1

DISORDERS OF THE THYROID GLAND

ANATOMY
A detailed knowledge of gross anatomy is mandatory for the surgeon who is to
operate on the thyroid gland.
The thyroid gland consists of right and left lobes connected by a narrow isthmus.
It is a very vascular organ, normally accounting for 5% of the cardiac output.
It is surrounded by a sheath derived from the pretracheal layer of deep fascia.
The sheath attaches the gland to the larynx and the trachea and so moves with
these structures on swallowing.
Each lobe is pear-shaped and the isthmus extends across the midline in front of
the 2nd,3rd and 4th tracheal rings.
Relations of the lobes
Antero-laterally
The sternothyroid muscles, superior belly of the omohyoid muscles, sternohyoid
and the anterior border of the sternocleidomastoid muscles.
Postero-laterally
The carotid sheath with the common carotid artery, internal jugular vein and
vagus nerve.
Medially
The larynx, trachea, the pharynx and oesophagus.
In the groove between the oesophagus and the trachea is the recurrent laryngeal
nerve which must be preserved during thyroid surgery.
The rounded posterior border of each lobe is related posteriorly to the superior
and inferior parathyroid glands.
Blood supply
Arterial supply
The superior thyroid artery, which is the first branch of the external carotid
artery, supplies the superior pole of the thyroid.
The inferior thyroid artery, which arises from the thyrocervical trunk as a branch
of the subclavian artery, supplies the lower pole of the gland.
A thyoidea ima artery occasionally arises from the aortic arch and connects to
the thyroid isthmus inferiorly.
Venous drainage
The superior thyroid and middle thyroid veins drain into the internal jugular
vein.
The inferior thyroid veins drain into the internal jugular vein or into the
innominate vein.
Innervation of the thyroid gland
The recurrent laryngeal nerve runs in the tracheooesophageal groove in intimate
relationship to the posteromedial aspect of the thyroid gland.
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On the right, the nerve recurs around the subclavian artery and runs an oblique
course from the lateral to medial, crossing the inferior thyroid artery before
entering the tracheooesophageal groove.
On the left, the nerve recurs around the aortic arch in the mediastinum and runs a
course parallel to the tracheooesophageal groove throughout its course in the
neck.
Injury to the recurrent laryngeal nerve most commonly occurs where the nerve
crosses the inferior thyroid artery or where it penetates the cricothyroid
membrane but injury can occur anywhere along its course.
Superior laryngeal nerve
The nerve is intimately intertwined with the branches of the superior thyroid
artery. The superior laryngeal nerve can be injured during mobilization of the
upper pole especially when the lobe is enlarged.
Injury results in voice weakness and can be avoided by ligation of the branches
of the superior thyroid artery at their junction with the gland rather than along
the course of the artery in the neck.
Development of the thyroid gland
The thyroid gland develops from the thyroglossal duct. As development
continues the duct elongates and its distal end becomes bilobed. The duct
becomes a solid cord and migrates down the neck. By the seventh week it
reaches its final position in relation to the larynx and trachea. Meanwhile, the
solid cord connecting the thyroid gland to the tongue breaks up and disappears.
The site of origin of the thyroglossal duct on the tongue remains as a pit called
the foramen cecum.

Normal thyroid function

The follicular cells produce the thyroid hormones T3 and T4.
Iodine and tyrosine combine to form T3 and T4.Both of these homones bind with
thyroglobulin and are stored on the gland until released onto the bloodstream.
Release is under the control of TSH from the pituitary and TRH (thyrotropin
releasing hormone) from the hypothalamus.
A feed-back mechanism regulating T3, T4 release is related to the level of
circulating T3 and T4.
Hormonal action
The thyroid hormones activate energy-producing respiratory processes, resulting
in an increase in the metabolic rate and an increase in oxygen consumption.
Increased glycogenolysis results in a rise in blood sugar.
The thyroid hormones also enhance metabolic, circulatory and somatic neuro-
muscular actions of catecholamines.
The result is:
-an increase in the pulse rate, cardiac output and blood flow
-nervousness,irritability, muscular tremour and muscle wasting can also occur
-these effects can be blocked by the use of beta-blockers such as propanolol.
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The parafollicular or C cells produce thyrocalcitonin. The principal physiologic

effect of thyrocalcitonin is to lower serum calcium and phosphate concentrations
through the inhibition of osteoclastic activity with a rersulting reduction in both
bone resorption and the release of calcium and phosphate into the extracellular
fluid. In the kidney, thyrocalcitonin accelerates calcium, phosphate and sodium
excretion.

CONGENITAL ANOMALIES

1. Agenesis of the thyroid gland may occur and is the commonest cause of
cretinism. Cretimism is arrested physical and mental development due to
congenital lack of thyroid secretion.

2. Incomplete descent of the thyroid gland may occur and the thyroid may be
found at any point between the base of the tongue and the trachea.
Lingual thyroid is the commonest form of incomplete descent.
It may be the only functioning thyroid tissue in the individual.

3. A thyroglossal duct may appear in childhood or young adults. It is due to a

persistence of a segment of the thyroglossal duct. The cyst occurs in the midline
of the neck at any point along the thyroglossal tract.

METHODS OF INVESTIGATION IN THYROID GLAND DISORDERS

Clinical investigation
Biochemical
Radiochemical
Ultrasonography
Biopsy
Immunological
Clinical investigation
Assessment of thyroid function by a careful history and observation of clinical
signs is still of fundamental importance.
A patient with thyroid disorder may be from functional point of vue:
hypothyroid, euthyroid or hyperthyroid.
Symptoms and signs of hypothyroidism
Symptoms Description
1. Diminished sweating
2. Dry skin
3. Cold intolerance Preference for a warm room, extraclothing
4. Weight increase Tightness of clothing
5. Constipation Use of laxative
6. Hoarseness
7. Parasthesia Numbness, tingling in hands
8. Deafness Progressive impairement of hearing
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Signs
1. Slow movements
2. Coarse skin
3. Cold skin
4. Periorbital puffiness
5. Slow pulse rate
6. Slowing of ankle jerk
Observe patient removing a buttoned
garment
Examine hands, forearms, elbows for roughness
Should obscure curve of malar bone
Under 75/min.
Elicit with patient kneeling a chair, grasping its
back.

