thyroidcarcinoma-170906130602.pdf

THYROID
MALIGNANCIES
Prof .HOD.Dr.D.Maruthupandian MS.,FICS.,FAIS.,
I SURGICAL UNIT
GRH,Madurai

Our Sincere Thanks to
• Dr.D.Latha M.S., D.A.,
• Dr.C.Saravanan M.S.,D.Ortho.,
• Dr.S.Thirumalai Kannan M.S.,D.Ch.,
• Dr.Ravichandran M.S.,

Introduction
• Thyroid Anatomy – Dr.Kundhavi P
• Physiology – Dr.Thalabathik Kumara Vikram
• Etiopathogenesis of thyroid malignancy – Dr.A.Srinivasan
• Work up and management of WDTC – Dr.R.Ashwin
• Follow up of WDTC – Dr.K.Sivachandran
• Thyroid malignancies other than WDTC – Dr.P.Jayakumar

Embryology
• Follicles develop by 8th
week
• Colloid is formed by 3rd
month
4th week
7-8th
week
(15%)

Ectopic Thyroid Tissue
• Can develop anywhere from Foramen caecum to
Mediastinum along thyroglossal tract:
• Lingual thyroid :-
total failure of descent
• Substernal aberrant thyroid- in Mediastinum
• Lateral thyroid Anlage – from 4th pharyngeal
pouch (from a lateral aberrant thyroid that failed
to fuse with Median thyroid lobule) now
considered as metastatic thyroid tissue
• Intra-tracheal thyroid rests (rare)

 Bounded by the Carotid sheath,
Sternocleidomastoid muscles laterally
on either side
 Overlies the Larynx & Trachea (2nd, 3rd
& 4th rings) medially.
 Lies beneath the skin, subcutaneous
fat, Platysma, superficial Cervical
Fascia (containing the External and
Anterior Jugular Veins & Transverse
cervical nerves) and Strap Muscles.

Deep Cervical Fascia: Condensed
well defined fibrous sheets:
 Investing Layer of deep Cervical fascia:
encloses Parotid & sub-mandibular salivary
gland (Note: Does not enclose Thyroid gland)
 Pre-tracheal fascia – surrounds the
thyroid gland ,Parathyroids and
Strap muscles.
 Pre-Vertebral layer- encloses the pre-
vertebral muscles.
Carotid Sheath- encloses the Common &
Internal Carotid Artery, IJV & Vagus Nerve,
Deep cervical LNs chain along IJV.

Ligament of
Berry:
Is a condensation of
pre tracheal fascia with
the thyroid capsule suspending
thyroid from trachea
in medial aspect of the lobes.

Tubercle of
Zuckerkandl:
o Lateral & posterior most part of
thyroid gland at the level of
cricoid cartilage.
o Lateral to RLN
o Anterior to the Superior
Parathyroids.

Vascular Anatomy:-
Superior Thyroid Artery:
• Arises from ipsilateral External carotid
Artery
Inferior Thyroid Artery:
• Arises from Thyrocervical trunk from
I part of Subclavian Artery
Arteria thyroidea Ima:-
• Direct branch of Aorta /Innominate
artery
• Present in 1-4%

Venous drainage
 Superior Thyroid Vein
(accompanies the Artery) drains
into IJV
 Middle thyroid veins
drain into IJV
 Occasionally a 4th vein is
observed between MTV and ITV
known as Kocher’s vein IJV
 Inferior thyroid plexus- drains
into Brachiocephalic Vein.

Nerves related to thyroid
VAGUS
Superior laryngeal nerve
External laryngeal nerve
Internal laryngeal nerve
Recurrent laryngeal nerve

Nerve Supply
Left Recurrent Laryngeal Nerve:
• Arises from inferior Ganglion of Vagus where
it crosses the Aortic Arch
• Loops around the Ligamentum arteriosum
Right Recurrent laryngeal Nerve:
• Arises from vagus at its crossing with Right
Subclavian Artery
Function:
• Sensory to larynx below the Vocal cord
• Motor to all laryngeal muscles except
Cricothyroid

RLN Identification :
 RLN lies within 3mm of Berry’s ligament
 Inferior cornu of thyroid cartilage indicates point of entry of nerve into
larynx
 Identification of the tubercle of Zuckerkandl shows the branches of
Inferior thyroid artery and its relation with the RLN.

Non recurrent Laryngeal Nerve
Does not hook around Subclavian Artery but enters
Tracheoesophageal groove directly.
It is commonly associated
with Vascular Anomalies.
If found on the Left it may be associated
with Situs inversus

Superior Laryngeal Nerve:
 Arises from vagus at the base of skull
 Traversus along Internal Carotid Artery
 Divides into 2 branches at level of Hyoid
Internal External
Sensory to supra-glottic larynx Descends along Supr Thy V
Innervate Cricothyroid muscle
(tensor of VC)

Identification of External laryngeal
nerve:
Triangle of Joll:

Cernea Classification
Relationship of External Laryngeal Nerve
to Superior Thyroid vessels:
Type I:- ELN crosses Artery ≥1cm above
the superior aspect of thyroid lobe
Type II:- ELN crosses < 1cm
a) Above the superior pole of thyroid
b) Below the superior pole of thyroid

Surgical Importance :
Superior thyroid vessel should not be ligated
enmasse.
Should be individually divided , low on
thyroid gland, dissected lateral to cricothyroid
muscle in order to avoid injury to the nerve.

Lymphatics:
 Extensive network of lymphatics connect both
lobes through the isthmus & drain into the
Central group & Lateral group.
LN stations:
Level I Submental&
submandibular nodes
Level II Upper Jugular nodes
Level III Middle Jugular nodes
Level IV Lower Jugular nodes
Level V Posterior Triangle LN
Level VI Central neck nodes
Level VII Anterior Mediastinal LN

Lymph Node Stations:
Level IA : Submental & Submandibular glands
IB Hyoid below, anterior to the posterior
edge of submandibular gland
Level II : lies superior to Level III
Level III : Superiorly Hyoid, inferiorly Cricoid,
laterally posterior border of Sternocleido
mastoid, anteromedially Level VI/carotid sheath,
Level IV : Lies inferior to Level III
Level V : posterior triangle LN, lateral to
lateral border of SCM
Level VI : Central group, Includes the Thyroid
gland, Superiorly Hyoid, inferiorly
Brachiocephalic Artery, laterally
carotid sheaths on either side.
Level VII : Pretracheal, Paratracheal, Superior
Mediastinal group of nodes.

Parathyroids:
Superior PT:
Relatively fixed, postero-lateral to RLN,
behind the thyroid capsule,
about 1cm above of Inferior Thyroid Artery
& RLN,
and within 2cm diameter.

