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

The most frequent typical localization of the process is the I, II, IV and VI segments of the right lung. The diameter of abscesses varies – from 2–3 mm to 6–10 cm or more.

Clinical picture. There are two periods in the clinical picture of the typically occurring ALA:

•abscess formation (before its rupture into the bronchus);

•rupture of the abscess into the bronchus.

In the period of abscess formation, the clinical picture is similar to that of severe pneumonia and is characterized by: an increase in body temperature up to 38–39 °C; pain in the chest in the affected side, increased with breathing; dry wheezing or coughing with a small amount of sputum; general severe condition due to intoxication.

The described symptoms become worse during the following 5–10 days, after which the second period comes – the rupture of the abscess into the bronchus. It is accompanied by a sudden onset of cough with the discharge of purulent sputum (up to 300–800 ml / day or more) with unpleasant smell (rarely – containing blood), large quantities of leukocytes, tissue dendrites and elastic fibers.

After the abscess drainage into the bronchus of a large diameter and in case of satisfactory immunoresistance, the condition of the patient is markedly improved: inflammation resolves, the temperature becomes normal, dyspnea disappears, the abscess cavity decreases as a result of its reduction and gradual filling of the granulation tissue.

Treatment. ALA conservative treatment includes the following:

•optimal drainage, sanation of the pulmonary destruction cavity and the tracheobronchial tree;

•adequate antibacterial therapy, taking into account the results of microbiological examination, resistance of microorganisms to antibiotics (AB);

•the best ways of antibiotics administration in case of ALA are: intravenous; selective (into the bronchial arteries); directly into the pathological focus by means of fibrobronchoscopy or percutaneous micro-tracheostomy;

•correction of vollemic, water-electrolyte disorders, acid-base state (ABS), hypoor dysproteinemia;

•disintoxication therapy by the introduction of forced diuresis, plasmapheresis, indirect electrochemical blood oxidation;

•increase in natural immunoresistance reaction and immune response by hyperimmune plasma substitution for specific pathogens or complex immunoglobulin remedies, activators of the T-system (imunofan, vylon) and / or macrophage-leukocyte (leiargunal, polyoxidonium) chain;

•enteral high-calorie nutrition (as indicated – parenteral nutrition, infusion of amino acids or some blood components).

To ensure adequate drainage, sanation of purulent focus and tracheobronchial tree doctors apply:

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•postural drainage (placing the patient to the position allowing the outflow of pus to flow naturally into a large lobar bronchus with subsequent active coughing);

•selective endotracheal sanation of the pulmonary destruction focus which allows the doctors to administer endofibro-bronchoscopic solutions of antiseptics, antibiotics, proteolytic enzymes for local enzyme therapy to achieve lysis of necrotic tissues, fibrin, sputum liquefaction and to reduce antibiotic resistance of microflora. For this purpose chymotrypsin, ribonuclease, lidazum, terrilytin, papain, acetylcysteine are most often used;

•percutaneous drainage of the abscess under the control of polypositional fluoroscopy, CT or ultrasound by means of microor macrodrainage under local anesthesia;

•selective occlusion of the “targeted” lobar bronchus, thoracoabscessoscopy and sanation of the abscess cavity with the application of videothoracoscopy, followed by the drainage with the Subbotin-Perthes system.

7.3. ACUTE PLEURA EMPYEMA

Acute pleural empyema (APE) is the acute inflammation of the pleural cavity with the involvement of its visceral and parietal layers and purulent exudate formation.

In the overwhelming majority of cases, the development of APE occurs due to the association of Gram-positive (Staphylococci, Streptococci, Pneumococci) and Gram-negative microflora, represented by Proteus, intestinal and Pseudomonas aeruginosa. In 20–30% of cases, bacteroides, fusobacteria, peptostreptococci, and other nonclostridial anaerobic pathogens may also join them.

In more than 95% of cases, APE is a secondary process due to endogenous or lymphogenic infection of the pleural cavity; only in some cases, it may be primary, due to penetrating chest injuries or thoracic interventions.

