2. HistoryHistory
GoiterGoiter
– Fist described in China in 2700 BCFist described in China in 2700 BC
Thyroid FunctionThyroid Function
– Da Vinci – thyroid is designed to fill empty spaces in the neckDa Vinci – thyroid is designed to fill empty spaces in the neck
– Parry – thyroid works as a buffer to protect the brain from surgesParry – thyroid works as a buffer to protect the brain from surges
in blood flowin blood flow
– Roman physicians – thyroid enlargement is a sign of pubertyRoman physicians – thyroid enlargement is a sign of puberty
CuresCures
– ““application of toadapplication of toad’’s blood to the necks blood to the neck””
– ““stroking of the thyroid gland with a cadaverous handstroking of the thyroid gland with a cadaverous hand””
3. Surgical advancesSurgical advances
500 AD500 AD
– Abdul Kasan Kelebis Abis performed the first goiter excision inAbdul Kasan Kelebis Abis performed the first goiter excision in
Baghdad.Baghdad.
– Procedure: unknownProcedure: unknown
12001200’’s ADs AD
– Advancements in goiter procedures included applying hot ironsAdvancements in goiter procedures included applying hot irons
through the skin and slowly withdrawing them at right angles. Thethrough the skin and slowly withdrawing them at right angles. The
remaining mass or pedicled tissue was excised.remaining mass or pedicled tissue was excised.
– Patients were tied to the table and held down to prevent unwantedPatients were tied to the table and held down to prevent unwanted
movement.movement.
– Most died from hemorhage or sepsisMost died from hemorhage or sepsis ..
1646 AD1646 AD
– Wilhelm Fabricus performed a thyroidectomy with standard surgicalWilhelm Fabricus performed a thyroidectomy with standard surgical
scalpels.scalpels.
– The 10 y/o girl died, and he was imprisonedThe 10 y/o girl died, and he was imprisoned
1808 AD1808 AD
– Guillaume Dupuytren performed a total thyroidectomy.Guillaume Dupuytren performed a total thyroidectomy.
– The patient died postoperatively ofThe patient died postoperatively of ““shockshock””
4. Surgical advancesSurgical advances
18661866
– ““If a surgeon should be so foolhardy as to undertake itIf a surgeon should be so foolhardy as to undertake it
[thyroidectomy] … every step of the way will be[thyroidectomy] … every step of the way will be
environed with difficulty, every stroke of his knife willenvironed with difficulty, every stroke of his knife will
be followed by a torrent of blood, and lucky will it bebe followed by a torrent of blood, and lucky will it be
for him if his victim lives long enough to enable him tofor him if his victim lives long enough to enable him to
finish his horrid butchery.finish his horrid butchery.””
–– Samuel David GrossSamuel David Gross
5. Surgical advancesSurgical advances
18831883
KocherKocher’’s performs a retrospective reviews performs a retrospective review
5000 career thyroidectomies5000 career thyroidectomies
Mortality rates decreasedMortality rates decreased
– 40% in 1850 (pre-Kocher & Bilroth)40% in 1850 (pre-Kocher & Bilroth)
– 12.6% in 187012.6% in 1870’’s (Kocher begins practice)s (Kocher begins practice)
– 0.2% in 1898 (end of Kocher0.2% in 1898 (end of Kocher’’s career)s career)
Many patients developed cretinism or myxedemaMany patients developed cretinism or myxedema
His conclusions ….His conclusions ….
6. Surgical advancesSurgical advances
In presentation to the German SurgicalIn presentation to the German Surgical
Congress …Congress …
““ ……the thyroid gland in fact had a function….the thyroid gland in fact had a function….””
- Theodor Kocher, 1883- Theodor Kocher, 1883
7. Medical AdvancesMedical Advances
1820 AD1820 AD
– Johann Straub and Francois Coindet found that useJohann Straub and Francois Coindet found that use
of seaweed (iodine) reduced goiter size andof seaweed (iodine) reduced goiter size and
vascularityvascularity
1830 AD1830 AD
– Graves and von Basedow describe a toxic goiterGraves and von Basedow describe a toxic goiter
condition they referred to ascondition they referred to as ““Merseburg TriadMerseburg Triad”” ––
goiter, exopthalmos, palpitations.goiter, exopthalmos, palpitations.
