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

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»

МИНСК «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 underly 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 – сholedocholithiasis

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.

Classification, 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-α), gamma interferon (γ-IF), producers of arachidonic acid or eicosanoids (5-HETE, leukotrienes, prostaglandins), oxygen and nitrogen metabolites (O2; H2O2; NO2; NO; OHˉ, 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.

Classification. 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.

Classification. 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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