Хирургические болезни. Практикум = Surgical diseases. Practice book

   С.А. Алексеев М.Н. Петрова



 ХИРУРГИЧЕСКИЕ БОЛЕЗНИ
        ПРАКТИКУМ


     SURGICAL DISEASES
         PRACTICE BOOK


Допущено Министерством образования Республики Беларусь в качестве учебного пособия для иностранных студентов учреждений высшего образования по специальностям «Стоматология», «Медико-профилактическое дело»












      миНС минск
      «ВЫШ «ВЫШЭЙШАЯ ШКОЛА»
2020

УДК 617-089(076.58)-054.6
ББК 54.5я78

    А47







    Р ец е нз енты: кафедра хирургических болезней № 2 УО «Гомельский государственный медицинский университет» (заведующий кафедрой доктор медицинских наук, профессор З.А. Дундаров); профессор кафедры хирургических болезней № 2 УО «Гродненский государственный медицинский университет», доктор медицинских наук, профессор С.М. Смотрин; доцент кафедры современных технологий перевода Минского государственного лингвистического университета, кандидат филологических наук, доцент Т.И. Голикова
































    Все права на данное издание защищены. Воспроизведение всей книги или любой ее части не может быть осуществлено без разрешения издательства.


ISBN 978-985-06-3163-3

                     © Алексеев С.А., Петрова М.Н., 2020 © Оформление. УП «Издательство

“Вышэйшая школа”», 2020

FOREWORD



   Clinical surgery is a fundamental area of medicine. It combines complementary knowledge of anatomy and operative surgery, physiology, microbiology, pathological anatomy and clinical pharmacology which under-ly professional training of doctors in any specialty.
   The main sources of information are textbooks in surgical diseases, guide books on specific topics, as well as lecture courses.
   The current book in English is prepared by the staff members of the departments of general surgery and foreign languages of Belarusian State Medical University based on their 25-year teaching experience. It includes the topics according to the curriculum in surgical diseases for the specialties “General Medicine”, “Dentistry” and “Preventive Medicine” and is an important additional source of developing information competence for the students of other faculties of higher medical education institutions.
   The book contains the test items grouped according to the topics of the curriculum: diseases of peripheral vessels, thyroid and mammary glands, rectum and paraproctium, purulent diseases of the lungs, emergency gastrointestinal diseases.
   It is designed for the students of higher medical education institutions in the specialties “General Medicine”, “Dentistry” and “Preventive Medicine”. It may be useful for the students of other faculties, clinical residents and PhD students of surgical specialties.
   In each thematic section of the book there is brief relevant information preceding the test items and providing insight into their essence.
   For technical support of test performance monitoring the information and the tests are presented in an electronic form that facilitates their use for self-preparation and enables the staff to prepare different variants for final exam in the subject area of surgical diseases.
   The authors express sincere gratitude to our reviewers: Professor, DMSc Z.A. Dundarov, Head of the Department of Surgical Diseases No.2 of Gomel State Medical University; Professor, DMSc S.M. Smotrin, Professor of the Department of Surgical Diseases No.2 of Grodno State Medical University for providing detailed feedback on the draft of the Practice Book which lead to significant improvements in its content and structure.
   We also benefited greatly from the observations, comments and useful suggestions made by T.I. Golikova, PhD, Associate Professor of the Department of Modern Translation Technologies of Minsk State Linguistic University.
   Finally, we would like to thank our academic colleagues, the staff members of the Foreign Languages Department of Belarusian State Medical University I.I. Tikhonovich and Olesya Sakhnova for advice on many specific points as we compiled the book.

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           LIST OF ABBREVIATIONS



