SURGICAL PATHOLOGY OF THYROID GLAND

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Thyroid gland is an endocrine glandule, situated in anterior cervical area,
formed by two lateral lobes and istmus. Weight – 30-35 g. Thyroid gland consists of
folliculus and connective stroma with good vascularization – arteria thyroidea
superior (from a. carotis externa) and inferior (from thyrocervical trunk). Sometimes,
there is arteria thyroidea ima (from brachiocephalic trunk or aorta arch).
Venous drainage is realized by v. thyroidea → v.jugularis externa → thyreo-
linguo-facial trunk.
Lymphatical drainage is realized by cervical and mediastinal ganglions.
Nerve laryngeal superior and recurrens inferior provide with sympathetic
innervation.
Thyroid gland produces thyroid hormones: T4 –thyroxine, T3- triiodthyronine,
thyrocalcitonine, which have following effects:
- control of cellular metabolism
- stimulate proteic and lipidic catabolism
- processes of neoglucogenesis
- increase the tissue consumption of oxygen
- decrease the plasmatic concentration of F and Ca 2+.

The stages of synthesis and secretion of thyroid hormones:

- the metabolism of iodine (nonorganic and organic stages)
- synthesis, accumulation and secretion of thyroid hormones
- transportation of hormones to receptors of target organs
- specific effects
- regulation of thyroid activity (feed-back relationship)

METHODS OF EXAMINATION OF THYROID PATHOLOGY

1. Clinic examination and anamnesis – competent and complex with

paraclinical examination in dependence of peculiarity of case or necessity of
differential diagnosis.
2. Biological analysis: hemogram, coagulogram, renal tests (urea, creatinine),
hepatic tests (bilirubin, ALAT, ASAT), glycemia, analysis of urine, etc.

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3. Radiologic examination and echography of glandule thyroidea: radiography
of thorax with barium esophageal transit, cervical radiography, computed
tomography and nuclear magnetic resonance.
4. Radioisotopic examination: thyroid scintigraphy with I131 or Tc99.
5. Functional examination: tests of inhibition with T 3 (Werner test), stimulation
test with TSH (Querido-Stamburi test); basic metabolism, reflexogram.
6. Doses of biohormones: T3 or T4; cholesterol, PBI (protein binding iodine),
antithyroid antibody (antiglobuline, antipyroxidase, anti-TSH); calcitonine;
tumor markers (carcinoembyonic antigen, prostaglandine E 1 and E2 etc).
7. Puncture-biopsy - different variants.
8. Lymphography, thermography and angiography of glandula thyroidea.

CLASSIFICATION OF THYROID GLAND PATHOLOGY

1. Endemic goiter:
- according to the dimensions of goiter – 0, I, II, III, IV, V.
- according to the shape – diffuse, nodular(50%) or mixed.
- according to functional state – hypothyroidism, euthyroidism and
hyperthyroidism.
- according to localization – unilateral, bilateral and retrosternal (5-10%),
sublingual (2-9%) and ectopic;
2. Sporadic goiter – the same classifications like endemic goiter.
3. Thyroid toxic adenoma (Plummer thyreotoxic adenoma)
4. Toxic diffuse goiter (Basedow-Graves disease), classification according to
severity – light, middle, severe.
5. Hypothyroidism – light, middle, severe.
6. Inflammatory disease of thyroid gland – thyroiditis, acute thyroiditis and
strumitis (purulent and non-purulent); subacute thyroiditis (de Querven);
chronic atrophic thyroiditis (Riedel and Hashimoto); specific thyroiditis
(tuberculosis, syphilis).
7. Parasitogenic disease (hydatic cyst, actinomycosis)
8. Thyroid cancer or malignant goiter:
A. Malignant epithelial tumors (90%) – carcinoma :
- differentiated tumor (80%): papillar (55-70%); follicular (15-20%)
- non-differentiated : anaplasic (5%), medullar (5-10%)

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 B. Connective tumors (10%) – sarcoma; lymphoma.
C. Metastatic cancer in thyroid gland.

ENDEMIC GOITER

Definition. Endemic goiter is a hypertrophy of the thyroid gland and is

conditioned by dystrophic hyperplasia of glandular folliculus or connective vascular
tissue.
It can be congenital or acquired (sporadic, endemic), with eu- hypo- or
hyperthyroidism.
This disease is spread mainly in mountainous area (Carpathians, Alps,
Himalayas) and in zones where is the geoclimatic deficit of iodine. According to WHO
statistics there are 200 million people with endemic goiter in the world.

