ENDEMIC AND SPORADIC GOITER .

DIFFUSE GOITER WITH HYPERTHYROIDISM.

INFLAMMATORY DISEASES OF THYROID GLAND.
THYROID CANCER.

Endemic goiter is the pathology of thyroid gland, which occurs in

biogeochemical regions with iodine deficiency in environment (regional
pathology).
Sporadic goiter is the disease of thyroid gland, which occurs in unendemic
for goiter regions.
Anatomy(Fig.1;Fig.2;Fig.3.)

Fig.1.Anatomy of thyroid gland:

1 – lobus pyramidalis gl. thyreoideae; 2 - lobus sinister gl. thyreoideae; 3 – trachea;
4 – isthmus gl. thyreoideae; 5 - lobus dexster gl. thyreoideae; 6 – cartilago
thyreoideae; 7 – membrana hyothyreoideae; 8 – os hyoides.
 Fig.2.Transversal section of the neck
on the thyroid gland level:
1 – mm. sternohyoideus et sternothyreoideus; 2 – m. sternocleidomastoideus;
3 – m. omohyoideus; 4 - gl. parathyreoidea; 5 – v. jugularis int.; 6 – a. carotis
communis i n. vagus; 7 – nn. recurrentes і стравохід; 8 – n. longus colli; 9 – fascia
praevertebralis; 10 - gl. parathyreoidea; 11 – вени; 12 – capsula thyreoidea int.; 13
- capsula thyreoidea ext.; 14 – platisma (by Welti).

Fig.3.Topography of recurrens nerve and art. thyreoidea inferior:

1 – a. thyreoidea inf.; 2 - n. recurrens.
 Etiology and pathogenesis

Except iodine deficiency, the goitrous endemia is contributed by excessive

contents of calcium in environment, deficiency of bromine, poor sanitary and
hygienic conditions. Decreased contents of cobalt, manganese, and zinc in
environment also influence on expression of goitrous endemia. The lack of iodine
in the organism blocks the synthesis of thyroid hormones. It results in
hypersecretion of thyroidstimulating hormone of hypophysis, which in turn leads
to hypertrophy and hyperplasia of thyroid epithelium that on initial stages can be
compensated, but further transformed into the goiter.
The gravity of endemia is assessed by such indexes:
1) relationship between men and women with goiter (if it approaches to 1,
the endemia is more severe);
2) predominance of the nodular form of goiter above its other forms;
3) presence of cretinism;
4) goiter in animals;
5) a number of persons with thyroid hyperplasia.
Sporadic goiter arises from relative iodine deficiency, which results from
disturbance of iodine ingestion, liver dysfunction.

Pathology

Macroscopically the goiter is divided onto diffuse, nodular and mixed.

According to histological structure distinguished parenchymatous and colloid ones.
Sometimes occur cystic transformation of the gland and calcification. The enlarged
nodes may result in atrophy of adjacent tissues and organs. So, the advanced forms
of goiter can cause compression of trachea and its softening (tracheomalacia). The
sings of hyperthyroid transformation of euthyroid goiter include: the
transformation of thyroid epithelium from squamous cell into cubic and
cylindrical, presence of papillomatous overgrowth, agglomeration of lymphocytes,
liquid vacuolated colloid.

Classification

According to the form of enlargement of thyroid gland distinguished:

1) diffuse goiter;
2) nodular goiter;
3) mixed goiter.
For determining of the degree of goiter used such scale:
0 - the thyroid gland is not palpated;
I - the isthmus of the gland is noticeable during swallowing and could be
palpated;
II - entire gland is noticeable during swallowing and could be palpated;
 III - the enlargement of gland results in evident thickening of neck ("a thick
neck");
IV – the gland considerably enlarged, and sharply deforms neck;
V - the enlargement reaches excessive size (goiter of major sizes).
According to the functional state of thyroid distinguished:
1) euthyroid goiter (normal function);
2) hyperthyroid goiter (excessive function);
3) hypothyroid (reduced function).
Diffuse enlargement of thyroid of I-II degrees without disturbances of
function and nodular transformation referred to compensatory hyperplasia of the
gland.
According to localization distinguished:
1) typical localization (anterior surface of neck);
2) retrosternal goiter;
3) ectopic goiter (goiter of the base of the tongue, intrathoracic goiter);
4) goiter of additional glands (aberrant goiter);
5) presternal goiter.

Symptomatology and clinical course

In the patients with endemic euthyroid goiter the clinical sings are
basically caused by mechanical and reflex influence of enlarged thyroid gland on
adjacent organs. Patients mainly complain of the presence of "tumour" and neck
deformity. Sense of tightness in the neck, difficult breathing, swallowing, and also
sudden attacks of cough (owing to compression of laryngeal nerves by goiter)
trouble them. In case of great goiter (particularly retrosternal,) periodical dyspnea
may develop (especially in the night), up to asphyxia, which is result of
compression and inflection of trachea. Retrosternal goiter frequently accompanied
with hoarseness, distended veins of face and neck.
The goiter with low thyroid function, as a rule, clinically manifests by
general weakness, malaise, sleepiness, hypomnesia, chilliness, dry skin and
edemas, particularly around eyes. Sometimes in such patients observed
constipation.
The patients with hyperthyroid goiter complain of irritability, heartbeat,
excessive sweating, and tremor of arms, sleeplessness, feeling of fever. Sometimes
observed loss of weight, diarrhea. The thyroid hyperfunction in endemic goiter
mainly slightly expressed, and not associated with exophthalmus.
Enlargement of thyroid gland in patients with endemic goiter mostly often
has nodular or mixed character, and only in small number of the patients (mainly
of younger age) observed diffuse enlargement of thyroid gland.
Nodular goiter is palpated as painless tumour with regular contours, smooth
surface, not connected with adjacent tissues and displaced during swallowing.
Such goiter is characterized by elastic or dense consistence. Long-term goiter leads
to formation of fibrosis and calcification, it becomes solid, and tuberous.
 The shape of diffuse goiter resembles the butterfly. It retains the contours,
its surface is smooth, consistence – mostly elastic, sometimes soft or dense. Mixed
goiters combine manifestations of the nodular and diffuse one, however tactically,
the mixed goiters refer to nodular group.
The separate nodes or entire goiter can partially or completely be displaced
behind breastbone. Palpation of such goiter requires the special devices. The
examination is performed when the patient is supine with the bolster under
scapulas. During the procedure the patient must force by himself or cough, that
causes the emergence of the upper pole or entire goiter above breastbone.

Variants of clinical course and complications

Features of the clinical course of endemic and sporadic goiter caused by its
form (nodular, diffuse, mixed), degree of thyroid enlargement, character of
functional state (euthyroid, hypothyroid, hyperthyroid), location (typical,
retrosternal, ectopic, aberrant goiter), constitutional features of the patient, duration
of the disease and character of previous treatment.
Complication: inflammation of the goitrous thyroid gland (strumitis),
hemorrhage in the tissue of goiter, asphyxia, malignancy.

