Хирургические болезни. Практикум = Surgical diseases. Practice book. Учебное пособие

Chapter 4

VASCULAR DISEASES. CHRONIC LYMPHOSTASIS OF EXTREMITIES

Chronic limphostasis of extremities (CLE) (synonyms: lymphedema, lymphatic edema) is a complex of pathological symptoms caused by a gradually developing lymphatic outflow disturbance due to various causes and accompanied by persistent edema, increase in the extremity size, fi- brosis of the skin and subcutaneous tissue.

Etiology. Chronic lymphostasis is based on congenital causes, which cause discrepancy between the volume of the lymphatic channel and the existing level of lymphogenesis, as well as secondary causes leading to the closure (obstruction) of lymphatic vessels or lymph nodes. The latter include:

•regional injury;

•inflammatory changes (including of recurrent erysipelas);

•surgical interventions including the removal of subcutaneous tissue or regional lymph nodes (more often oncological indications);

•growing neoplasms of this area;

•previously performed manipulations on the lymphatic system (including endolymphatic administration of antibiotics) or sessions of local radiation therapy;

•increased venous pressure in this area due to CVI (PTFB), which also accompanies lymphatic hypertension.

The presented etiological factors contribute to the increase of endolymphatic pressure and lead to the stretching of smooth muscle cells of lymphangion, the basic anatomo-functional structure of the lymphatic vessel supporting its regulation, tone and lymph flow.

Clinical picture. At the initial stage (the stage of compensation or reversible changes), by decreasing the pumping function of the lymphangia, transient edema in the ankles and lower third of the shins begins to appear, intensifying in the summer (due to heat and high humidity) and significantly diminishing in the morning.

In the congenital nature of CL, to which the primary lymphedema or Milroye’s disease is attributed, there appears hysterectomy, and then swelling of the lower third of both NK, while in the secondary CL only one limb flows.

In the stage of subcompensation (or transient), a constant soft edema of the limb with a “pit” is determined after its palpation (the so-called “trace” reaction). The skin becomes pale, poorly form the skin fold (Stammer’s symptom).

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The stage of decompensation (or irreversible changes) is accompanied by deep and irreversible structural and functional damage to the lymphangia with complete destruction of its structure and contractile apparatus. Clinically, this is manifested by the constant, dense lymphatic edema of the limb due to rapid sclerosis of the lymphatic vessels and surrounding tissues. After palpation of the altered ND tissues, there is no trace “fossa”, which indicates the development of fibrosis of the skin and subcutaneous tissue and marks the onset of the fibrodema stage.

Diagnosis. Among the additional methods of studying CLE are:

•dynamic lymphoscintigraphy by lymphotropic administration of 0.2 ml of serum albumin, labeled with rapidly disintegrating radioisotopes Tc99 (or J131), followed by graphic registration of the image of the lymph drainage pathways up to the inguinal lymph nodes) in both stops; 0.2 ml of serum albumin;

•radiopaque lymphography based on endolymphatic insertion into the previously dyed (1% of the formula of methylene blue or 0.4% of the rth of indigo carmine) and isolated at the rear of the foot a lymphatic vessel of water-soluble contrast agents (omnipak, urographine, verographin) followed by dynamic radiography of limbs (up to 24 images per minute) to establish their contractile activity (aplasia);

•selective tomography (ST) and magnetic resonance imaging (MRI). These techniques are combined with radiopaque endolymphatic admin-

istration of drugs and subsequent CT (MRI) assessment of the stage of the process, the state of lymph nodes, the prevalence of edema (fibrosis) of tissues.

Treatment. Conservative treatment of the first stage of CLE (with preservation of the structure and function of lymphangia) is carried out by including:

•physiotherapy methods: electrostimulation of lymphatic vessels with amplipulse therapy apparatus; electrophoresis with lidase (ronidase, chymopsin, glucocorticoid hormones); ultraviolet or cutaneous laser irradiation of blood; VLOK – intravenous laser irradiation of blood; local ozonotherapy or HBO – hyperbaric oxygenation;

•mechanical methods consisting of:

therapeutic complexes and gymnastic exercises;

lymphatic massage with the use of special devices FTL and pneumocompression (a procedure consisting in sequential alternation – compression of the limb under a certain pressure – “bottom up” and subsequent discharge);

constant wearing of compression knitwear (I–II classes);