Etiology factors.
– deficit of iodine
– goiter-stimulated substances
– disturbance of metabolism
– genetic and individual factors, age, sex and stress
Etiology factors → decrease synthesis and concentration of thyroid hormones
(T3, T4) in blood → deliberation of TRH at the level of hypothalamus (feed-back
relationship) → increase the secretion of TSH → stimulation of glandular growth and
activation of hormones synthesis → normalization of peripheral titre of thyroid
hormones.
Primary, it has the place a functional hypertrophy of thyroid gland, then the
hyperplasia of functional units of thyroid gland, with irreversible structure
modifications.
Clinical manifestations. Objective local examinations (inspection,
auscultation, palpation) give the information about topography (global, lobar, isthmic,
ectopic and abberant), volume, mobility and consistence of thyroid gland and
presence of latero-cervical adenopathy.
Clinical classification of process of parenchimatous hyperplasia based on
increase in volume of thyroid gland (0, I, II, III, IV, V – Swedish score)
0 – thyroid gland is invisible and non-palpated;
I – is invisible, but isthmus is palpated;

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 II – is visible (in swallowing), both lobes are palpable;
III – goiter is big, visible so-called “thick-neck”.
IV – voluminous goiter which changes the configuration of neck;
V – gigantic goiter with phenomenon of compression:
 laryngo-tracheal – dyspnea
 recurrent-syndrome – bitonal voice, grow hoarse
 jugular-syndrome – cyanosis of face, cephalgia, epistaxis
 esophageal-syndrome – dysphagia
 cervical sympathetic syndrome Claud Bernard-Horner –
miosis, exophthalm, palpebral superior ptosis
 pneumogastric syndrome – tachycardia, bradycardia
Diagnosis
►Cervico-thoracic radiography discover deviation or compression of trachea,
the presence of calcification or mediastinal goiter.
►Scintigraphy of thyroid gland gives information about volume of goiter and
discover generalization of process in Basedow disease or localization of “hot node” in
toxic thyroid adenoma and “cold node” in presence of one cyst, calcificate or thyroid
neoplasm.
►Echography – shows if the formation is solid or cystic, nodular or multinodular
and gives the possibility of biopsy or puncture of cyst.
►Radiocapture of thyroid gland increase in first 6 hours with slow normalization.
►Basic metabolism decrease in forms associated with hypothyroidism and
increase in forms with hyperthyroidism.
►Radioimmunologic method determines the dose of T3 and T4 in blood.
►Laryngoscopy shows the paresis of vocal chord in case of compression.

Evolution and complications. The evolution of simple goiter is chronic,

dependent on alimentation, treatment, physiological state and associated with
increase slow or regressive.
Complications: interstitial haemorrhage, strumitis, compressions,
malignisations in case of nodular forms.

Treatment. The treatment of goiters is prophylactic (salt with iodine, pill with
KI), medical (antithyroidean) and surgical. The treatment has certain goals:
1. Reestablishment of deficit of iodine

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 2. Normalization of level of thyroid hormones in blood
3. Liquidation of phenomenon of anatomical structures compression

Indications for surgery

 Non-effective medical treatment (after 6 months of correct treatment)
 Nodular goiters
 Gigantic compressive goiters
 Goiters with hyperthyroidism
 Goiters with strumitis
 Goiters with suspicion of malignization

Variants of operations
 Subtotal thyroidectomy (Kocher) or subfascial (Nicolaev) – 4-6 g of thyroid
gland reserved for support of hormones balance
 Hemithyroidectomy – lobectomy with isthmectomy
 Enucleoresection – extirpation of nodes or isolated cysts
 Total thyroidectomy (multinodular goiter)

Anesthesia can be local and general. Incision – cosmetic, arcuate, cervical

anterior, 2 cm cranially from fossa jugularis of sternum.

HYPERTHYROIDISM (Thyreotoxicosis)

Definition. It is a summary of visceral, hormonal, biochemical and clinical

manifestations, which results in acute or chronic intoxication by thyroid hormones.
Hyperthyroidism can be primary, secondary, tertiary and quaternary.
Principal affections which provoke the state of hyperthyroidism are:
 Diffuse toxic goiter (Basedow-Graves-Parry disease)
 Hyperfunctional thyroid adenoma (toxic adenoma Plummer)
 Multinodular hyperthyroid goiter

DIFFUSE TOXIC GOITER

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 Basedow-Graves disease is the autoimmune hyperthyroidism with general
incidence 1-2 cases/1000 people/year, mainly affects female.
Etiopathogenesis. Basedow disease is a form of thyrotoxicosis with
autoimmune pathogenesis, genetic determination.
Predisposal factors:
 State of stress, mental traumatism
 Preexisted thyroid affections (goiter, thyroiditis)
 Some infections (influenza, rheumatism, syphilis)
 Period of hormonal disbalance (puberty, pregnancy, menopause)
Thyroid stimulating immunoglobuline is a late action thyroid stimulator (LATS),
gammaglobuine 7S acts at the level of TSH–receptors (thyroid stimulating hormone).

