2Painful thyroid acute pyogenic or fungal thyroiditis subacute thyroiditishemorrhage into a cystAcute hemorrhagic degeneration in a nodule,Hashimoto’s disease with painful recurrencethyroid malignancy(lymphoma)amiodarone-induced thyroiditis or amyloidosis
5Acute Thyroiditis Causes May occur secondary to More common in HIV 68% Bacterial (S. aureus, S. pyogenes)15% Fungal9% MycobacterialMay occur secondary toPyriform sinus fistulaePharyngeal space infectionsPersistent Thyroglossal remnantsThyroid surgery wound infections (rare)More common in HIV
7Acute Thyroiditis Diagnosis Treatment FNA to drain abscess, obtain cultureRAIU normal&TFT NL (versus decreased in DeQuervain’s)CT or US if infected TGDC suspectedTreatmentHigh mortality without prompt treatmentIV AntibioticsNafcillin / Gentamycin or Rocephin for empiric therapySearch for pyriform fistulae (BA swallow, endoscopy)Recovery is usually complete
8Subacute Thyroiditis Subacute Most common cause of painful thyroiditis 20% of thyrotoxic casesDe Quervain’s thyroiditisGiant cell thyroiditisPseudogranulomatous thyroiditisSubacute painful thyroiditis
9characteristic 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.
10Sub Acute ThyroiditisViral (granulomatous) Mumps, coxsackie, influenza, adeno and echoviruses
11Subacute thyroiditis features 5:1 female predominanceAge of onset 20-60yProdrome (myalgias, fever, pharyngitis)Seasonal variation (correlation with enterovirus?)Fever/severe neck painDysphagia,odynophagia,hoaresnessThe 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 immunoglobulinsThyroid storm – case reports
12Subacute 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 maybe truly unilateral.The overlying skin may be warm and erythematous.
13Subacute Thyroiditis DeQuervain’s, Granulomatous FNA may reveal multinuleated giant cells or granulomatous change.CoursePain and thyrotoxicosis (3-6 weeks)Asymptomatic euthyroidismHypothyroid period (weeks to months)Recovery (complete in 95% after 4-6 months)2-9% with recurrent disease5% residual hypothyroidism
15Subacute Thyroiditis DeQuervain’s, Granulomatous DiagnosisElevated ESR usually>100Elevated/NL CBCAnemia (normochromic, normocytic)Low TSH, Elevated T4 > T3, Low anti-TPO/TgbLow RAI uptake (same as silent thyroiditis)TreatmentNSAID’s and salicylates.Oral steroids in severe casesBeta blockers for symptoms of hyperthyroidism, Iopanoic acid for severe symptomsPTU not indicated since excess hormone results from leak instead of hyperfunctionSymptoms can recur requiring repeat treatment
17Treatment: Subacute Thyroiditis large doses of aspirin (e.g., 600 mg every 4–6 h) or NSAIDsmarked 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.
