Chest Revision PDF

.Lung abscess. Definition: It is localized cavity containing pus or necrotic debris (and often air-fluid level), resulting from necrosis of lung tissue due to infection by pyogenic organisms. Classification: acute (< 6 weeks) or chronic (> 6 weeks), primary or secondary Causes: 1. Aspiration pne...

.Lung abscess. Definition: It is localized cavity containing pus or necrotic debris (and often air-fluid level), resulting from necrosis of lung tissue due to infection by pyogenic organisms. Classification: acute (< 6 weeks) or chronic (> 6 weeks), primary or secondary Causes: 1. Aspiration pneumonia (the most common) 2. Necrotizing pneumonia 3. Other causes: hematogenous spread (usually by S aureus), extension from adjacent structures, pre-existing lung disease as bronchiectasis, infected pulmonary infarct, trauma, immunodeficiency Causative organisms 1. Anaerobes in up to 93 % 2. Aerobes as Staph. aureus, Streptococcus pyogenes, K. pneumoniae, and P. aeruginosa 3. Other uncommon organisms as Nocardia spp., Paragonimus westermani Diagnosis ▪ Symptoms: cough with purulent foul odor or putrid sputum (indicative of anaerobic infection), high grade fever, dyspnea, pleuritic chest pain and hemoptysis that can occasionally be life-threatening. ▪ Chest X ray and CT: thick-walled cavity with air-fluid level. ▪ Blood cultures and sputum cultures Treatment 1. Antimicrobial therapy ▪ The treatment must be guided by microbiology and underlying cause ▪ Duration: A minimum of 4-6 weeks of antibiotics is recommended. ▪ Postural drainage and lung physiotherapy 2. Bronchoscopic or sonar-guided percutaneous drainage 3. Surgical resection of necrotic segments: Poor response to antibiotics (> 4 months), large abscesses (> 6 cm diameter), massive hemoptysis or airway obstruction (tumor or foreign body) that limits drainage..Bronchiectasis. Definition: abnormal and irreversible dilatation of thick-walled medium-sized bronchi. Causes and pathogenesis 1. Primary infection: as pneumonia, TB, HIV 2. Bronchial obstruction as tumor, aspirated foreign body, lymphadenopathy  3. Primary impairment of mucous clearance as cystic fibrosis, Kartagner syndrome 4. Developmental defects as α-1 antitrypsin deficiency, sequestrated segment 5. Immunodeficiency syndromes 6. Airway diseases as allergic bronchopulmonary mycoses (in asthma) 7. Autoimmune disease: as SLE, RA Clinical picture: ▪ Cough: persistent, copious, mucopurulent sputum, worse in the morning. ▪ Hemoptysis ▪ Dyspnea is regarded as a late symptom and usually indicates widespread lung disease with extensive destruction and fibrosis. Wheeze may occur. ▪ Acute exacerbations: increasing cough, dyspnea, and volume of sputum production, fever, hemoptysis, and chest pain ▪ General tiredness, malaise, weight loss and symptoms of underlying diseases. Pulmonary function tests: airflow obstruction in up to 80%. Sputum microbiology Investigations directed at underlying cause Chest X ray and CT: There may evidence of dilated bronchi: ring shadows, parallel lines, tubular opacities and appearances consistent with volume loss Management 1- Treatment of underlying cause 2- Mucolytic: as carbocysteine, bromhexine, recombinant human DNase 3- Chest physiotherapy: airway clearance techniques: postural drainage, forced expiration technique, … 4- Pulmonary rehabilitation 5- Airway drug therapy: bronchodilators & inhaled corticosteroids 6- Antibiotic therapy for exacerbations 7- Surgical management: ▪ Elective surgical treatment (resectional surgery): for patients with localized disease in whom symptoms are not controlled by medical treatment and no persisting systemic causal factor. ▪ Emergency surgery for hemoptysis: therapeutic bronchial artery embolization and/or resection ▪ Lung transplantation: indicated for end-stage disease. 8- Additional measures: such as vaccination and smoking cessation 9- Management of complications: such as oxygen for hypoxic patients and diuretic for decompensated cor pulmonale. tuberculosis. Tubercle bacillus: Human tuberculosis is caused by Mycobacteria tuberculosis (in most cases), M. bovis and M. africanum (in relatively few cases). Modes of infection: 1- Airborne infection: the main route of transmission of MTB infection. 