. Women are much more likely to develop hyperthyroidism than men.

The thyroid gland's production of thyroid hormones (T3 and T4) is triggered
by thyroid-stimulating hormone (TSH), which is made by the pituitary
gland.
What is the thyroid gland?

The thyroid is a 2-inch-long, butterfly-shaped gland weighing less than an

ounce. Located in the front of the neck below the larynx, or voice box, it is
composed of two lobes, one on each side of the windpipe.
The thyroid is one of the glands that make up the endocrine system. The
endocrine glands produce, store, and release hormones into the
bloodstream that travel through the body and direct the activity of the
body's cells. Thyroid hormones regulate metabolism-the way the body
uses energy-and affect nearly every organ in the body.

1
 Hormones Made by the Thyroid Gland

The thyroid gland makes two thyroid hormones, triiodothyronine (T3) and
thyroxine (T4). Thyroid hormones affect metabolism, brain development,
breathing, heart and nervous system functions, body temperature, muscle
strength, skin dryness, menstrual cycles, weight, and cholesterol levels.
A third hormone produced by the thyroid gland, calcitonin, is not
considered a thyroid hormone as such, but affects calcium levels in the
blood and controls the buildup of calcium in the bones.
Thyroid hormone production is regulated by thyroid-stimulating hormone
(TSH), which is made by another gland in the endocrine system called the
pituitary, located in the brain.

What causes hyperthyroidism?

Hyperthyroidism has several causes, including
 Graves' disease
 one or more thyroid nodules
 thyroiditis, or inflammation of the thyroid gland
 ingesting too much iodine
 overmedicating with synthetic thyroid hormone, which is used to treat
underactive thyroid
Rarely, hyperthyroidism is caused by a pituitary adenoma, which is a
noncancerous tumor of the pituitary gland. In this case, hyperthyroidism is
due to too much TSH.

Graves' Disease
Graves' disease, also known as toxic diffuse goiter, is the most common
cause of hyperthyroidism in the United States. Graves' disease is an
autoimmune disease, which means the body's immune system acts
against its own healthy cells and tissues. In Graves' disease, the immune
system makes an antibody called thyroid stimulating immunoglobulin
(TSI), which mimics TSH and causes the thyroid to make too much thyroid
hormone.

Thyroid Nodules
Thyroid nodules, also called adenomas, are lumps in the thyroid. Thyroid
nodules are common and usually noncancerous. About 3 to 7 percent of
the population has them. However, nodules may become overactive and
2

produce too much hormone. A single overactive nodule is called a toxic

adenoma.
When multiple nodules are overactive, the condition is called toxic
multinodular goiter. Often found in older adults, toxic multinodular goiter
can produce a large amount of excess thyroid hormone.

Thyroiditis
Several types of thyroiditis can cause hyperthyroidism. Thyroiditis does
not cause the thyroid to produce excess hormone. Instead, it causes
stored thyroid hormone to leak out of the inflamed gland and raise
hormone levels in the blood.

2
Subacute thyroiditis. This condition involves painful inflammation and
enlargement of the thyroid gland. Doctors aren't sure what causes
subacute thyroiditis, but it may be related to a viral or bacterial infection.
The condition usually goes away on its own in a few months. Many people
with subacute thyroiditis briefly develop hypothyroidism-when hormone
levels are too low-after the hyperthyroidism resolves but before the
thyroid gland is completely healed.
Postpartum thyroiditis. About 8 percent of women who have been
pregnant develop postpartum thyroiditis within a few months of giving
birth. Postpartum thyroiditis is believed to be an autoimmune condition
3

and causes hyperthyroidism that usually lasts for 1 to 2 months. The

condition is likely to recur with future pregnancies. As with subacute
thyroiditis, women with postpartum thyroiditis often develop
hypothyroidism before the thyroid gland is completely healed. In some
women, the gland does not heal and hormone levels remain low. These
women must take thyroid hormone replacement for the rest of their lives.
Silent thyroiditis. This type of thyroiditis is called "silent" because it is
painless, as is postpartum thyroiditis, even though the thyroid may be
enlarged. Like postpartum thyroiditis, silent thyroiditis is probably an
autoimmune condition and sometimes develops into permanent
hypothyroidism.

Iodine Ingestion
The thyroid gland uses iodine to make thyroid hormone, so the amount of
iodine you consume influences the amount of thyroid hormone your thyroid
makes. In some people, consuming large amounts of iodine may cause the
thyroid to make excess thyroid hormone. Sometimes significant amounts
of iodine are contained in medications-such as amiodarone, which is used
to treat heart problems-or in supplements containing seaweed. Some
cough syrups also contain large amounts of iodine.

Overmedicating with Thyroid Hormone

Some people who take thyroid hormone for hypothyroidism may take too
much. If you take synthetic thyroid hormone, see your doctor at least once
a year to have your thyroid hormone levels checked and follow your
doctor's instructions about the dose you take. Some medications may also
interact with your synthetic thyroid hormone to raise levels in your blood.
Ask your health care professional about drug interactions when starting
new medications.

