3. Contents of the training materials

Aetiology and pathogenesis of the disease.

Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities containing necrotic debris or fluid caused by microbial infection. The formation of multiple small (<2 cm) abscesses is occasionally referred to as necrotizing pneumonia or lung gangrene. Both lung abscess and necrotizing pneumonia are manifestations of a similar pathologic process. Failure to recognize and treat lung abscess is associated with poor clinical outcome.

Pathophysiology

Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by mouth anaerobes. The patients who develop lung abscess are predisposed to aspiration and commonly have periodontal disease. A bacterial inoculum from the gingival crevice reaches the lower airways, and infection is initiated because the bacteria are not cleared by the patient's host defense mechanism. This results in aspiration pneumonitis and progression to tissue necrosis 7-14 days later, resulting in formation of lung abscess.  Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, causing septic emboli (usually multiple) to the lung

Causes

The bacterial infection may reach the lungs in several ways. The most common is aspiration of oropharyngeal contents.

• Patients at the highest risk for developing lung abscess have the following risk factors:

  • Periodontal disease

  • Seizure disorder

  • Alcohol abuse

  • Dysphagia

• Other patients at high risk for developing lung abscess include individuals with an inability to protect their airways from massive aspiration because of a diminished gag or cough reflex, caused by a state of impaired consciousness (eg, from alcohol or other CNS depressants, general anesthesia, or encephalopathy).

• Infrequently, the following infectious etiologies of pneumonia may progress to parenchymal necrosis and lung abscess formation:

  • Pseudomonas aeruginosa

  • K pneumoniae

  • S aureus (may result in multiple abscesses)

  • Streptococcus pneumoniae

  • Nocardia species

  • Fungal species

• An abscess may develop as an infectious complication of a preexisting bulla or lung cyst.

• An abscess may develop secondary to carcinoma of the bronchus; the bronchial obstruction causes postobstructive pneumonia, which may lead to abscess formation

Symptoms and Diagnosis

History

Symptoms depend on whether the abscess is caused by anaerobic or other bacterial infection.

• Anaerobic infection in lung abscess

  • Patients often present with indolent symptoms that evolve over a period of weeks to months.

  • The usual symptoms are fever, cough with sputum production, night sweats, anorexia, and weight loss.

  • The expectorated sputum characteristically is foul smelling and bad tasting.

  • Patients may develop hemoptysis or pleurisy

• Other pathogens in lung abscess

  • These patients generally present with conditions that are more emergent in nature and are usually treated while they have bacterial pneumonia.

  • Cavitation occurs subsequently as parenchymal necrosis ensues.

  • Abscesses from fungi, Nocardia species, and Mycobacteria species tend to have an indolent course and gradually progressive symptoms

Physical

The findings on physical examination of a patient with lung abscess are variable. Physical findings may be secondary to associated conditions such as underlying pneumonia or pleural effusion. The physical examination findings may also vary depending on the organisms involved, the severity and extent of the disease, and the patient's health status and comorbidities.

• Patients with lung abscesses may have low-grade fever in anaerobic infections and temperatures higher than 38.5°C in other infections.

• Generally, patients with in lung abscess have evidence of gingival disease.

• Clinical findings of concomitant consolidation may be present (eg, decreased breath sounds, dullness to percussion, bronchial breath sounds, course inspiratory crackles).

• The amphoric or cavernous breath sounds are only rarely elicited in modern practice.

• Evidence of pleural friction rub and signs of associated pleural effusion, empyema, and pyopneumothorax may be present. Signs include dullness to percussion, contralateral shift of the mediastinum, and absent breath sounds over the effusion.

• Digital clubbing may develop rapidly.

Examination

Chest x-rays nearly always reveal a lung abscess. However, when an x-ray only suggests an abscess, computed tomography (CT) of the chest can confirm the presence of a lung abscess and possibly determine its cause. Cultures of sputum from the lungs may help identify the organism causing the abscess, but this test is not always useful.

• Chest radiograph

• A typical chest radiographic appearance of a lung abscess is an irregularly shaped cavity with an air-fluid level inside. Lung abscesses as a result of aspiration most frequently occur in the posterior segments of the upper lobes or the superior segments of the lower lobes.

• The wall thickness of a lung abscess progresses from thick to thin and from ill-defined to well-circumscribed as the surrounding lung infection resolves. The cavity wall can be smooth or ragged but is less commonly nodular, which raises the possibility of cavitating carcinoma.