Inferior PT:
Variable position , prone for ectopic sites.
 Most commonly anteromedial to RLN
 In thyrothymic ligament tissue
 Within thymus
 In carotid sheath

Platysma flap raised maintaining the subplatysmal avascular plane
Platysma is deficient in midline

Anterior Jugular Vein:-
• These vessels are retracted than divided to avoid edema of
upper neck & larynx.
• These veins may be greatly dilated in tumours of thyroid &
tumours compressing the IJV.

Strap muscles:
Arranged in two planes.
• Superficial plane: Sternohyoid &
superior belly of omohyoid
• Deep plane: Sternothyroid
Thyroid is exposed by, retracting the
superior belly of omohyoid ,
sternohyoid laterally and finally by
cutting the sternothyroid muscle.

Oblique line of thyroid:
Significance:-
 Site of origin of Thyrohyoid
& insertion of Sternothyroid.
 Boundary of Triangle of Joll.

Ansa
Cervicalis (Or Ansa
Hypoglossi )
• Loop from descending branch of
Hypoglossal N
• And C2,C3 spinal nerves.
• It lies superficial to the IJV in
the carotid triangle,
• On the anterior wall of carotid sheath,
close to the Superior thyroid Artery.
Its name means “Handle of the
neck" in Latin
Ansa
Cervicalis

So sectioning of strap above this
will spare the nerve supply of
strap muscles.
However, this concept is now
revised owing to segmental
innervation where we may divide
the strap muscles in the segment
where more exposure is required

THE THYROID GLAND
• The thyroid is a vitally important hormonal gland that
plays a major role in the metabolism, growth and
maturation of the human body.
• It helps to regulate many body functions by constantly
releasing a steady amount of hormones into the
bloodstream.
• The T4 and T3 hormones stimulate every tissue in the
body to produce proteins and increase the amount of
oxygen used by cells.

SYNTHESIS/STORAGE/SECRETION
• Following steps are involved synthesis, storage and secretion:
1. Thyroglobulin production by follicular cell
2. Iodine uptake by follicular cell from the blood
3. Attachments of iodine to tyrosine on thyroglobulin to form MIT and DIT
4. Coupling processes between the iodinated tyrosine molecules to form T4 and T3
in the colloid
5. Secretion (upon stimulation) of T4 and T3 occurs by endocytosis a piece of
colloid, uncouplingof T4 and T3 and diffusion out of the follicular cell into the
blood

• Dietary iodine is absorbed in the GI tract, then taken up
by the thyroid gland (or removed from the body by the
kidneys).
• The transport of iodide into follicular cells is dependent
upon a Na+/I- cotransport system.
• Iodide taken up by the thyroid gland is oxidized by
peroxide in the lumen of the follicle:
peroxidase
I- I+

• Major sources of iodine:
- iodized salt, iodated bread, dairy products, shellfish
• Minimum requirement: 75 micrograms/day
• 90% of secretion - T4.
• T4 T3
Liver, Kidneys
• In addition to T3, an equal amount of “Reverse T3” may
also be formed. This has no biological activity.
T3 MIT + DIT
Reverse T3 DIT + MIT

• T3 more active than T4. T3 is 4times more potent in its
biologic form than T4 and is the major hormone that
interacts with the target cells.
• Half life of T4 - 6 to 7 days and T3 -12 hours

• Thyroid hormones are lipid-soluble (Water Insoluble).
• Thus, they are found in the circulation associated with binding proteins:
- Thyroid Hormone-Binding Globulin (~70% of hormone)
- Pre-albumin (transthyretin), (~15%)
- Albumin (~15%)
• Less than 1% of thyroid hormone is found free in the circulation.
• Only free and albumin-bound thyroid hormone is biologically
available to tissues.

Metabolic rate and heat production:
– ↑ O₂ consumption
– BMR can ↑ by 60 – 100%
– Since ↑ metabolism results in ↑ heat production → thyroid hormone effects
is calorigenic
Sympathomimetic effect
– Sympathomimetic: any action similar to one produced by the sympathetic
nervous system
Thyroid hormone ↑ target cell responsiveness to catecholamines (SNS
and adrenal) by ↑ production of specific catecholamine target cell
receptors
The cardiovascular system:
– ↑ the heart’s responsiveness to circulating catecholamines (permissive
action)

Growth and the nervous system
• Effect on growth is manifested mainly in growing children
– Thyroid hormone stimulates GH secretion and promotes GH effects
– Lack of thyroid hormone → growth retardation but can be reversed
by thyroid replacement therapy
– Unlike excess GH, excess thyroid hormone does not produce
excessive growth
• Important in promoting growth and development of the brain
during fetal and postnatal life
– Thyroid hormone deficiency → mental retardation if therapy is not
administered days or weeks after birth

WOLFF
CHAIKOFF
•autoregulatory phenomenon that inhibits
synthesis of thyroxine when excess iodine is given
ESCAPE
PHENOMENON
•resumption of thyroxine synthesis upon
prolonged administration of iodine
JOD-BASEDOW
•iodine-induced hyperthyroidism typically in
patients with endemic goitre.

THYROID PROFILE
T3 1.2-3.1 nmol/lit
T4 55-150 nmol/lit
TSH 0-5 nmol/lit
Free T3 3-9 nmol/lit
(0.3%)
Free T4 8-26 nmol/lit
(0.03%)
Free T3 is the single best test in assessing hyperthyroidism

Thyroglobulin estimation
• During the release of thyroxine,a small amount of
thyroglobulin leaks into circulation.thyroglobulin as such
doesn’t have any function .Normal value is 0.5-50 μg/L or
ng/ml.
• It is the ideal follow up marker in WDTC after thyroidectomy.
• It should be done once in 3-6months.
• After thyroidectomy thyroglobulin secretion is stopped, hence
its level should not be traceable after total thyroidectomy.
• Rh TSH has redefined the efficacy of monitoring stimulated
Tg levels as evidence of recurrence.
• As many as 15% to 30% of patients with thyroid carcinoma
have anti-Tg antibodies, which seriously compromises the
use of Tg as a tumor marker

HYPERTHYROIDISM
• Apart from other causes of hyperthyroidism, Occasionally carcinoma
thyroid can present with hyperthyroidism.
• These hyperthyroid individuals should be brought to euthyroid state
before proceeding for surgery
• Carbimazole is the commonest drug used. It acts by blocking thyroid
hormone synthesis
• Dose is 5-10 mg, exactly 8th hourly (as T1/2 of carbimazole is 8 hrs).
• Other drugs used are methimazole, propylthiouracil, propranolol,
glucocorticoids, lugol’s iodine etc.