The diagnostic program

1. Physical examination of the neck, palpation of thyroid gland(fig.4.).
2. Sonography, computer tomography.
3. Determining of thyroid function (serum hormones, serum iodine, and
thyroid-iodine uptake)(Fig.5;Fig.6;Fig.7;Fig.8.).
4. According to indications: X-radiography of the neck (calcification,
ossified foci) with barium swallow (compression of esophagus, trachea,
their shift, and deformity).
5. Chest X-radiography, particularly of mediastinum, in two plains,
pneumomediastinography (intrathoracic goiter).
6. Puncture biopsy (Fig.9.)
Fig.4. Palpation of thyroid gland (right lobe)

Fig.5. Thyroid gland scanning

Fig.6. Scanogram of diffuse goiter

Fig.7. Scanogram of nodular goiter

Fig.8. Scanogram of mixed goiter

 Fig.9. Endemic nontoxic goiter. Macro follicular goiter with epithelium
proliferation.

Differential diagnostics

Endemic and sporadic goiter requires the differential diagnostics with

chronic autoimmune thyroiditis (Hashimoto's thyroiditis), Riedel's fibrous
thyroiditis, neck cysts, lipomas and other tumours of the neck and mediastinum,
malignant neoplasms of thyroid gland, metastases of tumours in cervical lymph
nodes.
Hashimoto's thyroiditis is characterized by specific immunological
indexes, diffuse density of thyroid, mosaic changes on sonogram and scintiscan,
reducing of the goiter in response to prednisolone assay.
In case of Riedel's goiter the gland is tuberous, of woody consistency, quite
often knitted with adjacent tissues (except skin).
The cysts, tumours of the neck, metastases in lymph nodes are well
defined on sonograms, do not displace at swallowing and accumulate radioactive
iodine.
The suspicion on thyroid cancer makes the necessity to carry out
morphological verification by puncture biopsy with further cytological
examination.

Tactics and choice of treatment

Endemic goiter is the subject for treatment in all its forms and all stages of
the development. The choice of treatment depends on type of the goiter (diffuse,
nodular, mixed), degree of enlargement of the thyroid (I-V) and character of
complications of the goiter (inflammation, hemorrhage, asphyxia, and
malignancy).
Conservative treatment includes the drugs of inorganic iodine, thyroidine
and pure hormonal drugs (thyroxine, triiodothyronine). Thyroxine is the most
effective one. The iodine drugs less effective and frequently are the cause of
secondary hyperthyroidism. The medicament treatment is administered in diffuse
thyroid enlargement without sings of compression of neck organs. Polynodular
goiter (particularly in elder women) sometimes complicated by malignancy and
consequently, even if the sings of compression of neck organs and hyperthyroidism
are absent, also treated by conservative agents. The important argument of
medicament treatment is their often recurrences after operation.
The surgical approach in endemic and sporadic goiter are determined by
their spread and character of the lesion. There used the principle that all
transformed into the goiter parenchyma should be removed, and healthy –
preserved as much as possible.
The nodular and mixed form of the goiter, despite its function and size, is
the subject for surgery. The hypothyroidism is not contraindication for operation,
as the removal of the goiter results in functional normalization of unaltered,
paranodular tissue. The operation, first of all, is indicated if present the sings of
compression of neck organs, goiter of the major sizes, secondary hyperthyroidism
and suspicion on malignancy. The goiter of additional thyroid glands (aberrant
goiter) is the subject for obligatory surgical removal. The operation consists of
removal of the aberrant gland with revision of the basic thyroid gland.
The intrathoracic goiter, which develops in retrosternal ectopy of thyroid
gland, also requires obligatory surgical removal(Fig.10.). The best access is the
longitudinal sternotomy. The cervical goiter is possible to remove by means of
cervical access without the special technical efforts.

Fig.10. Scheme of goiter formation (retrosternal, intrathoracic)

In tongue ectopy if there are no severe disturbances of speech, swallow and

breathe also possible observation and conservative treatment. Progressive growth
of the goiter, presence of sings of compression, dysphagia, traumatic bleeding and
suspicion on malignancy require the surgical treatment – removal of the goiter
mostly through a lateral pharyngeal incision.
The acute disturbance of breathing (asphyxia) requires performance of
urgent operation.
The optimal method of anesthesia is the endotracheal narcosis. This method
prevents mechanical asphyxia during operation resulting from compression or
inflection of trachea at the moment of mobilization and drawing out of the goiter.
The method permits to perform careful revision of entire gland and neck spaces,
first of all retrosternal, retrotracheal, retroesophageal, where there can be separate
thyroid nodes. It is necessary to consider a local anesthesia, and also other methods
of general anesthesia as reserve.
For removal of goiter used transversal incision by Kocher in the inferior part
of the neck above the sternoclavicular junctions. Operation on thyroid gland must
begin from careful revision and intraoperative diagnostics that permits to choose
the adequate operative tactics. Trachea must be mobilized by means of isthmus
dissection. It permits better orientation in topographic situation caused by the
goiter, and to perform tracheostomy at occurrence of asphyxia. Further isthmus and
pyramidal lobe must be removed as the most dangerous as for relapse of the goiter.
The volume of thyroid resection in endemic and sporadic goiter is
determined individually. The resection is performed subfascially that prevent the
removal of parathyroid glands and trauma of laryngeal nerves. The node is
necessary to eliminate together with paranodular tissue, as it is functionally failed.
It is justified also by oncologic reasons. The operation of nodular enucleation is
considered to be inadequate, thus never used. Meanwhile, in multinodular bilateral
goiter, when practically entire thyroid gland is affected, it is necessary to eliminate
separate nodes from healthy parenchyma, preserving its maximal amount, as the
parenchyma is mainly disposed as lamina on their surface. This layer of
parenchyma is necessary to dissect and draw aside by scissors out of node, having
preserved its vascularization.(Fig.11-15.)

Fig.11. Operative incision

Fig.12. Prepararation of upper layers of the skin

Fig.13. Transversal section of prethyroid muscles

 Fig.14. Sutures imposition and closing with thyroid stump

Fig.15.Sutures on prethyroid muscles and drainage of operative wound

In endemic and sporadic goiter applied saving, extent and subtotal resection
of the thyroid with obligatory indication of amount and site of leaving
parenchyma.
For oncologic standpoint it is necessary in all cases to carry out
intraoperative express cytology of the removed tissue.
For prophylaxis of goiter relapse after the operation necessary long-termed
institution of thyroid hormones with the purpose to block thyroid stimulation by
pituitary gland.
 DIFFUSE GOITER WITH HYPERTHYROIDISM

Diffuse goiter with hyperthyroidism (Grave's or Basedow's disease,

thyrotoxicosis, hyperthyroidism) is severe autoimmune and neuroendocrine disease
resulting from excessive secretion of thyroid hormones by diffuse-enlarged thyroid
gland with lesion of all organs and systems of the body.
The diffuse goiter with hyperthyroidism (thyrotoxicosis) mostly occurs at
women. In 5 % of persons with hyperthyroidism develop ophthalmopathy and
pretibial myxedema.

