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

Chapter 6

DISEASES OF THE MAMMARY GLANDS

6.1. CLASSIFICATION OF THE MAMMARY

GLANDS DISEASES

Diseases of the mammary glands (MG) are divided into developmental shortcomings, MG damages, inflammatory diseases of breast, intravenous disharmonious dysplasia and breast tumors.

1. Developmental shortcomings, including:

•amastia, i.e. absence of mammary gland (rarely);

•atelia, i.e. lack of a pacifier MG;

•polymastia, i.e. an excessive number of glands;

•polythelium, i.e. excessive number of nipples;

•additional mammary glands not associated with gland and, as a rule, do not have a excretory duct;

•micromastia, i.e. symmetrical underdevelopment of MG tissue in various endocrine diseases;

•macromastia, i.e. hypertrophy of MG tissue.

2. MG damage, which includes:

•closed injuries, hematomas and bruises accompanying the development of scar tissue;

•open injuries (wounds), accompanying the trauma of the milk ducts with the development of secondary mastitis or the formation of external fistulas.

3. Inflammatory diseases of breast, including:

•acute processes:

paramastitis, i.e. inflammation of the fat surrounding the breast;

mastitis is an acute inflammation of the glandular tissue of the MG;

•chronic processes:

chronic mastitis;

actinomycosis of MG;

tuberculosis;

syphilis.

4. Intravenous disharmonious dysplasia, including:

•fibro-cystic mastopathy (synonyms: fibroadenosis, fibrocystic disease);

•cysts (including single and multiple, called “galactocele”);

•gynecomastia (mammary gland hypertrophy in men).

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5. Breast tumors divided into:

•benign:

fibroadenoma;

cystoadenoma (i.e. a phylum tumor);

lipoma;

papilloma;

•malignant:

epithelial (or cancerous), accounting for 98–99% of the processes of this subgroup;

nonepithelial (or sarcomas), constituting about 1% of all malignant formations of MG.

6.2.DIAGNOSIS OF THE MAMMARY GLANDS DISEASES

Special methods for diagnosis of MG diseases are:

•mammography – X-ray examination of MG in direct and oblique lateral projections. There are two types of mammography: screening (used in the absence of symptoms for the purpose of early change in MF) and diagnosis mammography (used with the already identified changes in MG);

•ultrasound examination (95–96% informative). The disadvantage of the method is the impossibility of diagnosing MG-lesions with a diameter of less than 1 cm;

•FNAB (fine needle aspiration biopsy) – under an ultrasound or R- graphic (mammographic) control with the cytological examination (70–80% informative);

•trepanobiopsy – taking the material;

•computer and magnetic resonance imaging – to assess the prevalence of the process, the state of the intrathoracic lymph nodes, the presence of distant metastases in the lungs, the liver;

•positron emission tomography (PET) is a method of visualization of malignant tumors in MG, a diameter of less than 10 mm and intensively accumulating an ultrashort-acting (rapidly decaying) radionuclide preparation based on 18-fluorodeoxyglucose in relation to unchanged cells;

•determination of tumor markers (CEA and CA-15-3), the level of which correlates with the presence of bulk malignant MG formations.

6.2.1. Acute mastitis

Acute mastitis (AM) is an acute inflammation of the parenchyma and interstitial breast tissue. There are two forms of AM: lactate (above 85– 95% of all species) and nonlactate form, which cause women older than 35–40 years from the lactation period.

Classification. AM is classified by:

•ulcer localization:subcutaneous;

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intramammary (in the MG tissue);

retromammary (deeply localized abscess between the thoracic fascia and the MG);

subareolar (located in the projection of the sucking mug);

galacto-oophoritis;

•stage of development (by the nature of the inflammatory process):

nonsuppurative:

−serous;

−infiltrative;

suppurative:

−abscessing;

−infiltrative-abscessing;

−phlegmonous (according to the type of purulent soft tissue of the breast);

−gangrenous (proceeds on a background of a thrombosis of vessels of MG and a hypoxia of tissues);

prevalence of purulent inflammation:

−limited (localized within the limits of the 1st quadrant);

−diffuse (occupies 2–3 quadrants);

−total (occupies all 4 quadrants of MG).