What are the symptoms of hyperthyroidism?

Hyperthyroidism has many symptoms that can vary from person to person.
Some common symptoms of hyperthyroidism are
Symptoms of Hyperthyroidism
Gastrointestinal system • Weight loss in spite of increased appetite. •
Diarrhea (due to increased activity at ganglionic level).
Cardiovascular system • Palpitations. • Shortness of breath at rest or on
minimal exertion. • Angina. • Cardiac irregularity. • Cardiac failure in the
elderly (CCF).
Neuromuscular system • Undue fatigue and muscle weakness. • Tremor.
3
Skeletal system • Increase in linear growth in children
Genitourinary system • Oligoor amenorrhea. • Occasional urinary
frequency.
Integument • Hair loss. • Pruritus.
Psychiatry • Irritability. • Nervousness. • Insomnia.

Signs of Hyperthyroidism
Order of appearance of signs
Stellwag’s sign - Mild. First sign to appear.- Stellwag’s sign: Absence of
normal blinking—so starring look.
von Graefe’s Sign - Mild.-Lid lag sign is visible white sclera above the
corneal margin during lid lag.
Joffroy’s sign – Moderate- Absence of wrinkling on forehead when patient
looks up (frowns).
Moebius sign. – Severe- Lack of convergence of eyeball. Defective
convergence is due to lymphocytic infiltration of inferior oblique and
inferior rectus muscles in case of primary thyrotoxicosis. There will be
diplopia. It may be an early sign of eventual ophthalmoplegia.
EXOPHTHALMOS
• It is proptosis of the eye, caused by infiltration of the retrobulbar tissues
with fluid and round cells, with lidspasm of upper eyelid
. • Sclera can be seen clearly above the limbus of the eye.
• Proptosis can be measured by ophthalmometer.
• Exophthalmos is often self-limiting, but not always. Sleeping in propped
up position and lateral tarsorrhaphy will help to protect the eye.
Severe exophthalmos
• Eyelid edema, chemosis, conjunctival injection.
• Diplopia, ophthalmoplegia (complete weakness of all extraocular
muscles and so no movements possible).
• Corneal ulceration.
• Papilledema soon develops.
• Finally it may also cause loss of vision. It is called as malignant
exophthalmos.

Investigations
Your doctor will begin by asking you about your symptoms and performing
a thorough physical examination. Your doctor may then use several tests
to confirm a diagnosis of hyperthyroidism and to find its cause.

Thyroid-Stimulating Hormone (TSH) Test

4
The ultrasensitive TSH test will probably be the first test your doctor
performs. This test can detect even tiny amounts of TSH in the blood and
is the most accurate measure of thyroid activity available. The TSH test is
especially useful in detecting mild hyperthyroidism.
The TSH test is based on the way TSH and thyroid hormone work together.
The pituitary gland boosts TSH production when the thyroid is not making
enough thyroid hormone; the thyroid normally responds by making more
hormone. Then, when the body has enough thyroid hormone circulating in
the blood, TSH output drops. In people who produce too much thyroid
hormone, the pituitary shuts down TSH production, leading to low or even
undetectable TSH levels in the blood.
Generally, a TSH reading below normal indicates hyperthyroidism and a
reading above normal means a person has hypothyroidism.

Other Tests
If your doctor confirms you have hyperthyroidism, additional tests may be
needed to find the cause and determine the best treatment.
T3 and T4 test. This test will show the levels of T3 and T4 in your blood.
If you have hyperthyroidism, the levels of one or both of these hormones in
your blood will be higher than normal.
Thyroid-stimulating immunoglobulin (TSI) test. This test, also called a
thyroid-stimulating antibody test, measures the level of TSI in your blood.
Most people with Graves' disease have this antibody, but people whose
hyperthyroidism is caused by something else do not.
Radioactive iodine uptake test. The radioactive iodine uptake test
measures the amount of iodine your thyroid collects from the bloodstream.
Measuring the amount of iodine in your thyroid will help your doctor know
what is causing your hyperthyroidism. For example, low levels of iodine
uptake might be a sign of thyroiditis, whereas high levels could indicate
Graves' disease.
Thyroid scan. A thyroid scan shows how and where iodine is distributed in
your thyroid. This information helps your doctor diagnose the cause of
your hyperthyroidism by providing images of nodules and other possible
thyroid irregularities.

Treatment
Treatment depends on the cause of hyperthyroidism and how severe it is.
When choosing a treatment, doctors consider a patient's age, possible
allergies to or side effects of the medications, other conditions such as
pregnancy or heart disease, and the availability of an experienced thyroid
surgeon.
The aim of treatment is to bring thyroid hormone levels to a normal state,
thus preventing long-term complications, and to relieve uncomfortable
symptoms. No single treatment works for everyone. The three treatment
options are medications, radioiodine therapy, and surgery.

Medications
Antithyroid Drugs

• Carbimazole and propylthiouracil are the main drugs.

5
 • These interfere with T3 and T4 synthesis by inhibiting oxidation and coupling.