Etiology and pathogenesis

The scientific investigation and clinical examination testify that the diffuse
goiter with hyperthyroidism is autoimmune disease. This disease is commonly
results from infections, intoxication, craniocerebral injury, dysfunction of other
endocrine glands, first of all genital, acute and chronic mental disorder, sunstroke.
The disease develops under the influence of these factors directly on generically
predisposed to thyrotoxicosis organism.

Pathology

The thyroid gland is 2-5 times enlarged, moderately dense, on incision

pulpy, sanguineous, of grey-pink color. Histologically revealed a polymorphism of
follicles. Follicular epithelium is cylindrical with papillomatous growths. The
colloid is eosinophilic, contains plenty of resorptive vacuoles. In interstitial space –
lot of lymphocytes, which form follicles. The severe form of thyrotoxicosis results
in thyrotoxic heart, thyrotoxic liver cirrhosis, thyrotoxic ophthalmopathy,
osteoporosis, and cachexia.

Classification

According to the clinical course distinguished mild, moderate and severe

forms of the disease.
According to Milk's classification, there are four stages of hyperthyroidism.
I stage – neurotic, onset of thyrotoxicosis, slight enlargement of thyroid
gland.
II stage – neurohormone, marked sings of thyrotoxicosis, the thyroid is
noticeably enlarged in size.
III stage – visceropathic, is characterized by a thyrotoxic lesion of viscera.
IV stage – cachectic, is characterized by nonreversible dystrophy of organs
and systems.
 Symptomatology and clinical course

A diffuse toxic goiter affects practically all organs and systems and disturbs
all types of metabolism. Except described in 1842 by Basedow classical triad
(goiter, tachycardia and eye bulging), today is known about 70 signs, proper for
thyrotoxicosis, which can be combined in three basic syndromes: hyperthyroidism,
eye signs (ophthalmopathy) and lesion of skin (pretibial myxedema). By the may,
the hyperthyroidism is the permanent phenomenon, and ophthalmopathy and
pretibial myxedema occurs rather seldom (in 1-5 % of patients).
To initial sings of thyrotoxicosis can be regarded: general weakness, prompt
fatigability, decreased work ability and muscular force, nervousness, irritability,
sleeplessness, sweating and hyperemia of skin.
The basic signs of thyrotoxicosis are enlargement of thyroid gland (goiter),
palpitation, exophthalmos, tremor and progressing loss of weight. (Fig. 16)

Fig.16. Thyrotoxicosis

The thyroid gland in the patients with thyrotoxicosis is diffuse enlarged and
of moderate density. In some of them due to excessive blood supply it can pulsate.
After long treatment by iodine the gland becomes dense and painless. Such long-
term conservative treatment causes the development of sclerotic degenerative
processes, sometimes with nodular transformation of the tissue, and the degree of
thyroid enlargement frequently does not relate to the gravity of thyrotoxicosis.
Secretory activity of thyroid hyperplasia in the form of excessive releasing
of its hormones (triiodothyronine and thyroxine) underlies the hyperthyroidism.
The majority of effects of thyroid hyperfunction manifest through sympathetic
nervous system: palpitation, tremor of fingers, tongue, and whole body (sign of
"telegraphpole"), sweating. In the patients with thyrotoxicosis the protein,
carbohydrate and lipid metabolism is elevated, which manifests by simultaneous
excessive appetite and loss of weight.
The changes, which develop in organs of cardiovascular system and
manifests by tachycardia, high systolic and low diastolic pressure, increase of
pulse pressure and complete arrhythmia with the development of heart failure form
a syndrome of thyrotoxic heart.
The excessive formation of heat owing to intensive metabolism, which
results from the influence of thyroid hormones, leads to hyperthermal syndrome
(feeling of fever, high body temperature). The sings of nervous dysfunction include
irritability, anxiety, fear sensation, nervousness, sleeplessness, hyperactive tendon
reflexes. The dysfunction of genitals manifests by oligo- or amenorrhea, and in the
men by gynecomastia, which is the outcome of disturbed relation between
estrogens and androgens. Thereafter libido and potency are reduced.
The thyrotoxicosis without treatment results in loss of weight, in advanced
cases not only the subcutaneous fat disappears, but also a muscular tissue reduced,
down to cachexia. Degenerative changes in muscles, and lesion of peripheral
nervous system result in thyrotoxic myopathy.
In majority of patients develop characteristic eye signs. The predominant
one is the exophthalmos. By the way, eye bulging, which occurs in 50 % of cases,
frequently can be the initial manifestation of the disease, assigned by patient. Three
types exophthalmos are distinguished: slight (14-17 mm), moderate (17-20 mm)
and considerable (more than 20 mm). The exophthalmos in thyrotoxicosis is
symmetric, the eye trophic and movements of does not disturbed. Except
exophthalmos, there are lot of other eye signs observed in the patients with
thyrotoxicosis.
 Graefe's sign – the upper lid lag when the patient looks downward;
 Stellwag's sign – infrequent winking;
 Mebius' sign – a weakness of convergence;
 Dalrymple's sign - wide palpebral fissure;
 Kocher's sign – retraction of the upper eyelid at prompt change of view.
The eye signs of diffuse toxic goiter are necessary to differentiate from
ophthalmopathy (malignant exophthalmos), which observed approximately in 5 %
of the patients with thyrotoxicosis. Such exophthalmos simultaneously associated
with pain in the eyeballs, gritty sensation and eyewatering. Also detected lid
edema, ocular injection. In considerable ophthalmopathy the eyeballs bulge from
orbits, eyelids and conjunctiva are swollen, with sings of inflammation. It can
result in keratitis with corneal ulceration, which finally can lead to blindness. The
high orbital pressure caused by lymphoid infiltration, accumulation of fluid and
edema of retroorbital tissues result in not only eye bulging – exophthalmoses, but
also compression of optic nerve and loss of sight. It is necessary also to specify
that the ophthalmopathy in thyrotoxicosis, as a rule, develops on the background of
encephalopathy and has an autoimmune genesis. (Fig.17.)

Fig.17. Exophthalmoses

Pretibial myxedema arises on the anterior surface of lower legs. The skin
becomes dense, thickened, of purple-red color, and hair follicles jut out of its
surface.
Thyroid hypersecretion also negatively influences on the liver parenchyma.
In severe cases it can result in toxic hepatitis, jaundice and further hepatargy. It is
necessary to consider the toxic hepatitis in such patients unfavorable as for
prognosis.
Under the direct cytotoxic influence of thyroid hormones on intestinal
mucosa suppressed its enzymatic function that leads to intestinal hyperkinesis and
osmotic diarrhea – thyrotoxic enteric syndrome. It is accompanied by gluco- and
mineralocorticoid dysfunction of suprarenal gland, and leukopenia, granulocytosis
and lymphocytosis in blood.