9. Iodine transportIodine transport
NaNa++
/I/I--
symport proteinsymport protein
controls serum Icontrols serum I--
uptakeuptake
Based on NaBased on Na++
/K/K++
antiport potentialantiport potential
Stimulated by TSHStimulated by TSH
Inhibited byInhibited by
PerchloratePerchlorate
10. Thyroid hormone formationThyroid hormone formation
Thyroid Peroxidase (TPO)Thyroid Peroxidase (TPO)
– Apical membrane proteinApical membrane protein
– Catalyzes Iodine organification to tyrosine residues ofCatalyzes Iodine organification to tyrosine residues of
thyroglobulinthyroglobulin
– Antagonized by methimazole, PTUAntagonized by methimazole, PTU
Iodine coupled to ThyroglobulinIodine coupled to Thyroglobulin
– Monoiodotyrosine (Tg + one IMonoiodotyrosine (Tg + one I--
))
– Diiodotyrosine (Tg + two IDiiodotyrosine (Tg + two I--
))
Pre-hormones secreted into follicular spacePre-hormones secreted into follicular space
11.
12. Wolff-Chaikoff EffectWolff-Chaikoff Effect
Increasing doses of IIncreasing doses of I--
increase hormone synthesisincrease hormone synthesis
initiallyinitially
Higher doses causeHigher doses cause
cessation of hormonecessation of hormone
formation.formation.
This effect is countered byThis effect is countered by
the Iodide leak from normalthe Iodide leak from normal
thyroid tissue.thyroid tissue.
Patients with autoimmunePatients with autoimmune
thyroiditis may fail to adaptthyroiditis may fail to adapt
and becomeand become hypohypothyroid.thyroid.
13. Jod-Basedow EffectJod-Basedow Effect
Opposite of the Wolff-Chaikoff effectOpposite of the Wolff-Chaikoff effect
Excessive iodine loads induceExcessive iodine loads induce hyperhyperthyroidismthyroidism
Observed in hyperthyroid disease processesObserved in hyperthyroid disease processes
– GravesGraves’’ diseasedisease
– Toxic multinodular goiterToxic multinodular goiter
– Toxic adenomaToxic adenoma
This effect may lead to symptomatic thyrotoxicosis inThis effect may lead to symptomatic thyrotoxicosis in
patients who receive large iodine doses frompatients who receive large iodine doses from
– Dietary changesDietary changes
– Contrast administrationContrast administration
– Iodine containing medication (Amiodarone)Iodine containing medication (Amiodarone)
15. TRHTRH
Produced by HypothalamusProduced by Hypothalamus
Release is pulsatile, circadianRelease is pulsatile, circadian
Downregulated by TDownregulated by T33
Travels through portal venous system toTravels through portal venous system to
adenohypophysisadenohypophysis
Stimulates TSH formationStimulates TSH formation
16. TSHTSH
Produced by Adenohypophysis ThyrotrophsProduced by Adenohypophysis Thyrotrophs
Upregulated by TRHUpregulated by TRH
Downregulated by TDownregulated by T44, T, T33
Travels through portal venous system toTravels through portal venous system to
cavernous sinus, body.cavernous sinus, body.