Clinical manifestations. Cardinal symptoms of this disease are included in

Basedow’s triad: goiter, thyrotoxic syndrome and ophthalmopathy. It can be diffuse,
elastic, vascular, homogenous.
Thyrotoxic syndrome is represented in different grades and affects majority
of systems:
– Cardiovascular (99%)
– Nervous (90%)
– Digestive (50%)
– Other organs of internal secretion (50%)
– Ophthalmopathy Graves (60-80%):
 Absence of convergence of ocular globes (Moebius symptome)
 Photophoby
 Epiphora (running eyes)
 Rare winking (blinking)
 Fixed look (Stellwag I,II symptom)

Secondary symptoms of thyrotoxicosis: scleroderma, pigmentation,

urticaria, itch, infiltrative dermatopathy, disturbance of menstrual cycle, decrease of
libido, gynecomasty.

Diagnosis of thyrotoxicosis:
 hemogram – leucopenia, lymphocytosis, eosinophylia

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  level of T3, T4 in blood (increase)
 echography of thyroid gland (hyperechogenic structure of gland),
 scintigraphy: diffuse or local hyperplasy of thyroid gland with
phenomenon of hypercapture of I131
 basal metabolism (increased more then 30-90%)
 reflexogram
 histopathological examination – small folliculi with epithelial high cells and
lymphoplasmocitar infiltration

Treatment of thyrotoxicosis is complex and the goal is:

 decrease of secretion of thyroid hormones
 struggle with visceral and metabolic effects of thyronine
 sedation of cortico-diencephalo-hypophysial centers
 social and professional rehabilitation of patients

Therapeutical treatment: antithyroid substances, radioactive iodine and

surgery – every method has advantages and disadvantages.
Antithyroid substances (ATS, inhibitors of synthesis) – methylthiouracil,
propylthiouracil, benzyilthyouracil, carbimazol, metimazol, methylmercaptomedazol.
Treatment with ATS can be independent or associated with
immunosuppression (glucocorticoids), inhibitors of peripheral conversion (salt of
lithium), beta-adrenergic blockade (anapriline), anabolics, diuretics, tranquillizer.
Surgical treatment has advantages because of fast and persistent
therapeutic result. The success of surgical intervention depends on preoperative
preparation of patients and for this goal are indicated:
 alimentary regime with proteins and glucides
 neuromental sedation – bromate, barbiturate etc
 inhibition of hormones synthesis – Sol.Lugole 2% in progressive doses
 administration of sympathycolytic (guanitidine, reserpine, propranolole)
 administration of antithyroid drogs – 2-3 weeks before operation

The optimal criterion of successful operation is the state of euthyroidism:

1. The pulse 80-90 per minute
2. Increasing weight

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 3. Psychomotor sedation
4. Temperature and paraclinic analysis in limits of norma
Indications for surgery
1. Non-effective correct medical treatment or relapse
2. In case, when I131 is contraindicated
3. In severe forms at the beginning, age < 40 years
4. In forms complicated with cardiothyreosis and other phenomenon of
visceralization
5. Nodular goiters with hyperthyroidism
6. Hyperthyroidism with compressive or retrosternal hypertrophy of
thyroid gland

Operation technique – subtotal and subfascial thyroidectomy (Nicolaev).

TOXIC THYROID ADENOMA

TTA is represented by one-node with hypersecretion of thyroid hormones

(Plummer, 1993).
Etiopathogeny is not learned completely.
Clinical symptoms of this malady are the same as in Basedow’s disease, but
exophthalmos is absent.
Physical examination shows the uninodular goiter with clear borders, mobile.
Positive diagnosis:
1. Scintigraphy of thyroid gland: “hot node” hypercaptured
2. Echography determines the structure of node
3. Histology: cylindrical cells of follicule’s epithelium, often with atypia

Treatment in TTA is only surgical - enulcleation of node or subtotal lobectomy.

The iodine-containing pills are used for prophylaxis of recidives.

MULTINODULAR TOXIC GOITER

It is a variant of hyperthyroidism which appear in patients from endemic zones

with old polynodular goiters (non-functional nodes with hyperfixant (-functional) node,
which is the generator of thyrotoxicosis).