Variants of clinical course and complications

In clinical course of thyrotoxicosis distinguished the mild, moderate and

severe forms.
The mild form of thyrotoxicosis is characterized by following signs: pulse
100 beat/min, loss of weight approximately 3-5 kg, slight sweating, eye signs
absent or slightly expressed, normal arterial pressure, basal metabolism to +30 %,
elevated thyroid-iodine uptake, and the maximum of iodine accumulation, which
exceeds 30 % is detected after 24 hours.
The moderate gravity of the disease manifests by expressed
symptomatology: loss of weight to 8-10 kg, tachycardia 101-120 beat/min, systolic
pressure is elevated, and diastolic – decreased or normal. Frequently observed
exophthalmos, basal metabolism +31-50 %, thyroid-iodine uptake has been
excessive since first hours.
The severe form of thyrotoxicosis is characterized by the sharply expressed
symptomatology, which is caused by considerable visceral dysfunction. The pulse
rate in such patients exceeds 120 per minute, and complete arrhythmia develops.
Tremor and profuse sweating sharply expressed, pulse pressure considerably
elevated circulatory failure and ophthalmopathy frequently observed. The loss of
weight can overtop 10 kg, basal metabolism more than +50 %, the maximum of
radioactive iodine accumulation detected in 4-6 hours after taking of isotope, and
decreasing of accumulation curve exceed 24 hours.
According to the clinical course two forms of thyrotoxicosis distinguished:
а) thyrotoxicosis with slow development; б) acute form of diffuse toxic goiter,
which is characterized by an acute onset and prompt, sometimes within several
hours, development. The acute thyrotoxicosis seldom occurs and in most cases
ends lethally from thyrotoxic coma.
The clinics of acute thyrotoxicosis develop within some hours or days. Thus
the thyroid gland is not enlarged, high temperature, vomiting, diarrhea, sharp loss
of weight are observed.
The special forms of thyrotoxicosis include the thyrotoxicosis in childhood,
in pregnant, in climacteric women, and people of the elderly age.
Among complications during the course of disease the most dangerous for
the life is thyroid storm. It is observed in 0,02-0,05 % of the patients and develops,
mainly, as the outcome of the lesion of provoking factor. Among them considered
trauma (surgical intervention on thyroid gland or other organs), harsh palpation of
the gland, mental trauma, emotional stress, infections, pregnancy, labors and
radioiodine therapy.

The diagnostic program

1. Clinical examination, examination, palpation, auscultation of thyroid

gland.
2. Detecting of basal metabolism, serum lipids, ECG.
3. Detecting of thyroid hormone concentration (common free thyroxine –
Т4, common free triiodothyronine – Т3), serum iodine-binding globulin,
serum thyroidstimulating hormone of hypophysis.
4. Determining of thyroidstimulating antibodies – immunoglobulins,
antithyroid antibodies.
5. Sonography of thyroid gland.
 Differential diagnostics

The manifestation of initial, vague and slightly expressed forms of

thyrotoxicosis can resemble neuroses, rheumatic disease, tuberculosis,
chroniosepsis, postcastrate syndrome, diencephalic lesions, and also malignant
tumours. It particularly concerns those cases, when the enlargement of thyroid
gland is slight or it is failed to detect.
All the mentioned diseases are characterized by palpitation, heart pain
excessive sweating, subfebrile fever and loss of weight.
The acute development of thyrotoxicosis sometimes makes the necessity to
rule out such acute infectious diseases, as dysentery, influenza or camp-fever.
The thyrotoxicosis with exophthalmos is necessary to differentiate with
encephalitis, ophthalmopathy. Encephalitic exophthalmos is characterized by
combination of looking upward paresis with diplopia, corneal ulceration,
conjunctivitis, progressing, so-called malignant exophthalmos, which rather
frequently can result in loss of eye. By the way, this type of exophthalmos is
commonly unilateral.
Laboratory tests are important for differential diagnostics of thyrotoxicosis:
detecting of thyroid hormones, serum protein-bounded iodine, thyroid-iodine
uptake, biochemical, immunological investigations, sonography and scanning with
the radioiodine or technetium.
In particularly severe cases it is advisable to apply trial antithyroid therapy.