Symptoms and signs of hyperthyroidism

Symptoms Description
1. Dyspnea on effort Age of patient
2. Palpitation Occuring at rest or on moderate exertion
3. Tiredness Unusual tiredness after physical effort
4. Preference for cold Habit of sitting away from fire
5. Sweating Both thermal and emotional sweating
6. Nervousness Irritability, ”tenseness”easy loss of temper
7. Weight Decrease in weight.
8. Appetite Increased appetite
Signs
1. Palpable thyroid Should be visible and palpable
2. Thyroid bruit High-pitched systolic bruit
3. Exophtalmos Sclera seen between upper lid and iris
4. Lid lag Sclera appears when patient’s eyes moving from
above downwards fixed on examiner’s finger.
5. Hyperkinesis Rapid jerky movements
6. Finger tremor Fine tremor of outstretched hands with eyes
closed.
7. Hands Hot and moist
8. Pulse rate More than 90/min. or atrial fibrillation.

Biochemical investigation
Thyroid hormones
Measurement of thyroid hormones in the serum allows precise assessment of
thyroid status to confirm the clinical diagnosis or clarify a difficult diagnostic
problem.
The thyroid hormones, T3 and T4 are stored in thyroid colloid bound to
thyroglobulin.
In the circulation the thyroid hormones are bound to thyroxine-binding
globulin (TBG), thyroxine-binding pre-albumin (TBPA) and albumin.
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The metabolic effects of the thyroid hormones are due to unbound free T4 and
T3 which is below 1% of the total circulating hormones. Because almost all T4
and T3 is protein bound, measurement of total hormones is influenced by
conditions which change the serum levels of binding proteins.
Elevated levels are seen in pregnancy and in women taking oral contraceptives
and low levels in the nephrotic syndrome.
Radioimmunoassays for free T4 and T3 are now readily available and give a
precise assessment of thyroid function. T3 is the more active hormone with 80%
being produced in the periphery from T4.
TSH can also be measured, raised TSH levels are seen in primary
hypothyroidism (autoimmune thyroiditis) and after treatment of thyrotoxicosis
by surgery or radioiodine.
Reduced TSH levels occur in hyperthyroidism.
Radiochemical investigation
Radioisotopes of iodine make possible dynamic thyroid function studies.

Radioiodine uptake
The rate of incorporation of radioiodine into the thyroid after injection can yield
a lot of information about the function of the gland.
Measurement of the 4 and 24 hours uptake of an administered dose of
radioactive iodine123 is useful in the assessment of thyrotoxicosis, when
increase uptake is seen.

Thyroid isotope scanning

The thyroid gland can be scanned either with iodine 123 or technetium
99, classifying nodules into those that are non-functioning “cold”, normally
functioning ”warm” and hyperfunctioning “hot”.
Although the finding of a “hot” nodule is usually consistent with benign
pathology, more than 80% of nodules are cold and only 20% of these will be
malignant.

Isotope scanning identifies patients with metastatic thyroid tumours and aids
localisation of ectopic thyroid tissue.

Ultrasonography
Ultrasonographic scanning is of great vallue in determining something of the
nature of swellings within the thyroid, especially those that are “cold” on isotope
scanning.
This technique is capable of identifying impalpable nodules, will discriminate
cystic from solid lesions but cannot distinguish benign from malignant
disease. Cystic nodules constitute 25% of all thyroid nodules and when 4 cm or
more in diameter may have a malignancy rate of 20%.
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CT scanning and MRI

These techniques have an increasingly important role in the assessment of
thyroid disease particularly in the evaluation of retrosternal goitres and glands
producing significant pressure effects and distorsion of adjacent structures.

Biopsy
This technique is a most valuable complement to clinical examination
Particularly in the assessment of thyroid nodular disease.
There are two quite distinct types of needle biopsy.
1. Cutting needle biopsy
This method produces a core of tissue suitable for histological examination.
It has high diagnostic accuracy but is a painful procedure and may cause
hematoma, tracheal puncture and recurrent laryngeal nerve damage.
2. Fine needle aspiration cytology (FNAC)
This technique employs a fine needle to obtain a thyroid sample suitable
for cytological assessment.
It is now, universally accepted as being a highly accurate, cost-effective method
with low morbidity and good patient compliance. The method can accurately
diagnose: colloid nodules, thyroiditis, papillary carcinoma, medullary carcinoma,
anaplastic carcinoma and lymphoma.
Its major limitation is its inability to distinguish benign from malignant follicular
neoplasms, this distinction being dependent on histological criteria of capsular
and vascular invasion.

Immunological investigation
Autoimmune thyroiditis of which Hashimoto’s disease is the most severe form,
can be inferred by demonstrating antibodies to thyroglobulin. Techniques for
demonstration of the thyroid autoantibodies are of importance in research but not
generally available for diagnostic purposes.

DISORDERS OF THE THYROID STRUCTURE

GOITRE
The term goitre refers only to visible or palpable enlargement of the thyroid and
infers no particular alteration in thyroid function.
It takes three varieties:
1. Physiological goitre
Physiological goitre is the term applied to thyroid enlargement seen commonly
in girls at the menstrual cycle or in women during pregnancy. The cause is
unknown and normally the goitre regresses in time.
No treatment is required though the patient and her family will require
reassurance.
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2. Endemic goitre
Goitre was once endemic in certain geographical areas where diet is deficient in
iodine. The problem can be eliminated by the iodization of salt and remains a
significant problem only in those areas where this public health measure cannot
be applied.
Goitres may reach enormous size and complications may be seen as a
consequence of the size of the gland alone, from metabolic consequences such as
thyrotoxicosis or malignancy.
3. Sporadic goitre
Goitre may occur sporadically in non-goitrous regions and in the absence of
iodine deficiency.
The cause is uncertain, some are autoimmune in nature.
Such patients are more prone to develop secondary thyrotoxicosis and to have a
higher risk of thyroid cancer.
Surgery is reserved for pressure symptoms, thyrotoxicosis, development of an
thyroid cancer and cosmetic reasons.

The term goitre, derived from the Latin guttur, meaning throat, is used as a non-
specific term to indicate enlargement of the thyroid gland.