• Initial dose of carbimazole is 40 mg/day (10 mg 6 hrly) which can be gradually reduced to 20 mg/ day (10 mg
12 hrly) to maintain euthyroid state.

• Course of therapy ranges from 6 months-2 years during which time patient generally goes into remission.

• Side effects are skin rash and agranulocytosis that usually manifests as sore throat.

• In patients with mild symptoms, propranolol can be used in dosage of 10 mg two to three times a day. It is a
beta blocker and blocks peripheral receptors for thyroxine. It does not reduce serum levels of thyroxine.

Radioiodine Therapy
Radioactive iodine-131 is a common and effective treatment for
hyperthyroidism. Because your thyroid gland collects iodine to make
thyroid hormone, it will collect the radioactive iodine in the same way.
The radioactive iodine will gradually destroy the cells that make up the
thyroid gland but will not affect other tissues in the body.
Contraindicated in- Although iodine-131 is not known to cause birth
defects or infertility, radioiodine therapy is not used in pregnant women or
women who are breastfeeding. Radioactive iodine can be harmful to the
fetus' thyroid, and it can be passed from mother to child in breast milk.
.

Thyroid Surgery
The least-used treatment is surgery to remove part or most of the thyroid
gland. Surgery
• Make the patient euthyroid with antithyroid drugs before surgery.
• Potassium iodide (5 mg TDS) may be added about 10 days prior to
surgery to cause regression in size of the gland.
• Toxic adenoma—do lobectomy.
• MNG, large gland, relapse after medical treatment— do subtotal
thyroidectomy (about 5 gm gland left on each side).
• It is better to do more removal of gland because postoperative
hypothyroidism is easier to treat rather than recurrent thyrotoxicosis.

THYROID FUNCTION TESTS

THYROID FUNCTION TESTS Most of the thyroid function tests performed in the past are only of historical importance. As
a routine, only a small number of tests need to be performed.

6
Serum TSH, T3 and T4 Levels

If TSH level is within normal range, it is suggestive of euthyroid state and estimation of T3 and T4 is not required.

In euthyroid patient, T3, T4 and TSH levels will be within normal range. In hyperthyroid state, T3 and 4 levels will be high
and TSH levels are on lower side (even undetectable) due to increased negative feedback on pituitary gland.

In hypothyroid state, T3 and T4 levels will be low and TSH levels will rise due to decreased negative feedback on
pituitary gland (Box 23.2).

Normal values:

T3 – 3.5-7.5 p mol/lit.

T4 – 10-30 n mol/lit.

TSH – 0.3-3.3 mμ/lit.

Isotope Scan I123 or Tc99m is given in low dosage and its pick up by active thyroid tissue is demonstrated with gamma
camera. The findings in a case of thyroid nodule can be as follows:

a. Warm nodule: Nodule as well as surrounding normal thyroid tissue has normal and equal uptake of the isotope.

b. Cold nodule: Nodule has no uptake while surrounding thyroid tissue has normal uptake of the isotope

Cold nodule: Causes

• Cysts.

• Fibrosis.

• Hemorrhage.

• Carcinoma

c. Hot nodule: Nodule has increased uptake while surrounding thyroid tissue has decreased uptake of isotope. It is
suggestive of autonomous toxic nodule. The malignant nodules are mostly cold, but can also be hot sometimes.
Therefore, isotope scan is not diagnostic of thyroid malignancy.

• In toxic MNG, isotope scan demonstrates whether nodules or inter-nodular area are hyperactive that helps in deciding
the therapy.

• Isotope scan is useful in locating ectopic thyroid tissue (lingual, subhyoid, mediastinal, ovarian) and to look for
retrosternal extension of thyroid gland.

• Whole body isotope scanning is useful in locating metastases of thyroid malignancy since these areas have functional
activity. However, normal thyroid gland has to be removed (with surgery or radioiodine ablation) before the scan is
done since functional thyroid metastasis cannot compete with normal thyroid tissue in iodine uptake.

Thyroid Antibodies

Antibodies against thyroid are useful in determining the cause of thyroid dysfunction. The levels are high in autoimmune
thyroiditis and Graves’ disease.
7
 Goiter classification

1. SIMPLE NONTOXIC

a. Diffuse hyperplastic—

1. Physiological— a. Puberty. b. Pregnancy.

2. Primary iodine deficiency (Endemic; dietary intake less than 100ug/day).

3. Secondary iodine deficiency - Goitrogens of Brassica family, e.g. cabbage, soyabean - Excess dietary fluoride. - Drugs:
PAS, Lithium, Phenylbutazone, thiocyanates. - Dyshormonogenetic goiter.

b. Colloid goiter

c. Nodular goiter (Multinodular).

d. Solitary nontoxic nodule.

e. Recurrent nontoxic nodule.

2. TOXIC

a. Diffuse (Primary)—Graves’ disease.

b. Multinodular (Secondary)—Plummer’s disease.

c. Toxic nodule (solitary) (Tertiary).

d. Recurrent toxicosis.

3. NEOPLASTIC

a. Benign—Adenomas: Papillary, follicular, Hurthle cell, colloid.

b. Malignant—Carcinomas: Papillary, follicular, medullary, anaplastic, lymphomas.