• An interval of 6 weeks is needed postoperatively to go for
RAI uptake study.
• Till then no supplementation or suppression of thyroxine
is given
• Suppressive dose-300ug/day
• Supplementing dose-100ug/day

CALCITONIN
• Secreted by parafollicular/clear/C cells(neural crest
origin),which lie between thyroid follicles.
• Calcitonin together with parathormone and vitamin-D maintain
calcium homeostasis
• Half life : < 10 minutes.
• The routine use of calcitonin determination in the workup of
thyroid nodules is not recommended.
• In patients with thyroid masses and in whom multiple
endocrine neoplasia type 2 (MEN2) syndrome or isolated
medullary carcinoma is suspected, a baseline calcitonin level
can be obtained.

• The most common cause of hypoparathyroidism is
damage to the parathyroid glands during
thyroidectomy.Mostly it is temporary due to vascular
spasm of para thyroid glands
• Occurs in 2nd-5th postoperative day
• Signs and symptoms: perioral numbness and tingling in
the fingers, Anxiety or confusion, Tetany,Chvostek sign.
HYPOCALCEMIA

TREATMENT OF HYPOCALCEMIA
• A calcium gluconate infusion [10 ampules of calcium gluconate in 1
liter of NS] at a rate of infusion is 30 mL/hr, which needs to be
titrated according to symptoms and serial serum calcium levels
• 10 ml of 10% calcium gluconate can given IV 8th hourly
• Coincident electrolyte abnormalities, hypomagnesemia, need to be
corrected to facilitate correction of the hypocalcemia
• Oral calcium(calcium carbonate 500 mg 8th hourly) and vitamin D
analogues are used for long-term management
• After 3-6 weeks,serum calcium level is repeated.

• Rad-iso I131 half life is just 8 days. Then why people in chernobyl had
cancer even after so many years and still continuing???
• M/C mutation in Chernobyl disaster?? why??
• Is there any resistant organism in Chernobyl…!?

Etiopathogenesis of thyroid carcinoma
• Genetic alterations
• Environmental factors

GENETIC ALTERATIONS
• GAIN OF FUNCTION IN PROTO-
ONCOGENES
• LOSS OF FUNCTION IN TUMOUR
SUPPRESSOR GENES

GENES IN THYROID CANCER
TYPES GENES
Papillary carcinoma RET/PTC,PTC,BRAF
Follicular carcinoma RAS,PTEN,PAX8:PPA
RG
Medullary carcinoma RET
Anaplastic
carcinoma
P53, ẞ-CATENIN

RET PROTO ONCOGENE
• CHROMOSOME 10
• Receptor tyrosine kinase binds several
growth factors such as GDNF and NEURTURIN.

• Expressed in embryonic nervous tissue and
excretory system
• Disruption Enteric nervous system
• GERM LINE MUTATION: MEN2A,MEN2B,
FMTC
• SOMATIC MUTATION: MTC and
pheochromocytoma
Kidney

• 40% thyroid malignancy
• More in iodine deficient individuals
• K-RAS mutation --- radiation exposed individuals
• Follicular CA with RAS mutation --- more aggressive than
non RAS mutated ones

• Tumour suppressor gene
• Maintain genomic integrity
• Mutations are more common in undifferentiated
carcinoma than others

GENES INVOLVED IN THYROID CANCER

7 GENE MUTATION PANEL TESTING:
BRAF.
NRAS.
HRAS.
KRAS.
RET/PTC 1 OR PTC 3 WITH OR WITHOUT
PAX8:PPARG.
OTHERS:
mRNA.
miRNA marker.
TSH mRNA.
USES :
Pre-op for evaluation of follicular of unknown
significance.
Post-op for risk stratification..
GENETIC TESTING

AWARENESS RIBBON FOR THYROID
CANCER

ENVIRONMENTAL FACTORS
• Radiation
• Iodine deficiency

RADIATION
• Mainly <20yrs of age
• Risk max after 20 to 30 years after
exposure.
• Risk increases linearly from 6.5 to
2000cGy, beyond which the incidence
declines as the radiation causes
destruction of thyroid tissue.
• Most thyroid carcinoma following
radiation are papillary.

FAMILY HISTORY
• Risk for development of both MTC
and NMTC
• Familial : occurs as a part of MEN2
syndrome
• NMTC occur in association with
syndrome such as cowdens ,
werners, FAP, carney complex type1.

PAPILLARY CARCINOMA
• 80%of thyroid malignancy
• 25 - 50 yrs
• oncogenic pathway : mitogen activated proteins
• Translocation / inversion ---RET(20-
40%)/NTRK1(10%)
Fusion proteins – RET/PTC
• Point mutation –B RAF (V 600 E) 44%
• 85% Multi centric
• 40% LN spread

Variants
• Follicular
• Diffuse sclerosing
• Clear cell
• Trabecular
• Insular
• Columnar
• Tall cell
• Poorly differentiated.

Papillary
projections
Nuclear groove
Orphan Annie eye nuclei

FOLLICULAR CARCINOMA
• 10% of thyroid malignancy.
• 40-60years
• Oncogenic pathway: phosphatidyl inositol pathway
• MUTATIONS:
GOF mutation RAS
LOF PTEN
Amplification in PIK3CA
Fusion protein PAX 8:PPARG
• 5% LN spread

HURTHLE CELL VARIANT
• 60 to 70 yrs
• Multifocal
• Secretes thyroglobulin
• 30% multicentric
• 20% distant spread
• resembles FTC gross/HPE
• abundant oxyphilic cells
• Bony mets/aggressive
• worst prognosis

WHY THEY ARE CONSIDERED TO BE A
SEPARATE CLASS?
• MULTIFOCAL AND
BILATERAL (30%)
• DON’T UPTAKE RAI (5%)
• LN METS (25%)

HIFC
MIFC
FOLLICULAR CARCINOMA DIFFERS FROM
ADENOMA BY CAPSULOVASCULAR INVASION

TUMOR DE-DIFFERENTIATION
• The WDTC cells proliferate yet lose their ability to trap,
organify, store, & metabolize iodine.
• The presumed mechanism is an acquired mutation of the
Sodium Iodide Symporter (NIS) gene
• These cells are still able to synthesize Tg
• Redifferentiation can be tried with various agents
• Retinoic Acid Therapy (1mg/kg/day for 1st wk, followed by 1.5/kg/day
for 4 wks)- 20-30% response rate

Various Risk Stratifications
• AGES
• MACIS
• AMES
• DEGROOT

AMES SCORING
A-AGE,LESS THAN 40 YRS HAS BETTER PROGNOSIS
M-DISTANT METASTASIS
E-EXTENT OF THE TUMOUR
S-SIZE OF THE TUMOUR,LESS THAN 4 CM HAS BETTER PROGNOSIS