Classification. APE is divided by:

•a primary source of infection into:

primary: post traumatic (due to complications of chest injuries);

postoperative (caused by complications after thoracic surgery, incompetence of the bronchus stump, esophageal-intestinal anastomoses, infections of the postoperative wounds, osteomyelitis of the ribs and sternum or cases of purulent perichondritis development);

•infection routes:

contact, including:

parapneumonic (arising simultaneously with pneumonia); metapneumonic (join after pneumonia resolution);

perforating (due to the rupture of abscesses into the lung or the pleural cavity);

metastatic (hematogenic, from any pyemic extrapulmonary foci);

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Chapter 8

ACUTE APPENDICITIS

Acute appendicitis (AAp) is an acute inflammation of the appendix. It is the most common surgical pathology, occurring in 4–5 people per 1000 adult population. In Belarus AAp is diagnosed 1.8 to 2 times more often in women than in men. Most frequently appendectomies in the treatment of AAp are performed during two age periods: 15–19 years and 30–34 years, respectively.

Mortality rate in AAp is 0.05–0.3% and it has not declined significantly over the last 25–30 years.

In the last decade there has been a decrease in the total number of AAp patients in all developed countries of the world.

Classification. The following forms are distinguished:

•uncomplicated which include:

appendicular colic. It is diagnosed in the following cases: after the exclusion of AAp and other emergency pathology of the abdominal cavity (taking into account the data of the performed videolaparoscopy); after the intraoperative revision of the unchanged appendix; after 12-hour dynamic observation of the patient with positive clinical and laboratory dynamics (relief of pain syndrome, normalization of hemogram readings);

catarrhal (synonyms: simple or superficial) appendicitis;

phlegmonous (including empyema of the appendix) appendicitis;

gangrenous appendicitis;

perforated appendicitis;

•complicated, presented by:

periappendicular infiltrate;

periappendicular abscess;

retroperitoneal phlegmon;

peritonitis (local and generalized). Local peritonitis may occur in the diffuse or limited forms. Local limited forms of peritonitis include infiltrates and abscesses of the abdominal cavity of various localizations: pelvic, subdiaphragmatic, subhepatic, interintestinal, right iliac fossa;

abdominal sepsis (it is observed in generalized peritonitis in case of multi-organ failure);

pylephlebitis (purulent inflammation of the portal vein branches). Etiology. Acute appendicitis is a multietiologic disease the develop-

ment of which is associated with the invasion of pathogenic microflora;

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formation of coprolites, which cause stasis of intestinal contents; disorders of microcirculation of the intestinal wall; angiospasm of mesentery vessels; helminthic invasion.

These factors contribute to:

•the development of obstruction of the lumen of the appendix, stasis of the contents and the formation of a “closed” cavity caused by congenital or acquired processes, accompanied by secondary changes, narrowing or squeezing of the lumen from outside;

•enterogenous invasion of bacterial flora into the appendix (primarily

Escherichia coli, Enterococcus, Proteus, Bacteroides, pathogenic Anaerobic cocci) against the background of lymphoid tissue hyperplasia and reduction of local mucosal immunoreactivity. This, in turn, leads to incomplete phagocytosis, decrease in the synthesis of secretory immunoglobulin A; suppression of immune mechanisms of cells with the prevalence of local hyperimmune reaction due to prolonged hypersensitization. Much more rarely the penetration of microbes into the tissue of the appendix occurs hematogenously or lymphogenically from other infected organs;

•prolonged reflex spasm of mesentery vessels, lumen dilatation, microcirculatory damage to the wall followed by tissue ischemia.

Clinical picture. The clinical picture of acute appendicitis differs in the variety of manifestations and depends on:

•the degree of inflammatory changes in the appendix;

•localization of the appendix (typical localizations include: descending, lateral, medial, retrocecal, anterior or ventral ones);

•age;

•expression of the muscles of the anterior abdominal wall (determines the degree of manifestation of muscular defense);

•immunoreactivity;

•concomitant pathology.

The clinical picture of AAp is characterized by four main syndromes: painful, dyspeptic, inflammatory and peritonial characterized by specific features.

Treatment. With the confirmed diagnosis of acute appendicitis the only method of treatment is an emergency operation performed after short-term preoperative preparation.