2- Ingestion: Ingestion of infected milk (M. bovis) or sputum (M. tuberculosis) 3- Primary cutaneous TB: direct inoculation of bacilli into the skin or mucous membrane Tuberculin skin testing Interpretation: tuberculin test is positive when: Induration > 5mm: HIV, organ transplants, patients taking >15mg prednisolone for >1month or taking TNF-α antagonists, recent close contact with TB patient and persons with fibrotic changes on chest radiographs consistent with old TB Induration > 10mm: Persons with risk factors for tuberculosis other than the above: ▪ Foreign-born persons from high-prevalence countries, IV drug users, socially deprived or ethnic minority groups, homeless, laboratory personnel, residents and employees of long-term care facilities (prisons, nursing homes, and hospitals) ▪ Persons with medical conditions predisposing to tuberculosis, e.g. silicosis, DM, chronic renal failure, hematologic disorders as leukemias & lymphomas, specific malignancies (e.g., carcinoma of the head or neck and lung), immunosuppressive therapy, gastrectomy, and jejunoileal bypass Induration > 15mm: considered positive in all persons Treatment: short course chemotherapy for 6 months; initiation phase (2 month and 4 drugs), and continuation phase (4month and 2 drugs) Bronchial asthma Bronchial asthma is a heterogeneous disease usually characterized by chronic airway inflammation. It is defined by the history of respiratory symptoms such as wheezing, shortness of breath, chest tightness, and coughing that vary over time and in intensity together with variable expiratory airflow limitation (GINA 2022). Atopy: production of abnormal amounts of IgE in response to environmental allergens. Pathogenesis ▪ Asthma is an inflammatory disorder of the airways which involve several inflammatory cells and mediators ▪ Inflammatory cells: mainly eosinophils, mast cells, CD4 T lymphocytes ▪ Inflammatory mediators: chemokines, cytokines, histamine, prostaglandins, cysteinyl leukotreines, nitric oxide, platelet activating factor, bradykinines. Clinical manifestations: ▪ Asthma symptoms: episodic dyspnea, wheezing, cough and chest tightness ▪ Diagnostic criteria: more than one asthma symptoms that tend to be variable over time and intensity, worse at night or early morning, triggered by exercise, allergen, irritants, cold air, viral infection and respond to anti-asthma therapy. The attack ends  spontaneously or after treatment. The attack may persist as acute severe asthma that may be fatal or near fatal. ▪ In between attacks, the patient is clinically free except in chronic asthma. ▪ There are seasonal variability, diurnal variability, positive family history of asthma or allergy and history of atopic disease (allergic rhinitis, urticarial, eczema, hey fever and spring catarrh). Investigations: ▪ Spirometry: normal or obstructive pattern with reversible airflow limitation. ▪ Peak expiratory flow rate (PEFR): to examine variability of asthma ▪ Bronchial provocation tests ▪ The presence of allergic component: positive skin testing or high serum total and specific IgE. ▪ Markers of airway inflammation: sputum eosinophilia >2% & exhaled NO & CO. ▪ Other tests: Radiographic studies, blood tests, and more extensive lung function studies are used to exclude other conditions Medications for asthma that include ▪ Controllers (maintenance): inhaled corticosteroids (ICS), leukotriene modifiers, long acting β2 (inhaled and oral) agonists, sustained released theophylline, cromones, anti-IgE, systemic glucocorticosteroids and oral anti-allergic compounds ▪ Relievers (rescue medications): short acting β2 agonists (SABA), short acting anticholinergic (SAMA), systemic glucocorticosteroids. Route of Administration: inhaled, oral and parenteral (subcutaneous, IM or IV). Advantages of inhalation therapy: 1- High concentrations can be delivered to the airways 2- Minimal systemic absorption and side effects. 