A-AGE,AGE LESS THAN 40 YRS HAS BETTER PROGNOSIS
G-PATHOLOGIC GRADE OF THE TUMOUR
E-EXTENT OF THE TUMOUR
S-SIZE OF THE TUMOUR,SIZE LESS THAN 4 CM HAS BETTER PROGNOSIS
AGES SCORING

MEDULLARY CARCINOMA
• Sporadic 80% (MC)
• Familial 20%
– MEN syndrome
– FMTC
– RET mutations
• Origin from parafollicular c cells
• Common in upper lobe
• MEN 2A- favourable outcome than MEN2B
• bilateral /multicentric
• Amyloidosis
• Calcitonin/serotonin/PG/VIP

ANAPLASTIC
• Origin : denovo
de differentiation of well differentiated carcinoma
• P53 inactivation
• Beta-catenin active mutation

Giant cell variant spindle cell variant

PATHOLOGY REPORT
In addition to the basic tumor features required for AJCC/UICC thyroid
cancer staging including status of resection margins,
additional information helpful for risk assessment, such as
1. the presence of VASCULAR INVASION
2. the NUMBER of invaded vessels,
3. NUMBER OF LYMPH NODES examined and involved with tumor,
4. SIZE OF THE LARGEST METASTATIC FOCUS to the lymph node,
5. presence or absence of EXTRANODAL EXTENSION of the metastatic
tumor.
(Strong recommendation, Moderate-quality evidence)

• Rad - iso I 131 half life is just 8 days. Then why people in chernobyl had
cancer even after so many years and still continuing???
• IODINE get deposited in animals, plants
and soil.
• M/C mutation in Chernobyl disaster??why??
• RET/PTC fusion proteins (frequency
more due to radiation).
• Is there any resistant organism in Chernobyl…!?
• ARABIDOPSISTHALIANA (Resist
methylation )

Work up and
management of
Well differentiated
thyroid cancer
Dr. Ashwin

Clinical Presentation
Differentiated
tumors present
most commonly as
a solitary nodule
(60%)

Lymph node
metastasis at
presentation (10%)
Metastatic lesion
Clinical Presentation

Examination
Surface
Consistency
Mobility

Examination
Carotid invasion
(Berry’s sign)
Tracheal
deviation

Examination
Horner’s
syndrome
Retrosternal
extension

Examination
• Complete evaluation of lymphnodes
• Signs of
hyperthyroidism
(5%)

Madonna of Carnation
By Leonardo Da Vinci

Investigations
To evaluate the nodule
• Serum TSH
• US Thyroid
• Fine Needle Aspiration
To assess the extent of lesion
• Xray Neck
• Contrast CT
• Laryngeal examination

Thyrotropin (TSH)
• Initial biochemical investigation
TSH
HIGH OR NORMAL
LOW
RADIONUCLEOTIDE
SCAN
PROCEED TO
FNAC

USG Thyroid
Characteristics of malignancy
• Irregular margins
• Microcalcifications
• Taller than wide shape
• Extra thyroidal extension

Nodule and node characteristics in malignancy
- USG
NODULE
• Hypoechogenecity
• Central vascularity
• Microcalcification
• Solid echotexture
• Taller than wide
NODE
• Hyper – echogenecity
• Peripheral vascularity
• Microcalcification
• Cystic areas
• Rounded shape

Risk stratification with USG
High suspicion Solid hypoechoic nodule
With one or more:
IM/ MC/ TW/ ETE
RISK
> 70 – 90
%
Intermediate
suspicion
Hypoechoic nodule without
IM/MC/ TW/ ETE
10 – 20 %
Low suspicion Isoechoic or hyperechoic
nodule
5-10 %
Very low suspicion Spongiform or party cystic <3 %
Benign Completely cystic <1 %

TI-RADS
• Taller than wide
• Irregular margins
• Microcalcifications
• Marked hypogenecity

FNAC
• Not mandatory in purely cystic nodules
• USG every 6-12 months for 1-2 years and
then yearly for 3-5 years
High suspicion
Intermediate suspicion
≥ 1 cm
Low suspicion ≥ 1.5cm
Very low suspicion
(spongiform nodule)
≥ 2 cm

FNAC
• USG guided FNAC –
posteriorly located nodules
> 50% cystic
In cases of multiple nodules, each nodule must be
evaluated separately (independent malignancy risk)
FNAC from individual nodules using USG

FNAC thyroglobulin washout
To confirm lymph nodal metastasis where
• Cytological evaluation inadequate
• Cystic nodes
• Tg concentration >1ng/ml – suspicious

Bethesda system
1
• Carcinoma (papillary, medullary, or anaplastic) or suspicious for
carcinoma
2
• Follicular or Hürthle cell neoplasm
3
• Atypia of undetermined significance (AUS) or follicular lesion of
undetermined significance (FLUS)
4
• Thyroid lymphoma
5
• Benign (ie, nodular goiter, colloid goiter, hyperplastic/adenomatoid
nodule, Hashimoto’s thyroiditis)
6
• Insufficient biopsy (nondiagnostic)

Radionucleotide scan (I123)
Indicated when TSH is below normal
Hyper functioning/Hot Greater uptake than
surrounding normal thyroid
Iso functioning/ Warm Uptake equal to surrounding
thyroid
Non functioning/ Cold Less uptake than
surrounding tisssue

Role of Contrast CT
• Bulky tumours with clinically palpable nodes
• Difficult to visualise mediastinum, infra clavicular,
retropharyngeal, parapharyngeal regions in USG
• Tracheal compromise
• Iodine excreted in 4-8 weeks
• No concerns regarding RAI

Laryngeal examination
• Detailed history – pre existing conditions
• Voice assessment - subjective and objective
• Correlation with clinical findings
• Degree of compensation

Other investigations
• Routine thyroglobulin (Tg) measurement not
recommended - non specific for thyroid cancer
• Calcitonin - Medullary thyroid carcinoma
• Preoperative FDG-PET scan not recommended

“Nothing is more delightful to
contemplate than this great
miracle of nature”
- Versalius

Management of thyroid malignancy

Goals of therapy
• Removing the primary tumour and accessible locoregional
disease is the mainstay even in metastatic disease
• Minimise the risk of recurrence and metastasis
• Facilitate post operative treatment with RAI
• Permit accurate staging and risk stratification
• Minimize treatment related morbidity

Thyroidectomy – Definitions
Total thyroidectomy Removal of all visible
thyroid tissue
Near total
thyroidectomy
<1g of thyroid tissue is
left in situ
Subtotal thyroidectomy >1g of thyroid tissue is
left in situ

Pre operatively detected/ Biopsy proven
malignancy the only treatment is total
thyroidectomy