Etiology. The causative agent of AM is most often Staphylococcus aureus (up to 90% of cases); less often Epidermal staphylococcus, E. coli, streptococcus, enterococcus, proteus, Pseudomonas aeruginosa (usually in association with staphylococcus).

Factors contributing to the development of AM are:

•lactostasis (85% of all factors);

•stiffness and cracked nipples;

•mastopathy in the history;

•anatomical features of the structure of the breast and nipple (convoluted and thin milk ducts);

•noncompliance with breastfeeding or personal hygiene;

•purulent-septic diseases in the anamnesis;

•pathology in the period of pregnancy, childbirth (use of oxytocin or prostaglandins) or early postpartum period;

•decreased immunity and changes in the immune status (associated with a number of concomitant diseases, advanced labor, complicated by the course of the postpartum period).

These factors contribute to both the activation of inflammation, and the disorder of venous and lymphatic outflow in the MG tissue. In turn, the increasing swelling of the interstitial tissue causes the secondary compression of the milk ducts of neighboring, unchanged regions – the lobules of the breast and is accompanied by the development of lactostasis with the progression of the inflammatory process to the entire MG.

Treatment. Conservative treatment of mastitis in the stage of serous-

infiltrative inflammation is:

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•improvement of milk separation by the use of myotropic spasmolytic agents (no-spa, drotaverin, spasmalgon, duspatalin) and oxytocin (0,5 ml every 5 min before feeding);

•carrying out a short retro mammary novocain blockade according to A.V. Rozhkov (1922) consisting of : 150 ml of 0.25% solution of novocaine with a broad-spectrum antibiotic (semisynthetic penicillins of 4–5 generations or cephalosporins 3–4 generations) + corticosteroid preparations (175 mg hydrocortisone) + protease inhibitors counter 20,000 units or gordox 120,000 units or gabexat);

•IM introduction of broad-spectrum antibiotics and antihistamines;

•the use of immunocorrectors of monocyte-macrophage and T-cell links and natural immunorequency – (12 мg of polyoxidonium, 1 ml of 0,0005% of imunofan, 2 ml of erbisol); the introduction of hyperimmune preparations of serums and immunoglobulins (indicated only to a specific causative agent);

•aseptic dressings-applications with 25% dimexide gel in combination with indovazin (1 : 1); local application of semi-alcoholic compresses or chloroethyl blockade;

•conducting FTL – ultrasound, magnetolaser therapy or UniSPOK (on the area of the MF infiltrate).

Surgical treatment of AM is performed in its purulent forms more often under general anesthesia and includes the basic principles of surgical treatment of a purulent focus (HOGO).

6.2.2. Fibro-cystic mastopathy

Fibro-cystic mastopathy (FCM) is a disease based on a dyshormonal benign process that combines various disorders in the proliferation of epithelial and connective tissue components of the MG resulting from an imbalance of circulating and / or locally produced female sex hormones.

The presented disorders affect both proliferative (hyperplasia, proliferation of lobes and ducts, growth of connective tissue), and the regressive nature of changes in the MG, including atrophy, fibrosis, and cyst formation.

Classification. There are two forms of FCM:

•diffuse, representing diffuse fibrosis of connective tissue with the formation of small cysts. As a rule, it results from:

predominance of the fibrous component;

predominance of the cystic component;

combination of the above disorders;

sclerosing adenosis;

•nodal, which is a single nodal MG formation of various sizes. Typically, proceeds according to the type:

adenofibroma;

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fibroadenomas;

adenosis;

fibromatosis.

Etiology. The risk factors for FCM are:

•functional disorders of the neuroendocrine system (including various psychogenic disorders: stress, neurosis, depression, thyroid dysfunction, metabolic syndrome, diabetes, polycystic ovary syndrome, etc.);

•reproductive factors (include the history of multiple pregnancies, childbirth or abortion, predisposing age, existing menstrual irregularities, or gynecological diseases);

•diseases of the liver and biliary tract;

•genetic predisposition;

•diseases of a sexualorgans;

•MG injury in history.

As a result of the influence of the presented factors on the side of the MG tissue, there are observed:

•the onset of fibrosis of the stroma of the connective component;

•proliferation of duct epithelial cells with the formation of papillomatous structures;

•widening of the intracanalicular ducts with the formation of cysts;

•the onset of apocrine metaplasia (up to intraepithelial calcification);

•proliferation of connective tissue in the lobules of the breast with the formation of sclerosing adenosis.