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 Clinical manifestations. Symptoms of moderate thyrotoxicosis (muscular
asthenia, tachyarrhythmia, atrial fibrillation). Non-homogenous goiter, polynodular
with variable volume I-IV grades, with compressive phenomenons.
Diagnosis:
Scintigraphy and echography: non-homogenous aspect.
Laborator: confirmation of thyrotoxicosis.
Treatment – subtotal thyroidectomy is used.

THYROIDITIS

Definition. Inflammation of thyroid gland with normal structure is called

thyroiditis, but inflammation of one goiter is called strumitis.

Acute thyroiditis

Etiology is varied – microbian infection, viruses, amygdalitis, phlegmon of

neck etc.
Clinical manifestations – pain at the cervical anterior area with temperature
38-40°C, shivering, aglutition. Local – tumor, rubor, color, dolor, fluctuation and the
palpation (abscess).
Diagnosis – leukocytosis, ESR ↑, scintigraphy and thermography show the
“cold zone” (abscess).
Treatment – antiinflamatory and antiinfectious. Surgical treatment is indicated
in phase of abscess – incision in point of maximal fluctuation, evacuation, drainage.

Granulomatous subacute thyroiditis de QUERVEN

It is a non-supurative inflammation of thyroid gland of viral etiology with

subacute evolution and with anatomo-clinical peculiarities, appears after one episode
of intercurrent infection of superior respiratory tract, appears mainly in female.

Clinical manifestations – temperature, asthenia, adynamia, myalgia, later

appear rapid increase in volume of thyroid gland and violent pain with reflection in
head, neck or superior thorax. Patients have anxiety, palpitation, insomnia.

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 Positive diagnosis – clinic, lymphocytosis, capture of Tc 99↓, increased ESR.
Puncture-biopsy of thyroid gland shows the infiltration with gigantic cells, polynuclear
cells and macrophages, granulation tissue (granuloma).

Evolution – the spontaneous recovery in 70% of cases (1-3 months),

sometimes the malady relapses and transforms in chronic lymphomatous or fibrous
thyroiditis.

Treatment is medical and the goal is to limit inflammatory process:

 AIN
 Corticotherapy is extremely efficient (prednisolon according to scheme)
 Local anti-inflammatory roentgenotherapy (in severe cases)
 Symptomatical treatment: sedatives, beta-adrenergic blockers

Lymphomatous chronic thyroiditis HASHIMOTO

It is a chronic inflammatory process which is characterized by infiltration of

thyroid gland with lymphoid cells.

Etiopathogenesis. Female/male - 8/1. This disease has the familial

character. There is a production of antibody against components of thyroid gland
which determine the autoimmune manifestation (rheumatoid polyarthritis, lupus
erythematosus, myasthenia gravis, sclerodermia).

Morphopathology. Thyroid gland is big due to diffuse or nodular increasing

and has following microscopic characteristics:
 inflammation of stroma with lymphoid cells
 follicular epithelium is replaced by big cells, oxyphylic so-called
Askanazy-Girtle cells

Clinical manifestations. Homogenous goiter, solid, pain-free with high local

temperature, which provokes discomfort in cervical anterior area. The symptoms of
thyroid gland hypofunction appear very often (weariness, increase in weight) and
compressive phenomenon.

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 Diagnosis: clinic, increase of serologic titre of antithyroid autoantibodies,
increase of ESR, state of hypothyroidism (50% cases). Reliable method of diagnosis
is puncture with echo-guided biopsy.

Treatment is medical (thyroid hormones, corticosteroids) and surgical in case

of compression phenomenon (subfascial subtotal thyroidectomy + thyroid hormones
in postoperative period).

Chronic fibrous thyroiditis RIEDEL

Thyroid gland is replaced by fibrous sclerosed tissue, solid (dense), which

extends on neighboring organs (trachea, nerves, vessels).

Etiopathogenesis is not studied completely. It is considered that thyroiditis

Riedel presents the final stage of thyroiditis Hashimoto or granulomatous de
Querven. In can be associated with other fibrous idiopathic pathology (retroperitoneal
fibrous, sclerosing cholangitis, fibrous mediastinitis).

Clinical manifestations. The main symptoms are connected with

compression of trachea, esophagus or recurrent nerve. The finally hyperthyroidism,
recurrent paralysis, stridor, dyspnea and deglutitive problems appear.

Diagnosis. Physical examination determines a solid goiter, fixed, arborescent.