      AAb - acute abscess
      AAI - acute arterial insufficiency
      AAO - acute arterial obstruction
      AAp - acute appendicitis
      AAWH - anterior abdominal wall hernias
      AAW - anterior abdominal wall
      ABB - acid-base balance
      ABS - acid-base state
      ABT - antibacterial therapy
      AB - antibiotics
      ACC - acute calculous cholecystitis
      AC - abdominal cavity
      AD - arterial diseases
      AF - anal fissure
      AGDB - acute gastroduodenal bleeding
      AH - abdominal hernia
      AIO - acute intestinal obstruction
      ALA - acute lung abscess
      AM - acute mastitis
      ApAb - appendicular abscess
      APC - argon-plasma coagulation
      APE - acute pleural empyema
      AP - acute pancreatitis
      APp - acute paraproctitis
      AVI - acute venous insufficiency
      BC - breast cancer
      BD - bile ducts
      BED - bronchiectatic disease
      BE - bronchiectasis
      BLD - bacterial lung destruction
      CAO - chronic arterial obstruction
      CCE - cholecystectomy
      CDL - choledocholithiasis
      CDM - colour duplex imaging
      CFV - common femoral vein
      ChPP - chronic periproctitis
      ChP - chronic pancreatitis
      ChT - chemotherapy
      CLE - chronic lymphostasis of extremities
      CL - cholelithiasis
      CNLD - chronic nonspecific lung diseases
      CRF - chronic renal failure
      CRI - chronic renal insufficiency

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      CSF - colony-stimulating factors
      CS - cephalosporins
      CT - chemotherapy
      CVI - chronic venous insufficiency
      CVP - central venous pressure
      DFA - deep femoral artery
      DP - diffuse peritonitis
      DTG - diffuse toxic goiter
      EBT - electro-beam theraty
      ECP - epithelial coccygeal passage
      EG - endemic goiter
      EIS - enteral insufficiency syndrome
      EI - endogenous intoxication
      EPST - endoscopic papillosphincterotomy
      ERPS - endoscopic retrograde papillosphincterotomy
      EVLC - endovascular laser coagulation
      FCM - fibro-cystic mastopathy
      FNAB - fine needle aspiration biopsy
      GB - gallbladder
      GIT - gastrointestinal tract
      GSV - great saphenous vein
      Gy - gray (radiation unit)
      HBO - hyperbaric oxygenation
      HIV - human immunodeficiency viruse
      HR - heart rate
      HT - hormone therapy
      IL - interleukins
      IO - infenstinal obstruction
      IR - intestinum rectum
      IVC - inferior vena cava
      LA - laparoscopic appendectomy
      LE - lower extremity
      LSV - large saphenous vein
      LS - lymphatic system
      MDP - major duodenal papilla
      MG - mammary glands
      MOF - multiple organ failure
      MRA - magnetic resonance angiography
      MRI - magnetic resonance imaging
      NAA - nonspecific aorto-arteritis
      OALEV - obliterating atherosclerosis of the lower extremity vessels
      ODLEV - obliterating diseases of the lower extremity vessels
      OJ - obstructive jaundice
      OTp - obliterating thromboangiitis
      PAF - platelet activating factor
      PC - pilonidal cyst
      PDR - pancreatoduodenal resection

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           PET - positron emission tomography
           PE - pulmonary embolism
           PIC - postoperative infensive care
           PM - periappendiceal mass
           PoP - preoperative preparation
           PTD - post-thrombophlebitic disease
           PTFE - polytetrafluoroethylene
           PTS - post thrombotic syndrome
           PUD - peptic ulcer desease
           PVC - premature ventricular contraction
           PVD - peripheral vascular disease
           RP - rectal prolapse
           RT - radiotherapy
           SCT - spiral computed tomography
           SEF - syndrome of enteric failure
           SH - strangulated hernia
           SIRS - systemic inflammatory response syndrome
           SPV - selective proximal vagotomy
           SSV - short saphenous vein
           ST - selective tomography
           SVC - superior vena cava
           TG - thyroid gland
           TPS - intrahepatic portocaval shunt
           TRH - thyrotropin-releasing hormone
           TSH - thyroid stimulating hormone
           TTH - thyrotrophic hormone
           UPDS - ulcerative pyloroduodenal stenosis
           US - ultrasound
           UVI - ultraviolet irradiation
           VD - venous diseases
           VOS - venous obstruction syndrome
           VT - venous thrombosis
           VVLE - varicose veins of lower extremities

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                Chapter 1




            VASCULAR DISEASES.
            LOCAL MANIFESTATIONS
            OF CIRCULATORY DISORDERS


  Peripheral vascular diseases (PVD) are divided into arterial diseases (AD) associated with impaired arterial flow, venous diseases (VD) leading to venous drainage obstruction and diseases of the lymphatic system (LS) occurring with impaired lymphatic drainage.
  In turn, peripheral arterial diseases may occur with the development of the syndrome of acute arterial obstruction (AAO) or chronic arterial obstruction (CAO). Diseases of veins respectively result in acute venous obstruction syndrome (VOS) and chronic venous insufficiency (CVI). Diseases of the peripheral lymphatic system cause the onset of chronic lymphatic insufficiency (lymphostasis).