Tactics and choice of treatment

The thyrotoxicosis revealed for the first time, and also its severe and
moderate forms require institutional treatment. Three methods of treatment of
thyrotoxicosis are commonly employed: а) antithyroid drugs; b) treatment by
radioactive iodine; c) surgery.
The antithyroid drug therapy of the patients with thyrotoxicosis, first of
all, should be directed to ameliorate hyperthyroidism. This is gained by the usage
of iodine and thyrostatic agents, particularly mercasolil – synthetic antithyroid
drug. In severe cases the treatment begins from 45-60 mg (9-12 tablets) per day, in
the moderate form – from 30 mg (6 tablets), in mild – from 15 mg (3 tablets) per
day. The maximal initial dose ordered within 2-4 weeks to gain expressed clinical
relief of the disease (decrease of irritability, normalization of pulse rate, increase of
weight). After that, if the state of the patient gradually improves, the dosage is
reduced every 3-4 weeks by 1-2 tablets per day to supportive dose (1 or 1/2 tablets
per day during 2-3 months). Commonly, the course of the treatment by mercasolil
should be lasted for 1-1,5 years. Among complications, which can arise during the
treatment, it is necessary to mention leukopenia, agranulocytosis and allergy.
In case of allergic response to mercasolil or development of complications
used a reserve drug – lithium carbonate.
 Such long conservative treatment of thyrotoxicosis is desirable in those
patients, who gained euthyoidism in 1-3 months, that is the gradual reduce of
goiter and eye signs. If during the treatment periodically exacerbation occurs,
which manifests by thyroid enlargement, development of encephalopathy,
activation of ophthalmopathy the surgery is indicated.
More recent studies showed that the treatment by radioactive iodine is a
radical method of therapy of thyrotoxicosis. The radioactive iodine, which deposits
in thyroid gland, irradiating its parenchyma, results in destruction of the active
thyrocytes with their further replacement by connective tissue (bloodless
thyroidectomy). The standard dosage is 0,1 mCi per gram of thyroid tissue, and it
can be introduced at one time or partly.
Nevertheless such therapy has series of essential drawbacks. The lack of
precise methods of determining the weight of the gland results in miscalculations
at selection of total dose of the isotope. It is also impossible to exclude the harmful
influence of the isotope on the genetic kettle of the patient. Almost in 70 % of the
patients the hypothyroidism develops after the treatment by radioactive iodine and
there is a potential threat of the development of radioactive thyroid cancer. That's
why the indication for application of this method rather restricted.
The treatment by radioactive iodine is commonly indicated for the patients
with thyrotoxicosis after 40, with recurrent thyrotoxicosis, and after operations
particularly, in combination with severe concomitant diseases and in case of refuse
of surgery. It is not justified at young age, pregnancy and during lactation,
thyrotoxic multinodular adenoma, expressed leukopenia, and kidney dysfunction
or at severe acute thyrotoxicosis.
Sometimes introduction of radioactive iodine can cause the exacerbation of
thyrotoxicosis, up to the development of thyroid storm. Thus, before administration
of the radioactive iodine, particularly in patient with severe form of thyrotoxicosis
in order to relieve thyrotoxicosis it is necessary to institute antithyroid drugs.
The surgical method of treatment is considered to be radical and the most
effective. The operation almost always allows to liquidate the manifestations of
hyperthyroidism together with its morphological base. The efficiency of this
method in the specialized clinics reaches 95-97 %.
The indications for surgery include thyrotoxicosis of moderate gravity when
the conservative treatment is inefficient during 2-3 months, severe forms of
thyrotoxicosis, goiter of IV-V degree despite the gravity of thyrotoxicosis, and also
nodular transformation of toxic goiter.
The surgical method is not recommended for the patients with thyrotoxicosis
with severe concomitant diseases and dysfunction of vital systems.
The obligatory requirement of successful surgery of the patients with
thyrotoxicosis is the careful preoperative preparation, which goal is the
liquidation or decreasing of hyperthyroidism, that achievement of euthyroid state.
Preoperative preparation should be complex, pathogenically proved and individual.
The appropriate place in preoperative period should possess psychological
preparation. The patients stay in chambers together with patients recovering after
operation. In severe form of thyrotoxicosis a strict bed regime is ordered. The diet
should be high-caloric, rich with proteins, vitamins. The patient must take
antithyroid drugs under the control of general blood analysis. To prevent
leukopenia and agranulocytosis instituted leukopoetic agents. Besides antithyroid
therapy, are advisable reserpin that characterized by hypotensive, sedative and
antithyroid activity, beta-blockers and tranquilizers for decreasing stimulation of
CNS.
In severe form of thyrotoxicosis, at presence of hypoproteinemia is
advisable the intravenous infusion of protein substitute solutions (albumin, protein,
plasma). With the purpose of detoxycation applied neohaemodes, neocompensan.
For exhausted patients beside high-caloric diet applied parenteral infusion of
glucose, intralipid, amino acids and vitamins, particularly of B-group. The patient
with sings of heart failure simultaneously should take cardiac glycosides and other
cardiac agents. One of the measures in preoperative preparation is the regulation of
reduced function of suprarenal glands. Glycocorticoids (hydrocortisone etc.)
administered in daily dosage of 25-50 mg 2-3 times per day during 3-4 days before
the operation and 2-3 days after it. Preoperative preparation should also include
regulation of hemostatic dysfunction (vicasol, aethamsylat, dicynon, inhibitors of
proteases).
The preoperative preparation is considered to be sufficient, if the state of the
patient is regarded to euthyroid or approximate to it. It is testified by normalization
of pulse (90-80 per minute), increase of weight on 3-5 kg, liquidation of
nervousness and irritability, disappearance of tremor, regulation of function of
cardiovascular system, liver, suprarenal glands, CNS and basal metabolism.
Anesthesia. The method of choice is endotracheal narcosis.
Operation. The most effective and rational surgery approach for
thyrotoxicosis is the subtotal subfascial resection of the thyroid (O.V.Nickolayev,
1951) or thyroidectomy. The main difference of this procedure is the refuse of
ligation of thyroid vessels before they enter the gland and subfascial resection of
the gland. The goal of this technique is to gain bloodless and atraumatic procedure
of operation, to prevent damage (removal) of parathyroid glands and laryngeal
nerves. This procedure also favors the formation of a gland stumps in the site of
parathyroid glands and passage of recurrent nerves. The volume of resection and,
consequently, the size of the gland stamp must be based on the account of gravity
of thyrotoxicosis, age of the patient, duration of the disease, previous treatment,
morphology of the organ and immune state of the patient. (Fig.18)
 Fig.18. Subtotal resection of thyroid gland by Welti

It is generally accepted, that the more severe the form of thyrotoxicosis,

more young the patient, more short duration of the disease, more intensive
vascularization, more dark color of the gland, the smaller tissue remnant is
necessary to leave (mainly less 6 g, on 1-3 g from each side). Morphologically in
such patients revealed hyperfunctional type of histogram and autoimmune
processes on initial stage of the development.
The elderly age of the patients with long conservative treatment, reduced
blood supply of the gland, expressed plasmolymphatic infiltration of the tissue
requires to leave greater thyroid remnant (6-10 g). Morphologically in such
patients detected regenerate type of histogram.
Sometimes a long anamnesis and conservative treatment, in association with
expressed sclerosis of the gland or its nodular or cystic transformation requires
performing of thyroidectomy.
Postoperative period. The clinical course of early postoperative period in
the patients undergone the operation mainly depends both on quality of
preoperative preparation, and on technique of the surgical intervention. In some
patients, particularly with severe form of thyrotoxicosis, during first days after the
operation it is possible to observe exacerbation of thyrotoxicosis – postoperative
thyrotoxic response.
There are three degrees of postoperative thyrotoxic response: mild, moderate
gravity and severe.
Characteristic sings of mild degree is the tachycardia up to 120 per minute,
fever as high as 38°С, satisfactory state of the patient, tachypnea.
The moderate gravity of thyrotoxic response manifests by mild psychomotor
excitement. They complain of general weakness, headache, fever sensation, rapid
pulse to 120-140 per minute (rhythmic, tense), sometimes extrasystole.
Temperature raises as high as 38,5-39°С. Characteristic the considerable sweating,
tachypnea, superficial sleep.
Severe degree of thyrotoxic response is characterized by expressed
psychomotor excitement. The patients are restless, frequently change positions in
the bed, they complain of considerable sweating, permanent fever sensation and
expressed tremor. Hyperemia of the face, pulsate vessels of the neck and cyanosis
of leaps are evident. The pulse rate usually exceeds 140 per minute, irregular and
soft. The breathing is superficial. Body temperature is 39-40°С. The sleeplessness
in such patients is almost impossible to liquidate by hypnotic and narcotics agents.