4. THYROIDITIS Hashimoto’s autoimmune thyroiditis. de-Quervain’s autoimmune thyroiditis. Reidel’s thyroiditis.

5. RARE CAUSES: Bacterial (suppurative), amyloid.

Multinodular goitre

8
It is the end stage of hyperplastic goiter and is irreversible. It is more common in females and usually presents in 4-5th
decade of life.

Symptoms and Signs

• Asymptomatic neck mass (Fig. 23.8).

• Dyspnea and dysphagia may occur in a large MNG due to compression of trachea and esophagus respectively.

• Firm nodular thyroid that moves on deglutition.

Complications of MNG

• Secondary thyrotoxicosis (30%).

• Follicular carcinoma of thyroid.

• Hemorrhage in a nodule.

• Tracheal obstruction.

• Cosmetic problem

Investigations • Routine investigations (Hb, BT, CT, Urine)

• Blood urea, blood sugar

• ECG, chest X-ray

• X-ray soft tissue neck: AP and lateral view are done to look for tracheal deviation and tracheal compression (scabbard
trachea*) respectively. It is important from anesthetist’s point of view while doing endotracheal intubation during
anesthesia.

• Indirect laryngoscopy: To see and document the status of vocal cords (for medicolegal reasons).

9
•T 3T4 and TSH levels.

• FNAC of thyroid nodule to rule out malignancy.

Treatment

Surgery is the mainstay of treatment. Indications for surgery are:

• Cosmetic reasons

• Pressure symptoms

• Risk of malignant change

Types of Surgery

1. Subtotal thyroidectomy: Remove most of the bulk of the gland leaving a normal size thyroid (size of thumb) in
tracheo-esophageal groove on both sides taking care not to injure recurrent laryngeal nerve and parathyroid glands.
Although postoperative thyroxin is given routinely in these cases, it doesn’t prevent recurrence of thyroid nodules.

2. Total thyroidectomy: There are chances of recurrence after subtotal thyroidectomy since etiological factors persist.
In such cases reoperation is very difficult and hazardous. So another option, especially in younger patients, is total
thyroidectomy with preservation of bilateral recurrent laryngeal nerves and at least one parathyroid gland. The patient
is put on lifelong thyroxin replacement.

3. Lobectomy: If only one lobe of thyroid gland is involved and the other lobe is not palpable, treatment is removal of
involved lobe only (Figs 23.10A to C)

Toxic goiter
a. Diffuse (Primary)—Graves’ disease.

b. Multinodular (Secondary)—Plummer’s disease.

c. Toxic nodule (solitary) (Tertiary).

d. Recurrent toxicosis.

. Diffuse Toxic Goiter

• Also known as Graves’ disease or primary thyrotoxicosis .

• It is most common cause of thyrotoxicosis (70% cases).

• It is an autoimmune disorder

• Production of thyroid stimulating antibodies (TSAb) leads to diffuses hypertrophy and hyperplasia of thyroid gland.

• It involves young females and mostly patients have eye signs.

• Disease is known to have remissions and exacerbations.

II. Toxic Multinodular Goiter

• Also known as Plummer’s disease or secondary thyrotoxicosis (Box 23.7).

• It is mostly seen in older patients with long standing MNG.

• Mostly internodular area is active and nodules are inactive. Rarely nodules may become overactive.

• The clinical features are usually mild and eye signs are absent.

III. Toxic Adenoma

10
• It is a solitary nodule in the thyroid which is autonomous and overactive.

• Excess release of thyroxin from the toxic nodule leads to decrease in TSH levels by negative feedback mechanism. This
in turn leads to suppressed normal thyroid tissue around the nodule that is seen as ‘hot spot’ on thyroid scan.

IV. Rare Causes

• Thyroiditis

• Metastatic thyroid carcinoma

• Exogenous iodine/thyroid hormone

• Thyrotoxicosis factitia—due to overdose of thyroxine.

• Jod-Basedow’s thyrotoxicosis—iodine induced toxic goiter.

• Struma ovarii—ectopic thyroid tissue in malignant ovarian tumor. • Drugs—amiodarone (antiarrhythmic drug

NOTE- SYMPTOMS SAME AS HYPERTHYROIDISM

Signs

• Tremors: Tongue tremors (Fig. 23.11), Finger tremors (Fig. 23.12)

• Warm, moist skin

• Tachycardia (High sleeping pulse rate)

• Atrial fibrillation

• Cardiac failure

11
• Goiter with bruit

• Lid lag, lid retraction.

Specific to Graves’ Disease

• Ophthalmopathy (see thyroid eye disease)

 Grittiness

 Periorbital edema

 Conjunctival edema (chemosis)

 Bulging eyes (proptosis)

 Diplopia (extraocular muscle involvement)

 Impaired vision (optic nerve compression)

• Pretibial myxoedema (nonpitting edema, thick skin of pretibial region)

• Thyroid acropathy (finger clubbing)

• Thyroid myopathy (weakness of proximal limb muscles)

DIAGNOSIS FOR THYROTOXICOSIS

• Investigations- MENTION NAMES OF INVESTIGATIONS FOR HYPERTHYROIDISM( as described earlier)

• Most of the times, diagnosis of thyrotoxicosis is easily made on clinical findings. In doubtful cases thyrotoxicosis should
always be suspected in following situations:

 Children with behavior problems, CNS symptoms.

