Antibiotics (Properties, Application, Interactions) - M.P. Cherenko 1999

Acute purulent infection
Purulent diseases of serous membranes

Acute purulent Pleurisy (pleuritis purulenta acuta) is a diffuse or localized purulent inflammation of the visceral and parietal Pleura, resulting in the accumulation of pus within the pleural cavity.

The pleura is a thin serous membrane that lines the inner walls of the thoracic cavity (parietal pleura) and covers the Lungs (visceral pleura). In the region of the lung ROOT, both pleural layers converge, forming a closed cavity.

The parietal pleura is subdivided into costal, diaphragmatic, and mediastinal parts. In the costophrenic region, the parietal layer forms a space known as the costodiaphragmatic recess (sinus). A similar space (costomediastinal recess) is located at the transition of the costal pleura into the mediastinal pleura. The volume of these spaces fluctuates during respiration.

Under normal conditions, the pleural cavity contains 20—25 ml of serous fluid, which facilitates smooth lung movement during breathing.

The cupula of the pleura lies above the clavicle, projecting posteriorly at the level of the VII cervical vertebra and anteriorly 2—3 cm above the clavicle. The lower BOUNDARIES OF THE pleural cavities are located as follows: along the mid-clavicular line—at the level of the VII rib, along the mid-axillary line—at the level of the X rib, and along the paravertebral line—at the level of the XII rib.

Depending on the etiological factor, pleurisy can be specific (most commonly of tuberculous origin) or non-specific, caused by streptococci, staphylococci, pneumococci, or anaerobic non-clostridial microflora. Occasionally, the infection is mixed. This section focuses on acute non-specific pleurisy. This condition is typically secondary. It may complicate Pneumonia, suppuration of a parasitic (echinococcal) cyst, disintegrating Lung Cancer, various thoracic surgeries, rib Osteomyelitis, pericarditis, mediastinitis, or pulmonary gangrene. Sometimes, the infection is seeded hematogenously or lymphogenously from distant inflammatory foci.

Primary pleurisy is less common; it usually develops following open chest trauma, when the infection gains direct entry into the pleural cavity.

Pathomorphological changes in pleurisy primarily affect the visceral and parietal pleural layers. They thicken, lose their luster, the surface becomes dull, and the endothelium is destroyed. Initially, serous exudate accumulates in the pleural cavity, followed by serofibrinous and ultimately purulent exudate. It is thick in the lower regions, fluid in the middle, and may remain transparent in the upper parts. Due to fibrinous deposits, adhesions form between the pleural layers.

In malignant tumors of the lungs and pleura, the effusion acquires a hemorrhagic tint.

If left untreated, the exudate infiltrates through the intercostal Muscles into the subcutaneous tissue, forming a Phlegmon. Through lymphatic pathways, the infection invades the lungs and Bronchi, causing purulent melting of the bronchial wall with The formation of a bronchopleural fistula.

The inflammatory process may involve the entire pleural cavity (total pleurisy) or be confined to specific areas (encysted pleurisy).

Clinical presentation. When pleurisy complicates pneumonia, its onset is gradual, whereas in the rupture of an abscess or a suppurating infected cyst into the pleural cavity, it is sudden. The disease is characterized by a deterioration of the patient's general condition, the onset of pain in the affected hemithorax, which intensifies during respiration and coughing. Body Temperature rises to 39—40 °C, pulse and respiration accelerate, and acrocyanosis appears. Objective Examination of the chest reveals an enlargement of the affected hemithorax and widening of the intercostal spaces. The chest lags behind in the act of breathing. Percussion reveals a dull sound over the exudate. Occasionally, a space with increased acoustic conductivity can be detected in the paravertebral zone between the pleural exudate and the spine (Garland's triangle). The lower boundary of fluid accumulation on the anterior chest wall is lower than on the posterior wall, forming the so-called Ellis-Damoiseau line. On the healthy side, a triangular area of dullness corresponding to the displacement of mediastinal Organs is determined—Grocco-Rochfuss triangle.