Complication of a postoperative period

1. Thyroid storm is the severe complication of postoperative period in the

patients with thyrotoxicosis (thyrotoxic crisis, acute postoperative thyrotoxicosis).
The crisis develops mainly on the second or third day after the operation. If is
failed to liquidate it in a day after the onset, the patient can die.
The clinical development of such crisis is acute or fulminant. It manifests by
excitement, up to psychosis and coma, motor disorders, tachycardia (pulse rate –
150-200 per minute), complete arrhythmia, fever as high as 40°С and more,
hyperemia of the face, neck, limbs, cyanosis, extremely sweating, diarrhea.
Pathogenically thyroid storm is caused by excessive releasing of thyroid
hormones. It can arise as the result of rough palpation of the thyroid, treatment by
antithyroid drugs, radioactive iodine, infections and traumas.
The crisis requires an urgent and complex treatment. Infusion therapy
includes transfusion of haemodes, solutions of glucose with vitamins, plasma, and
albumin. Major doses of glycocorticoids, narcotics, neuroleptanalgesia are
instituted. Also desirable administration of sedative antihistamine drugs, adrenergic
blockers, cardiac glycosides, oxygenotherapy, hypothermia, particularly on regions
of major vessels, medical narcosis, extracorporal method of detoxycation.
The prophylaxis of thyroid storm suggests an adequate preoperative
preparation in order to gain euthyroid state of the patient, and also atraumatic
performance of surgical intervention.
2. The damage of laryngeal nerves is the severe complication of operations
on thyroid gland. Thus the paralysis of laryngeal nerves can be unilateral or
bilateral, temporary or permanent. The basic causes of the paralysis: cutting off the
nerve, its crushing or ligating, distention or compression. It is also necessary to
specify that the bilateral injury of inferior laryngeal nerves is particularly
dangerous.
The prophylaxis of the damages of laryngeal nerves basically consists of
careful technique of subfascial resection of thyroid gland. It is always necessary
gently manipulate in the region of inferior poles and "dangerous zone". The
hemostasis in order to obtain "dry" operative wound should be carried out only
under the visual control.
The development of asphyxia requires an urgent intubation of trachea, or
tracheostomy.
 3. Asphyxia. It is caused, except bilateral injury of inferior laryngeal nerves,
by the damage of trachea, tracheomalacia, laryngeal edema or inflection of trachea.
The tracheal wall injuries must be sutured by atraumatic needle with further
muscular plastics. Tracheomalacia requires supporting sutures on trachea or
application of prosthetics from synthetic material. Sometimes it is necessary to
perform temporary tracheostomy.
4. Air embolism. The cause of this infrequent complication is the entering
of air in the neck veins owing to suctional activity of chest and negative venous
pressure. The prophylaxis of such complications consists of clamping of veins
before cutting.
5. Parathyroid tetany is a difficult postoperative complication, which is
hardly to undergo rehabilitation. The basic cause parathyroid tetany is the removal
of parathyroid glands together with thyroid tissue. Besides it can result from
impaired blood supply of the glands after the operation. The tetany develops on the
base of mineral metabolism disorders, first of all, extremely reduced serum
calcium (less 2,5 mEq/l)
It manifests by acute attack of wide-spread or localized cramps of separate
groups of muscles of the upper or lower limbs. The most dangerous in this plan is
the development of laryngospasm or tonic contraction of diaphragm.
Early clinical manifestation of parathyroid tetany is the Chvostek's signs
(percussion near mandible angle causes muscular contractions of the face),
Ttrousseau (occurrence of paresthesias and the sign of "obstetrician's" hand" after
applying of tourniquet on brachium.
The treatment of parathyroid tetany consists of prompt administration of
calcium agents. The usage of parathormone in complex with vitamin D is usually
beneficial. Simultaneously with conservative treatment also performed
transplantation of bony tissue.
The careful technique of subfascial resection of thyroid gland prevents the
damage of parathyroid glands (except cases of their thyroid ectopy).
6. Bleeding. The cause of intra- and postoperative bleedings is insufficient
mechanical hemostasis.
The postoperative bleedings are observed within first hours after operation
as the result of unreliable hemostasis or slipping of ligature from vessels.
Bleedings are clinically characterized by the prompt enlargement of swelling in the
region of neck, considerable sopping of bandage by blood. Meanwhile, the patients
complain of feeling of tightness in the neck, fear, tachycardia, cyanosis and
dyspnea. The treatment of this complication is only surgical. The goal consists of
complete disclosure and revision of the wound, carrying out of careful hemostasis.
The prophylaxis of postoperative bleeding includes a complex of measures,
the most important of which is a subfascial technique of thyroid resection, careful
reliable hemostasis and anatomic operating. The special attention is necessary to
pay on lateral thyroid veins (Kocher's veins), which are short and empty directly
into interior jugular vein. If the vessels are sclerosed, fragile and easily broken,
they should be tied at once after cutting, instead of leaving on clamps up to the end
of gland removal.
 The damage of larynx, esophagus, major vessels of neck, lymph duct and
pleura very seldom occurs. The laryngeal defects are sewed up with further
covering by muscles. The esophageal wound is sewed up tightly, and feeding of the
patient during 7 days is carried out through the tube.

INFLAMMATORY DISEASES OF THYROID GLAND

PURULENT THYROIDITIS

The purulent thyroiditis is a suppurative septic lesion of thyroid

parenchyma. There are also cases of purulent inflammation goitrous thyroid gland
– acute purulent strumitis.

Etiology and pathogenesis

The purulent thyroiditis arises owing to invasion of the thyroid by bacterial

infection which spreads by hematogenous or lymphogenous way. The infecting
agent most often represented by pyogenic streptococcus or staphylococcus aureus.

Pathology

Morphologically according to the character of inflammation distinguished

the plain and specific thyroiditis, according to the course – acute, subacute and
chronic.
The acute thyroiditis mainly develops in one lobe. Histologically revealed
formation of the necrotic foci, hemorrhages, leukocytic infiltration of stroma with
admixture of lymphocytes and macrophages.
The subacute thyroiditis (de Kerven) is histologically represented by the
developments granulomatous inflammation. The stroma is commonly infiltrated by
lymphocytes, leukocytes and large cells, which remind the cells of foreign bodies.
The chronic thyroiditis can manifest in the form of Hashimoto's and Riedel's
goiter or specific thyroiditis caused by tuberculosis, lues or actinomycosis.
Hashimoto's goiter is characterized by predominant lymphocytic infiltration
with formation follicles (lymphocytic goiter). Riedel's goiter ("iron” goiter, fibrous
thyroiditis) is represented by growth of fibrous tissue.
In specific thyroidites revealed specific granulomas.

Classification
 Distinguished acute purulent thyroiditis as diseases, which arise in unaltered
thyroid gland, and acute purulent strumitis – the lesion of the goitrous transformed
thyroid gland.

Symptomatology and clinical course

The onset of the disease is usually acute. It manifests by spontaneous sharp

pain in the region of the neck, which amplifies at movements, speech and
swallowing, fever, chills, weakness, sweating and tachycardia. On examination it is
possible to note local reddening and swelling. Palpation reveals tissue tension,
thyroid enlargement, density, with fluctuation in the site of lesion. In blood
observed neutrophil leukocytosis and increased erythrocyte sedimentation rate.

Variants of clinical course and complications

The clinical course of the disease is characterized by the sings of purulent

septic pathology of the neck. The process spreads outside the thyroid. Late
diagnostics and inappropriate treatment result in discharge of the abscess outside,
development of neck phlegmon, mediastinitis and sepsis. Nevertheless, in general,
the outcome is favorable, on the site of abscess replaced by fibrous tissue, and the
function of gland tends to norm.