Total vs less-than Total
• Multifocal nature of disease
• Facilitates post operative RAI
• No need for resurgery
• No increase in morbidity?
• Revision procedure simple?
• No need for thyroxine
supplementation
• USG and Tg levels can be
used post operatively

• > 1cm
• Extra thyroidal
extension
• Regional or distant
metastasis
• <1 cm in size
• Clinically N0
• No extra thyroidal
extension
• No locoregional
metastasis
Management options
Lobectomy +
isthmusectomy
Near total/ Total
Thyroidectomy

Thyroidectomy –
operative
considerations

Operative considerations
Kocher’s incision

Tracing the RLN
Inferior
approach
After
identification of
the ITA

Tracing the RLN
Lateral
dissection

Tracing the RLN
Near the
Berry’s
ligament

Preservation of parathyroids
• Slips within pad of fat
• A small area lateral to the
parathyroid is left intact

Role of neck dissection
• Therapeutic neck dissection for clinically involved nodes
• Prophylactic central neck dissection
• T3 or T4 lesions with clinically N0
• Clinically involved lateral neck nodes

Boundaries for neck dissection
Central neck dissection:
• Hyoid bone, bilateral carotids, suprasternal notch
Lateral neck dissection
• MRND TYPE III
• Structures excised: submandibular gland
• Structures preserved: SCM/ AN/ IJV

FOLLOW UP OF DIFFERENTIATED
THYROID CANCERS

Goals of follow up
• To improve overall and disease specific survival
• Reduce the risk of persistant or recurrent disease
• Monitor TSH levels
• Provide thyroxine suppression or replacement therapy
• Low risk patients
• Less aggressive management
• Use High Specificity tests
• High risk patients
• More aggressive management
• Early detection of recurrent disease

RECURRENCE
• Local- Thyroid bed
• Regional- Cervical Lymph node
• Distant
• Clinical Recurrence- Physical examination or chest X-ray
• I131 Scan – New area of Iodine uptake or increased area of
concentration

145
Pre operative
Assessment
Surgery
Dynamic Risk
Stratification
Clinical
Follow up

Less aggressive and more aggressive variants
• Pure papillary variant
• Mixed papillary and follicular
variant
• Follicular variant of papillary
• Tall cell
• Insular
• Columnar
• Diffuse sclerosing
• Clear cell
• Trabecular
• Poorly differentiated

Pathology report
In addition to the basic tumor features required for AJCC/UICC thyroid
cancer staging including status of resection margins,
additional information helpful for risk assessment, such as
1. the presence of vascular invasion
2. the number of invaded vessels,
3. number of lymph nodes examined and involved with tumor,
4. size of the largest metastatic focus to the lymph node,
5. presence or absence of extranodal extension of the metastatic tumor.
(Strong recommendation, Moderate-quality evidence)

Various Risk stratifications
• AGES
• MACIS
• AMES
• DEGROOT

Papillary thyroid ca (with all of the following):
RECOMMENDED
• No local or distant metastases;
• All macroscopic tumor has been resected
• No tumor invasion of loco-regional tissues or
structures
• No vascular invasion
• No aggressive histology (e.g., tall cell, hobnail
variant,columnar cell carcinoma)
• No 131 I uptake outside the thyroid bed on the
ﬁrst posttreatment whole-body RAI scan
Proposed modifications 2015 ATA guidelines
incremental benefit to be established
• Clinical N0 or ≤ 5 pathologic N1 micrometastases
(<0.2 cm in largest dimension)
• Intrathyroidal, encapsulated follicular variant of
papillary thyroid cancer
• Intrathyroidal, well differentiated follicular thyroid
cancer with capsular invasion and no or minimal (<4
foci) vascular invasion
• Intrathyroidal, papillary microcarcinoma, unifocal or
multifocal, including BRAFV600E mutated (if known)
LOW RISK

RECOMMENDED
• Microscopic invasion into perithyroidal soft
tissues
• RAI-avid metastatic foci in the neck on the first
post treatment whole-body RAI scan
• Aggressive histology (e.g., tall cell, hobnail
variant, columnar cell carcinoma)
• Papillary thyroid cancer with vascular invasion
• Clinical N1 or >5 pathologic N1 with all involved
lymph nodes <3 cm in largest dimension
• Multifocal papillary microcarcinoma with ETE and
BRAFV600E mutated (if known)
INTERMEDIATE RISK

HIGH RISK
RECOMMENDED
• Macroscopic tumor invasion into the
perithyroidal soft tissues (gross ETE)
• Incomplete tumor resection
• Distant metastases
• Postoperative serum thyroglobulin
suggestive of distant metastases
• Pathologic N1 with any metastatic lymph
node ≥3 cm in largest dimension
• Follicular thyroid cancer with extensive
vascular invasion (> 4 foci of vascular
invasion)

Follow up
• Clinical
• Physical examination
• Biochemical
• TSH
• Tg
• Anti Tg antibodies
• Whole body radio iodine scan
• Radiological
• CXR
• USG
• CT/MRI
• PET

4-6 weeks following surgery
Assess Post op disease status (i.e., the presence or absence of
persistent disease) for deciding further management
Clinical examination
Chest X Ray
TSH Values
Serum Tg values
Anti Tg Antibodies (NCCN)
USG Neck (central and lateral compartment)
Whole body diagnostic RAI scan

TOTAL THYROIDECTOMY
EVALUATION OF POST OP DISEASE STATUS
RAI REMNANT ABLATION NOT ROUTINELY RECOMMENDED
INITIAL TSH GOAL
EVALUATE RESPONSE TO
THERAPY
EXCELLENT RESPONSE INCOMPLETE / INDETERMINATE
RESPONSE
SERUM Tg
Diagnostic RAI Scan and/or USG
Suppressed Tg
<0.2ng/ml
Suppressed Tg
≥0.2ng/ml
Maintain TSH
0.5-2.0 mU/L
Maintain TSH
0.1-0.5 mU/L
SERUM Tg, USG NECK
Diagnostic I131 not recommended routinely
LOW RISK DTC

LOW RISK DTC
LOBECTOMY
RAI REMNANT ABLATION NOT ROUTINELY RECOMMENDED
INITIAL TSH GOAL
0.5-2.0 mU/L
THERAPY
RESPONSE
SERUM Tg
USG NECK
USG NECK
Consider Tg Testing

INTERMEDIATE RISK DTC
TOTAL THYROIDECTOMY
THERAPEUTIC NECK DISSECTION ±
PROPHYLACTIC central NECK
DISSECTION
RAI ABLATION
INITIAL TSH GOAL
0.1-0.5 mU/L
THERAPY
RESPONSE
SERUM Tg
REMNANT
ABLATION 30 mCi
Adjuvant therapy
upto 150 mCi
SERUM Tg,
USG NECK
Whole body RAI scan