X-ray Examination makes it possible to determine the localization and extent of the process, the volume of pus, the condition of the lungs (following evacuation of the exudate), and the displacement of thoracic organs.

The Diagnosis of purulent pleurisy is confirmed by diagnostic thoracentesis (puncture). Its site is determined based on the results of physical and radiological examination Methods. Following the puncture, the pleural cavity is irrigated with an antiseptic solution, and the exudate is subjected to cytological and Bacteriological examination. Thus, pleural puncture serves both diagnostic and therapeutic purposes.

Treatment of acute purulent pleurisy. Since acute pleurisy is predominantly a secondary condition complicating the course of other diseases, treatment must begin with the sanitation of the primary focus.

Two methods—closed and open—are used to treat acute pleurisy. Treatment begins with the former. It can be conservative or surgical. The conservative method consists of repeated aspiration punctures of the pleural cavity. Pus is aspirated, the pleural cavity is irrigated with antiseptic agents (furatsilin, solafur, dioxidine, chlorhexidine), and Proteolytic Enzymes (Trypsin, Chymotrypsin, streptase) are instilled into it.

In the absence of efficacy, the closed surgical method of treatment is indicated. It involves drainage of the pleural cavity using a tube inserted either via the trocar used for pleural puncture or through the bed of a resected rib segment. The tube is inserted into the pleural cavity in the 8th–9th intercostal space along the posterior axillary line. The soft Tissues around the tube are closed tightly, and the tube itself is secured to the Skin to prevent dislodgement. Its outer end is connected to active or passive suction, which may include underwater drainage (Bülau's method), siphon drainage, Water pumps, or an electric aspirator.

Concurrently with pus evacuation, detoxification and general supportive therapy, Blood transfusions, parenteral administration of Antibiotics, and other measures are carried out.

If the aspiration method proves ineffective within 1–2 months, the open surgical method is indicated (thoracotomy with resection of one or two Ribs at the lowest point of pus accumulation, removal of pus and fibrin clots, irrigation of the pleural cavity with an antiseptic solution, and drainage with a wide tube, and sometimes with tampons soaked in the same antiseptic).

Intensive antibacterial therapy is continued in the postoperative period.

Acute purulent Peritonitis. Peritonitis is an inflammation of the parietal and visceral layers of the Peritoneum, accompanied by a severe General condition of the Organism and frequently by irreversible changes in individual organs.

The peritoneum is a smooth, shiny, thin serous membrane of a bluish-pink color. Its surface area is 21,000 cm². It comprises parietal (lining the abdominal walls) and visceral (covering the Abdominal cavity organs) layers. The thickness of the peritoneum ranges from 0.7 to 1.1 mm. During inflammation, it sometimes thickens by 2–8 times. The peritoneum features a well-developed network of blood and Lymphatic vessels and nerves. The vascular bed of the peritoneum acts as a blood depot; during peritonitis, a large volume of blood accumulates within it, severely disrupting systemic hemodynamics.

The peritoneum both absorbs and secretes fluid, absorbing and eliminating about 70 liters daily. Not all Regions of the peritoneum absorb fluid equally: the peritoneum of the upper divisions is the most active in this regard, whereas the pelvic region is the least active.

The peritoneum also possesses significant plastic properties. When inflammatory exudate forms, fibrin is deposited on its surface, which facilitates the formation of adhesions that wall off the inflammatory process.

Etiology AND Pathogenesis. The cause of acute peritonitis is the action of microbes and their toxins on the peritoneum, and less frequently, aseptic fluids (blood, Lymph, Bile).

Infection can enter the abdominal cavity As a result of traumatic injury (including surgical interventions), acute abdominal conditions (such as acute appendicitis, cholecystitis, or pancreatitis), by metastatic spread—when infection extends to the peritoneum from adjacent organs (e.g., pelvic osteomyelitis or inflammation of the abdominal wall)—or hematogenously from distant sources of infection (such as tonsillitis, Influenza, or pneumonia).