Classification of goitre
1. Simple goitre (endemic or sporadic)- diffuse hyperplastic goitre
- nodular goitre

2. Toxic goitre - diffuse (Graves’disease)

- toxic multinodular goitre
- toxic solitary nodule

3. Neoplastic goitre - benign

- malignant
4. Thyroiditis - subacute (granulomatous)
( de Quervain’s)
- autoimmune (Hashimoto’s)
- Riedel’s- invasive fibrous thyroiditis
- acute suppurative
5. Miscellaneous - chronic infections: TB, syphilis
- actinomycosis
- amyloidosis

Simple goitre
Simple goitre is the result of TSH stimulation, usually secondary to
inadequate levels of circulating thyroid hormones.
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TSH stimulation causes diffuse hyperplasia of the thyroid and an elevation in

hormone output.
Iodine deficiency is a key factor in simple endemic goitre,associated with a low
iodine content of water and food. The minimum daily requirements of iodine are
of 50-100 mg.
Endemic goitrous areas are in the mountainous regions such as the Alps, Andes,
and Hymalayas.
Iodine deficiency in its most extreme form is associated with cretinism,
congenital hypothyroidism and mental impairment.
The natural history of thyroid stimulation by TSH is such that there are
fluctuating levels of stimulation but eventually active and inactive lobules co-
exist. At this stage nodules form throughout the thyroid; there are changes of
hyperplasia, cystic degeneration, hemorrhage, colloid-filled follicles, fibrosis and
later calcification.
All types of goitre occur more often in women.
Prevention and treatment of simple goitre
Prevention of the development of simple endemic goitre can be achieved by
addition of iodine to table salt.
At the prenodular stage a hyperplastic goitre can be made to regress in size by
giving thyroxine 0,1-0,15 mg. daily often continuing for several years.
Thyroidectomy may be indicated for pressure effects, thyrotoxicosis,
development of a thyroid cancer.

THYROID NODULES
Thyroid nodules are common, being a feature of many different thyroid disease.
Although the vast majority of thyroid nodules are benign and include colloid
lesions, follicular adenomas, nodular thyroiditis and degenerative cysts, the
essential clinical problem, particularly when the lesion is solitary, remains the
distinction between benign and malignant disease.
Clinical assessment and diagnosis
1. Most thyroid nodules are asymptomatic but the acute development of a painful
swelling in the thyroid usually suggests hemorrhage into a pre-existing colloid
nodule. This is an important condition to recognise as spontaneous resolution,
sometimes aided by aspiration, will occur in a few weeks without any action.
2. Rapid growth of an existing nodule with discomfort radiating into the face or
jaw may be due to malignancy. A malignant nodule, however, may grow slowly
over many years before a diagnosis is made.
Thyroid nodules also occur more often in women but a solitary nodule in a male
carries a greater risk of malignancy.
In the elderly, a rapid growing firm painful lesion is likely to be an anaplastic
carcinoma.
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Irradiation increases the incidence of benign thyroid nodules but the reported
risk of malignancy in a palpable nodule found in a previously irradiated thyroid
ranges from 20-50%. High dose external irradiation to the neck for conditions
such as Hodgkin’s lymphoma may also increase the risk of thyroid malignancy.
The latent period for developing post-irradiation tumours ranges from 6 to 35
years.
3. A preliminary clinical examination of the patient is directed towards
assessment of thyroid status, although most patients with a solitary thyroid
nodule are euthyroid.
4. A nodule in a hyperthyroid patient is highly unlikely to be malignant.
5. A hard fixed nodule is likely to be malignant but it is not uncommon for
papillary lesions to be cystic and follicular lesions to be soft as a result of
hemorrhage.
6. A very hard lesion may be an entirely benign calcified colloid nodule.
7. Lymphadenopathy in the paratracheal groups or in the lateral deep cervical
region is a common finding in papillary and medulary carcinomas.
8. Although voice change and hoarseness may be non-specific, a proven
recurrent laryngeal nerve palsy on the side of a palpable thyroid nodule is likely
to indicate malignant infiltration.
Rarely direct pressure from a benign lesion produces vocal cord paralysis.
Although the presence of pressure symptoms, tracheal deviation or retrosternal
extension will not aid the distinction of malignant from benign lesions these
features will be considerations in the selection of patients for surgery.
9. The thyroid status will be confirmed by measurement of T4 and TSH.
Radiograph of the neck and CXR- delineate retrosternal extension or airway
distortion.
10. Isotope scanning-may reveal if the nodule is cold, warm or hot.
11. Ultrasonography of the thyroid gland may add some informations about the
structure .
12. Needle biopsy and aspiration cytology-this highly accurate and cost-effective
technique is the method of choice for precisely diagnosing most patients with
thyroid nodular disease.

Surgical treatment for thyroid nodules

The minimum surgical procedure for adequate treatment of the solitary thyroid
nodule is a unilateral lobectomy with removal of the isthmus and pyramidal lobe.
This is a safe operation with minimal risk of damaging either the parathyroids or
the recurrent laryngeal nerve.
Frozen section histology can be used to confirm the preoperative diagnosis and
aid decision making particularly with respect to benign pathology where
lobectomy alone will be sufficient.
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THYROID CYSTS
Confirmation of the diagnosis of a thyroid cyst is usually made by fine needle
aspiration and this simple technique can be both diagnostic and therapeutic.
If a cyst refills it is appropriate to reaspirate but after two or three such
manoevres surgery is likely to be indicated.
A large cyst (greater than 4 cm. in diameter), a significantly blood-stained
aspirate, cytological findings of neoplasia or a previous history of irradiation are
all indications for surgery.

MULTINODULAR DISEASE
The usual indications for surgery are cosmetic or pressure effects, a dominant
nodule increasing in size or showing cytological features which raises the
possibility of malignancy, thyrotoxicosis or retrosternal extension.
The surgical procedure will be tailored to the situation found at surgery,
frequently a bilateral subtotal thyroidectomy is appropriate.
Total thyroidectomy is indicated when the multinodularity is both bilateral and
extensive often with no normal thyroid tissue to be left as a remnant.

RETROSTERNAL GOITRE
Asymptomatic- found as a coincidental observation on a chest radiograph.
Symptomatic- pressure symptoms- dyspnea
- dysphagia
- hoarseness of voice
- SVC compression syndrome
- thyrotoxicosis
Diagnosis is made on CXR, CT or MRI
Treatment-surgery-to remove the risk of progressive airway obstruction resulting
from growth of the gland or from hemorrhage into a benign colloid lesion.