Treatment. In the diffuse form, after the final verification of the diagnosis, a therapeutic treatment is prescribed, including:

•elimination of provoking etiological factors determining pathogenesis of the process;

•multivitamins (A, C, E, group B) and minerals (selenium, copper, zinc,

iron);

•administration of nonsteroid anti-inflammatory drugs (one week before mensis);

•administration of drugs that improve venous outflow (cyclo 3-fort, detraleks, flebodia, venoruton, etc.);

•in the presence of indications – hormonal treatment (antiestrogens (phareston, tamoxiren, danazol)); gestagens; inhibitors of prolactin (dopinex); gonadotropin activators (LHRH));

•phytotherapy and homeopathic remedies (feocarnin, mammokram, cyclodion, climadion, mastodion, etc.) continuously for more than 5–6 months;

•long-term enzyme therapy (at least 3 months) with vobenzim, fl uen-

zyme.

With the nodular form (after the final verification of the diagnosis and the establishment of the proliferation of the epithelium without atypia),

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an economical removal of the node with biopsy is shown; in mastopathy suspected atypia a sectoral resection with a histological intraoperative studis performed.

6.2.3. Phyllodes tumor of the mammary glands

Phyllodes tumor of the mammary glands (MG) (i.e. leaf-shaped cystadenoma – cystadenoma phyllodes) is a type of fibroadenoma of the MG, consisting of connective tissue and the epithelium of the MG.

This tumor looks like “cabbage leaves” on the cut or sheets of a folded book, which determined its primary name.

It is characterized by the rapid growth of existing cells, up to very large formations, reaching 30–40 cm in diameter, the skin over which is thinned and acquires a cyanotic staining. It occurs in 0.2–0.3% of all cases of MG tumors; in 10–20% of cases sarcoma is malignant, in 15% gives metastases, in 20–30% is complicated by reoccurrence after surgical treatment.

Classification. Morphologically three types of tumors are distinguished: benign, borderline, and malignant.

Process options are:

•a forming tumor;

•a classical course with the presence of intracanal FA; with the growth of connective tissue in the lumen of dilated ducts covered with epithelium;

•leaf-shaped tumor with the presence of sarcomatous stroma along the edges, requiring FNAB with a cytological study of the tumor to confirm atypical cells.

Treatment. The treatment of a phylloid tumor of breast cancer is surgical. The operation of choice is a sectoral resection of MG with an urgent biopsy; if intraoperative biopsy confirms the third option, go for a radical mastectomy with lymphodissection.

6.2.4. Breast cancer

Breast cancer is a malignant neoplasm of MG, originating from the cells of the ductal epithelium and the parenchyma of the breast. It is responsible for about 20–30% of all malignant tumors of any other localizations. It is the most common tumor in women above 40; the peak incidence falls on the age of 60–65.

Classification. Classification of breast cancer according to the type of tumor growth:

•nodular form;

•diffuse forms, consisting of:

swelling-infiltrate;

shell;

inflammation (including mastitis, and erysipelas form).

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Etiology. Predisposing risk factors for breast cancer include:

•nulliparous women with high socio-economic status;

•late first childbirth (> 30 years), early menarche (< 12 years); late menopause (> 55 years);

•mastopathy in the anamnesis;

•replacement hormone therapy in postmenopause due to excess estrogens and prolactin;

•morbid obesity;

•ionizing radiation;

•being tall (more than 170 cm).

The genetic factors that affect the development of breast cancer include:

•mutation of BRCA-1 genes (increases the risk of breast cancer to 70% in women to 70 years of age) and BRCA-2 (found only in men, causing a risk of developing breast cancer in 80% of cases);

•genetic predisposition (with anamnestic confirmation of breast cancer in the mother the risk increases 4 times, in the sibling – more than 8 times).

Presented predisposing and genetic factors contribute to the disruption of the interaction between the neuroendocrine and immune systems, promote the development of hyperestrogenemia, followed by the accumulation of genetic damage of target cells, which the epithelium of the breast refers to. There are two types of molecular damage – induction of cell proliferation and DNA mutation.

Treatment. Treatment of breast cancer is combined and consists of surgical intervention in combination with chemotherapy or radiation.