•medicines consisting of:

flavanids, agents that improve microcirculation, metabolic processes;

antihypoxants (actovegin, solcoseryl, reamberin, cytoflavin);

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Chapter 5

DISEASES OF THE THYROID GLAND

5.1. CLASSIFICATION OF THE THYROID DISEASES

Diseases of the thyroid gland (thyroid diseases) are divided into: 1. Congenital defects, including:

•aplasia, hypoplasia, ectopia;

•position anomalies (ectopia, dystopia);

•nonhealing diseases of the lingual-thyroid duct (middle cysts, neck fistula).

2. Nodular nontoxic goiter. It is subdivided by:

•the extent of thyroid gland enlargement:

0 – G is not visually determined or palpated;

I – G is not visualized while swallowing; only the isthmus is palpated;

II – G is visualized while swallowing and palpation;

III – G has the appearance of a “thick neck”;

IV – characteristic changes in the configuration of the neck are observed;

V – goiter of a large size (gigantic) is present.

•morphological features:

parenchymal goiter;

colloid goiter;

adenomatous goiter;

vascular goiter.

3.Toxic goiter (synonyms: thyrotoxicosis, Graves’ disease, Basedov’s disease). Thyrotoxicosis is a clinical syndrome that occurs in case of toxic goiter due to a number of reasons leading to excessive amount of thyroid hormones in the blood, regardless of the source of their origin.

4.Hypothyroidism. It is a clinical syndrome caused by a decrease in the thyroid function due to a decreased production of T3 and T4 hormones.

Hypothyroidism may be:

• primary, observed in 95% of cases. It is due to:

congenital defects caused by hypoplasia, thyroid aplasia or hereditary thyroid biosynthesis disorders;

developmental causes (often postoperative);

post-radiation effects arising after inflammation of the thyroid gland; use of thyreostatics, or in case of neoplastic lesions;

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•secondary, due to the defect of the pituitary area and the decrease in TSH (thyroid-stimulating hormone) secretion. Most frequently it is of inflammatory character due to pituitary diseases, traumas and brain tumors;

•tertiary, due to the defect of the hypothalamus and the decrease in the secretion of thyroliberin (thyrotropin-releasing hormone – TRH), contributing to the development of inflammatory processes in the hypothalamus, it may rarely occur after the treatment with serotonin drugs;

•peripheral due to inactivation of thyroid hormones in tissues or due to reduced sensitivity of tissue receptors to thyroid hormones.

5. Inflammatory thyroid diseases include:

•acute thyroiditis (strumit);

•subacute granulomatous goiter de Kerven-Krail (viral thyroiditis);

•chronic Ridelea thyroiditis (synonyms: fibrous or woody);

•chronic autoimmune thyroiditis (synonyms: Hashimoto’s goiter, lymphomatous thyroiditis);

•rare inflammatory thyroid diseases of a specific nature (tuberculosis, syphiliactinomycosis).

6. Thyroid injuries include:

•open injuries (wounds);

•closed injuries (bruises).

7. Thyroid benign tumors include:

•adenomas:

follicular tumors;

papillary tumors;

oxyphilocellular tumors;

clear cell tumors;

functioning tumours or Plummer disease;

•non-adenomatous formations (teratoma, hemarthroma, chemodectoma, neurofibroma).

8. Thyroid malignant tumors include:

•follicular cancer;

•medullary cancer;

•papillary cancer;

•undifferentiated carcinoma;

•other types of malignant tumors (sarcoma, lymphoma, epidermoid carcinoma).

5.2. SPECIFIC METHODS OF THYROID DISEASES

DIAGNOSIS

Specific methods of thyroid diseases diagnosis include:

•identification of the main thyroid gland hormones;

•Х-ray study of the thyroid gland to determine the size, shape, tissue volume and blood supply intensity;

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•scintigraphy with preliminary introduction of I125 or Tc99 isotopes (technetium pertechnetate), enable make it possible to clarify the function of the thyroid gland on the basis of isotope accumulation in its various sites;

•radiography of the chest with a contrasting substance, enable to make it possible to indirectly assess the size of the goiter by the shadow of the esophagus and the thyroid gland;

•computed tomography or magnetic resonance imaging is a highly informative diagnostic technique in substernal goiter localization;

•puncture with a fine needle aspiration biopsy under ultrasound control (informative value is over 95%).