Scheme of Management for Thyroid Nodules

Solitary Thyroid Nodule
1. Hyperthyroid- FNAC and I 131 scan
- greater than 3 cm-surgery
- less than 3 cm- I 131 therapy
2. Euthyroid- FNAC
- benign- no pressure symptoms- observe, repeat FNAC in 6 months, discharge if
benign again.
- benign with pressure symptoms- tracheal deviation, increasing size-surgery
- thyroiditis- T4 treatment
- suspicious- surgery
- malignant- surgery
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- inadequate FNAC- repeat FNAC

- cystic- bening- observe,review in 6 weeks- no recurrence-discharge
- recurrence- repeat FNAC, review in 6 months.
- malignant- surgery

Scheme of Management for Multinodular Goitre

1. Hyperthyroid- I scan- large gland- antithyroid drugs and surgery
- small gland- I therapy
2. Euthyroid- no dominant nodule, no pressure symptoms-observe, discharge
- dominant nodule- FNAC- benign, no symptoms-observe
- malignant- surgery
- suspicious- surgery
- inadequate- repeat FNAC
- retrosternal- surgery
- cosmetic- surgery

Study questions

1. What are the anatomical structures in close proximity of the thyroid gland
which must be preserved during thyroid surgery?
2. At which level the recurrent laryngeal nerve might be injured ?
3. A 32 year old lady complains of palpitation, sweating, nervousness. On
physical examination the thyroid is palpable, diffusely enlarged, pulse rate
of 110/min.regular. What diagnosis would you make on clinical grounds?
4. What investigations would you ask to confirm your clinical diagnosis?
5. What investigation is the most important in a thyroid solitary nodule?

DISORDERS OF THYROID FUNCTION

HYPERTHYROIDISM
Hyperthyroidism is a condition in which there are increased levels of thyroid
hormones in the blood and one for which surgical correction is frequently
appropriate.
Causes of thyrotoxicosis
Common causes: - diffuse toxic goitre (Graves’s disease)
- toxic multinodular goitre (Plummer’s disease)
- toxic solitary nodule
- nodular goitre with hyperthyroidism due to exogenous
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iodine.
- exogenous thyroid hormone excess
- thyroiditis
Rare causes: - metastatic thyroid carcinoma
- pituitary tumour secreting TSH

Graves’s disease
It is the most common cause of hyperthyroidism, it is an immunological disorder
in which thyroid stimulating antibodies of the Ig.G type bind to the TSH receptor
and stimulate the thyroid cell to produce and secrete an excess of thyroid
hormones.
The thyroid gland hypertrophies producing diffuse enlargement.
Most of the symptoms and signs of thyrotoxicosis result from excess thyroid
hormones, stimulating metabolism, heat production and oxygen consumption.
It is especially common in young women between 20 and 40 years of age.
Ophthalmopathy has two major components:
1- non infiltrating ophthalmopathy resulting from sympathetic activity leading to
upper lid retraction, a stare and infrequent blinking.
2- infiltrative ophthalmopathy causing oedema of the orbital contents, lids and
periorbital tissues, cellular infiltration and deposition of mucopolysaccharide
material within the orbit.
Diplopia results from weakening and paralysis of the external ocular muscles.
The cornea is vulnerable to damage and ulceration may occur.
Investigations:
- measurement of free T4, T3, TSH will confirm the diagnosis.
- a radioactive iodine or technetium scan is not essential in patients with

Graves’s disease although it is necessary in the assessment of toxic solitary and

multinodular goitre to determine the site of nodular overactivity.
- radioactive iodine uptake studies are particularly appropriate revealing an
increased uptake.

Treatment
In Graves’s disease three treatment modalities can be used either alone or in
combination to restore the euthyroid state:
- antithyroid drugs
- radioactive iodine
- surgery

Antithyroid drugs
These drugs interfere with the thyroid hormones synthesis.
Medical treatment with antithyroid drugs has two principal roles:
- treatment of newly diagnosed patients with Graves’disease in the hope of
inducing a permanent remission
- to render the toxic patient euthyroid in preparation for surgery.
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Beta-adrenergic blockers
Many of the manifestations of hyperthyroidism, particularly those relating to the
cardiovascular system, can be ameliorated by the administration of beta-blockers
such as metoprolol.
Beta-blockers are usually used in combination with one of antithyroid drugs in
patients who are severely toxic and in those patients being prepared for surgery.

Radioactive iodine
I 131 used to control thyrotoxicosis achieves its effect by destruction of
overactive thyroid tissue.
There would appear to be no adverse effects of I 131 treatment with respect to
leukemia, thyroid carcinoma, fetal damage or genetic mutation.
An ablative dose will render more than 60% of patients hypothyroid in one year.
Regular long-term surveiilance is required and thyroxine replacement given as
necessary.

Surgery
Thyroidectomy in patients with Graves’s disease is safe and rapidly renders the
patient euthyroid. The principal indications for surgery are:
- relapse after an adequate course of antithyroid drugs
- severe thyrotoxicosis with a large goitre
- difficulty in controlling toxicity with antithyroid drugs
The surgical procedure: bilateral subtotal thyroidectomy leaving about 4 g.
posterior remnant of thyroid tissue on each side of the trachea or total
thyroidectomy.

Toxic multinodular goitre

Antithyroid drugs are of no value as a long-term treatment because thyrotoxicity
is due to autonomy and will recur once any medication is discontinued.
I 131 can be used for small goitres but usually a subtotal thyroidectomy is most
appropriate after achievement of the euthyroid state or total thyroidectomy.