Stimulates several processesStimulates several processes
– Iodine uptakeIodine uptake
– Colloid endocytosisColloid endocytosis
– Growth of thyroid glandGrowth of thyroid gland
18. Thyroid HormoneThyroid Hormone
Majority of circulating hormone is TMajority of circulating hormone is T44
– 98.5% T98.5% T44
– 1.5% T1.5% T33
Total Hormone load is influenced by serum bindingTotal Hormone load is influenced by serum binding
proteinsproteins
– Albumin 15%Albumin 15%
– Thyroid Binding Globulin 70%Thyroid Binding Globulin 70%
– Transthyretin 10%Transthyretin 10%
Regulation is based on the free component of thyroidRegulation is based on the free component of thyroid
hormonehormone
19. Hormone Binding FactorsHormone Binding Factors
Increased TBGIncreased TBG
– High estrogen states (pregnancy, OCP, HRT, Tamoxifen)High estrogen states (pregnancy, OCP, HRT, Tamoxifen)
– Liver disease (early)Liver disease (early)
Decreased TBGDecreased TBG
– Androgens or anabolic steroidsAndrogens or anabolic steroids
– Liver disease (late)Liver disease (late)
Binding Site CompetitionBinding Site Competition
– NSAIDNSAID’’ss
– Furosemide IVFurosemide IV
– Anticonvulsants (Phenytoin, Carbamazepine)Anticonvulsants (Phenytoin, Carbamazepine)
25. GoiterGoiter
GoiterGoiter: Chronic enlargement of the thyroid gland not due: Chronic enlargement of the thyroid gland not due
to neoplasmto neoplasm
Endemic goiterEndemic goiter
– Areas where > 5% of children 6-12 years of age have goiterAreas where > 5% of children 6-12 years of age have goiter
– Common in China and central AfricaCommon in China and central Africa
Sporadic goiterSporadic goiter
– Areas where < 5% of children 6-12 years of age have goiterAreas where < 5% of children 6-12 years of age have goiter
– MultinodularMultinodular goitergoiter in sporatic areas often denotes the presencein sporatic areas often denotes the presence
of multiple nodules rather than gross gland enlargementof multiple nodules rather than gross gland enlargement
FamilialFamilial
26. GoiterGoiter
EtiologyEtiology
– HashimotoHashimoto’’s thyroiditiss thyroiditis
Early stages only, late stages show atrophic changesEarly stages only, late stages show atrophic changes
May present with hypo, hyper, or euthyroid statesMay present with hypo, hyper, or euthyroid states
– GravesGraves’’ diseasedisease
Due to chronic stimulation of TSH receptorDue to chronic stimulation of TSH receptor
– DietDiet
Brassica (cabbage, turnips, cauliflower, broccoli)Brassica (cabbage, turnips, cauliflower, broccoli)
CassavaCassava
– Chronic Iodine excessChronic Iodine excess
Iodine excess leads to increased colloid formation and can preventIodine excess leads to increased colloid formation and can prevent
hormone releasehormone release
If a patient does not develop iodine leak, excess iodine can lead to goiterIf a patient does not develop iodine leak, excess iodine can lead to goiter
– MedicationsMedications
Lithium prevents release of hormone, causes goiter in 6% of chronicLithium prevents release of hormone, causes goiter in 6% of chronic
usersusers
– NeoplasmNeoplasm
27. GoiterGoiter
PathogenesisPathogenesis
– Iodine deficient areasIodine deficient areas
Heterogeneous response to TSHHeterogeneous response to TSH
Chronic stimulation leads to multiple nodulesChronic stimulation leads to multiple nodules
– Iodine replete areasIodine replete areas
Thyroid follicles are heterogeneous in their growth and activityThyroid follicles are heterogeneous in their growth and activity
potentialpotential
Autopsy series show MNG >30%.Autopsy series show MNG >30%.
Thyroid function evaluationThyroid function evaluation
– TSH, T4, T3TSH, T4, T3
– Overt hyperthyroidism (TSH low, T3/T4 high)Overt hyperthyroidism (TSH low, T3/T4 high)
– Subclinical hyperthyroidism (TSH low, T3/T4 normal)Subclinical hyperthyroidism (TSH low, T3/T4 normal)
Determination of thyroid state is key in determining treatmentDetermination of thyroid state is key in determining treatment
28. Non-Toxic GoiterNon-Toxic Goiter
Cancer screening in non-toxic MNGCancer screening in non-toxic MNG
– Longstanding MNG has a risk of malignancy identical toLongstanding MNG has a risk of malignancy identical to
solitary nodules (<5%)solitary nodules (<5%)
– MNG with nodules < 1.5 cm may be followed clinicallyMNG with nodules < 1.5 cm may be followed clinically
– MNG with non-functioning nodules > 4cm should be excisedMNG with non-functioning nodules > 4cm should be excised
No FNA needed due to poor sensitivityNo FNA needed due to poor sensitivity
Incidence of cancer (up to 40%)Incidence of cancer (up to 40%)
– FNA in MNGFNA in MNG
Sensitivity 85% - 95%Sensitivity 85% - 95%
Specificity 95%Specificity 95%
Negative FNA can be followed with annual USNegative FNA can be followed with annual US
Insufficient FNAInsufficient FNA’’s should be repeateds should be repeated
Incoclusive FNA or papillary cytology warrants excisionIncoclusive FNA or papillary cytology warrants excision
– Hyperfunctioning nodules may mimic follicular neoplasm onHyperfunctioning nodules may mimic follicular neoplasm on
FNAFNA
29. Non-Toxic GoiterNon-Toxic Goiter
Treatment optionsTreatment options (no compressive symptoms)(no compressive symptoms)
– US follow-up to monitor for progressionUS follow-up to monitor for progression
– Thyroid suppression therapyThyroid suppression therapy
May be used for progressive growthMay be used for progressive growth
May reduce gland volume up to 50%May reduce gland volume up to 50%
Goiter regrowth occurs rapidly following therapy cessationGoiter regrowth occurs rapidly following therapy cessation
– SurgerySurgery
Suspicious neck lymphadenopathySuspicious neck lymphadenopathy
History of radiation to the cervical regionHistory of radiation to the cervical region
Rapid enlargement of nodulesRapid enlargement of nodules
Papillary histologyPapillary histology
Microfollicular histology (?)Microfollicular histology (?)