Peritonitis is most commonly caused by Escherichia coli, and less frequently by staphylococci, enterococci, streptococci, Pseudomonas aeruginosa, and non-clostridial anaerobes.

Harmful agents act upon the peritoneum, damaging it and triggering an inflammatory process. Blood flow slows within dilated Blood Vessels, leading to the leakage of fluid into the abdominal cavity (exudation). Initially, the exudate is serous, but it subsequently becomes purulent, accompanied by the formation of fibrinous deposits. Toxic products are then absorbed into the dilated blood vessels.

The exudate accumulating in the abdominal cavity irritates a multitude of nerve receptors, which can lead to painful Shock on the one hand, and causes dehydration alongside protein and electrolyte imbalances on the other.

Intestinal atony (paralytic ileus) plays a major role in the pathogenesis of acute peritonitis. Large volumes of fluid accumulate within the dilated intestinal loops, contributing to further fluid loss. Intestinal paralysis sharply intensifies intoxication.

Death in peritonitis results from traumatic or bacterial shock, hepatorenal failure, and cardiovascular collapse.

Classification of peritonitis. Peritonitis is classified as primary or secondary. Primary peritonitis is rare (1%) and occurs when infection is introduced into the abdominal cavity exogenously in women via the fallopian tubes, or via hematogenous or lymphogenous routes.

Secondary peritonitis is much more common (resulting from trauma or acute inflammatory processes in abdominal organs).

Peritonitis is also categorized as acute or chronic (most frequently tuberculous).

Depending on the extent of the inflammatory process, peritonitis can be localized (circumscribed or uncircumscribed) or generalized (diffuse, widespread, or total).

In localized circumscribed peritonitis, the inflammatory process is walled off and separated from the free abdominal cavity by adhesions. Localized uncircumscribed peritonitis is confined to a single region of the abdominal cavity (such as the iliac or subhepatic region). In diffuse peritonitis, the inflammatory process involves one or two floors of the ABDOMINAL CAVITY AND tends to spread. In widespread peritonitis, more than two floors of the abdominal cavity are affected. When the pathological process involves all sections of the parietal and visceral peritoneum, the condition is termed total peritonitis.

Peritonitis is further distinguished into aseptic (non-bacterial) and septic (infectious).

Based on the character of the exudate, peritonitis may be serous, fibrinous, purulent, hemorrhagic, biliary, or putrid, and various combinations of these types are also observed.

Clinical Presentation and diagnosis. The clinical course of peritonitis comprises three stages: reactive, toxic, and terminal.

The reactive stage spans the first 24 hours (up to 12 hours in cases of hollow viscus perforation) from the onset of the disease. During this stage, the patient complains of severe abdominal pain and vomiting. In certain types of peritonitis, particularly those resulting from hollow organ perforation, the clinical picture of shock may be observed: the skin is pale and covered in cold sweat, the pulse is rapid and of low volume, the Abdominal muscles are rigid, and blood pressure is reduced.

Upon examination, the anterior abdominal wall is scaphoid or asymmetrical, and participates poorly or not at all in the respiratory act. Palpation reveals localized or generalized rigidity of the anterior abdominal wall (depending on the extent of the inflammation). Occasionally, the abdominal wall becomes rigid "like a board." Percussion of the abdomen elicits maximal pain

and dullness in the flanks, indicating fluid accumulation in those areas.

When the anterior abdominal wall is slowly depressed with the fingers and then suddenly released, the patient experiences a sharp increase in pain (a positive Blumberg's sign).

Additional Diagnostic Methods aid in the diagnosis of peritonitis. Blood tests reveal alterations: leukocytosis, a left shift in the leukocyte differential, an elevated ESR, and anemia.

The toxic stage of peritonitis lasts from 24 to 72 hours. During this phase, local symptoms subside somewhat, while systemic manifestations intensify. Pain and rigidity of the anterior abdominal wall decrease, and Blumberg's sign becomes less pronounced. Concurrently, intestinal atony worsens, and abdominal distension increases.