Toxic solitary nodule

This condition caused by a single autonomous thyroid can be treated by either a
unilateral thyroid lobectomy or I 131.
Follow-up
Because of the risk of developing postoperative hypothyroidism patients who
have undergone any form of treatment for hyperthyroidism must be followed on
a long-term basis with regular clinical and biochemical assessment.
Preparation for surgery
Classically the patient comes to surgery in the euthyroid state, controlled by a
period of antithyroid drug therapy. Because the antithyroid drugs block the
synthesis of thyroxine but do not inhibit the release of the hormone from existing
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colloid stores the time required for symptomatic improvement may vary
widely from two weeks to as long as three months.
There has been a lot of interest in carrying out the operation of thyroidectomy for
thyrotoxicosis in patients prepared for operation by beta-adrenergic blockade
with metoprolol. When the patient has become euthyroid, iodine given as
Lugol’s solution is administered for ten days before surgery for the good reason
to induce a firmity of the gland and reduce the hemorrhagic risk at operation.
The operation is often made easier by avoidance of antithyroid drugs which are
to a degree goitrogenic. Beta-blockers may be reduced after surgery and
discontinued by 7 days after operation.

Postoperative complications

1. Postoperative bleeding
There is always a risk of postoperative bleeding after thyroid surgery.
It is rare but sometimes dramatic and fatal. The bleeding may occur in one of
two sites:
- deep to the myofascial layer in relation to the thyroid remnant or vessels.
Evacuation must be done quickly but it will usually be possible to do this under
general anesthesia in the operating theatre.
- bleeding deep to the skin flaps is the more common and usually arises from
veins. Bleeding is slow but a substantial hematoma may develop and produce
pressure on the airway. Evacuation is mandatory. If hematoma is seen within 12
hours of operation it should probably be evacuated to prevent respiratory
embarrassment developing. Little is to be gained by observation.

2. Postoperative thyrotoxic crisis

Thyrotoxic crisis is a serious complication but it should not be seen where there
has been adequate preoperative preparation.
It occurs within the first 24 hours of thyroidectomy with the patient becoming
confused and hyperactive with a high temperature, profuse sweating and rapid
heart rate.
Treatment must be vigorous with beta-adrenergic blockade, intravenous
hydrocortisone and iodine.

3. Postoperative voice changes

Rarely are voice changes due to any damage to recurrent laryngeal nerves since
this occur in less than 1% of cases when thyroidectomy is carried out by
experienced thyroid surgeons.
Damage to the recurrent laryngeal nerve which may run between the bifurcation
of the inferior thyroid artery as it enters the gland.
Probably minor changes in the muscles around the cricoid and thyroid cartilages
are the most important and it is to some extent, inevitable that there will be some
changes with the mobilization of the gland.
 15
Trauma to the external laryngeal nerve supplying the cricothyroid muscle can
lead to voice changes because of difficulty in achieving vocal cord tension if the
muscle is paralysed.
Damage to the internal laryngeal nerve is also serious and can occur where there
is difficulty in mobilizing the superior pole. This leads to desensitization of the
appropriate side of the larynx and spilling over, especially of liquids, during
swallowing.

4. Hypoparathyroidism
The commonly encountered hypocalcemia of the first few days after
thyroidectomy probably has little to do with hypoparathyroidism and is more
likely to be a consequence of the metabolic changes taking place with re-entry of
calcium into bone demineralized by hyperthyroidism (“hungry bones”).
The operation of thyroidectomy is designed to leave a large amount of thyroid
capsule and with it the parathyroids.
However, parathyroids are very small and are not always easy to identify at
thyroidectomy. The incidence of hypoparathyroidism after surgery for
thyrotoxicosis should be less than 1%.

5. Hypothyroidism
All forms of treatment for thyrotoxicosis will produce a population of patients
prone to develop hypothyroidism, greatest after radioiodine therapy but seen
after all forms of treatment.

MALIGNANT DISEASE OF THE THYROID GLAND

Primary malignancies of the thyroid can be classified according to the element

from which they arise:

Tumours of thyroid follicular epithelium

1- papillary carcinoma
2- follicular carcinoma
3- anaplastic carcinoma
Tumours of parafollicular cells
1- medullary carcinoma
Tumour of lymphoid element
1- lymphoma

Papillary carcinoma
This is the commonest thyroid tumour which shows an increased incidence in
iodine-rich areas and usually affects children and young adults. Previous neck
irradiation particularly in the young may predispose to thyroid cancer.
Pathology
 16
This tumour which has a propensity for lymphatic spread both within the
thyroid and to the paratracheal and cervical lymph nodes is usually a hard
whitish lesion infiltrating the thyroid gland and presents as a thyroid nodule.
The lesion is frequently multifocal, rarely encapsulated and blood-borne spread
is usually a late feature.
These tumours can be divided into three main types based on their size and
extent: - minimal- these are lesions 1 cm. or less in size, usually not clinically
obvious. They readily metastasise to regional lymph nodes.
- intrathyroidal- these lesions are larger than minimal tumours, have a less
favourable prognosis, are situated totally within the thyroid.
- extrathyroidal- this a locally advanced condition extending through the
thyroid capsule often involving adjacent structures as the trachea, oesophagus
and recurrent laryngeal nerve.
Clinical presentation
The commonest presentation of papillary carcinoma is a thyroid nodule
frequently associated with enlarged cervical lymph nodes.
Involvement of the adjacent structures by a locally invasive tumour may cause
hoarseness of the voice due to recurrent laryngeal nerve palsy, airway symptoms
because of tracheal involvement and dysphagia as a result of esophageal
invasion.
Less than 1% of patients at the time of initial presentation will show features of
distant metastases.
Diagnosis is based on a combination of careful clinical assessment and fine
needle aspiration cytology.

Follicular carcinoma
This tumour, less common than papillary carcinoma, has a higher incidence in
iodine-deficient areas due to chronic TSH stimulation and can also be caused by
previous irradiation.

The disease has a female to male ratio of 3:1, affects an older age group (mean
age 50 years) than papillary carcinoma.
Pathology
Follicular carcinoma is invariably encapsulated, solitary, readily exhibiting
vascular invasion and spread via the bloodstream.
Follicular carcinoma is classified into two types according to histopathological
features:- minimally invasive- histology demonstrates only slight capsular or
vascular invasion
- frankly invasive- histology demonstrates venous extension particularly
into the middle thyroid and internal jugular veins.
Clinical features
Follicular thyroid cancer presents as a discrete solitary thyroid nodule increasing
in size. Although many tumours are firm a follicular carcinoma is often soft
because of hemorrhagy within the lesion.
 17
Metastatic disease may already be present at the time of diagnosis with bone
and lung involvement.
Diagnosis
Unlike papillary thyroid carcinoma, follicular carcinoma cannot be diagnosed
precisely by FNAC. The cytology report will describe a follicular tumour,
usually showing a microfollicular pattern, the majority of such lesions being
entirely benign.
Only 20% of these will be subsequently identified as follicular carcinoma.
Treatment of differentiated thyroid cancer
There is general agreement that thyroidectomy is the treatment of choice.
The treatment objectives are:
- to eradicate primary tumour
- reduce the incidence of distant or local recurrence.
Total thyroidectomy has been advocated because of its ability to treat multifocal
tumour, decrease local and distal recurrence.
In the case of papillary carcinoma there is a high incidence of multifocality
which clearly would not be treated by a unilateral or even near total
thyroidectomy.
Retrospective studies of thyroidectomy for papillary tumours have demonstrated
a reduced local recurrence rate when total thyroidectomy was performed
compared with a subtotal resection.
Thyroidectomy must always include clearance of pretracheal and paratracheal
lymph nodes.