    1.1. NECROSIS

  Necrosis is the most common local outcome of PVD or circulatory disorders. The word “necrosis” comes from Greek - “nekros” (dead), indicating the death of part of a living organism (cell, tissue or organ). Types of necrosis including gangrene (necrosis in contact with the external environment) and infarction (from the Latin word - “infarctus” - “stuffed into”) - necrosis of the inner organs, which are not in contact with the external environment.
  Classifi cation, etiology. Depending on predisposing etiological factors necrosis is divided into external and internal.
  External necrosis is caused by direct influence of various external factors such as mechanical, chemical, microbial, enzymatic, acidic, fermentative and others.
  Internal necrosis is a consequence of various circulatory disorders: a) arterial flow; b) venous and lymphatic drainage; c) neurotrophic factors; d) microcirculatory manifestations and more rarely - reduced central hemodynamics.
  Pathogenesis. Pathogenesis of necrosis encompasses the following disorders:
  •    the effect of initiating factors (external and internal) results in reduced oxygen supply of the tissues;
  •    reduced partial pressure of oxygen (pO₂) below 30 mmHg is accompanied by the development of the metabolic acidosis and mediated patho

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physiologic mechanisms which include: the opening of arteriovenous shunts; humoral imbalance of regulatory systems; activation of antiinflammatory cellular mechanisms involving synthesis of proinflammatory cytokines (interleukins - 1, 2, 6, 8); tumor necrosis factor (TNF-a), gamma interferon (Y—IF), producers of arachidonic acid or eicosanoids (5-HETE, leukotrienes, prostaglandins), oxygen and nitrogen metabolites (O₂; H₂O₂; NO₂; NO; OH", etc.), biogenic kinins. Presented mediators cause the buildup of ischemic edema followed by the onset of an ischemic syndrome and the formation of tissue destruction areas.
    Two types of necrosis developing in tissues are distinguished:
    1.    Dry necrosis, which is formed in case of minor (local) circulatory disorders, most commonly due to direct exposure of etiologic factors; its development has a gradual onset. The skin surface looks like dark blue or black epidermal blisters with reduced sensitivity of the skin over them. In the course of scab rejection the granulation tissue is formed. This type of necrosis develops in tissues with low levels of fat, as well as hypoproteinemia in the elderly.
    2.    Wet necrosis is characterized by deep lesions, widespread and frequent involvement of subfascial structures; the presence of extended edema and increased organ size, as well as the absence of demarcation line. Most often it occurs in tissues with lots of fluid and enriched adipose tissue.
    They are accompanied by rapid development of purulent (pyogenic) infection and severe endogenous intoxication.
    Gangrene (dry and wet). Gangrene is extensive necrosis in contact with the external environment. It is characteristic of diseases of hollow organs of the alimentary tract (intestine, appendix, gall bladder), the respiratory tract and the lungs. The development of this type of necrosis in organs activates hemoglobin decomposition and due to the acidic environment (hypoxia) hydrochloric hematin is produced, imparting dirty graygreen or black-brown color to the tissues.
    Dry gangrene is characterized by slow development in CAO and acid burns. It is accompanied by the formation of coagulation necrosis with disintegration of cell nuclei. The tissues acquire dark brown or black color with mummification. In the necrosis area there is no inflammation and leukocyte infiltration, the formation of demarcation line occurs due to leukocyte infiltration, subsequent emergence of granulations and growth of connective tissue. Slow independent tissue rejection occurring after 4-5 weeks leads to the formation of a deep defect whose bottom is the granulation tissue.
    Development of purulent inflammation in dry gangrene is characteristic during the initial period - before the formation of the demarcation line or after the rejection of necrosis due to secondary infection.
    Wet gangrene is characterized by its rapid development against the background of AAO or alkali burns due to colliquative necrosis. Necrotic

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tissues in such a type of gangrene contain an excessive amount of fluid that in the presence of bacterial infection (over 10⁵ cfu / l g tissue) leads to their putrification.
   Demarcation processes, in view of total leukocyte infiltration, are absent. This contributes to active absorption of endo-, exotoxins, the decay products enter into the bloodstream followed by reperfusion and resorption mechanisms and cause endogenous intoxication (EI).
   Treatment. Treatment of necrosis (gangrene) includes:
   •     removal of devitalized tissue (necrectomy) and subsequent activation of reparative processes with early plastic replacement of existing defects;
   •     in dry necrosis, after necrectomy, there is a need for maximum preservation of the organ, and in relation to the lower limb - its supportive ability;
   •     in wet necrosis (gangrene) treatment involves conversion into a dry form of necrosis; in the absence of such conditions (rapid progression against the background of increasing EI) - radical surgery with limb amputation (organ extirpation) at the level of obviously unchanged tissues.