 Elderly with cardiac problems (arrhythmia, CHF)

 Unexplained diarrhea and weight loss.

• On investigations, TSH is decreased and T3, T4 levels are high.

• Levels of TSAb are high in Graves’ disease.

• On thyroid scan, hot nodule is seen in toxic adenoma, diffuse increase in uptake is seen in Graves’ disease and patchy
uptake is seen in toxic MNG.

TREATMENT There are three modalities of treatment, namely antithyroid drugs, surgery and radioiodine

Note-Same as for hyperthyroidism

Malignant goitre
Pathology Types of malignant tumors are:

1. Differentiated thyroid carcinoma

 Papillary carcinoma

 Follicular carcinoma

2. Undifferentiated (anaplastic) carcinoma

12
 anaplastic carcinoma

3. Medullary carcinoma

4. Lymphoma.

Clinical Features

• Thyroid cancer usually presents as a lump in the neck which clinically may be a solitary nodule or multinodular goiter.
• About 10% of thyroid nodules are malignant.

• Dominant nodule in MNG has same cancer risk as solitary nodule.

• A thyroid nodule should be viewed with suspicion if it has following features:  Family history of thyroid cancer.

 History of neck irradiation in past

.  Age <15 years or > 65 years, especially male patient.

 Recent origin.

 Rapid increase in size.

 Hoarseness of voice.

 Firm, fixed, irregular nodule in thyroid.

 Along with enlarged cervical lymph nodes.

DIFFERENTIATED THYROID CARCINOMA

i. Papillary Carcinoma (10)***

• Most common form of thyroid carcinoma (60-80%).

• Most papillary tumors are mixture of papillary and follicular neoplasm, but they are treated as papillary carcinoma.

• Most common in children and young adults.

• Histologically, papillary projections are seen with calcified areas (psammoma bodies). Cells contain pale and empty
looking nuclei (Orphan Annie eyed nuclei).

• Tumor is multifocal involving one or both lobes due to rich intrathyroidal lymphatic plexus.

• Metastasis occurs commonly by lymphatic spread to cervical lymph nodes. The blood born metastasis is unusual.
However, lymph node involvement does not worsen the prognosis

• The tumor not palpable clinically and detected on histopathology (up to 1.5 cm) is called occult tumor. Clinically it may
present with only cervical lymphadenopathy (lateral aberrant thyroid)).

• The preoperative diagnosis is usually made by FNAC of thyroid nodule and/or enlarged cervical lymph node.

• A patient is considered low/high-risk based on absence or presence of ‘AMES criteria’

metastatic cervical lymph nodes

• Lower deep cervical nodes are usually involved on the side of lesion.

• Firm or cystic in consistency.

• Mobile or fixed.
13
• Only cervical nodes may be palpable with non-palpable thyroid in occult tumor (lateral aberrant thyroid).

• Lymph node metastasis does not worsen the prognosis.

• Modified radical neck dissection is the treatment of choice.

• Berry picking (removal of only enlarged lymph nodes) is not practised these days.

‘AMES criteria’ for differentiated thyroid carcinoma (Papillary and Follicular)

The prognosis is poor in:

A: Old age (>50 years female, >40 years male)

M:Presence of distant metastasis

E: Extra thyroidal extent (tumor extending outside the capsule of thyroid).

S: Size >5 cm.

ii. Follicular Carcinoma (5)***

• Constitute 10-20% of all thyroid cancers.

• Higher incidence in endemic areas (Fig. 23.16).

• It is not multifocal and lymph node involvement is rare.

• Presence of capsular and vascular invasion differentiates is from follicular adenoma.

• Metastasis is blood borne to lungs and skeleton. Metastasis is functional and takes up radioiodine (Box 23.13C).

• FNAC is not helpful in making diagnosis of follicular carcinoma because FNAC cannot identify presence of capsular and
vascular invasion. Hence, the diagnosis of follicular carcinoma is established on excision biopsy (lobectomy).

• The patients are divided into low/high-risk groups based on absence or presence of ‘AMES criteria’

• Hurthle cell neoplasm is a variant of follicular carcinoma and is rich in oxyphilic cells. It has unpredictable behavior
because benign and malignant neoplasm is difficult to distinguish. Moreover, it does not take up radioactive iodine.
Hence, total thyroidectomy is the treatment of choice. Comparison between two types of differentiated thyroid
carcinoma is shown in

Follicular carcinoma—skeletal metastasis

• Due to hematogenous spread.

• Grows very rapidly.

• Involves flat bones (skull, sternum, ribs, vertebrae) due to presence of red marrow.

• Presents as  Pulsatile mass  Pathological fracture.

• X-ray shows osteolytic lesion.

• Increased alkaline phosphatase levels.