At present, depending on the technical possibilities, both traditional (open) and laparoscopic interventions to remove the inflamed appendix are used.

Traditional (open) appendectomy. More than 20 different surgical accesses to the appendix are known. The most common is the access of Volkovich-Dyakonov (Mac-Burney) performed through a conditional point connecting the right anterolateral axis of the ileum to the navel and the line perpendicular to it between the outer and middle third of this distance.

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Less commonly used are the right suprapubic (transverse along the “bikini” line); pararectal (access of Lenander) and lower-middle laparotomy accesses. Any of them should provide maximum convenience during the operation and minimize possible postoperative complications.

The typical features of the traditional operation (appendectomy) are:

•the search for a vermiform appendage, the landmark of which is the site of the fusion of three longitudinal muscular bands (taeniae coli) in the region of the dome of the cecum; after finding it the latter is delivered into the operative wound;

•bandaging the mesentery of the appendix at its base;

•appendectomy with immersion of the appendiceal stump into pursestring and Z-shaped sutures;

•closure of the operative wound in layers.

Laparoscopic appendectomy (LA). Special endovideoscopic equipment (videolaparoscopic set and instruments introduced through separate punctures of the anterior abdominal wall) is used.

The varieties of appendectomy are:

•laparoscopically – assisted appendectomy. In this case the stage of isolation of the appendix is performed laparoscopically, then, after delivering it into the wound typical appendectomy is performed;

•laparoscopically – supplemented appendectomy is characterized by the fact that after the stage of diagnostic videolaparoscopy, in order to determine the location of the appendix, mini-access is made up to 2.5 cm in length and then the appendix is delivered into the wound and typical appendectomy is performed;

•appendectomy from the “mini-access”. It can be performed in the following ways:

by transverse access up to 2–3 cm in length according to L.G. Kurtenko’s method with the help of traditional general surgical instruments;

with the help of a set of “Mini-assistant” which includes a ring with a retractor and wound widening speculum fixed on it, an illuminator and special tools curved at a certain angle (the method proposed by M.D. Prudkov);

•NOTES – appendectomy, referring to the new surgical approach (Natural Orifice Transluminal Endoscopic Surgery (2008)), based on the principle of appendectomy (or other abdominal surgery) with the use of a flexible endoscope – manipulator inserted through natural openings or through the wall of the hollow organ into the abdominal cavity during the videolaparoscopy. Nasotransgastral or transvaginal accesses (in women) are most frequently used.

Complications. Periappendiceal mass (PM). A tumor-like formation without clear boundaries which is painful on palpation is detected in the

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right ileac region during an objective examination of PM. Positive symptoms of irritation of the peritoneum can also be revealed here. The laboratory findings include moderate leukocytosis and a shift of white blood count to the “left”.

Treatment for PM is determined individually: in severe tenderness and irritation of the peritoneum an emergency operation (appendectomy) is indicated; in other cases conservative treatment is administered.

In case of dense periappendiceal mass formation the intensity of the pain syndrome decreases until it completely disappears. Moderate pains while walking or changes in body position are distinguished. Body temperature falls to subfebrile or returns to the norm.

On palpation a slightly painful, densely-elastic (more often immobile) tumor-like mass delimited from the free abdominal cavity is determined in the right iliac region.

On percussion dullness and, most often, negative symptoms of peritoneal irritation are revealed above it. The characteristic readings on the hemogram are slight leukocytosis, moderate neutrophil shift to the “left” and accelerated ESR.

Ultrasound examination confirms the presence of limited rounded mass with heterogeneous contents (without anechogenic inclusions), in the center of which an oval structure with indistinctly differentiated, uneven thickened walls of the appendix is visualized. In complicated cases MRI or HCT (helical computer tomography) are used.

Therapeutic tactics in the diagnosed dense PM is conservative. On the first day local hypothermia, intrapelvic novocaine blockade on the right according to Shkolnikov-Selivanov with the introduction of broad-spec- trum antibiotics are used.

The outcome of PM is its resorption (involution) within 25–30 days or suppuration with the formation of a periappendiceal abscess.