• The extent of the air-fluid level within a lung abscess is often the same in posteroanterior or lateral views. The abscess may extend to the pleural surface, in which case it forms acute angles with the pleural surface.

• Anaerobic infection may be suggested by cavitation within a dense segmental consolidation in the dependent lung zones.

• Lung infection with a virulent organism results in more widespread tissue necrosis, which facilitates progression of underlying infection to pulmonary gangrene.

• Up to one third of lung abscesses may be accompanied by an empyema

• CT scan

• CT scan of the lung may help visualize the anatomy better than the chest radiograph. It is very useful in identification of concomitant empyema or lung infarction.

• On CT scan, an abscess often is a rounded radiolucent lesion with a thick wall and ill-defined irregular margins.

• The vessels and bronchi are not displaced by the lesion as they are by an empyema.

• The lung abscess is located within the parenchyma compared to loculated empyema, which may be difficult to distinguish on chest radiograph.

Treatment

Prompt, complete healing of a lung abscess requires the administration of antibiotics. These are initially given intravenously in most cases and later by mouth when the person has improved and the fever has resolved. Antibiotic treatment continues until the symptoms disappear and a chest x-ray shows that the abscess has disappeared. Such improvement usually requires several weeks or months of antibiotic therapy. Postural drainage may be used to help drain the abscess.

Bronchoscopy is performed to confirm the presence of an obstruction when the cause is thought to be a blocked airway due to a tumor or a foreign object. Bronchoscopy may also be used to remove a foreign object or to help drain a lung abscess that does not respond to antibiotics.

About 5% of people with lung abscesses need additional treatment. Occasionally, an abscess requires drainage through a tube inserted through the chest wall and into the abscess. More often, infected lung tissue may have to be removed surgically. Sometimes an entire lobe of a lung or even an entire lung has to be removed.

The death rate for people with lung abscesses is about 5%. The rate is higher when the person is debilitated or has an impaired immune system, lung cancer, or a very large abscess.

Surgical Care: Surgery is very rarely required for patients with uncomplicated lung abscesses. The usual indications for surgery are failure to respond to medical management, suspected neoplasm, or congenital lung malformation. The surgical procedure performed is either lobectomy or pneumonectomy.

When conventional therapy fails, either percutaneous catheter drainage or surgical resection is usually considered. Endoscopic lung abscess drainage was considered if an airway connection to the cavity could be demonstrated. Success of this treatment represents an additional option other than percutaneous catheter drainage or surgical resection.

Bronchiectasis

Bronchiectasis is defined as localized irreversible dilatation of part of the bronchial tree. Involved bronchi are dilated, inflamed, and easily collapsible, resulting in airflow obstruction and impaired clearance of secretions.

Pathophysiology

By definition, bronchiectasis demonstrates localized, irreversible dilatation of bronchi > 2 mm in diameter that results from destruction of the muscular and elastic components of bronchial walls. Damage to these 2 bronchial wall components is caused by an infectious organism and also by the inflammatory cytokines, nitric oxide, and neutrophilic proteases released by the host's immune response to the organism. Additionally, peribronchial alveolar tissue may be damaged, resulting in diffuse peribronchial fibrosis. The result is abnormal bronchial dilatation with bronchial wall destruction and transmural inflammation. The involved bronchi are not only dilated but also inflamed and easily collapsible, resulting in airflow obstruction and impaired clearance of secretions.

The most important functional finding of altered airway anatomy is severely impaired clearance of secretions from the bronchial tree. This altered airway anatomy causes colonization and infection with pathogenic organisms, contributing to the common purulent expectoration observed in patients who have bronchiectasis. The result is a cycle of bronchial damage, bronchial dilatation, impaired clearance of secretions, recurrent infection, and more bronchial damage.

Diseases associated with bronchiectasis are as follows:

•Infection: Typical organisms include Klebsiella species, Staphylococcus aureus, Mycobacterium tuberculosis, Mycoplasma pneumoniae, nontuberculous mycobacteria, Mycobacterium avium-intracellulare complex, measles, pertussis, influenza, respiratory syncytial virus, herpes simplex virus, and certain types of adenovirus.

•Bronchial obstruction: Obstruction occurs as a result of endobronchial tumors, broncholithiasis, bronchial stenosis resulting from infections, encroachment of hilar lymph nodes, and foreign body aspiration.