HIGH RISK DTC
TOTAL THYROIDECTOMY
THERAPEUTIC NECK DISSECTION ±
PROPHYLACTIC central NECK
DISSECTION
RAI ABLATION
INITIAL TSH GOAL
< 0.1 mU/L
THERAPY
RESPONSE
SERUM Tg
Known structural disease 100-200 mCi
Old age >70 yrs 100-150 mCi
Dosimetry guided dosing
Adjuvant therapy
upto 150 mCi
SERUM Tg (if >10ng/ml),
USG NECK
Whole body RAI scan
CT or MRI and /or FDG PET

DYNAMIC RISK RESPONSE STRATIFICATION
Category Imaging
USG/ RAI
Suppressed Tg Stimulated Tg Anti Tg
Antibody titre
Excellent <0.2 ng/ml <1.0 ng/ml
Biochemical
incomplete
≥1.0 ng/ml ≥10 ng/ml Rising
Structural
incomplete
Any Any ±
Indeterminate Non specific
findings or faint
RAI uptake in
thyroid bed
< 1 ng/ml < 10 ng/ml Stable or
declining

Long term Follow up of excellent response
Low Risk , Intermediate Risk
Primary follow up every 12-24
monthly intervals
• Clinical examination
• TSH monitoring 0.5-2 mU/L
• Non stimulated Tg
• Periodic USG (based on Tg)
High Risk
Primary follow up every 6 months
(for atleast 5 yrs)
• Clinical examination
• TSH monitoring 0.1-0.5 mU/L
• Non stimulated Tg
• Periodic USG/CT/MRI

Structurally Incomplete or Biochemically
Incomplete or Indeterminate responses
Surgical incomplete
Additional work
up and further
management
regarding
localization/resec
tability
Biochemical incomplete
• Continue observation
with TSH suppression
• Raising Tg and Anti Tg
antibody needs
further work up
Indeterminate response
• Serial imaging
• Tg monitoring
• Nonspecific findings that
become suspicious over
time can be further
evaluated with additional
imaging or biopsy

WHOLE BODY SCANNING (WBS)
• To evaluate the residual,
recurrent & metastatic
disease after primary
surgery
• Residual Disease –
if the uptake is >8%
it is defined as residual disease

How to prepare for RAI study
Thyroxine withdrawl
• LT4 should be withdrawn for 3–4
weeks
• LT3 should be withdrawn for at
least 2 weeks
• If LT4 is withdrawn for 4 or more
weeks, substitute it with LT3
• Maintain Serum TSH > 30mU/L
RhTSH supplementation
• Any risk DTC with Comorbidity
• Acutely exacerbated with
hypothyroidism
• Pituitary failure patients
• Inability to mount an adequate
endogenous TSH response

Recombinant TSH
The use of rhTSH in DTC is FDA-approved for diagnostic testing only,
and not for therapy
• Advantage
• No need to stop Thyroxine
• Disadvantage
• Expensive
• Not easily available
• Not approved for distant metastases
• Schedule
Day 1
• 0.9 mg im
Day 2
• 0.9 mg im
Day 3
• RAI
Day 4
• Rest
Day 5
• Evaluation

I123 or I131 STUNNING EFFECT
DEFINITION
• Scanning dose of I131 may induce follicular cell damage , decreasing uptake in the
thyroid remnant or remnant of metastasis thus impairing the therapeutic efficacy of
subsequent I131
• Stunning exists at cellular level, Higher the dose of I131, increase in incidence
Scintigraphy for detection of thyroid metastasis consists of obtaining images of the body,
• 1–3 days following the oral ingestion of I-131,
• 6 to 48 hours after I-123.
• To avoid stunning
• Smaller dose of Iodine131
• Use of iodine 123
• Shorter interval between diagnostic & therapeutic dose( <72 hrs)

POST ABLATION SCAN
• It is a must following ablative
therapy
• Done usually 4 to 10 days later.
• New metastatic foci (20-25%)
will be revealed
• Preferably combined with
TG Assay

Thyroglobulin
• Ideally Serum Tg and anti Tg antibody should be assessed
longitudinally in the same laboratory using the same assay for a given
pt.
• Tg reaches its nadir usually 3-4 weeks postoperatively in most
patients.

Anti Tg Antibodies
• Presence of anti Tg antibodies limits the assay.
• Tg assay may not be reliable and misleading .
• 25 % of DTC patients will have anti Tg antibodies.
• 10 % of normal population have anti Tg antibodies.
• Tg Abs rise even before Tg start rising
• Presence of anti Tg antibodies 1 year after thyroidectomy after RAI
indicates the presence of residual disease and increase the recurrence.

INTERPRETATION OF Tg ASSAY
• Proceed for localisation
Tg detectable during
Thyroxine treatment
• look for stimulated level after rhTSH or
stopping thyroxine
Tg normal during
Thyroxine treatment
• Localisation
Stimulated Tg level >
1 ng/ml
• Follow up
Stimulated Tg level <
1 ng/ml

Usg as a follow up tool
Suspicious lymph nodes ≥ 1cm
• Biopsy
• Tg measurement in the needle
washout fluid.
Suspicious lymph nodes
<1cm follow up
• Consider FNA or intervention
• if there is growth of node
• if the node threatens vital
structures.

Role of CT/MRI
• Cross-sectional imaging of the neck and upper chest (CT, MRI) with IV
contrast should be considered
• Bulky recurrent nodal disease
• Aerodigestive tract invasion
• when neck USG is felt to be inadequately visualizing neck nodes (high Tg,
negative neck USG).

Role of CT / MRI of other organs
High risk DTC with negative neck and chest imaging, RAI could not be
performed
Imaging of other organs considered
• MRI brain
• MR skeletal survey
• CT or MRI of the abdomen

Role of FDG PET
Highrisk DTC patients with elevated serum Tg (generally >10 ng/mL)
with negative RAI imaging
• Degree of FDG uptake directly proportional to
• Tg synthesis
• Degree of tumor dedifferentiation
• Level of TSH stimulation
• FDG uptake indicates tumor dedifferentiation
• prognosis is poor in positive FDG uptake
• Sensitivity of the scan increases as the serum TG level increases
• Fusion scan- FDG PET-CT

TUMOR DE-DIFFERENTIATION
• The WDTC cells proliferate yet lose their ability to trap, organify, store, &
metabolize iodine.
• The presumed mechanism is an acquired mutation of the Sodium Iodide
Symporter (NIS) gene
• These cells are still able to synthesize Tg
• Redifferentiation can be tried with various agents
• Retinoic Acid Therapy (1mg/kg/day for 1st wk, followed by 1.5/kg/day for 4 wks)- 20-
30% response rate

Tg positive & I-131 negative
Causes
• Inadequate TSH stimulation
• Small tumor size
• Iodine contamination
• Tumor dedifferentiation