• Treatment-  Palliative (Radioiodine/RT)

14
Treatment of Differentiated Thyroid Cancer

The strategy of surgical treatment for differentiated thyroid cancer is decided on the basis of low or high

Box risk group patient (AMES criteria).

In low-risk group patients, hemithyroidectomy (lobectomy + isthmusectomy) is sufficient,

while high-risk group patients require total thyroidectomy..

i. Papillary Carcinoma Following are the principles of surgical treatment:

• Patient with 1 cm tumor with no palpable lymph nodes  hemithyroidectomy

• Patient with tumor > 1 cm  Total thyroidectomy

• Patient with multifocal or bilateral disease, node positive  Total thyroidectomy.

• In patients with enlarged cervical nodes, modified radical neck dissection is done where internal jugular vein,
accessory nerve and sternomastoid muscles are preserved.

ii. Follicular Carcinoma Following are the principles of surgical treatment:

• All follicular neoplasms involving one lobe are initially treated with hemithyroidectomy.

• Lesions with no capsular and vascular invasion— no further treatment.

• Lesions with minimal capsular invasion—suppressive thyroxine therapy.

• Lesions with vascular invasion or local fixity—total thyroidectomy.

• Hurthle cell tumor—total thyroidectomy. Postoperative Management

• After surgery, thyroxine replacement is given to prevent hypothyroidism and to suppress TSH since differentiated
tumors are TSH dependent.

• In differentiated thyroid tumors, radioactive iodine scanning is done after surgery because these tumors take up
iodine.

• Isotope scanning is not needed in low-risk patients where hemithyroidectomy is sufficient

• In high-risk patients (extra-thyroidal tumor, positive nodes, distant spread), scanning is done six weeks after surgery.
Scanning is not able to pick up distant metastasis if substantial thyroid tissue is left in place. If residual thyroid tissue
and/or metastases are picked upon scan, then the patient is given a therapeutic dose of radioiodine.

• In preparation for scan, allow endogenous TSH to increase by stopping thyroxine for 4 weeks before the scan.

• After ablation with radioiodine, the patient can be followed-up by monitoring serum thyroglobulin levels (tumor
marker) and a rising level will indicate residual or recurrent disease.

15
ANAPLASTIC CARCINOMA

It is an uncommon tumor and affects elderly patients (>60 years) and has higher incidence in areas of endemic goiter.
Many cases arise from pre-existing, undiagnosed well-differentiated tumors.

There is long standing history of goiter that suddenly starts enlarging rapidly.

Tumor rapidly infiltrates adjoining structures and metastasizes by blood and lymphatics.

Pressure symptoms like dyspnea, dysphagia and hoarseness of voice predominate.

The tumor carries a very poor prognosis and most patients die within one year.

This feature emphasizes need for adequate treatment of welldifferentiated tumors and full evaluation of all goiters.
FNAC is helpful in making the diagnosis.

Thyroidectomy is usually not possible due to wide spread disease.

Treatment is palliative for relief of symptoms.

For airway obstruction, tracheostomy should be avoided and tracheal pressure can be relieved by division of isthmus.
External beam radiotherapy helps in local control

MEDULLARY CARCINOMA

• It is a rare tumor that arises from parafollicular or C-cells of thyroid gland (neural crest origin).

• It is not TSH dependent and does not take up radioiodine.

• Its hormone marker is calcitonin.

• It can present in sporadic and familial form.

• Sporadic presents as unilateral tumor while familial is almost always bilateral.

• In familial form (MEN type II) it is associated with other endocrine tumors of adrenal and parathyroid gland. It is
essential to exclude co-existing pheochromocytoma in these cases before planning surgery (Box 23.18).

• The clinical presentation is usually as thyroid swelling with enlarged cervical lymph nodes. Patient may complain of
diarrhea due to hormones and peptides secreted by the tumor. Distant spread may occur to lungs, liver and bones.

• Diagnosis is made by FNAC and raised serum calcitonin levels. Microscopically, hyperchromatic nucleus with amyloid
stroma are characteristic features.

• Treatment is primarily surgical.

Total thyroidectomy and central compartment lymph node clearance is recommended for all patients. In case lateral
lymph nodes are involved, modified radical node dissection is required. Prognosis and survival depends on presence or
absence of lymph node metastasis.

• In familial cases, genetic screening for the RET oncogene mutation can identify cases who will develop medullary
carcinoma later in life. Prophylactic total thyroidectomy should be considered in such cases at the age of 5-7 years.

16
SOLITARY THYROID NODULE

• Well-circumscribed, single nodule is palpable in thyroid while remaining gland is not palpable

• In 50% cases, underlying pathology is multinodular goiter having one dominant nodule while remaining nodules are
microscopic, hence not palpable.

• In remaining cases, the causes are adenoma, carcinoma (papillary or follicular) and thyroiditis.

• In case of toxic adenoma (autonomous nodule), it is almost never caused by malignant nodule.

• FNAC is the investigation of choice for determining underlying pathology

•If FNAC is inconclusive and the nodule is suspicious it should be subjected to hemithyroidectomy.

