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ENDEMIC AND SPORADIC GOITER

June 6, 2024

Endemic and sporadic goiter .

Diffuse goiter with hyperthyroidism.

Inflammatory diseases of thyroid gland

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 and esofageus; 8 – n. longus colli; 9 – fascia praevertebralis; 10 – gl. parathyreoidea; 11 – veins; 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.

Fig . Anatomy of thyreoid gland. Lateral side.

Fig . Anatomy of thyreoid gland. Back side. 1- vagus nerve; 2- esophageus; 3- trachea; 4- recurrens nerve; 5- a. thyreoidea sup.; 6- glandula parathyroidea; 7- glandula thyroidea; 8- a. thyreoidea inf.

Fig . Anatomy of thyreoid gland. Lymphatic nodes.

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.

2. Sonography, computer tomography.

3. Determining of thyroid function (serum hormones, serum iodine, and thyroid-iodine uptake).

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.4. Palpation of thyroid gland(right lobe)

Fig.5. Palpation of thyroid gland(left lobe),

Fig.6. Palpation of thyroid gland

Fig. Thyroid gland scanning

Fig. Scanogram of diffuse goiter

Fig. Scanogram of thyreoid gland. Equal accumulation of isotop

Fig. Scanogram of nodular goiter

Fig. Scanogram of thyrotoxic adenoma

Fig. Scanogram of mixed goiter

Fig. Scanogram of thyreoid gland. Hypothyreosis

Fig. Scanogram of thyreoid gland. “Cold” nodle

Fig. 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.

Fig. Nodular goiter. Destruction in a center. Sonogram

Fig. Cyst of thyreoid gland. Sonogram

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. Scheme of goiter formation (retrosternal, intrathoracic)

Fig. Antesternal goiter formation

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. Anatomy of n.recurrens.

Fig. Stages of subtotal operative incision

Fig. Operative incision

Fig. Prepararation of upper layers of the skin

Fig. Transversal section of prethyroid muscles

Fig. Sutures imposition and closing with thyroid stump

Fig.Sutures on prethyroid muscles

and drainage of operative wound

Fig.16. Scheme of operation of retrosternal goiter

Fig. Large retrosternal goiter dislocated into the wound

Fig. Retrosternel goiter.

Fig. Intrathoracic goiter

Fig. Polynodes goiter

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 operatioecessary 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.

Fig. Diffuse toxic goiter. Lymphoplasmocytic infiltration of stroma.

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. Thyrotoxicosis

Fig. Diffuse toxic goiter. 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 iot 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. 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.

Diagnosing Hyperthyroidism

Fig. Algorithm for diagnosing hyperthyroidism. (TSH = thyroid-stimulating hormone; T4= thyroxine; T3= triiodothyronine.)

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.

Antithyroid drugs act principally by interfering with the organification of iodine, thereby suppressing thyroid hormone levels. Methimazole (Tapazole) and propylthiouracil (PTU) are the two agents available in the United States. Remission rates vary with the length of treatment, but rates of 60 percent have been reported when therapy is continued for two years. Relapse can occur in up to 50 percent of patients who respond initially, regardless of the regimen used. A recent randomized trial indicated that relapse was more likely in patients who smoked, had large goiters, or had elevated thyroid-stimulating antibody levels at the end of therapy.

Methimazole

Methimazole usually is the drug of choice ionpregnant patients because of its lower cost, longer half-life, and lower incidence of hematologic side effects. The starting dosage is 15 to 30 mg per day, and it can be given in conjunction with a beta blocker. The beta blockade can be tapered after four to eight weeks and the methimazole adjusted, according to clinical status and monthly free T4 or free T3 levels, toward an eventual euthyroid (i.e., normal T3 and T4 levels) maintenance dosage of 5 to 10 mg per day. TSH levels may remain undetectable for months after the patient becomes euthyroid and should not be used to monitor the effects of therapy. At one year, if the patient is clinically and biochemically euthyroid and a thyroid-stimulating antibody level is not detectable, therapy can be discontinued. If the thyroid-stimulating antibody level is elevated, continuation of therapy for another year should be considered. Once antithyroid drug therapy is discontinued, the patient should be monitored every three months for the first year, because relapse is more likely to occur during this time, and then annually, because relapse can occur years later. If relapse occurs, radioactive iodine or surgery generally is recommended, although antithyroid drug therapy can be restarted.

Propylthiouracil

PTU is preferred for pregnant women because methimazole has been associated with rare congenital abnormalities. The starting dosage of PTU is 100 mg three times per day with a maintenance dosage of 100 to 200 mg daily. The goal is to keep the freeT4 level at the upper level of normal.

Complications

Agranulocytosis is the most serious complication of antithyroid drug therapy and is estimated to occur in 0.1 to 0.5 percent of patients treated with these drugs. The risk is higher in the first several months of therapy and may be higher with PTU than methimazole. It is extremely rare in patients taking less than 30 mg per day of methimazole. The onset of agranulocytosis is sometimes abrupt, so patients should be warned to stop taking the drug immediately if they develop a sudden fever or sore throat. Routine monitoring of white cell counts remains controversial, but results of one study showed that close monitoring of white cell counts allowed for earlier detection of agranulocytosis. In this study, patients had white cell counts every two weeks for the first two months, then monthly. In most cases, agranulocytosis is reversible with supportive treatment. Minor side effects (e.g., rash, fever, gastrointestinal symptoms) sometimes can be treated symptomatically without discontinuation of the antithyroid drug; however, if symptoms of arthralgia occur, antithyroid drugs should be discontinued because arthralgia can be a precursor of a more serious polyarthritis syndrome.

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.

The treatment dosage of radioactive iodine has been a topic of much debate. A gland-specific dosage based on the estimated weight of the gland and the 24-hour uptake may allow a lower dosage and result in a lower incidence of hypothyroidism but may have a higher recurrence rate. Higher-dose ablative therapy increases the chance of successful treatment and allows the early hypothyroidism that results from this regimen to be diagnosed and treated while the patient is undergoing close monitoring. Some studies have shown that the eventual incidence of hypothyroidism is similar regardless of the radioactive iodine dosage. The high-dose regimen is clearly favored in older patients, those with cardiac disease, and other groups who need prompt control of hyperthyroidism to avoid complications. Patients with toxic nodular goiter or toxic adenomas are more radio resistant and generally need high-dose therapy to achieve remission. They have a lower incidence of eventual hypothyroidism because the rest of the gland has been suppressed by the toxic nodules and protected from the effects of radioactive iodine.

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 (percussioear 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 iorm), 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 beeoticed, 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.

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Підготував Доброродній А.В.