• Inhalation injuries

• Injury from noxious fumes, gases, or particles

• Inhalation of stomach acid and food particles

•Young syndrome - patients have bronchiectasis (often predominant in the lower lobes), sinusitis, and obstructive azoospermia

• Hereditary conditions

  • Cystic fibrosis - CF and its variants are likely the most common cause of bronchiectasis in the United States and other industrialized nations. CF is an autosomal recessive disease. CF is a multisystem disorder that affects the chloride transport system in exocrine tissues, primarily secondary to a defect in the CF transmembrane regulator (CFTR) protein.

  • Primary ciliary dyskinesia - manifested by immotile or dyskinetic cilia and/or sperm

  • Marfan syndrome

•Allergic bronchopulmonary aspergillosis - Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to inhaled Aspergillus antigen that is characterized by bronchospasm, bronchiectasis, and immunologic evidence of a reaction to Aspergillus species.

•Immunodeficiency states: The most common congenital conditions involve B-lymphocyte functions—specifically, hypogammaglobulinemia. An aggressive form of bronchiectasis has been described in patients with acquired immunodeficiency syndrome (AIDS).

•Congenital anatomic defects

◦Bronchopulmonary sequestration

◦Williams-Campbell syndrome (congenital cartilage deficiency)

◦Mounier-Kuhn syndrome (tracheobronchomegaly)

◦Yellow nail syndrome

•a 1 -Antitrypsin deficiency

•Lung and bone marrow transplants

•Rheumatoid arthritis and Sjögren syndrome

•Traction bronchiectasis associated with pulmonary fibrosis

In bronchiectasis, mucus production increases, the cilia are destroyed or damaged, and areas of the bronchial wall become chronically inflamed and are destroyed.

Anatomy

Bronchiectasis usually involves bronchi of medium size (>2 mm diameter). The proximal (main, lower, and segmental) bronchi are less affected, because they contain more cartilage than the distal bronchi and because they are more resistant to dilation. However, in patients with allergic bronchopulmonary aspergillosis and cystic fibrosis, the proximal bronchi are typically involved.

Although bronchiectasis caused by bacterial and viral infections usually affects the lower pulmonary lobes, the upper lobes are more frequently affected in patients with allergic bronchopulmonary aspergillosis and tuberculosis. Bronchiectasis is more diffuse in patients with cystic fibrosis and those with immunodeficiency states.

In advanced cases of bronchiectasis, dilated, medium-sized bronchi extend close to the pleura, without side branches and with few normal surrounding lung parenchyma. Focal destruction of part of the bronchial wall, increased mucus secretion and retention, and peribronchial fibrosis occur; the surrounding lung shows volume loss, fibrosis, emphysema, and nodular inflammatory foci.

Symptoms

History

The classic triad of symptoms (chronic cough, excess purulent sputum production, repeated infections) is seen only in the most severely affected patients. Total daily sputum production has been used to characterize severity of bronchiectasis:

• 10 mL/d is defined as mild bronchiectasis.

• 10-150 mL/d is defined as moderate bronchiectasis.

• 150 mL/d is defined as severe bronchiectasis.

Many patients have only mild or intermittent symptoms. Some patients with mild forms of bronchiectasis, as revealed on high-resolution computed tomography (HRCT) scans, may have no symptoms.

Hemoptysis is common and may occur in as many as 50% of patients. Episodic hemoptysis with little to no sputum production (dry bronchiectasis) is usually a sequela of tuberculosis. However, massive hemoptysis may occur; bleeding usually originates in dilated bronchial arteries, which contain blood at systemic (rather than pulmonary) pressures.

Less-specific symptoms include dyspnea, pleuritic chest pain, wheezing, fever, weakness, and weight loss. Significant airway obstruction may occur as a result of the bronchitis, bronchiolitis, or emphysema that frequently accompanies bronchiectasis. Repeated bronchial infection and pneumonia are common.

Physical examination

Findings are nonspecific and may be attributed to other conditions. Most commonly, crackles, rhonchi, wheezing, and inspiratory squeaks may be heard upon auscultation. General findings may include digital clubbing, cyanosis, plethora, wasting, and weight loss. Nasal polyps and signs of chronic sinusitis may also be present. In advanced disease, the physical stigmata of cor pulmonale may be observed.

• Crackles and rhonchi are often observed in association with active infections and acute exacerbations.

• Scattered wheezing may be heard in approximately one third of patients. Wheezing may be due to airflow obstruction from secretions, destruction of the bronchial tree leading to airway collapsibility, or concomitant conditions.

• Digital clubbing is an inconsistent finding in approximately 2-3% of patients. It is more frequent in patients with moderate-to-severe bronchiectasis.