30. Non-Toxic GoiterNon-Toxic Goiter
Treatment optionsTreatment options (compressive symptoms)(compressive symptoms)
– RAI ablationRAI ablation
Volume reduction 33% - 66% in 80% of patientsVolume reduction 33% - 66% in 80% of patients
Improvement of dysphagia or dyspnea in 70% - 90%Improvement of dysphagia or dyspnea in 70% - 90%
Post RAI hypothyroidism 60% in 8 yearsPost RAI hypothyroidism 60% in 8 years
Post RAI GravesPost RAI Graves’’ disease 10%disease 10%
Post RAI lifetime cancer risk 1.6%Post RAI lifetime cancer risk 1.6%
– SurgerySurgery
Most commonly recommended treatment for healthyMost commonly recommended treatment for healthy
individualsindividuals
31. Toxic GoiterToxic Goiter
Evaluate forEvaluate for
– GravesGraves’’ diseasedisease
Clinical findings (Pretibial myxedema, Opthalmopathy)Clinical findings (Pretibial myxedema, Opthalmopathy)
Anti-TSH receptor AbAnti-TSH receptor Ab
High RAUIHigh RAUI
– ThyroiditisThyroiditis
Clinical findings (painful thyroid in Subacute thyroiditis)Clinical findings (painful thyroid in Subacute thyroiditis)
Low RAUILow RAUI
– Recent Iodine administrationRecent Iodine administration
AmiodaroneAmiodarone
IV contrastIV contrast
Change in dietChange in diet
FNA evaluationFNA evaluation
– Not indicated in hyperthyroid nodules due to low incidence ofNot indicated in hyperthyroid nodules due to low incidence of
malignancymalignancy
– FNA of hyperthyroid nodules can mimic follicular neoplasmsFNA of hyperthyroid nodules can mimic follicular neoplasms
32. Toxic GoiterToxic Goiter
Risks of hyperthyroidismRisks of hyperthyroidism
– Atrial fibrillationAtrial fibrillation
– Congestive Heart FailureCongestive Heart Failure
– Loss of bone mineral densityLoss of bone mineral density
– Risks exist for both clinical or subclinical diseaseRisks exist for both clinical or subclinical disease
Toxic GoiterToxic Goiter
– Toxicity is usually longstandingToxicity is usually longstanding
– Acute toxicity may occur in hyperthyroid states (Jod BasedowAcute toxicity may occur in hyperthyroid states (Jod Basedow
effect) witheffect) with
Relocation to iodine replete areaRelocation to iodine replete area
Contrast administrationContrast administration
Amiodarone (37% iodine)Amiodarone (37% iodine)
33. Toxic GoiterToxic Goiter
Treatment for Toxic MNGTreatment for Toxic MNG
– Thionamide medicationsThionamide medications
Not indicated for long-term use due to complicationsNot indicated for long-term use due to complications
May be used for symptomatic individuals until definitiveMay be used for symptomatic individuals until definitive
treatmenttreatment..