    1.2.  BEDSORES (DECUBITUS)

   Bedsores are a variety of chronic ulcers that develop as a result of compression, friction, or displacement of the skin in patients with sensitivity disorders. The most frequent places of localization of bedsores are: occipital region, scapula, waist, sacrum, sciatic tubercles, calcaneus and buttocks, as well as great trochanter, i.e. the areas where the thickness of the skin and subcutaneous tissue is minimal over the adjacent bony protuberances. Due to this, compression of soft tissues occurs under the influence of the patient’s own weight. About 96% of decubitus is located in the lower parts - the sacrum, the sciatic tubercles (67-70%), the lower extremities (~ 30%) in patients who are forced to be in the supine (lying) position.
   Classifi cation. According to their size there are:
   •     bedsores in the form of a fistula - a small defect in the skin with a significant underlying cavity accompanied by osteomyelitis;
   •     small bedsores - up to 5 cm in diameter;
   •     medium bedsores - from 5 to 10 cm in diameter;
   •     large bedsores - from 10 to 15 cm;
   •     giant bedsores - over 15 cm in diameter.
   Etiology. The factors contributing to the formation of bedsores are:
   •     mechanical action leading to critical skin ischemia at a constant pressure of more than 70 mm Hg for more than 2 hours;
   •     absence of motor activity (with loss of consciousness, severe alcohol intoxication, after spine or spinal cord traumas, or in the early postoperative period), as well as excessive moisturizing of the skin, especially in elderly and senile patients.


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    1.3.  TROPHIC ULCER (ULCUS)

   Trophic ulcer (ulcus) is a defect in the skin or mucous membranes developing as a result of rejection of necrotic tissues and persisting as a result of poorly expressed regeneration without a tendency to spontaneous healing.
   Classifi cation. Depending on the use of surgical tactics, all ulcer defects are subdivided according to their size and area into:
   •  small ones - up to 10 cm²;
   •  medium - from 11 to 26 cm2;
   •  large - from 27 to 50 cm2;
   •  extensive - over 50 cm2.
   In trophic ulcers more than 27-30 cm2 chronic defects with callous edges are formed, replacing the granulation in the bottom area with connective tissue.
   Etiology. The formation of trophic ulcers is associated with the causes underlying the emergence of primary necrosis, which extends the regeneration period by more than 8-10 weeks.
   Clinical picture. The characteristic features of trophic ulcers include:
   •  the lack of tendency to spontaneous regeneration and healing;
   •  appearance of destructed tissue in the center of the focus;
   •     occurrence of false granulations of pale pink color, cyanotic character covered with fibrinous coating;
   •  development of secondary infection with a recurrent course.
   The following stages of trophic ulcers are distinguished:
   •  I - preulcers (ulceration reaches the layer of the dermis);
   •      II - characterized by dystrophic changes, necrosis and inflammation of all layers of the skin and adjacent tissues with the appearance of granulations. In the long course of their development, granulations in the area of the bottom of the ulcerative defect do not fill it entirely; they acquire a hypertrophic character of pale pink and purple-red color with fibrinous purulent content;
   •      III - fibrous consolidation of the bottom and edges of the ulcerative defect;
   •  IV - appearance of marginal epithelization;
   •  V - ulcer clearance (detersion) and the beginning of regeneration;
   •  VI - epithelization and scar formation.
   Treatment. Treatment of trophic ulcers includes the following:
   •  elimination of etiopathogenetic factors contributing to their formation;
   •  sanation of purulent focus - ulcerative defect and surrounding tissues;
   •     stimulation of reparative processes by activation of local immunoresistance and correction of immune status;
   •     in medium, large and extensive ulcerative defects after their cleansing, early autodermoplasty is used with the application of various techniques.

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