A unilateral lobectomy and isthmusectomy is adequate for minimal (less than 1

cm.) lesions.

Follicular tumours if minimal lesion then a unilateral lobectomy is all that is

required.
An invasive follicular tumour requires a total thyroidectomy.

Lymph node dissection is not routinely performed for follicular tumours. A

decision to proceed to a total thyroidectomy can often be made at the time of
surgery on the basis of the macroscopic appearance of the lesion and especially
when the tumour size is in excess of 4 cm.

Postoperative treatment
Thyroxine
Any patient who has undergone total thyroidectomy will require replacement
treatment with thyroxine.

Thyroglobulin measurement
It is a sensitive indicator of residual or recurrent differentiated thyroid cancer
when a total thyroidectomy has been performed and the patient is on full
replacement thyroxine dosage.
 18
This measurement is now performed routinely and has markedly reduced the
need for routine serial radioactive iodine scanning.
Radioactive iodine
Radioactive iodine is a most useful means of detecting metastatic disease when
total thyroidectomy has been performed for differentiated cancer.
Postoperatively, patients are initially placed on T3 and sent home to await an I
131 scan six weeks later.
T3 is discontinued two weeks before the scan to allow a rise in TSH level before
administering 2-5mCi of I 131.
If there are no metastases and the total thyroidectomy has been succesful the
uptake at 24h.should be less than 1%.
When there is significant uptake in the thyroid bed this can be ablated with
radioiodine and many metastatic disease subsequently treated with a therapeutic
dose of 150-200mCi I 131.
The maximum cumulative dose of I 131 should be no greater than 800-1000mCi.

Anaplastic carcinoma
This highly aggressive tumour usually affects the elderly with a peak incidence
between 60 and 70 years of age.
The tumour has a higher incidence in areas of endemic goitre. The tumour
rapidly infiltrates local structures and metastases via the bloodstream and
lymphatics.

The frequent finding of foci of papillary or follicular carcinoma in anaplastic

tumours suggests that this disease originates in an unrecognised or untreated
differentiated tumour.

The clinical findings are typically those of an elderly female often with a long
history of goitre that suddenly starts to grow rapidly with hoarseness, dysphonia,
dysphagia and a compromised airway.
Confirmation of clinical diagnosis may be obtained by FNAC, the aspirate
showing bizzare giant cells, multinucleated cells.

Resection of the thyroid is rarely possible because of the local extent of disease.
Incision biopsy for diagnostic purposes should be avoided for fear of infiltrating
an uncontrollable local spread of the disease.
If surgery is possible it should relieve an obstructed airway by excision of the
of the isthmus.
Radiotherapy and doxorubicin are the main modalities of treatment but
invariably the tumour rapidly progresses usually leading to death of the patient
within six months.
 19

Medullary carcinoma
This is a tumour which arises from the C-cells, derived from neural ectoderm,
and accounts for approximately 8% of malignant thyroid tumours.
This is a solid non-follicular carcinoma that arises from the parafollicular C-cells
which secretes calcitonin, a peptide capable of lowering the blood calcium and
amenable to measurement by radioimmunoassay.
Pathology
Medullary carcinoma is a solid tumour located in the upper two thirds of the
thyroid and is usually both multicentric and bilateral.
The tumour grows locally but readily spreads by lymphatics to regional nodes
and via the bloodstream to distant sites such as liver, lungs, bones.
This tumour produces and secretes calcitonin, a most valuable histochemical
marker for medullary carcinoma. Carcinoembryonic antigen (CEA) is another
tumour marker.
Clinical features
The disease tipically presents as a mass in the neck often with enlarged cervical
and mediastinal lymph nodes.
Involvement of adjacent organs and the recurrent laryngeal nerve may cause
respiratory or swallowing difficulties and voice changes.
Sporadic disease has a peak incidence at 40-50 years of age whereas inherited
familial disease is usually seen at a younger age.
Diarrhea is often a prominent clinical feature but the ability of this tumour to
secrete a range of hormones and peptides including calcitonin, prostaglandins, 5-
hydroxytryptamine and ACTH can give rise to a range of clinical syndromes
which may include Cushing’s syndrome.

Diagnosis
Clinical assessment and the taking of a careful family history are fundamental to
establishing a precise diagnosis and confirmation is obtained by FNAC and
measurement of serum calcitonin.

Because of the close association of phaeochromocytoma and MC in the MEN

familial forms measurement of urinary VMA and metanephrines should be
carried out in all patients with MC before progressing to any invasive measures
such as surgery.
Treatment
Total thyroidectomy is the appropriate procedure to adequately treat multicentric
and bilateral disease.
The central and paratracheal lymph nodes are cleared from the level of the
thyroid cartilage to the upper mediastinum.
The lateral nodes in the carotid sheath are sampled and if involved with tumour a
modified radical node dissection is performed preserving the internal jugular
vein, sternomastoid muscle and spinal accessory nerve.
 20
Even when the primary tumour is extensive the recurrent laryngeal nerve can
usually be preserved. Because of the multifocal nature of hereditary tumours a
bilateral lymph node clearance is advised.
Prognosis
The presence or absence of distant metastases and lymph node positivity are
major factors in determining the ultimate prognosis.
When lymph node metastases are present this survival rate is reduced to 45% at
10-years suevival.
Follow-up
After surgery regular clinical and biochemical follow-up is carried out with
measurement of the two tumour markers calcitonin and carcinoembryonic
antigen (CEA).
When raised levels of these agents persist after thyroidectomy or develop at a
later stage this may signify persistent and recurrent disease.
Ultrasonography, CT, MRI and scanning with other isotopes such as
dimercaptosuccinic acid (DMSA) and meta-iodobenzyl guanidine (MIBG) can
be utilised to detect this disease.
For recurrence, external irradiation can occasionally produce some benefit but
chemotherapy with doxorubicin is both toxic and disappointing.