Tg positive & I-131 negative
How to proceed…??
• Iodine contamination
• TSH level to be checked
• USG / CT/MRI of neck – local recurrence/nodes
• CT lungs/ Bone scan
• Imaging with other agents – FDG PET

TREATMENT OF METASTASIS - LOCALISED
•If Resectable – Resection
•If unresectable
• WBS +ve – Ablative RAI
• WBS –ve – EBRT

For tumour involving upper aerodigestive
tract
For Superficial invasion
Shaving a tumor off the trachea or
esophagus
For Deep Invasion
Tracheal resection and
anastomosis or
laryngopharyngoesophagectomy

Pulmonary metastasis (Micro and Macro)
• More frequent in young patients with PTC
• Lung is the only site in children
• Solitary mets – resection
• Multiple mets – Ablative radio iodine

Pulmonary metastasis (Micro and Macro)
RAI therapy
Repeat every 6– 12 months till there is clinical response.
Micromets – good reponse Macromets – poor survival

Bone metastasis
• More common in older patients and in FTC
• Pain, swelling & fracture in 80%
• Osteolytic lesions - difficult to detect on X-ray
• Bone scintigraphy, CT,MRI better

Bone metastasis – Various options
• Resection / RAI / EBRT / Biphosphanates / therapeutic embolisation
• Although RAI is rarely curative.
• RAI therapy of iodine-avid mets associated with improved survival
• Empirical (100–200 mCi) or dosimetry.
• Diffuse / symptomatic bone mets from RAI Refractory DTC
• Bisphosphonates and denosumab

CNS METASTASIS
1. Surgical resection
2. Stereotactic EBRT
3. Role of RAI – if it is AVID, Give EBRT First Then RAI
4. Multiple CNS Lesions – Resection And /Or IGRT
5. Progressive Disease – Lenvatinib, Sorafenib

TREATMENT OF METASTASES - NON LOCALISED
• Empirical RAI
• 100–200mCi for regular patients.
• 100–150 mCi for patients ≥70 years old
• DOSIMETRY LIMIT
• Whole-body retention to 80 mCi at 48 hours
• Bone marrow 200 cGy.
• Repeat RAI till post ablation scan normalizes or no clinical
response is being observed
• Maximum cumulative dose is 1000 mCi – 1500 mCi

SUPPRESSIVE THYROXINE THERAPY
• Initial effective dose is about 2.5µg/kg in adults
• Titrated dose - No deleterious effects on heart or bone
• Toxicity of TSH suppression
• Elderly – cardiac tachyarrythymias
• Post menopausal – bone demineralisation
• Supplementation with vitamin D – 1000 U /Day
• Calcium – 1200 mg/day

Risk of second malignancy with RAI
• Minimal risk
• Does not warrant specific screening.

Men and pregnant women side effects
• Women of childbearing age – R/O pregnancy prior to RAI
• Avoid pregnancy for 6–12 months after RAI
• Deferred during lactation and 3 months thereafter.
• Men Infertility risk - ≥ 400 mCi.

RAI Refractory DTC – No role for further RAI
The malignant/ metastatic tissue does not ever concentrate RAI
Kinase Inhibitors
• Sorafenib, Lenvatinib, Vandetanib
• Affects quality of life – Cautious use
• Not recommended for indolent disease
Chemotherapy
• Doxorubicin recommended

Other Primary Thyroid Malignancies

CLASSIFICATION
PRIMARY:
• Follicular epithelium –
Well differentiated
Papillary
Follicular
Hurthle cell
Undifferentiated
Anaplastic
• Parafollicular cells (C-cells)
Medullary
• Lymphoid cells
Lymphoma

Undifferentiated(anaplastic) thyroid carcinoma
• UTC are malignant tumours that histologically appear wholely or
partially composed of undifferentiated cells that exhibit
immunohistochemical or ultrastructural features indicative of
epithelial differentiation

• Usually elderly
• 5% of thyroid malignancies
• Presentation:
– rapidly growing mass
– hoarseness
– dysphagia
– dyspnea
– usually extrathyroidal extension

• Rapid evolution:
– massive growth in neck
– infiltration of ribbon muscles, esophagus, trachea, skin, and
contiguous bones
– commonly nodal and distant metastases
– cause of death usually involvement of vital structures in the
neck
– extremely poor prognosis, with many patients surviving less
than 6 months following diagnosis

Pathogenesis
• Usually a result of
anaplastic
transformation of
a pre-existing
well-differentiated
tumor (or a
metastatic focus):
– commonly papillary
carcinoma
Anaplastic thyroid
carcinoma showing residual
papillary carcinoma.

Gross anaplastic thyroid carcinoma showing a large yellow, tan, white
mass with areas of hemorrhage.

HISTOPATHOLOGY
• Squamoid
• Sarcomatoid:
spindle cell
giant cell

• Sarcomatoid: spindle cell and giant cell:
• These two patterns, often seen together
may exhibit:
– a fascicular or storiform growth pattern
– heavy neutrophilic infiltration
– prominent vascularization
– cartilaginous/osseous metaplasia
• May be osteoclast-like multinucleated giant
cells:
– giving an appearance reminiscent of giant
cell tumor of bone or soft tissues

Anaplastic carcinoma of the spindle cell type.

Anaplastic carcinoma of giant cell type

Special Stains and Immunohistochemistry
• Keratin 50-100%
• CEA 50%
• Throglobulin 5%
• Vimentin: (consistently present in the spindle cell component)
• TTF-1 (generally negative)

Management
• When resectable mass, thyroidectomy may lead to a
small improvement in survival, especially in younger
individuals
• Combined radiation and chemotherapy as adjuvant in
patients with resectable disease has been associated with
prolonged survival
• Tracheostomy may be needed for airway obstruction

Medullary carcinoma
• Thyroid malignancy with C(parafollicular) cell
differentiation. C-cells derived from the ultimobranchial
bodies, rich in superolateral lobe of thyroid.
• 5-10 % of thyroid neoplasms
• secrete calcitonin,
• elaborate other polypeptide hormones, such as serotonin,
ACTH, vasoactive intestinal peptide (VIP), calcitonin gene–
related peptide, histaminadases and prostaglandins E2 and
F2.

• Two forms:
– sporadic (approximately 80% of cases)
– familial
• The remainder 20% occurs in the setting of MEN syndrome 2A or
2B
• Cases associated with MEN types 2A or 2B occur in younger
patients, and may even arise during the first decade of life.
• sporadic as well as familial medullary carcinomas are lesions of
adulthood, with a peak incidence in the 40s and 50s.