Signs of intoxication progressively worsen in the patient. Facial features become sharp, the skin takes on a gray hue, and the eyes and Cheeks are sunken (facies Hippocratica); blood pressure drops, and breathing becomes shallow and rapid. Urine output decreases, and signs of renal failure gradually develop. Blood laboratory parameters deteriorate.

If the patient is not operated on for any reason, the peritonitis transitions into its final, terminal stage. In this stage, both local and systemic manifestations of the disease progress severely. The abdomen is markedly distended and tender upon palpation. Bowel sounds are absent. Free fluid can be percussed in dependent areas. The pulse is thready, and blood pressure is drastically reduced. The patient is lethargic and poorly responsive. The skin is cyanotic, and oliguria is present.

Treatment. In acute peritonitis, therapy consists of timely surgical intervention preceded by brief (2–3 hours) intensive preoperative preparation. This includes: administration of analgesics (promedol, norphine, tramal), infusion therapy involving intravenous administration of 5–10% glucose solution, 0.89% sodium chloride solution, polyglucin, rheopolyglucin, plasma, albumin, protein, blood transfusions, and administration of 4% sodium bicarbonate solution. If blood pressure is low, Hormones (hydrocortisone, prednisolone) are administered, alongside antibiotics and cardiac medications.

The surgery is performed under endotracheal anesthesia. The abdominal cavity is opened via a midline incision (along the linea alba). The exudate is evacuated, and the source of peritonitis is identified and addressed (removal of an inflamed Appendix, Gallbladder, etc.). The abdominal cavity is lavaged with an antiseptic solution and drained. The choice of drainage depends on the extent of the inflammatory process. In serous localized uncircumscribed peritonitis, the insertion of one or two polyvinyl tubes into the abdominal cavity may suffice. In widespread purulent peritonitis, the abdominal cavity is drained through small counter-incisions in four Abdominal Regions (two iliac and two subcostal) using rubber drains and polyvinyl tubes. Occasionally, the anterior abdominal wall is left unclosed (so-called programmed laparostomy) and covered with a special biological film to facilitate subsequent pus removal and periodic lavage of the abdominal cavity.

To achieve decompression of the digestive tract at the end of the operation, a multi-lumen polyvinyl tube with side openings (such as a Abbott or Miller tube) is inserted nasally into The Stomach, duodenum, and Small Intestine.

In the postoperative period, conservative therapy is continued, the intensity of which depends on the spread of peritonitis and The Nature of the exudate. It is carried out in several directions.

1. Combating infection by administering antibiotics locally (via drainage tubes into the abdominal cavity), intramuscularly, and intravenously.

2. Relief of paralytic intestinal obstruction is achieved through intestinal intubation and gastric drainage, as well as peridural and paranephral blockades. Drugs that stimulate intestinal peristalsis (cerucal, prostigmine/proserine) are administered, and siphon enemas are prescribed.

3. Detoxification therapy, restoration of circulating blood volume, and correction of water-electrolyte balance disorders. To this end, intravenous infusion therapy is performed, just as in the preoperative period. On average, the patient should receive 3–4 liters of fluid per day.

4. Adequate parenteral Nutrition is provided through the intravenous administration of hydrolysates, amino acid mixtures, and fat emulsions. It is gradually reduced, and once peristalsis resumes and the patient begins to eat independently, intravenous fluid administration is discontinued.

5. Improvement of cardiovascular and Respiratory system Functions (cardiac medications, breathing exercises, patient rubbing, inhalations, cupping, mustard plasters, Oxygen therapy). In recent years, Hyperbaric Oxygenation has been increasingly used to treat oxygen deficiency in peritonitis patients.

6. Management of increased blood clotting. Peritonitis is invariably accompanied by hypercoagulation. To counteract this, early physical exercises, massage, and anticoagulants are prescribed.

7. Stimulation of the body's immunological reactivity: blood transfusions, anti-staphylococcal plasma administration, Introduction of gamma-globulin, staphylococcal toxoid, T-activin, and pentoxyl.

As the patient's general condition improves and the signs of peritonitis subside, The Scope of conservative therapy is gradually reduced.