THYROIDITIS

The thyroid gland may be subject to inflammatory change in a variety of

conditions, the process being either focal or diffuse and often associated with
thyroid dysfunction.

Subacute thyroiditis
This condition, often called granulomatous or de Quervain’s thyroiditis is
probably of viral origin.
It is characterised by painful swelling of one or both thyroid lobes with
associated malaise and fever.

Frequently there is a preceding history of sore throat or viral infection a week or

two before the onset of thyroid symptoms.
Approximately one third of patients are asymptomatic apart from enlargement of
the thyroid gland but 15% have a more acute illness with symptoms and signs of
hyperthyroidism.
Thyroid hormone levels are raised but in contrast to Graves’disease there is low
uptake of radioactive iodine on scintigraphy. The ESR is raised.
The disease process of subacute thyroiditis is usually self-limiting with
resolution of local symptoms and thyroid dysfunction.
A few patients, however, pass through a mild hypothyroid phase.
Local symptoms can be controlled with aspirin but if severe and prolonged a
course of steroids can be helpful.
The transient hyperthyroidism does not require treatment with antithyroid drugs.
 21

Autoimmune thyroiditis
This condition was described by Hashimoto and occurs as a diffuse process
throughout the thyroid gland which usually enlarges to several times normal size.
Although clasically the gland enlargement is diffuse there may be nodularity and
lobulation making distinction from simple multinodular goitre or even malignant
disease difficult.
Histologically there is infiltration of the thyroid by lymphocytes and plasma
cells, frequently secondary lymphoid nodules and adjacent stromal fibrosis.
The condition is due to an immunological disorder characterised by thyroid
antibodies in the serum.
A positive family history of other autoimmune disease such as pernicious
anaemia, gastritis, thyrotoxicosis is frequently obtained.
As a result of destructive changes within the infiltrated thyroid,hypothyroidism
usually ensues and when present requires treatment with thyroxine.
This medication supresses TSH and leads to shrinkage of the thyroid gland with
relief of any symptoms.
Surgery is not usually required since pressure symptoms and involvement of
adjacent structures occurs rarely.
Occasionally a satisfactory reduction in the size of the goitre can be achieved by
the administration of steroids.
When the thyroid, involved with autoimmune disease, is seen to rapidly enlarge
or develop a firm asymmetrical nodular area, exclusion of lymphoma by FNAC
or core biopsy is required.

Riedel’s thyroiditis
This condition,sometimes called invasive fibrous thyroiditis, is characterised by
a dense fibrous inflammatory infiltrate throughout the thyroid, sometimes
extending through the capsule to involve adjacent structures.
The condition is rare but is important because the clinical picture mimics thyroid
malignancy.
Needle biopsy is likely to be required to free a compromised airway.
Steroid medication has been tried without much success and recently there have
been reports of benefit from tamoxifen.

Acute suppurative thyroiditis

The thyroid can be infected by a variety of bacterial or fungal agents producing
clinical features of an acute painfully inflamed gland.
Confirmation of diagnosis and bacteriology is obtained by needle aspiration and
appropriate antibiotics administered.

DISORDERS OF THE PARATHYROID GLANDS

The parathyroid glands are important to surgeons for two reasons.

First, because surgeons treat patients with symptomatic hyperparathyroidism
they must know the cause and management of various hyperparathyroid
 22
conditions and second during operations in the neck, it is imperative that the
intergrity of the parathyroids be preserved to avoid permanent
hypoparathyroidism.
Ther is no satisfactory replacement for endogenously produced parathyroid
hormone and the patient with hypoparathyroidism is doomed to a lifelong
process of episodic, symptomatic hypocalcemia despite calcium and vit.D
therapy.

Anatomy
The superior parathyroid glands usually lie at the junction of the upper and
middle third of the thyroid gland on its posteromedial surface and in the
tracheooesophageal groove.
The inferior parathyroid glands lie close to the inferior poles of the thyroid
gland.
Sometimes they are found some distance caudal to the thyroid gland in
association with the inferior thyroid veins.

Parathyroid hormone (PTH)

PTH is a major regulator of calcium matabolism. It acts in conjunction with
calcitonin and activated vitamin D3 to regulate the plasma concentration of the
ionized form of calcium.

As serum calcium falls, the secretion of PTH increases.

As serum calcium rises, the secretion of PTH decreases.

PTH exerts its biologic effect on bone, intestine and kidney:

- it increases the mobilization of calcium and phosphate from bone.
- it acts synergistically with D3 to increase the absorbtion of calcium and
phosphorus from the gut.
- it promotes the active reabsorbtion of calcium in the distal nephron.
- it inhibits phosphate reabsorbtion in the proximal tubule.
Increased PTH secretion has the following clinical effects on bone, intestine and
kidney:
- hypercalcemia
- hypocalciuria initially due to increased calcium reabsorbtion, then in a chronic
state hypercalciuria
-hypophosphatemia
-hyperphosphaturia

Laboratory tests
Serum PTH levels can be measured by radioimmunoassay.

Hyperparathyroidism
Primary hyperparathyroidism
Incidence. It may occur sporadically but may occur as:
 23
- part of a multiple endocrine adenomatosis syndrome
- familial hyperparathyroidism
- ectopic tumour
Etiology and pathology
- 90% of primary HPT cases are due to a solitary adenoma of one of the four
glands.
- about 10% are due to four-gland hyperplasia
- parathyroid carcinoma accounts for 1% of primary hyperparathyroidism cases.
Clinical presentation
Most patients with primary HPT are asymptomatic.
When patients are symptomatic, the symptoms are:
-renal lithiasis
-osteitis fibrosa cystica
-psychiatic manifestations
-peptic ulcer disease, usually associated with hypergastrinemia that results from
hypercalcemia
-cholelithiasis or pancreatitis may occur.
-non-specific symptoms: weakness, easy fatigability, constipation, arthralgia.