20Thyroiditis Time Course Williams Text of Endocrinology, Fig 11.50
21Thyroid nodule Risk 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 CaFamily Hx or h/o diseases associated with thyroid Ca: Cowden’s and Gardner syndromes, FAP, Pheo and HyperparathyroidismSize > 4 cmPrior h/o thyroid Ca
22Thyroid nodule Sign of malignancy: Rapid growth Hard nodule Fixated Vocal cord paralysisEnlarged lymph nodesFamily h/o thyroid CaSymptoms of invasionAll - 71% risk of malignancyDx of follicular neoplasm on FNA: % thyroid CaNCCN Practice Guidelines 2003J. Hamming. Arch Intern Med 1990R. Wein, Otolaryngology Clinics of NA 2005
23US signs of malignancy Microcalcifications BenignnoduleMicrocalcificationsSolid nodule / marked hypoechogenicityIrregular marginsAbsence of a hypoechoic halo around the noduleLymphadenopathy and local invasion of adjacent structuresHigh vascularity on Doppler flow
26Radioactive Iodine Uptake (RAIU) A small amount of 131I is given orally, and 4 & 24 hr dosimetry readings are taken from the thyroidNormal range: ~5-30%Increased RAIUGraves DiseaseToxic Multinodular GoiterThyroid AdenomaDecreased RAIUSubacute or Silent ThyroiditisIodine-InducedFactitious
27Ultrasonography Findings suggestive of malignancy: No Presence of haloIrregular borderPresence of cystic componentsPresence of calcificationsHeterogeneous echo patternExtrathyroidal extensionNo findings are definitive
28Silent Thyroiditis Post-partum Thyroiditis 2-21% of pregnanciesCan occur up to one year post partumUsually transient and returns to euthyroid stateTreatHypothyroidismSymptoms with ‘hyperthyroidism’Presence of TPO AB increases risk of long term hypothyroidism
29Silent Thyroiditis Post-partum Thyroiditis Silent thyroiditis is termed post-partum thyroiditis if it occurs within one year of delivery.ClinicalHyperthyroid symptoms at presentationProgression to euthyroidism followed by hypothyroidism for up to 1 year.Hypothyroidism generally resolvesDiagnosisMay be confused with post-partum Graves’ relapseTreatmentBeta blockers during toxic phaseNo anti-thyroid medication indicatedIopanoic acid (Telopaque) for severe hyperthyroidismThyroid hormone during hypothyroid phase. Must withdraw in 6 months to check for resolution.
30Chronic Thyroiditis Hashimoto’s Autoimmune Initially goiter later very little thyroid tissueRarely associated with painInsidious onset and progressionHashimoto’sWomen 3.5/1000Men 0.8/1000Frequency increases with ageFamilial historyAssociated with autoimmune diseasesMost common cause of hypothyroidismTPO abs present (90 – 95%)
31Hashimoto’s Thyroiditis Most common cause of goiter and hypothyroidism in the U.S.PhysicalPainless diffuse goiterLab studiesHypothyroidismAnti TPO antibodies (90%)Anti Thyroglobulin antibodies (20-50%)Acute Hyperthyroidism (5%)TreatmentLevothyroxine if hypothyroidTriiodothyronine (for myxedema coma)Thyroid suppression (levothyroxine) to decrease goiter sizeContraindicationsStop therapy if no resolution notedSurgery for compression or pain.
32Riedel’s Thyroiditis Insidious painless Symptoms due to compression Rare disease involving fibrosis of the thyroid glandMiddle aged womenInsidious painlessSymptoms due to compressionDense fibrosis developUsually no thyroid function impairmentDiagnosisThyroid antibodies are present in 2/3Painless goiter “woody”Open biopsy often needed to diagnoseAssociated with focal sclerosis syndromes (retroperitoneal, mediastinal, retroorbital, and sclerosing cholangitis)TreatmentResection for compressive symptomsChemotherapy with Tamoxifen, Methotrexate, or steroids may be effectiveThyroid hormone only for symptoms of hypothyroidism
33Drug-Associated Thyroiditis Most cases of thyroiditis associated with various therapeutic agents appear to be caused by drug-induced exacerbation of underlying autoimmunedisease.AmiodaroneIL-2, interferon-α,granulocyte/macrophage colony-stimulating factor (GM-CSF)lithiumGnRH 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
34exacerbations of Hashimoto’s disease may be difficult to distinguish from subacute thyroiditis. Lack of elevation of the erythrocyte sedimentation rate and high titers ofthyroid autoantibodies strongly suggest the former condition.Acute pyogenic thyroiditis is distinguished by thepresence 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
35Comparison of Thyroiditis CharacteristicSilent thyroiditisSubacute thyroiditisAge of onset (yr)5-9320-60Sex ratio (F:M)2:15:1EtiologyAutoimmuneViralPathologyLymphocytic infiltrationGiant cells, granulomasProdromePregnancyViral illnessGoiterNon-painfulPainfulFever/malaiseNoYesTPO/thyroglobulin ABHigh and risingLow, absent or transientESRNormalHighRAIU<5%RelapseCommonRarePermanent hypothyroidismInfrequent