• Cyanosis and plethora are rare findings secondary to polycythemia from chronic hypoxia.

• Wasting and weight loss are suggestive of advanced disease but are not diagnostic of bronchiectasis.

• In severe cases, findings are consistent with cor pulmonale. Right-sided heart failure may be observed, including peripheral edema, hepatomegaly, and hypoxia. This can ultimately lead to progressive respiratory failure.

Examination

Chest radiography is usually the first imaging examination, but the findings are often nonspecific and the images may appear normal. High-resolution computed tomography (HRCT) scanning has become the imaging modality of choice for demonstrating or ruling out bronchiectasis and its extent. HRCT scanning also helps clinicians evaluate the status of the surrounding lung tissue and exclude other lesions such as neoplasms/

Bronchography was the classic modality used and, until the advent of HRCT scanning, was the only imaging method to demonstrate bronchiectasis. Bronchography is performed by instilling an iodine-based contrast material via a catheter or bronchoscope, but it is rarely, if ever, performed today, as HRCT scanning has replaced it as the diagnostic modality of choice. HRCT scanning is noninvasive and has a sensitivity of 96% and a specificity of 93%.

Laboratory testing may be helpful:

• Results of sputum culture and analysis may reinforce the diagnosis of bronchiectasis and add significant information regarding potential etiologies.

• Complete blood counts are often abnormal in patients who have bronchiectasis.

• Quantitative immunoglobulin (Ig) levels, including levels of the IgG subclasses, IgM, and IgA, are used to exclude hypogammaglobulinemia.

• Quantitative a₁ -antitrypsin levels are used to exclude deficiency.

• Pilocarpine iontophoresis (sweat testing) is used to detect cystic fibrosis.

• Pulmonary function test results may be normal or abnormal but can be useful in making a functional assessment of the patient. The most common abnormality is an obstructive airway defect.

Bronchoscopy is not helpful in diagnosing bronchiectasis, but it may be used to identify underlying abnormalities, such as tumors and foreign bodies.

Medical Care

The goals of therapy are to improve symptoms, to reduce complications, to control exacerbations, and to reduce morbidity and mortality. Early recognition is essential in bronchiectasis and associated conditions. Additionally, management of underlying conditions, which may include the use of intravenous immunoglobulin or intravenous AAT therapy, is essential to the overall treatment.

Antibiotics and chest physiotherapy are the mainstay modalities. Other modalities (beyond those for specific associated conditions) may include bronchodilators, corticosteroid therapy, dietary supplementation, and oxygen or surgical therapies. Admitting patients with severe exacerbations of bronchiectasis to the hospital and treating them with intravenous antibiotics, bronchodilators, aggressive physiotherapy, and supplemental nutrition is not uncommon. Available treatment guidelines include:

• General therapy

  • Patients should stop smoking.

  • Patients should avoid second-hand smoke.

  • Patients should have adequate nutritional intake with supplementation, if necessary.

  • Immunizations for influenza and pneumococcal pneumonia are recommended.

  • Immunizations for measles, rubeola, and pertussis should be confirmed.

  • Oxygen therapy is reserved for patients who are hypoxemic with severe disease and end-stage complications, such as cor pulmonale.

  • Patients with CF should be cared for at specialized CF treatment centers that address all aspects of the disease, including nutritional and psychologic aspects.

• Antibiotics

  • Oral, parenteral, and aerosolized antibiotics are used, depending on the clinical situation.

  • In acute exacerbation, broad-spectrum antibacterial agents are generally preferred. However, if time and the clinical situation allows, then sampling respiratory secretions during an acute exacerbation may allow treatment with antibiotics based on specific species identification.

  • Acceptable choices for the outpatient who is mild to moderately ill include amoxicillin, tetracycline, trimethoprim-sulfamethoxazole, a newer macrolide (eg, azithromycin or clarithromycin ), a second-generation cephalosporin, or one of the fluoroquinolones. In general, the duration is 7-10 days.

  • For patients with moderate-to-severe symptoms, parenteral antibiotics, such as an aminoglycoside (gentamicin, tobramycin) and an antipseudomonal synthetic penicillin, a third-generation cephalosporin, or a fluoroquinolone, may be indicated. Patients with bronchiectasis from CF are often infected with mucoid Pseudomonas species, and, as such, tobramycin is often the drug of choice for acute exacerbation.