Diagnosis
Lab. tests
An elevated serum calcium level is the cornerstone of diagnosis.
While primary HPT is a relatively common cause of hypercalcemia, other causes
must be excluded, such as metastatic bone disease, myeloma, sarcoidosis the use
of thiazide diuretics, thyrotoxicosis and Addison’s disease.
A serum PT hormone level is high, disproportionately.
In patients with metastatic bone disease,hypercalcemia occurs without a
disproportionate elevation of PH.
In patients with secondary HPT, the serum PTH level is high and the serum
calcium is low.
In patients with hypoparathyroidism the serum calcium and serum PTH are both
low.
The serum phosphorus level is decreased, hyperphosphaturia.

Radiographic studies
X-ray of the skull may show a “ ground-glass” appearance in the outer 2/3 of the
skull. Skull X-ray are also obtained to search for enlargement of the sella turcica
due to pituitary tumour.
X-rays of the proximal ends of the long bones may demonstrate bony
reabsorbtion.
Indications for surgery
Once the diagnosis of primary hyperparathyroidism is confirmed biochemically
patients should be selected for operation.
1. All symptomatic patients with biochemically proven HPT should be
considered for surgery.
 24
2. Operation is also advised for an asymptomatic patient whose serum calcium
levels exceed 11 mg/dl, especially if the patient has a decrease in bone density,
hypercalciuria or a decrease in renal function due to other diseases such as
hypertension or diabetes mellitus.
Methods of preoperative localization
- ultrasonography
- scanning of the neck after administering Thallium 201
- thyrocervical angiography by Seldinger technique
- CT and MRI
Surgical treatment
Solitary adenoma- removal of adenoma
Four-gland hyperplasia- two options:
- subtotal parathyroidectomy- 5% recurrence rate after it
- total parathyroidectomy with autotransplantation of minced parathyroid
tissue into a well vascularized accessible forearm muscle.

THYMUS

The thymus gland has right and left lobes closely bound together which may
overlap each other to some extent. It lies anteriorly in the superior mediastinum
and extends both superiorly into the neck in front of the left brachiocephalic vein
and also inferiorly into the anterior mediastinum where its lower poles are
closely related to the pericardium.

After puberty the thymus undergoes fatty degeneration to a varying extent.

It derives a blood supply from the internal thoracic arteries and the venous
drainage is into the left brachiocephalic vein.
The function of the thymus gland has been the subject of an enormous amount of
research over the last 20 years and has still not been completely clarified.
Some aspects of its function are of considerable relevance to surgeons.
The thymus, plays a vital role,particularly in childhood in determining the
immunological competence of the individual. The thymic cells influence other
lymphocytes, the B-cells to produce immunoglobulins in response to antigenic
stimulation. The lymphocytes are from the bone marrow initially and develop
into the two distinct populations, T-cells and B-cells.
T-cells develop develop their identity in the neonatal period after passing
through a thymic phase. The T-cells then migrate to colonize the T-cell area of
the lymph nodes and spleen.
T-cells have been identified: helper and suppressor, which influence the B-cell
accordingly. The normal ratio of helper and suppressor T-cells is 2:1, this ration
is reversed in the immunocompromised patient

Myasthenia gravis
Myasthenia gravis is an acquired autoimmune disorder which involves
autoimmune blockage of postsynaptic nicotinic cholinergic receptors. The
 25
disease is related to the production of an antibody which blocks the effect of
acetylcholine at the motor end-plate. The neuromuscular transmission is
compromised the clinical result being muscular weakness and fatigability.
The sourse of these autoantibodies is the abnormal thymus in the majority of
cases.
The pathological appearance of the thymic gland in the majority of myasthenics
shows some degree of hyperplasia of the lymphoid elements but 10-20% of
myasthenics are reported to have thymomas.
Affected patients experience weakness which worsens by exertion and improves
by rest.
Occular muscle involvement induces ptosis and diplopia, facial muscle
involvement induces loss of facial expression and jaw drop. Bulbar muscle
involvement induces nasal speech, choking on foods, dysphagia.
Abnormal fatigability of the limb muscles causes difficulty in combing hair,
lifting objects, climbing stairs, walking and running.

Diagnosis is based on the characteristic history of progressive weakness of the

voluntary muscles, on physical examination which shows no neurological
abnormality but impaired muscles strength and specific investigations.
Anticholinesterase tests with edrophoniu or neostigmine which shows
improvement of the muscle strength after injection.
Electromyography- supramaximal stimulation of a motor nerve results in a 10%
decrement of the amplitude of the evoked muscle action potential. In mysthenics
the decrement is more than 10%.
CT of the thorax may show enlarged thymic gland or a thymic tumour located in
anterior-superior mediastinum.
Thymectomy is an effective treatment for this disease in most patients.

Thymoma without myasthenia

The majority of such patients are asymptomatic.
When symptoms occur they are often non-specific: chest pain, cough and
occasionally breathlessness.
Chest X-rays and CT scan should document the lesion.
Any opacity suspected of being a thymoma should be surgically excised.
The contraindication is clear-cut evidence of invasion of the great vessels
demonstrated either by the presence of caval obstruction with a cavogram
supporting invasion rather than compression or by an arteriogram indicating
invasion of the aorta or its branches.
Radiochemotherapy is useful in inoperable patients or in postoperative
recurrence of a thymoma.
 26

Study questions

1. A 35 years-old lady, underweight in spite of her good appetite went to her

G.P. being concerned of sleeplessness, anxious state and palpitation. On physical
examination her G.P. revealed a BP of 15/8 cm Hg, PR 90/min. and palpated a
slightly enlarged painless thyroid gland. He prescribed sleeping tablets and
tranquilizers (anti-anxiety agents). Did he manage well this patient?
2. What treatment should be done in the toxic solitary nodule ?

3. A 42 years-old lady complains of 2 weeks history of voice change and

dysphagia along with a rapid growing painless neck lump. She is from Ukraine
and it passed 10 years from Cernobil nuclear blast. How would you manage this
patient?
4. How could you know that a total thyroidectomy for papillary carcinoma
has been performed in the past by another surgeon if the patient cannot
remember or lost her medical discharge form and now she came with a lateral
neck lump?