The diagnostic program

1. Clinical examination, palpation.

2. General blood analysis.
3. Sonography of thyroid gland.
4. Diagnostic puncture of thyroid gland.
5. Bacteriological investigation of exudate.

The purulent thyroidites must be differentiated from simple thyroiditis and

strumitis. The stormy course and transformation of plane inflammation into
purulent that detected clinically, and by means of diagnostic puncture (purulent
exudate) distinguish acute thyroiditis from the other inflammatory processes in
thyroid gland.

Tactics and choice of treatment

Diagnostic puncture is necessary in order to confirm the diagnosis. If present

fluctuation and purulent exudate it is necessary to carry out surgical management
(drainage of suppurative focus). Such patients require antibiotics, analgesics,
antiinflammatory and sedative agents.
 AUTOIMMUNE THYROIDITIS
Autoimmune (lymphomatous) thyroiditis is the disease described by
Hashimoto in 1912. In most cases it occurs in women of age 40-50.

Etiology and pathogenesis

The basic etiologic factor in the development of autoimmune thyroiditis is

the release and entering of thyroid antigens into the blood as the result of
inflammatory processes and traumas combined with surgical operations on thyroid
gland. It has been found the presence of antibodies to thyroglobulins, colloidal
component of thyroid gland and microsomal fraction. However the presence of
antithyroid antibodies not always results in the damage of the thyroid. The
cytotoxic properties of these antibodies manifest only after their interaction with Т-
lymphocytes and HLA antigens.

Pathology

The histological sign of autoimmune thyroiditis is the diffuse or focal

thyroid infiltration by lymphocytes and plasma cells, which results in destruction
of follicles and their basal membranes. Further thyroid tissue is replaced by
connecting that leads to the focal fibrosis, which resemble nodes.

Classification

Distinguished diffuse and focal, and also hypertrophic and atrophic form of
autoimmune thyroiditis.

Symptomatology and clinical course

Hashimoto's thyroiditis is characterized by the slow growth of goiter, the

thyroid density, and gradual hypothyroidism. Besides develops the
symptomatology, resulting from compression of organs and tissues of the neck by
goiter. The patients complain of enlargement of thyroid gland, sense of tightness in
the neck, difficult swallowing and breathing, pain in the region of gland and
general weakness.
Enlargement of the thyroid is symmetric, it, as a rule, of dense consistence,
and on palpation detected its nodular character. During pressing on one of the lobe
of thyroid gland the elevation of contrlateral lobe is observed (the sign of "swing").

Variants of clinical course and complications

 Autoimmune thyroiditis is characterized by the development of
hypothyroidism. Nevertheless there are also atypical clinical forms of the disease:
autoimmune thyroiditis with thyrotoxicosis (Hashitoxicosis) with gradual
transferring into hypothyroidism, lesion of one lobe with clinical course according
to the nodular type of euthyroid or hypothyroid goiter. The autoimmune thyroiditis
can arise in thyroid stump after surgery for different forms of goiter. The
combination of autoimmune thyroiditis with thyroid adenoma or cancer and its
transferring into chronic rarely occur.
Autoimmune thyroiditis can complicated with hypothyroidism, compression
of neck organs, in some cases - malignancy.

The diagnostic program

1. Clinical examination of the patient (palpation of thyroid gland).

2. Detecting of thyroid hormone concentration and thyrotropin.
3. Sonography of thyroid gland.
4. Detecting of antibodies to different thyroid components.
5. Biopsy of thyroid gland.

Fig.19. Hashimoto's thyroiditis sonography picture

Differential diagnostics

It should be carried out with endemic and sporadic goiter, Riedel's fibrous
goiter and thyroid cancer.
Symmetric enlargement of thyroid gland, its dense consistence, nodular
character, presence of autoimmune diseases in family history, high antibody
capacity to thyroglobulins and microsomal fraction, development of
hypothyroidism, positive response as reducing of goiter at prednisolone assay (20
mg of prednisolone during 7-10 days) – all these distinguish autoimmune
thyroiditis from endemic and sporadic goiter, Riedel's thyroiditis. It is usually
impossible to differentiate autoimmune thyroiditis from thyroid cancer on the base
of clinical, instrumental and laboratory findings. In this case exclusive value has
the morphological investigation – biopsy of thyroid gland or express histological
investigation during operation. Macroscopically the gland is of pale-pink- greyish
color with yellowish tone (instead of red-brown in norm), with atrophic sheath and
thin-walled veins.

Tactics and choice of treatment

There is no specific therapy of autoimmune thyroiditis for today. The

phenomena of hypothyroidism require nominating of replaceable therapy by
thyroid hormones (thyroidine, thyroxine). Glycocorticoids and antihistamine
agents are used in subacute form of autoimmune thyroiditis.
Surgery is applied in case of compression of the neck organs and suspicion
on malignant tumour of the thyroid. The volume of operation has been still
controversial. Preserving operation (isthmusectomy in combination with wedge-
like resection of lateral lobes, resection of thyroid gland) expedient only on initial
stages of the disease with maintained thyroid activity. Taking into account a reality
of malignancy, often relapses of goiter after small resections, the role of thyroid
remnants as the foci of autoimmune aggression, the thyroidectomy is performed.
After such operation the patients till the end of life should take substitution therapy
by thyroid hormones. Is has been noticed, that after thyroidectomy, in comparison
with thyroid resection, the patients considerably better response to substitution
therapy by thyroid hormones.

RIEDEL'S THYROIDITIS

Invasive fibrous Riedel's thyroiditis (synonyms – Riedel's goiter, "woody"

goiter) is the extremely rare pathology, which consist of 0,005 % of persons
undergone the surgery for different thyroid lesions. The disease described by
Riedel in 1894 and 1897, occurs mainly in males.

Etiology and pathogenesis

The etiology of the disease is still unknown. There is the hypothesis that the
Riedel's thyroiditis is the similar to such diseases, as idiopathic fibrous
mediastinitis, sclerosing cholangitis and retrobulbar fibrosis. It gives the
suggestion that the fibrous lesions of different organs can be the manifestation of
one disease. Some authors suggest its infectious origin, though there are no reliable
findings.

Pathology

This disease is represented by the development of connective tissue in

thyroid gland with further transformation into a thick-fibber fibrous tissue.
Between its layers there are small foci of adenomatous parenchyma, mainly of a
microfollicular structure. The fibrous connective tissue spreads outside the thyroid,
penetrates into muscles of the neck, untimely adherents to esophagus and trachea,
causing their constriction and deformity.