5.3. ENDEMIC GOITER

Endemic (nontoxic) goiter (EG) is a disease manifested by a limited or diffuse enlargement of the thyroid gland caused by compensatory hyperplasia of its tissue in response to insufficient iodine intake due to regional iodine deficiency.

Iodine deficiency and the presence of thyroidogenic factors lead to inadequate production, and then to a decrease in the secretion of the thyroid hormones, causing compensatory stimulation of the thyroid hormone production by the pituitary gland with the subsequent growth of the thyroid tissue.

The development of EG is a kind of adaptive reaction of the organism in response to a lower intake of iodine at the level of “hypothalamus-hy- pophysis-thyroid hormones”, enable to make it possible (to a certain time) to restore the levels of synthesized T3 and T4, and to recreate the euthyroid state (at the onset of the disease).

With the goiter growth its state changes from the physiological to the pathological one leading to hypothyroidism, and in severe cases it results in myxedema and cretinism.

Treatment. In patients over 60 with a small size of the thyroid gland, its diffuse increases up to I–II stage and without disrupting its function, conservative treatment with iodine preparations (including potassium iodide, iodomarine), thyroid hormones (L-thyroxine or euthyriox) is used. When the function of the thyroid gland is increased, cytotoxic drugs are used in combination with iodine preparations.

Surgical treatment of EG is indicated in case of:

•TG nodular pathology or in diffuse-nodal forms;

•large (IV–V stage) diffuse or mixed goiter, which causes compression of the trachea, vessels and neck organs;

•diffuse goiter with thyrotoxicosis of moderate and high severity;

•substernal goiter.

In the treatment of EG the following methods are most frequently applied:

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•sparing (limited) thyroid resection under ultrasound control, including diathermocoagulation or cryodestruction of the nodes;

•hemithyroidectomy – subtotal removal of one of the TG lobes (in case of unilateral lesion);

•subtotal subfascial resection of the thyroid tissue (according to O. Nikolaev’s method, 1952) or the so-called thyroid tissue resection within the intrasternal fascia;

•minimally invasive interventions, including video-assisted operations, less often percutaneous injections of sclerosants using 96.4% ethanol or other chemicals.

5.4. DIFFUSE TOXIC GOITER

Diffuse toxic goiter (DTG) is an autoimmune, hereditary condition of the thyroid gland, with its uniform increase and excessive secretion of thyroid hormones, leading to thyrotoxicosis and endocrine ophthalmopathy (40–50%) due to the formation of specific thyroid-stimulating autoantibodies.

Classification. Depending on the severity of thyrotoxicosis, four stages of DTG are distinguished:

•neurotic with functional impairment;

•neurhormonal with disorders of iodine metabolism;

•visceropathic with organic lesions of internal organs;

•dystrophic (cachectic) with irreversible changes in organs and tissues against the background of more than 40% body weight loss.

According to the severity 3 degrees of DTG are distinguished:

•mild (heart rate is 80–100 beats / min, no atrial fibrillation, weight loss is up to 10%, increase in basal metabolism up to 30%;

•moderate (heart rate is 100–120 beats / min, decrease in weight loss by more than 10%, increase in basal metabolism up to 60% of the norm);

•severe (heart rate is more than 120 beats / min, ciliary arrhythmia and severe muscular weakness and dystrophy of parenchymal organs are revealed).

Etiology. The combination of various exogenous factors (acute and chronic infections, mental traumas, insolation, pregnancy, severe somatic diseases) with predisposing mechanisms (constitutional, genetic and neurohumoral), accompanied by the excessive secretion of thyroid-stimulat- ing immunoglobulins, simulating the effect of thyrotrophic hormone (TTH), are considered to be the main etiological factors of DTG development.

The incidence of DTG is 5–6 new cases per 100,000 adults per year. The disease is 8 times more common in women aged 30–50, due to the periods of dyshormonal disorders.