– RadioiodineRadioiodine
Primary treatment for toxic MNGPrimary treatment for toxic MNG
Large ILarge I131131
dose required due to gland sizedose required due to gland size
Goiter size reduction by 40% within 1 yearGoiter size reduction by 40% within 1 year
Risk of hypothyroidismRisk of hypothyroidism 11% - 24%11% - 24%
May require second doseMay require second dose
– SurgerySurgery
Used for compressive symptomsUsed for compressive symptoms
Hypothyroidism occurs in up to 70% of subtotal thyroidectomyHypothyroidism occurs in up to 70% of subtotal thyroidectomy
patientspatients
Pre-surgical stabilization with thionamide medicationsPre-surgical stabilization with thionamide medications
Avoid SSKI due to risk for acute toxic symptomsAvoid SSKI due to risk for acute toxic symptoms
34. GravesGraves’’ DiseaseDisease
Most common cause of thyrotoxicosis in the industrialized worldMost common cause of thyrotoxicosis in the industrialized world
Autoimmune condition with anti-TSHr antibodiesAutoimmune condition with anti-TSHr antibodies
Onset of disease may be related to severe stress which alters theOnset of disease may be related to severe stress which alters the
immune responseimmune response
DiagnosisDiagnosis
– TSH, TTSH, T44, T, T33 to establish toxicosisto establish toxicosis
– RAIU scan to differentiate toxic conditionsRAIU scan to differentiate toxic conditions
– Anti-TPO, Anti-TSAb, fTAnti-TPO, Anti-TSAb, fT33 if indicatedif indicated
RAIU in Hyperthyroid StatesRAIU in Hyperthyroid States
High UptakeHigh Uptake Low UptakeLow Uptake
GravesGraves’’ Subacute ThyroiditisSubacute Thyroiditis
Toxic MNGToxic MNG Iodine ToxicosisIodine Toxicosis
Toxic AdenomaToxic Adenoma Thyrotoxicosis factitiaThyrotoxicosis factitia
35. GravesGraves’’ DiseaseDisease
TreatmentTreatment
– Beta blockers for symptomsBeta blockers for symptoms
– Thionamide medicationsThionamide medications
May re-establish euthyroidism in 6-8 weeksMay re-establish euthyroidism in 6-8 weeks
40% - 60% incidence of disease remission40% - 60% incidence of disease remission
20% incidence of allergy (rash, itching)20% incidence of allergy (rash, itching)
0.5% incidence of potentially fatal agranulocytosis0.5% incidence of potentially fatal agranulocytosis
– Radioiodine ablationRadioiodine ablation
10% incidence of hypothyroidism at 1 year10% incidence of hypothyroidism at 1 year
55% - 75% incidence of hypothyroidism at 10 years55% - 75% incidence of hypothyroidism at 10 years
Avoid RAI in children and pregancyAvoid RAI in children and pregancy
– SurgerySurgery
Large goiters not amenable to RAILarge goiters not amenable to RAI
Compressive symptomsCompressive symptoms
Children, pregnancyChildren, pregnancy
50% - 60% incidence of hypothyroidism50% - 60% incidence of hypothyroidism
36. Toxic AdenomaToxic Adenoma
ThyrotoxicosisThyrotoxicosis
– Hyperfunctioning nodules <2 cm rarely lead toHyperfunctioning nodules <2 cm rarely lead to
thyrotoxicosisthyrotoxicosis
– Most nodules leading to thyrotoxicosis are >3 cm.Most nodules leading to thyrotoxicosis are >3 cm.
Treatment IndicationsTreatment Indications
– Post-menopausal femalePost-menopausal female
Due to increased risk of bone lossDue to increased risk of bone loss
– Patients over 60Patients over 60
Due to high risk of atrial fibrillationDue to high risk of atrial fibrillation
– Adenomas greater than 3 cm (?)Adenomas greater than 3 cm (?)
37. Toxic AdenomaToxic Adenoma
TreatmentsTreatments
– Antithyroid medicationsAntithyroid medications
Not used due to complications of long-term treatmentNot used due to complications of long-term treatment
– RadioiodineRadioiodine
Cure rate > 80% (20 mCi I131)Cure rate > 80% (20 mCi I131)
Hypothyroidism risk 5% - 10%Hypothyroidism risk 5% - 10%
Second dose of I131 needed in 10% - 20%Second dose of I131 needed in 10% - 20%
Patients who are symptomatically toxic may require control withPatients who are symptomatically toxic may require control with
thionamide medications before RAI to reduce risk of worseningthionamide medications before RAI to reduce risk of worsening
toxicity.toxicity.