Sporadic medullary carcinoma
• Occurs in adults (mean age 45 years)
• Almost always solitary
• Presents as a thyroid mass that is cold on thyroid scan
• Sometimes accompanied by intractable diarrhea or Cushing's
syndrome

Familial medullary carcinoma
• Autosomal dominant inheritance with virtually complete
penetrance.
• Becomes clinically apparent at mean age 35 years
• Most cases in children are familial medullary carcinoma
• Often multiple and bilateral

• Multiple endocrine neoplasia IIa (Sipple’s Syndrome):
• MTC, Pheochromocytoma, parathyroid hyperplasia
• Multiple endocrine neoplasia IIb (Wermer’s Syndrome):
• MTC, Pheochromocytoma, multiple mucosal neuromas, marfanoid
body habitus

Macroscopically
• Typically:
– solid
– firm
– nonencapsulated
– relatively well
circumscribed
– in the midportion or
upper half of the
gland, corresponding
to a greater
concentration of C
cells in this region
Unencapsulated quality, solid
appearance, and yellowish tan
color

Histopathology
• Classically:
– Solid proliferation of round to
polygonal cells with:
• granular amphophilic cytoplasm
• medium-sized nuclei
– highly vascular stroma
– hyalinized collagen
– amyloid
– coarse calcification
Low-power microscopic view
showing solid pattern of growth
and deposition of amyloid.

Diagnosis
• Family history, physical examination, raised serum calcitonin,
or CEA levels, and FNAB cytology
• Labs: 1) basal and pentagastrin stimulated serum
calcitonin levels (>300 pg/ml)
2) serum calcium
3) 24 hour urinary catecholamines
(metanephrines, VMA, nor-metanephrines)
4) carcinoembryonic antigen (CEA)

• Fine-needle aspiration
• Genetic testing of all first degree relatives
RET proto-oncogene
• Calcitonin and CEA are used to identify
persistent or recurrent MTC
• Calcitonin is a more sensitive tumor marker, but
CEA is a better predictor of prognosis

Special Stains and Immunohistochemistry
• Calcitonin+ 95 %
• CEA++100%
• Chromogranin+100
• Keratin AE 1/3+100
• TTF-1+90
• Thyroglobulin
• NSE
• Synaptophysin
• Medullary carcinoma showing
immunocytochemical positivity for calcitonin
and congo red

Metastases
• Cervical and mediastinal lymph nodes
• Distant organs, particularly lung, liver, and skeletal
system
• More common with sporadic and multiple
endocrine neoplasia (MEN)-IIB than MEN-IIA
• May be the first manifestation and a source of
confusion

Management
• When found to have a pheochromocytoma,
this must be operated on first
• Total Thyroidectomy(>50% bilateral Disease, high incidence of
multicentricity, aggressive course& I 131 not effective)
• B/L Central Neck Node Dissection (Central compartment nodes
involved bilateral central neck node dissection should be
routinely performed).
• Palpable cervical nodes or involved central neck nodes at
ipsilateral or bilateral, modified radical neck dissection is
recommended

• Prophylactic lateral neck dissection
• Tumors >1 cm, ipsilateral prophylactic modified radical
neck dissection is recommended because >60% of these
patients have nodal metastases
• If ipsilateral nodes are positive, a contralateral node
dissection should be performed.
• Locally recurrent or metastatic disease, tumor debulking
is done, not only to ameliorate symptoms of flushing
and diarrhea, but also to decrease risk of death from
recurrent central neck or mediastinal disease
Management

• External beam radiotherapy is controversial, but is
recommended for patients with unresectable residual or
recurrent tumor.
• No effective chemotherapy regimen
• Tyrosine kinase inhibitors
-STI571 (imatinib) No promising result in phase II
-ZD6474 (Zactima) was more effective in phase II
partial responses in 27% of patients, with reduction
in both calcitonin and CEA levels
• Anti-CEA monoclonal antibody (labetuzumab)
shown antitumor response in a small group of patients

• At the time of thyroidectomy Obviously enlarged parathyroid
glands should be removed.
• Normal parathyroids preserved.
• When vascular pedicle can't be maintained -> Biopsied &
autotransplanted to forearm of the nondominant arm
• Liver metastases >1.5 cm - Radiofrequency ablation done

Prophylactic Total Thyroidectomy
• Indicated in RET mutation carriers once mutation confirmed
• Performed before age 6 in MEN2A patients
• Before age 1 year old in MEN2B patients
• Central neck dissection avoided in children who are RET –positive
and calcitonin-negative with a normal ultrasound examination
• If calcitonin is increased or the ultrasound suggests thyroid cancer,
prophylactic central neck dissection is indicated

Postoperative Follow-Up
• Serial calcitonin and CEA
- 2 weeks postop
- 3/month for one year
• Followed by annual measurements of calcitonin and CEA levels,
in addition to history and physical examination
• To localize recurrent disease include ultrasound, CT, MRI,
and more recently FDG(Flurodeoxyglucose) PET scans.

Malignant Lymphoma
• Involve as part of systemic lymphoma (secondary
lymphoma) or may arise primarily in the thyroid
• 1% to 3.5% thyroid cancers are malignant lymphomas.
• Primary malignant lymphoma of the thyroid usually arises
in an immunologically abnormal gland, usually one
affected by chronic lymphocytic thyroiditis

• Clinically, thyroid lymphoma affects women
more frequently than men (ratio of 2.5 to
8.4:1).
• Most patients are elderly (age 50 to 80
years).
• The most common histologic subtype is
diffuse large-B cell lymphoma

Diffuse large-cell lymphoma arising in thyroid

Management
• Combined treatment with radiotherapy and chemotherapy
is often recommended.
• Thyroid lymphoma respond rapidly to chemotherapy
(CHOP—cyclophosphamide, doxorubicin, vincristine, and
prednisone).

ROLE OF SURGERY IN LYMPHOMA
• Thyroidectomy and nodal resection – not responding
rapidly to CHOP regimen / RT
• To alleviate the symptoms of airway obstruction

Prognosis
• MTC - 10-year survival approximately 80% but decreases
to 45% in patients with lymph node involvement, worst
survival of 35% at 10 years for MEN2B
• Anaplastic Carcinoma- Few patients surviving 6 months
beyond diagnosis
• Lymphoma- 5-year survival rate is about 50%; patients
with extrathyroidal disease have markedly lower survival
rates

• SECONDARY/METASTATIC:
-Kidney
-Breast
-Colon
-Direct extension
-Melanoma
• Teratoma
• Plasmacytoma
• Peripheral nerve sheath
tumors
OTHER THYROID TUMORS
• Paraganglioma
• Solitary fibrous tumor
• Follicular dendritic cell
tumor
• Langerhans cell
histiocytosis
• Ectopic thymoma
• Angiosarcoma
• Smooth muscle tumors

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