3- Fast onset of action of bronchodilators. Management of asthma exacerbations Definition: acute or subacute worsening in symptoms and lung function from the patient usual status that is sufficient to require change in treatment. Severity of exacerbations ▪ The severity of asthma exacerbations may range from mild to life threatening. ▪ Features of life-threatening attacks are severe dyspnea, bradycardia, central cyanosis, confusion, drowsiness, silent chest, paradoxical thoraco-abdominal movement & disturbed ABG (PaCO2>50mmHg, PaO2 55%) to keep SaO2 ≥ 90 % 5- Non-invasive ventilatory support: for persistent day-time hypercapnia 6- Surgical Treatments ▪ Bullectomy and lung volume reduction surgery ▪ Lung transplantation: for end stage COPD.Management of acute COPD exacerbations. Definition: acute worsening of respiratory symptoms result in additional therapy. Causes: exacerbations are mainly triggered by viral respiratory infection. Bacterial infection and environmental factors may initiate these events. Classification: ▪ Mild: treated with short acting bronchodilators only ▪ Moderate: treated with SABA/SAMA plus antibiotic ± oral steroid ▪ Severe: require hospitalization or emergency visit and associated with acute RF. Differential diagnosis: including pneumonia, congestive heart failure, pneumothorax, pleural effusion, pulmonary embolism, and cardiac arrhythmia. Symptoms: increased dyspnea is often accompanied by wheezing and chest tightness, increased cough and sputum, change of the color and/or tenacity of sputum, and fever. Treatment: 1. Bronchodilators: increase doses & frequency of short-acting bronchodilator, combine SABA and SAMA, use spacers or air-driven nebulizers. 2. Glucocorticoids: 40 mg prednisone per day for 5-7 days is recommended. Methylprednisolone 60-125mg 2-4 times daily for severe exacerbations. 3. Antibiotics: antibiotics are recommended when patients have clinical signs of bacterial infection as increased purulence of sputum. 4. Adjuvant therapies: as diuretics, prophylactic anticoagulants, treatment of comorbidities and fluid and nutritional support Respiratory support 1. Controlled oxygen therapy by venture mask: target O2 saturation 88-92 % 2. Ventilatory support: non-invasive or invasive ventilation Respiratory failure Definition of respiratory failure: Clinically: RF is defined as a PaO2 < 60 mmHg and/or a PaCO2 > 49 mmHg measured at rest at sea level. Types of respiratory failure: type I (hypoxemic) or type II (hypoxia and hypercapnea). Causes of type I RF: 1- Alveolar filling diseases: ARDS, pulmonary edema, pneumonia, alveolar hemorrhage, lung contusion, alveolar proteinosis, BOOP, aspiration, … 2- Interstitial lung diseases 3- Pulmonary vascular diseases: pulmonary embolism, pulmonary hypertension and pulmonary vasculitis 4- Pleural diseases: tension pneumothorax 5- Airway diseases: alpha-1 antitrypsin deficiency, acute severe asthma Causes of type II RF (alveolar hypoventilation): 1- Obstructive hypoventilation: COPD, acute severe asthma with respiratory muscle fatigue, bronchiectasis 2- Restrictive hypoventilation: morbid obesity, chest wall bony diseases (as kyphoscoliosis) and chest wall neuromuscular diseases (as myopathies, myasthenias, neuropathies, AHC, brain stem and brain diseases) Management of respiratory failure 1- Maintain a patent airway 2- Ensure adequate alveolar ventilation and oxygenation (prevent tissue hypoxia) by either oxygen therapy or eventually mechanical ventilation 3- Treat the primary condition and complications if possible. Goal of oxygen therapy: The goal of oxygen therapy is to prevent tissue hypoxia. The goal of oxygen therapy is to achieve a target saturation of 94–98% for most acutely ill patients not at risk of hypercapnic RF or 90–92% for those at risk of hypercapnic respiratory failure without causing significant oxygen toxicity Indications of chest tube insertion 1. Pneumothorax 2. Complicated parapneumonic effusion or empyema 3. Hemothorax 4. Chylothorax 5. Symptomatic pleural effusion 6. Bronchopleural fistula 7. chemical pleurodesis for benign and malignant conditions; 8. Postoperative use in thoracic/cardiac surgery; and 9. Penetrating chest trauma; 10. Severe blunt chest trauma; Causes of obstructive pattern 1. COPD (irreversible or partially reversible) 2. Bronchial asthma (reversible, variable) 3. Bronchietasis including cystic fibrosis 4. Some causes of bronchiolitis 5. Upper airway obstruction Causes of restrictive pattern ▪ Pulmonary causes: Interstitial lung diseases and lobectomy / pneumonectomy ▪ Extra-pulmonary (chest wall) causes 1. Obesity / OHS (obesity hypoventilation syndrome) 2. Skeletal abnormalities: as kyphoscoliosis, severe pectus excavatum, severe pectus carinatum, flail chest, … 3. Neuromuscular diseases: as myopathies, myasthenias, neuropathies, anterior horn cell diseases, brain and brain stem diseases