In response to the diverse etiological factors, B-lymphocytes and plasma cells in the body begin to erroneously recognize its own TTH thyroid

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receptors as foreign antigens, which is accompanied by the production of thyroid-stimulating autoantibodies.

The latter, by binding to thyroglutriate TTH receptors trigger an adenylate cyclase reaction with stimulation of the thyroid function. As a result, both the mass and vascularization of the thyroid gland increases thus raising the production of thyroid hormones.

A diffuse toxic goiter is characterized by a clinical triad – presence of goiter, signs of thyrotoxicosis and endocrine ophthalmopathy.

Treatment. Therapeutic treatment of DTG is recommended in the newly discovered forms of DTG. It includes:

•reduced psychoemotional and physical exertion, complete refusal from insolation;

•use of radioactive iodine-131 (applied only in case of contraindications for surgical treatment, not used in nodal forms, for children and pregnant women);

•use of iodine preparations and bromide (they block formation of THG hormones), neuroleptics;

•use of thyreostatics (mercazolil, thymazole, propylthiouracil), prescribed for 12 months in combination with levothyroxine to prevent the thyroidogenic effect (normalization of the thyroid function occurs in 30–40% of patients);

•use of the adrenal cortex hormones (prednisolone) and β-adreno- blockers (atenolol, propranolol) in case of cardiovascular system changes.

The course of DTG treatment lasts from 1 to 1.5 years. A positive effect is observed in 50–70% of patients.

Surgical treatment of DTG is recommended in case of:

•ineffectiveness of conservative therapy for 1 year;

•DTG with thyrotoxicosis of moderate and severe forms;

•compression of the neck organs (large size of the thyroid gland, causing tissue compression);

•nodal and mixed forms of toxic goiter (the so-called toxic adenoma). Operations in case of DTG are performed after the achievement of

drug compensation (euthyroid state) in the volume of subtotal subfascial resection (according to the method offered by O.V. Nikolaev, 1952).

5.5. THYROID CANCER

It occurs in about 1–2% of all malignant neoplasms or 5–6 new cases per year per 100,000 adults. In 70% of cases thyroid cancer occurs at the age of 40–60 mainly in women.

In the Republic of Belarus the incidence of thyroid tumors has doubled due to differentiated forms over the past 20 years.

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Classification. There are the following types of thyroid cancer:

•epithelial:

originating from follicular A-cells:

−papillary adenocarcinoma (80–85% of cases);

−follicular adenocarcinoma (10% of cases);

−undifferentiated (anaplastic) cancer (2.5% of cases);

originating from follicular B-cells (Ashkinazi-Gurtle) – 3–5% of all tumor cases;

originating from parafollicular C-cells – solid cancer with stromal amyloidosis or medullary cancer (1.5% of cases);

•originating from embryonic elements of the thyroid duct or metaplastic epithelium: squamous cell carcinoma (0.5% of cases);

•nonepithelial tumours: fibrosarcoma, neurosarcoma;

•mixed:

secondary (metastatic) carcinomas;

malignant lymphoma;

malignant hemangiendothelioma.

All thyroid malignancies are divided into 2 large groups – differentiated (papillary and follicular adenocarcinomas originating from A and B cells) and nondifferentiated (from any thyroid cells, and medullary cancer originating from parafollicular (C)cells).

Etiology. Etiological factors contributing to the development of thyroid cancer include the following:

•lack of iodine;

•secondary hypothyroidism;

•diseases associated with high levels of TSH in the pituitary gland;

•long-term administration of thyreostatics (timazole);

•presence of nodular goiter, adenomas or various types of chronic thyroiditis (including autoimmune);

•courses of radiotherapy in medical history;

•long stay in areas with a high level of ionizing radiation;

•combination with tumors of other localizations.

The above etiological factors contribute to the molecular-genetic transformation of thyroid cells, accompanied by activation of oncogenes (met) mutation; changes in the activity of suppressor growth genes (p53); increase in the expression of proteoglycans (CD 44, mdm 2).

Clinical picture. Thyroid cancer has no pronounced pathognomonic signs at the early stages. Later on, as the tumor increases, four groups of symptoms are revealed:

•associated with tumor growth:

rapid growth of nodular goiter;

presence of dense or uneven structure formation;

tuberosity of nodes in the area of goiter;

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