Treatment

If it is a nontoxic nodule due to any cause, hemithyroidectomy with complete removal of lateral lobe and whole of the
isthmus is done

. If it is papillary carcinoma thyroid, then near total thyroidectomy is done along with suppressive dose of L-thyroxine
given 0.3 mg OD daily.

If it is a toxic nodule, radioiodine therapy, I131 – 5 milli curie is given orally, if the age of the patient is more than 45
years.

If age is less than 45 years, then initially toxicity has to be controlled by antithyroid drugs, always followed by surgery—
Hemithyroidectomy

17
THYROIDITIS

It is a group of heterogenous disorders where common feature is inflammation of thyroid gland. It mainly affects
women and clinical course may be acute, subacute or chronic. Patients may present with euthyroidism, transient
hyperthyroidism or hypothyroidism and sometimes all three thyroid states may occur during the course of disease.

Hashimoto’s Thyroiditis (Chronic Autoimmune or Lymphocytic Thyroiditis)

 It is most common cause of thyroiditis. Histologically, there is diffuse lymphocytic infiltration, follicular
destruction, colloid depletion and fibrosis.
 Clinically, most patients present with a painless, diffuse goiter of variable consistency (rubbery, firm or hard)
depending on the cellularity and the degree of fibrosis.
 In patients of Hashimoto’s thyroiditis, sudden growth of goiter should raise the suspicion of malignant
change (lymphoma, papillary carcinoma).
 Initially, patients may have transient hyperthyroidism but ultimately, hypothyroidism occurs in most
patients.
 Diagnosis is mostly made on FNAC. Thyroid antibody titers are raised in most cases.
 Treatment is with thyroxine replacement therapy (0.2 mg/day) in patients with hypothyroidism.
 If goiter is increasing in size, steroid therapy may help. However, increasing goiter should raise the
suspicion of malignant change.
 In large goiter causing discomfort and cosmetic deformity, thyroidectomy is indicated.
 Treatment(5)

 The treatment of choice for Hashimoto thyroiditis (or hypothyroidism from any cause) is thyroid
hormone replacement. The drug of choice is orally administered levothyroxine sodium, usually
for life.
 Tailor and titrate the dose of levothyroxine sodium to meet the individual patient's
requirements. The goal of therapy is to restore a clinically and biochemically euthyroid state.
The standard dose is 1.6-1.8 mcg/kg lean body weight per day, but the dose is patient
dependent. The free T4 and TSH levels are within reference ranges in the biochemically
euthyroid state, with the TSH level in the lower half of the reference range.
 Patients younger than 50 years who have no history or evidence of cardiac disease can usually
be started on full replacement doses.
 Start patients older than age 50 years and younger patients with cardiac disease on a low dose
of 25 mcg (0.025 mg) per day, with clinical and biochemical reevaluation in 6-8 weeks. Carefully
titrate the dose upward to achieve a clinical and biochemical euthyroid state. Rarely, it may not
be possible to achieve a euthyroid state in a patient with baseline cardiac dysrhythmic disease
without worsening his or her cardiac status. In such cases, the astute clinician is content to
achieve the clinically euthyroid state and to accept a slightly elevated TSH level.
 Elderly patients usually require a smaller replacement dose of levothyroxine, sometimes less
than 1 mcg/kg lean body weight per day.
 Elderly patients and patients on androgens for various reasons usually require decreased
levothyroxine replacement dosing.

18
 Patients who have undergone bowel resection and have short-bowel syndrome (or
malabsorption for any reason) often require increased doses of levothyroxine to maintain the
euthyroid state.
 In their previously described study of 830 patients with Hashimoto thyroiditis, Tagami et al
found that, following treatment with small doses of levothyroxine in 32 of the study's patients
with subclinical hypothyroidism, significant decreases occurred in the patients' total cholesterol,
LDL, and non-HDL levels, as well as in their LDL/HDL ratios. [11]
 Combination therapy
 One popular treatment, more so among patients than physicians, is the combined use of
liothyronine (T3) and levothyroxine in an effort to mimic more closely thyroid hormone
physiology. However, a literature review found that out of 9 controlled clinical trials, only 1
indicated that combined therapy seemed to improve the mood, quality of life, and psychometric
performance of patients more than did levothyroxine alone. [18]
 Until investigators can demonstrate a definite advantage to the administration of levothyroxine
plus liothyronine, the use of levothyroxine alone should remain the treatment of choice for
replacement therapy in hypothyroidism


 THYROIDECTOMY—OPERATIVE STEPS
 • Patient is operated in supine position under general anesthesia.
 • A small sandbag is placed between the shoulders to extend the neck and head is supported upon a ring.
 • A ‘collar incision’ (necklace incision) is made in the neck along skin creases 1" above the sternum
extending between the lateral borders of sternomastoid muscles.
 • The flaps of skin and platysma are raised; upper flap upto thyroid cartilage and lower flap upto sternum.

• The investing layer of deep fascia is incised vertically in midline, the ribbon muscles are retracted laterally and
the thyroid gland is exposed.