In cases of positive dynamics – appendectomy is performed routinely in 2.5–3 months. In case of the preservation of the palpable infiltrate for more than 1–1.5 months additional differential diagnosis with tumors of the cecum, specific processes (tuberculosis, actinomycosis), nonspecific diseases of the colon (Crohn’s disease) is carried out.

Appendicular abscess (ApAb). Appendicular abscess is a consequence of suppuration of the periappendiceal mass.

In case of suppuration of the infiltrate the pain in the right iliac region becomes worse and at times acquires a pulsating character. The body temperature rises up to hectic figures and is accompanied by chills against the background of increased perspiration and tachycardia. Objectively, the symptoms of intoxication are revealed: dry and coated tongue, thirst, lethargy, adynamia, apathy. On dynamic palpation the boundaries of the infiltrate become widen and indistinct; a sharp tenderness over its projection is determined. In case of a close “location” of ApAb to the anterior abdomi-

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Chapter 9

DISEASES OF THE GALLBLADDER AND EXTRAHEPATIC BILE DUCTS

9.1. CHOLELITHIASIS

Gallstone disease (CL or Cholelithiasis) is a disease caused by metabolic disturbances resulting in the formation of stones in the gallbladder (cholecystolithiasis) or in the bile duct (choledocholithiasis).

The incidence of CL averages 10–15% of the total adult population. CL is found in 6–29% of autopsy cases, i.e. one case in five women and one case in ten men.

Classification. CL is classified by:

•localization of stones:

in the gallbladder;

common bile duct;

intrahepatic ducts;

•gallstone composition:

cholesterol;

bilirubin (pigment);

mixed;

•clinical course:

latent;

dyspeptic form;

hepatic (bile) colic;

atypical forms.

Clinical stages. The following stages of cholelithiasis are distinguished:

1.Initial (biliary sludge). The characteristic manifestations include thick ointment-like bile accompanied by the formation of biliary sludge and the presence of microlites.

2.Gallstone formation.

3.Acute and chronic calculous cholecystitis (recurrent, primary chronic, chronic residual).

Forms of CL. Hepatic (biliary) colic is a form of cholelithiasis characterized by the onset of pain syndrome after eating spicy and fatty food, less often, on physical exertion. The pain is mainly localized in the right hypochondrium or epigastrium (visceral pain) and associated with the stretching of the walls of the gallbladder (in the form of spastic contraction);

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Chronic calculous cholecystitis is a form of CL course presented by attacks of hepatic colic associated with the inflammatory syndrome (with elevated body temperature, moderate leukocytosis and shift of the leukocyte formula “to the left”, accelerated ESR) and absence of signs of acute inflammation (according to ultrasound data GB wall is less than 3 mm, no “double contour”, signs of a chronic process are determined: constrictions in GB with chronic impairment of outflow, S-shaped deformation, sclerosis of the wall).

Complications cholecystitis include (at the end) the following types:

•empyema and edema of the gallbladder;

•perivesical infiltrate and abscess;

•choledocholithiasis;

•mechanical (obstructive) jaundice;

•acute cholangitis;

•cicatricial strictures;

•acute or chronic pancreatitis;

•internal biliodigestive fistulas;

•bile peritonitis.

9.2.COMPLICATIONS OF THE DISEASES OF THE GALLBLADDER AND EXTRAHEPATIC BILE DUCTS

9.2.1. Acute calculous cholecystitis

Acute calculous cholecystitis (ACC) is a complicated form of CL caused by acute (nonspecific) inflammation of GB, which is a consequence of the obstruction of bile outflow with concrements.

Classification. ACC forms include:

•catarrhal – in this form the inflammatory process is limited to the mucosa or area of the primary Aschoff inflammation and / or submucous membranes;

•phlegmonous – it is characterized by inflammation of all layers of the gallbladder wall and often by the ulceration of portions of mucosa (phleg- monous-ulcerative inflammation). Clinical varieties of this form include empyema and edema;

•gangrenous – it is characterized by necrosis (local or total) of the GB

wall;

•complicated.

According to the complications ACC there are the following types of ACC:

• perforation of the GB wall and the development of local or widespread peritonitis. In some cases bile peritonitis can develop without the perforation

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