  • Infection with MAC provides special treatment challenges. For the treatment of MAC in the setting of bronchiectasis, the American Thoracic Society recommends a 3- to 4-drug treatment regimen with clarithromycin, rifampin, ethambutol, and possibly streptomycin that is continued until the patient's culture results are negative for 1 year. The typical duration of therapy may be 18-24 months.

  • Additionally, some patients with chronic bronchial infections may need regular antibiotic treatment to control the infectious process. Some clinicians prefer to prescribe antibiotics on a regular basis or for a set number of weeks each month. The oral antibiotics of choice are the same as those mentioned previously. Potential regimens include daily antibiotics for 7-14 days of each month, alternating antibiotics for 7-10 days with antibiotic-free periods of 7-10 days, or a long-term daily dose of antibiotics. For patients with severe CF and bronchiectasis, intermittent courses of intravenous antibiotics are sometimes used.

  • In the past several years, the nebulized route of antibiotic administration has received more attention because it is capable of delivering relatively high concentrations of drugs locally with relatively few systemic adverse effects. This is particularly beneficial in treating patients with chronic infection from P aeruginosa. Currently, inhaled tobramycin is the most widely used nebulized treatment for patients with bronchiectasis from either CF or non-CF causes of bronchiectasis. Gentamicin and colistin have also been used.

• Bronchial hygiene

  • Postural drainage with percussion and vibration is used to loosen and mobilize secretions. Other devices available to assist with mucus clearance include flutter devices, intrapulmonic percussive ventilation devices, and incentive spirometry. However, consistent benefits from these techniques are lacking and vary with patient motivation and knowledge.

  • Nebulization with sodium chloride solutions appears to be beneficial, particularly in patients with CF-related bronchiectasis. Mucolytics, such as acetylcysteine, are also often tried but a universal benefit does not seem to exist. However, maintaining adequate general hydration, which may improve the viscidity of secretions, is important.

• Bronchodilators

  • Bronchodilators, including beta-agonists and anti-cholinergics, may help some patients with bronchiectasis, presumably reversing bronchospasm associated with airway hyperreactivity and improving mucociliary clearance.

• Anti-inflammatory medication

  • The rationale is to modify the inflammatory response caused by the microorganisms associated with bronchiectasis and subsequently reduce the amount of tissue damage. Inhaled corticosteroids, oral corticosteroids, leukotriene inhibitors, and nonsteroidal anti-inflammatory agents have all been examined. Although evidence tends to support some benefit from the use of these agents, findings are not universally definitive.

Surgical Care

• Surgery is an important adjunct to therapy in some patients with advanced or complicated disease. Surgical resection for bronchiectasis can be performed with acceptable morbidity and mortality in patients of any age.  In general, surgery should be reserved for patients who have focal disease that is poorly controlled by antibiotics. The involved bronchiectatic sites should be completely resected for optimal symptom control. Other indications for surgical intervention may include the following:

  • Reduction of acute infective episodes

  • Reduction of excessive sputum production

  • Massive hemoptysis (Alternatively, bronchial artery embolization may be attempted for the control of hemoptysis.)

  • Foreign body or tumor removal

  • Consideration in the treatment of MAC or Aspergillus species infections

• Complications of surgical intervention include empyema, hemorrhage, prolonged air leak, and persistent atelectasis.

• Single- or double-lung transplantation has been used as treatment of severe bronchiectasis, predominantly when related to CF. In general, consider patients with CF and bronchiectasis for lung transplantation when forced expiratory volume in 1 second (FEV₁) falls below 30% of the predicted value. Female patients and younger patients may need to be considered even sooner.

4. Plan and organizational structure of educational sessions on discipline.

№ з/п	Stages of class	Time distribu-tion	Types of control	Equipment training
1.	The starting phase	15%
1.1.	Organizational matters	20-25 min.
1.2.	Formation of motivation
1.3.	Control of entry-level training		─ written computer testing; ─ oral questioning by the standardized list of questions.	─ textbooks treatment of internal diseases; ─ guidelines; ─ situational problem in therapy of internal medicine; ─ tests "Step 2";
2.	The main stage ─ demonstration of the patient - his clinical examination (history, physical examination, additional methods of investigation); ─ interpretation received symptoms	65% 120-130 mn.	─ practical skills at the bedside (collecting complaints, history of illness, physical examination, assessment of results of additional methods investigation); ─ interpretation of the results.	─ themed patients.
3.	The final stage	20%
3.1.	Control of the final level of training	25-30 min.	─ situational tasks; ─ structured written work.
3.2.	The total score of student workload
3.3.	Informing students about the topic the next lesson