• The middle thyroid vein is ligated and divided first and the lobe is delivered.

• Superior thyroid vessels are ligated and divided at upper pole taking care not to injure superior laryngeal
nerve.

• Inferior thyroid vessels are ligated and divided at lower pole taking care not to injure recurrent laryngeal
nerve.

• Current practice is to ligate individual branches of inferior thyroid artery after it has given supply to the
parathyroid glands so as to avoid ischemic damage to the parathyroid glands.

• The thyroid lobe is completely mobilized and divided at isthmus (Lobectomy).

• In total thyroidectomy same procedure is repeated on the other side taking care to preserve at least one
parathyroid gland.

19
• Hemostasis is achieved and the wound is closed after putting a closed suction drain in the thyroid bed.

 COMPLICATIONS OF THYROIDECTOMY
 Nerve Damage External branch of superior laryngeal nerve is the most commonly damaged nerve.
1) Injury results in loss of vocal cord tension leading to decreased pitch of voice (important for singers). This
damage often remains unrecognized.
2) Recurrent laryngeal nerve damage affects motor supply to vocal cords leading to vocal cord palsy.
3) Vocal cords allow phonation, protect airways and facilitate coughing. Hence, recurrent laryngeal nerve
should be identified and protected in all cases (Fig. 23.18).
4) Unilateral recurrent laryngeal nerve injury causes hoarseness of voice and reduced force of coughing. In
most cases, there is partial injury (neuropraxia) and recovery occurs in 3 weeks time.
5) Patients with permanent injury and no improvement may improve with teflon injection in vocal cords and
speech therapy.
6) Bilateral recurrent laryngeal nerve injury leaves both the vocal cords in paramedian position. It is because
of unopposed adducting action of cricothyroid muscles that are supplied by superior laryngeal nerves (also
see Chapter 16: Diseases of Larynx). Hence, patient develops respiratory obstruction on removal of
endotracheal tube after surgery. In such situation, airway is restored by doing tracheostomy.
7) Wait for 6 months to 1 year till recovery may occur. After 1 year, recovery is unlikely and treatment is vocal
fold lateralization procedure in form of Arytenoidectomy—removal of arytenoid cartilage or Lateral
arytenoidpaxy—suturing arytenoid cartilage laterally.
 Postoperative Bleeding It causes laryngeal compression and respiratory obstruction. Treatment is
immediate re-exploration under GA, evacuation of clots and suture ligation of bleeding vessels.
 Hypocalcemia It occurs after bilateral thyroid surgery due to inadvertent vascular injury to parathyroid
glands. Treatment is injection calcium gluconate 10 ml intravenous slowly followed by oral calcium and
vitamin D supplement.
 Hypothyroidism It can occur after bilateral thyroid surgery. Monitoring is done with thyroid function tests
and treatment is with thyroxine.

 Thyrotoxic Crisis It usually occurs if thyroid surgery is performed in a patient with uncontrolled
thyrotoxicosis. Patient presents with acute manifestations of thyroid over activity in form of high grade
fever, sweating, hypotension, tachycardia and prostration. Treatment is with intravenous fluids, cold
sponging, intravenous propranolol, steroids and neomercazole.
 Scarring and Keloid Formation It is especially seen in dark skin persons.
 Wound Infection It is seen rarely.
 Tracheomalacia Large goiter may cause prolonged tracheal compression leading to tracheomalacia. After
surgery, patient develops tracheal collapse and respiratory obstruction requiring tracheostomy

RETROSTERNAL GOITER

Usually arises from the lower pole of a nodular goiter.

Common in short neck individuals. Due to negative intrathoracic pressure, nodule gets drawn into the
superior mediastinum. Sometimes it may also be an ectopic thyroid.

20
Types 1. Substernal type: Part of the nodule is palpable in the lower neck.

2. Plunging goiter: An intrathoracic goiter is occasionally forced into the neck by increased intrathoracic
pressure.

3. Intrathoracic goiter itself.

Clinical Features

1. Dyspnea at night.

2. Cough and stridor (stridor is harsh sound on inspiration).

3. Dysphagia.

4. Engorgement of neck veins and superficial veins on the chest wall.

5. Pembertones‘ sign is positive. The patient is asked to raise the arm above the shoulder level. Dilated veins
are seen over neck and upper part of chest wall. Stridor and rarely dysphagia may occur. When patient raises
the arm above the shoulder level, retrosternal goiter compresses over the easily compressible structures like
SVC and trachea causing dilated veins and dyspnea respectively).

6. Dull note over the sternum on percussion.

7. Retrosternal goiter can be either nodular, toxic or malignant.

Differential Diagnosis Mediastinal tumor.

Investigations

• Chest X-ray shows soft tissue shadow under the sternum.

•I 123 study is diagnostic. • CT scan is useful.

Treatment

• Surgical removal of retrosternal thyroid is done. Commonly it can be removed through an incision in neck
(as blood supply of retrosternal goiter is from neck), but in case of large retrosternal extension or malignant
type median sternotomy is required.

• Radioiodine therapy is not accepted in retrosternal goiter.

21