– SurgerySurgery
Preferred for children and adolescentsPreferred for children and adolescents
Preferred for very large nodules when high I131 doses neededPreferred for very large nodules when high I131 doses needed
Low risk of hypothyroidismLow risk of hypothyroidism
– Ethanol InjectionEthanol Injection
Rarely done in the USRarely done in the US
May achieve cure in 80%May achieve cure in 80%
39. HypothyroidismHypothyroidism
Cause is determined by geographyCause is determined by geography
– HashimotoHashimoto’’s in industrialized countriess in industrialized countries
– May be due to iodine excess in some costal areasMay be due to iodine excess in some costal areas
DiagnosisDiagnosis
– Low FTLow FT44, High TSH (Primary, check for antibodies), High TSH (Primary, check for antibodies)
– Low FTLow FT44, Low TSH (Secondary or Tertiary, TRH, Low TSH (Secondary or Tertiary, TRH
stimulation test, MRI)stimulation test, MRI)
TreatmentTreatment
– Levothyroxine (TLevothyroxine (T44) due to longer half life) due to longer half life
– Treatment prevents bone loss, cardiomyopathy,Treatment prevents bone loss, cardiomyopathy,
myxedemamyxedema
41. HashimotoHashimoto’’ss
(Chronic, Lymphocytic)(Chronic, Lymphocytic)
Most common cause of hypothyroidismMost common cause of hypothyroidism
Result of antibodies to TPO, TBGResult of antibodies to TPO, TBG
Commonly presents in females 30-50 yrs.Commonly presents in females 30-50 yrs.
Usually non-tender and asymptomaticUsually non-tender and asymptomatic
Lab valuesLab values
– High TSHHigh TSH
– Low TLow T44
– Anti-TPO AbAnti-TPO Ab
– Anti-TBG AbAnti-TBG Ab
Treat with LevothyroxineTreat with Levothyroxine
43. HashimotoHashimoto’’s Thyroiditiss Thyroiditis
Most common cause of goiter and hypothyroidism in the U.S.Most common cause of goiter and hypothyroidism in the U.S.
PhysicalPhysical
– Painless diffuse goiterPainless diffuse goiter
Lab studiesLab studies
– HypothyroidismHypothyroidism
– Anti TPO antibodies (90%)Anti TPO antibodies (90%)
– Anti Thyroglobulin antibodies (20-50%)Anti Thyroglobulin antibodies (20-50%)
– Acute Hyperthyroidism (5%)Acute Hyperthyroidism (5%)
TreatmentTreatment
– Levothyroxine if hypothyroidLevothyroxine if hypothyroid
– Triiodothyronine (for myxedema coma)Triiodothyronine (for myxedema coma)
– Thyroid suppression (levothyroxine) to decrease goiter sizeThyroid suppression (levothyroxine) to decrease goiter size
ContraindicationsContraindications
Stop therapy if no resolution notedStop therapy if no resolution noted
– Surgery for compression or pain.Surgery for compression or pain.
44. Silent ThyroiditisSilent Thyroiditis
Post-partum ThyroiditisPost-partum Thyroiditis
Silent thyroiditis is termed post-partum thyroiditis if it occurs withinSilent thyroiditis is termed post-partum thyroiditis if it occurs within
one year of delivery.one year of delivery.
ClinicalClinical
– Hyperthyroid symptoms at presentationHyperthyroid symptoms at presentation
– Progression to euthyroidism followed by hypothyroidism for up to 1 year.Progression to euthyroidism followed by hypothyroidism for up to 1 year.
– Hypothyroidism generally resolvesHypothyroidism generally resolves
DiagnosisDiagnosis
– May be confused with post-partum GravesMay be confused with post-partum Graves’’ relapserelapse
TreatmentTreatment
– Beta blockers during toxic phaseBeta blockers during toxic phase
– No anti-thyroid medication indicatedNo anti-thyroid medication indicated
– Iopanoic acid (Telopaque) for severe hyperthyroidismIopanoic acid (Telopaque) for severe hyperthyroidism
– Thyroid hormone during hypothyroid phase. Must withdraw in 6 monthsThyroid hormone during hypothyroid phase. Must withdraw in 6 months
to check for resolution.to check for resolution.
45. Subacute ThyroiditisSubacute Thyroiditis
DeQuervainDeQuervain’’s, Granulomatouss, Granulomatous
Most common cause of painfulMost common cause of painful
thyroiditisthyroiditis
Often follows a URIOften follows a URI
FNA may reveal multinuleatedFNA may reveal multinuleated
giant cells or granulomatousgiant cells or granulomatous
change.change.
