyroidism’
Presence of TPO AB increases risk of long term hypothyroidism
Silent ThyroiditisPost-partum Thyroiditis Silent thyroiditis is termed post-partum thyroiditis if it
occurs within one year of delivery. Clinical
Hyperthyroid symptoms at presentation Progression to euthyroidism followed by hypothyroidism for
up to 1 year. Hypothyroidism generally resolves
Diagnosis May be confused with post-partum Graves’ relapse
Treatment Beta blockers during toxic phase No anti-thyroid medication indicated Iopanoic acid (Telopaque) for severe hyperthyroidism Thyroid hormone during hypothyroid phase. Must withdraw in
6 months to check for resolution.
Chronic ThyroiditisHashimoto’s
Autoimmune Initially goiter later
very little thyroid tissue Rarely associated with
pain Insidious onset and
progressionHashimoto’s
• Women 3.5/1000• Men 0.8/1000• Frequency increases
with age• Familial history• Associated with
autoimmune diseases
Most common cause of hypothyroidism
TPO abs present (90 – 95%)
Hashimoto’s Thyroiditis Most common cause of goiter and hypothyroidism in the U.S. Physical
Painless diffuse goiter Lab studies
Hypothyroidism Anti TPO antibodies (90%) Anti Thyroglobulin antibodies (20-50%) Acute Hyperthyroidism (5%)
Treatment Levothyroxine if hypothyroid Triiodothyronine (for myxedema coma) Thyroid suppression (levothyroxine) to decrease goiter size
• Contraindications• Stop therapy if no resolution noted
Surgery for compression or pain.
Riedel’s Thyroiditis Rare disease involving fibrosis of the thyroid glandMiddle aged women Insidious painless Symptoms due to compression Dense fibrosis develop Usually no thyroid function impairment
Diagnosis Thyroid antibodies are present in 2/3 Painless goiter “woody” Open biopsy often needed to diagnose Associated with focal sclerosis syndromes (retroperitoneal, mediastinal, retroorbital, and sclerosing
cholangitis)
Treatment Resection for compressive symptoms Chemotherapy with Tamoxifen, Methotrexate, or steroids may be effective Thyroid hormone only for symptoms of hypothyroidism
Most cases of thyroiditis associated with various therapeutic agents appear to be caused by drug-induced exacerbation of underlying autoimmunedisease.• Amiodarone • IL-2, interferon-α, • granulocyte/macrophage colony-stimulating factor (GM-CSF)• lithium• GnRH agonist leuprolide, but the pathophysiology is obscure.
Thyroiditis has been found in association with the useof a multitargeting kinase inhibitor, sunitinib, in patientswith gastrointestinal stromal tumors or renal cell carcinoma
Drug-Associated Thyroiditis
exacerbations of Hashimoto’s disease may be difficult to distinguish from subacute thyroiditis. Lack of elevation of the erythrocyte sedimentation rate and high titers of
thyroid autoantibodies strongly suggest the former condition. Acute pyogenic thyroiditis is distinguished by the presence of a septic focus
elsewhere,bygreaterinflammatoryreaction in the tissues adjacent to the thyroid, andby much greater leukocytic and febrile responses .The RAIU and thyroid function are usually preserved in acute pyogenic thyroiditis. Rarely, widespread infiltrating cancer of the thyroid can manifest with aclinical and laboratory picture almost indistinguishable from that of subacute thyroiditis. Ultrasonography and fine-needle aspiration should be performed if this is a consideration
Comparison of ThyroiditisCharacteristic Silent thyroiditis Subacute thyroiditisAge of onset (yr) 5-93 20-60Sex ratio (F:M) 2:1 5:1
Etiology Autoimmune ViralPathology Lymphocytic infiltration Giant cells, granulomasProdrome Pregnancy Viral illness
Goiter Non-painful PainfulFever/malaise No Yes
TPO/thyroglobulin AB High and rising Low, absent or transientESR Normal HighRAIU <5% <5%
Relapse Common RarePermanent
hypothyroidismCommon Infrequent