Scintigraphy with I131 shows non-homogenous decreased capture. Echography of
thyroid gland shows one hyperechoic node with non-regulate outline. Cytology
reveals follicular cells circled (included) by fibrous tissue, lymphoid elements,
macrophages and gigantic polynuclear cells.

Treatment is surgical and has following indications:

 grave phenomenon of compression
 impossibility of differential diagnosis with thyroid cancer

Surgical technique – total unilateral lobectomy with isthmectomy in case when

one lobe is affected or thyroidectomy with next substitution therapy with hormones in
case of total damage of thyroid gland.

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 POSTOPERATIVE COMPLICATIONS AFTER OPERATIONS
ON THYROID GLAND

 Haemorrhage, haematoma of thyroid bed – reopening of cervical wound,

evacuation of haematic collection.

 Attack of thyrotoxicosis – acute intoxication of body with thyroid hormones

(tachycardia, pulse >160’, arrhythmia, high blood pressure, fever 40-41ºC,
diarrhea, vomiting, myastenia, state of agitation, confusion, hallucinations,
coma). It is indicated hypotensive, beta-adrenergic blockers, antiarrhythimic,
thyrostatic, corticosteroids, sedative.

 Paralysis of recurrent nerve appears by compression, ligature or section of

recurrent nerve, as a result appear definitive or passing injuries, uni- or
bilateral (aphonia, dyspnea, cyanosis, hoarse, modifications of voice). The
treatment includes proserin, lasix, vitaminotherapy, inhalations. Bilateral
paralysis leads to asphyxia – urgent tracheostomy.

 Hypothyroidism appears after radical thyroidectomy and is characterized by

asthenia, increasing weight, intellectual deterioration, palpebral oedema,
lethargy. It is indicated substitutive hormonotherapy.

 Hypoparathyroidism – can be passing or permanent, and is caused by injuring

or accidental dissection of parathyroid gland. Clinic manifestations –
parathyroprive progressive and severe syndrome → paraspasm of face,
muscular cramps, muscular contraction of extremities and masseters. It is
administrated CaCl2, parathyroidine, implantation of parathyroid gland or
implantation of alogen subcutaneous bone tissue (20-30g).

 Wounds infection – in form of cellulitis or phlegmon of thyroid bed.

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The thyroid gland. A. The gland has been presented as a transparent structure to show the
relationship to the vessels and nerves. The path of the inferior thyroid artery can be followed.
B.Cross-section through the isthmus of the thyroid gland. C. The thyroid gland viewed from the
left side. The gland is in relation to two nerves (recurrent and external laryngeal), two tubes
(esophagus and trachea), and two muscles (inferior constrictor and cricothyroid).

Drawing demonstrating the possible locations of thyroglossal cysts. (A) In front of foramen cecum;
(B) at foramen cecum; (C) suprahyoid; (D) infrahyoid; (E) area of thyroid gland; (F) suprasternal.

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Graves' ophthalmopathy may present in association with thyrotoxicosis or in isolation (euthyroidal or ophthalmic Graves'
disease). Eye signs demonstrated in this patient are exophthalmos with proptosis, supraorbital and infraorbital swelling,
congestion, and edema of the conjuctiva.

The goiter in Graves' disease is diffusely enlarged and smooth. Evidence that the whole gland is enlarged may be confirmed by
palpation of the pyramidal lobe of the thyroid as it crosses the cricoid cartilage. The goiter illustrated here was large enough to
be viewed from behind the patient.

Radioiodine scan (123I) in a patient with thyrotoxic Graves' disease demonstrating uniform uptake throughout the gland.

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The iodide cycle. Ingested iodide is trapped in the thyroid gland, oxidized, and bound to tyrosine to
form iodotyrosines in thyroglobulin. Coupling of iodotyrosyl residues forms T4 and T3. Hormone
secreted by the gland is transported in the serum. Some T4 is deiodinated to T3. The hormone
exerts its metabolic effect on the cell and is ultimately deiodinated. The iodide is reused or excreted
by the kidneys. A second cycle goes on inside the thyroid gland with deiodination of iodotyrosines
generating iodide, which is reused without leaving the thyroid.

Schema of the homeostatic regulation of thyroid function. Secretion of TSH is regulated by a

negative feedback mechanism acting directly on the pituitary and is normally inversely related to the
concentration of unbound hormone in the blood. Release of TSH is induced by TRH secretion, which
sets the level of the pituitary feedback mechanism. Factors regulating secretion of TRH are uncertain
but may include the free hormone in the blood and stimuli from higher centers. Autoregulatory
control of thyroid function also is shown.

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