In breast cancer, the following types of interventions are used:

•Halstead radical mastectomy, that consists in the removal of the breast with both pectoral muscles, regional (axillary, subscapular and subclavian) lymph nodes and fatty tissue in a single block. Given the high traumatism and unsatisfactory cosmetic result after this intervention, the main indications to it are limited by the germination of the tumor into the large pectoral muscle;

•Patey radical mastectomy. It differs from the previous intervention by preserving the large pectoral muscle (only the small pectoral muscle is removed);

•Madden radical mastectomy. It consists in the removal of the MG with fascia, intermuscular fiber and a block of subclavian, axillary, and subscapular lymph nodes (lymphadenectomy) while preserving large and small pectoral muscles;

•Different types of organ-preserving operations (including removal from 1/3 the amount to lumpectomy, quadrantectomy or sectoral resections of MG with obligatory lymphadenectomy). The implementation of these interventions became possible only through video-assisted interventions.

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Chapter 7

PURULENT DISEASES OF THE LUNGS

AND PLEURA

7.1. BRONCHIECTASIS. BRONCHIECTATIC DISEASE

Bronchiectasis (BE) is irreversible morphological and functional changes in the bronchi, causing their expansion and deformation.

Bronchiectatic disease (BED) is a disease accompanied by a complex of pulmonary and extrapulmonary changes due to acquired bronchoectasis.

The course of the disease is characterized by three stages of disorders:

1.Reversible changes in bronchi.

2.Onset of irreversible morphostructural changes in the bronchial wall.

3.Peribronchial complications.

It is characterized by pneumosclerosis and chronic foci of peribronchial inflammation.

Сlassification. Bronchiectasis is divided by:

•origin:

congenital (primary) is the consequence of genetically determined factors of elastic, cartilaginous structures and elements of smooth muscle pathology, as well as the surfactant system damage. They appear on the background of inflammatory changes in the bronchi or due to bronchial patency impairment;

acquired (secondary), resulting from bronchitis, pneumonia, pulmonary tuberculosis, tumors, chronic abscesses or foreign bodies revealed in the bronchopulmonary system;

•the form of expansion:

cylindrical;

saccular;

cystoid;

mixed;

•clinical manifestations:

without obvious clinical signs;

mild;

moderately severe;

severe;

clinically complicated (with or without atelectasis);

•stages of the clinical course:

remission;

exacerbation.

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7.2. ACUTE LUNG ABSCESS

Acute lung abscess (ALA) is a form of bacterial lung destruction (BLD) representing a limited purulent-destructive process in the pulmonary tissue with a satisfactory state of the patient’s immunoreactivity system being more common in men aged 20–50 (80–90% of all ALA cases).

Classification. ALA is divided by:

•pathogenesis into:

post-, metapneumonic (develop after or simultaneously with pneumonia);

postraumatic;

aspiratory;

hematogenous-embolic;

obturative;

lymphogenous;

•localization:

single;

multiple (one or two-sided);

•in relation to the lung gates they may be:

central;

peripheral;

•the nature of complications:

with the development of bronchopleural communication (fistula);

with pulmonary hemorrhage;

with the development of sepsis.

Etiology. An important role in the development of ALA is played by polymicrobial associations of pathogenic aerobes (Ps. aeruginosa, Staph. aureus, E. coli, Klebsiella pneumoniae, Enterobacteria and Proteins), and less often by nonspore-forming nonclostridial anaerobes (Bacteroides, Fusobacterium, Peptococcus, Peptostreptococcus); rarely (in the period of 2007–2010) – by influenza A, “bird fly” or “swine fly” viruses, adenoviruses, fungal (more often noncandidous) flora.

ALA predisposing factors:

•chronic nonspecific lung diseases (CNLD), which contribute to the impairment of bronchial patency and the formation of atelectasis include: bronchial asthma, chronic obstructive bronchitis (more often in smokers), BED;

•diseases accompanied by a decrease in immunoresistance: hypovitaminosis, severe trauma, diabetes, alcoholism, HIV infection, hepatitis, anemia;

•diseases accompanied by consciousness pathology (including those with cough and epiglottis reflexes): alcoholism, smoking, drug addiction, severe craniocerebral traumas, general anesthesia, cerebral coma, epilepsy.

Most often (more than 70% of cases) ALA develops in men who abuse smoking, alcohol consumption and in those leading antisocial lifestyle.

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