CourseCourse
– Pain and thyrotoxicosis (3-6Pain and thyrotoxicosis (3-6
weeks)weeks)
– Asymptomatic euthyroidismAsymptomatic euthyroidism
– Hypothyroid period (weeks toHypothyroid period (weeks to
months)months)
– Recovery (complete in 95%Recovery (complete in 95%
after 4-6 months)after 4-6 months)
46. Subacute ThyroiditisSubacute Thyroiditis
DeQuervainDeQuervain’’s, Granulomatouss, Granulomatous
DiagnosisDiagnosis
– Elevated ESRElevated ESR
– Anemia (normochromic, normocytic)Anemia (normochromic, normocytic)
– Low TSH, Elevated T4 > T3, Low anti-TPO/TgbLow TSH, Elevated T4 > T3, Low anti-TPO/Tgb
– Low RAI uptake (same as silent thyroiditis)Low RAI uptake (same as silent thyroiditis)
TreatmentTreatment
– NSAIDNSAID’’s and salicylates.s and salicylates.
– Oral steroids in severe casesOral steroids in severe cases
– Beta blockers for symptoms of hyperthyroidism, Iopanoic acid for severeBeta blockers for symptoms of hyperthyroidism, Iopanoic acid for severe
symptomssymptoms
– PTU not indicated since excess hormone results from leak instead ofPTU not indicated since excess hormone results from leak instead of
hyperfunctionhyperfunction
– Symptoms can recur requiring repeat treatmentSymptoms can recur requiring repeat treatment
– GravesGraves’’ disease may occasionally develop as a late sequellaedisease may occasionally develop as a late sequellae
47. Acute ThyroiditisAcute Thyroiditis
CausesCauses
– 68% Bacterial (S. aureus, S. pyogenes)68% Bacterial (S. aureus, S. pyogenes)
– 15% Fungal15% Fungal
– 9% Mycobacterial9% Mycobacterial
May occur secondary toMay occur secondary to
– Pyriform sinus fistulaePyriform sinus fistulae
– Pharyngeal space infectionsPharyngeal space infections
– Persistent Thyroglossal remnantsPersistent Thyroglossal remnants
– Thyroid surgery wound infections (rare)Thyroid surgery wound infections (rare)
More common in HIVMore common in HIV
48. Acute ThyroiditisAcute Thyroiditis
DiagnosisDiagnosis
– Warm, tender, enlarged thyroidWarm, tender, enlarged thyroid
– FNA to drain abscess, obtain cultureFNA to drain abscess, obtain culture
– RAIU normal (versus decreased in DeQuervainRAIU normal (versus decreased in DeQuervain’’s)s)
– CT or US if infected TGDC suspectedCT or US if infected TGDC suspected
TreatmentTreatment
– High mortality without prompt treatmentHigh mortality without prompt treatment
– IV AntibioticsIV Antibiotics
Nafcillin / Gentamycin or Rocephin for empiric therapyNafcillin / Gentamycin or Rocephin for empiric therapy
– Search for pyriform fistulae (BA swallow, endoscopy)Search for pyriform fistulae (BA swallow, endoscopy)
– Recovery is usually completeRecovery is usually complete
49. RiedelRiedel’’s Thyroiditiss Thyroiditis
Rare disease involving fibrosis of the thyroid glandRare disease involving fibrosis of the thyroid gland
DiagnosisDiagnosis
– Thyroid antibodies are present in 2/3Thyroid antibodies are present in 2/3
– Painless goiterPainless goiter ““woodywoody””
– Open biopsy often needed to diagnoseOpen biopsy often needed to diagnose
– Associated with focal sclerosis syndromes (retroperitoneal,Associated with focal sclerosis syndromes (retroperitoneal,
mediastinal, retroorbital, and sclerosing cholangitis)mediastinal, retroorbital, and sclerosing cholangitis)
TreatmentTreatment
– Resection for compressive symptomsResection for compressive symptoms
– Chemotherapy with Tamoxifen, Methotrexate, or steroids mayChemotherapy with Tamoxifen, Methotrexate, or steroids may
be effectivebe effective
– Thyroid hormone only for symptoms of hypothyroidismThyroid hormone only for symptoms of hypothyroidism