Symptomatology and clinical course

The patients complain of goiter, dysphagia, difficult respiration and changes

of a vote quality (chestvoice) down to aphonia. The gland becomes of woody or
iron consistence, with change of configuration. Frequently observed the signs of
tracheal and esophageal compression.
The disease is characterized by severe "malignant" course with aggressive
growth of a fibrous tissue, which can go on even after thyroid resection and after
repeated operations for goiter relapse.
The function of the gland commonly preserved, though occasionally the
course of disease complicated with hypothyroidism.
The most common complication of the disease is compression of organs and
tissues of the neck, which results in dysphagia, dyspnea, and vocal changes.

The diagnostic program

1. Clinical examination of the patient (palpation of thyroid gland).

2. Sonography of thyroid gland.
3. Scanning of thyroid gland.
4. Puncture biopsy of thyroid gland.
5. Morphological investigation of thyroid tissue during surgical
management.

Differential diagnostics

Riedel's thyroiditis is necessary to differentiate with thyroid cancer. Such

sings as nodular character, metastases in lymph nodes of neck and paralysis of
recurrent nerves, are characteristic for cancer. Owing to high density of Riedel's
thyroiditis a puncture biopsy of the thyroid is usually hardly performed. Thus, it is
necessary to carry out intraoperative histological investigation.
 Macroscopically the adhesion of neck muscles with thyroid capsule is
observed. The tissue of the gland is grey, with pink foci, according to consistence
resemble cartilage and homogeneous on incision.

Tactics and choice of treatment

The treatment of invasive fibrous Riedel's thyroiditis only surgical and

consists of complete removal of affected thyroid tissue. The advantage should be
given to thyroidectomy.

THYROID CANCER
The thyroid cancer accounts 1-2 % of all malignant neoplasms. Recently
observed the tendency of increasing its frequency.

Etiology and pathogenesis

Etiologically, thyroid carcinoma has been linked to radiation exposure.

Atomic bomb survivors and patients exposed to radiotherapy for thymic and / or
tonsillar hyperplasia have been found to be at increased risk for developing thyroid
carcinoma with long latency period following irradiation. Also hormone disorders,
excessive contents of thyroidstimulating hormone of hypophysis in blood, iodine
deficiency and application of antithyroid agents contribute to thyroid cancer
occurrence. The particular value is given also influences of the genetic and
neuroendocrine factors.

Classification of thyroid cancer

According to cytological sings thyroid cancer is divided on:

I. Differentiated carcinomas:
1. Cancer from A and B cells:
- follicular adenocarcinoma;
- papillary adenocarcinoma;
- mixed adenocarcinoma.
2. Cancer from C-cells (medullary cancer with amyloidosis of stroma).
3. Squamous cell carcinoma.
II. Undifferentiated cancer.
1. Small cell cancer.
2. Large cell cancer.
3. Spindle cell cancer.
4. Polymorph cell cancer.
ІІІ. Suspicion of cancer.
 Variants of clinical course

The papillary carcinomas are the most common type of thyroid cancer.
Clinically, the papillary and mixed carcinomas are frequently grouped together.
The prognosis varies according to size of the tumour and the age of the patient. In
particular, large papillary carcinomas that cannot be completely resected as a result
of local invasion have a higher recurrence rate. Generally, the prognosis for
papillary carcinoma is excellent with a death rate of under 5%.
Follicular carcinoma is associated with a worse prognosis with associated
mortality rate of 5-15 %. Smaller tumours in young patients have a more favorable
prognosis.
Medullary carcinomas account for 5-10 % of thyroid cancer. Medullary
carcinoma can occur sporadically or in a familial form as part of the multiple
endocrine neoplasia syndrome II.
Medullary carcinoma tends to involve lymph nodes more frequently; in
addition, the basal calcitonine level is frequently elevated.
Finally, anaplastic thyroid carcinoma is a rare malignancy. It carries an
extremely poor prognosis as a result of rapid tumour growth with high locoregional
persistence and recurrence rates, as well as an overwhelming propensity to develop
distant metastases.

Clinical classification of thyroid cancer according to stages

I stage – single tumour, which does not grow through the capsule, the gland
preserves the form and mobility. There are no regional and distant metastases.
II stage – single or multiple thyroid tumours without growth into the capsule
and with preserved mobility; there are no distant metastases.
III stage – a) the tumour grow through the thyroid capsule into adjacent
tissues or compresses the neck organs (paresis of recurrent nerve, compression of
trachea, esophagus); the mobility of the gland is restricted; b) thyroid tumour
within the gland, but present bilateral movable metastases in cervical lymph nodes,
or fixed metastases in ipsilateral cervical nodes.
ІV stage – the tumour grows into adjacent tissues and organs with
metastases in cervical lymph nodes or tumour of any size with distant metastases.
The IV stage includes also all types of undifferentiated cancer

Symptomatology and clinical course

The thyroid cancer commonly occurs at women aged 40-50. Nevertheless,

this disease often occurs in young people. The clinical course is influenced by age
of the patient, morphological structure of the tumour, presence and character of
metastatic spread, general state of the patient and character of complications.
There are no characteristic sings for initial stages of thyroid cancer. The
most suspicious as for thyroid cancer are the single dense nodes of low
echointensity, which promptly enlarge in sizes. Among objective sings of thyroid
cancer is the prompt growth of the tumour and occurrence of induration and
tuberosity.
Aberrant goiter also needs to be differentiated from thyroid cancer or
metastasis in lymph node. Pain sensation is vague, and hoarseness, dysphagia,
dyspnea and hemoptysis are the late sings of thyroid cancer.
The diagnosis of thyroid cancer is confirmed by fine needle biopsy. Under
the check of sonography the aspiration needle is precisely inserted into the
pathological focus of thyroid gland or in lymph node.
During operation for thyroid pathology all the removed tissue undergo
urgent histological investigation. Its results determine the volume of further
surgical intervention.

Differential diagnostics

Differential diagnostics of thyroid cancer is based on the principle, that any

nodular, mixed or diffuse transformation of thyroid tissue, independently to a
functional state of the gland, should be suspicious on malignant neoplasm with
morphological verification. Clinical, laboratory, tests}, which allow to rule out
thyroid cancer, are absent.

Morphological diagnostics

Morphological diagnostics is performed on three levels: before operation by

means of puncture biopsy, during operation (investigation of smears, urgent
histological examination of the frozen sections of suspicious tissue) and after
paraffin investigation of specimens.

Tactics and choice of treatment

The therapy of will-differentiated thyroid carcinomas is based on the use of

surgery. Typically, a total or near-total thyroidectomy is performed. This procedure
should include a modified ipsilateral neck dissection. Patients with metastatic
tumours may undergo treatment with 131I. In these procedures patients are allowed
to become hypothyroid in order to optimize TSH stimulation of metastatic
(responsive) disease, which is followed by administration of 131I. External beam
radiotherapy is used for locoregional persistence or recurrence of thyroid tumour.
Chemotherapy is used for metastatic thyroid cancer. In particular, it has been
used in patients with anaplastic carcinomas, where doxorubicin has been
administrated and shown to result in occasional response. Doxorubicin is also used
for other metastatic thyroid malignancies.