Pulmonary Sepsis PDF Lecture Notes

🫁 Pulmonary Sepsis Lecturer Lecture Notes Type Objectives 1. Outline the normal defence mechanisms of the respiratory tract 2. Distinguish between up...

🫁 Pulmonary Sepsis Lecturer Lecture Notes Type Objectives 1. Outline the normal defence mechanisms of the respiratory tract 2. Distinguish between upper and lower respiratory infections 3. Describe the aetiology and pathogenesis of upper and lower respiratory infections organisms at risk individuals 5. Discuss methods of classification of pneumonia 5. Mention the common organisms responsible for pneumonia 6. Distinguish between bronchopneumonia and lobar pneumonia on the basis of morphology and clinical course describe the gross and microscopic differences 7. Discuss the complications of pneumonia 8. Explain the pathogenesis of lung abscess and bronchiectasis 9. Briefly outline how to investigate pneumonia 10. Be able to chose the right antibiotic Respiratory tract Pulmonary Sepsis 1  What are the defences of the respiratory tract? nasal hair, turbinates saliva filtering function of nasopharynx cough reflex - important in preventing aspiration. Not present in those under anaesthesia, w head injuries, inebriated w alcohol. mucociliary apparatus - action towards mouth secretion of IgA antibodies ( in lamina propria) phagocytic activity by alveolar macrophages alveolar fluid - surfactant, Igs, complement cell mediated immunity Airways have a well developed lymphoreticular system (local) to stop further spread. Pulmonary Sepsis 2  Which organisms cause infections? Primary: viral, bacterial, atypical bacteria (mycoplasma), fungi Secondary: infection has preceded it → made it easier for other organisms to infect that tissue Suppression of the cough reflex → reflux of gastric contents into airway Upper Respiratory tract infections Not a priority to give antibiotics for URTI What structures are affected? Nose, sinuses, larynx, trachea What are the common characteristics of URTI? Common Trivial or mild Transient Viral URT sepsis Viral: Common cold - rhinovirus Viral sore throat - adenovirus → pharyngitis, conjunctivitis (congestion & watery exudate) Secondary infection → purulent Influenza - influenza virus → few progress to pneumonia (primary influenzal pneumonia or secondary bacterial) Symptoms: fever, lassitude, depression Laryngotracheobronchitis - RSV (in children) Bacterial: healthy individuals, secondary to conditions which depress resistance (viral infections, chronic bronchitis, bronchiectasis) Strep pyogenes & other bacteria colonising the nose & throat Pulmonary Sepsis 3  Acute sinusitis & nasopharyngitis - Strep pyogenes → sudden death in young people Acute laryngitis - Haemophilus influenzae (type B) or Strep pyogenes Symptoms: swelling & mechanical inability to breathe Acute laryngitis & tracheitis - irritation by pollutants → oedema + obstruction Acute bronchitis in COPD Chronic bronchitis - specific Lower respiratory tract infections What structures are affected? Bronchi, bronchioles, lung parenchyma (alveolar spaces) The type of epithelium up till the terminal bronchioles - is designed to produce mucus and move that mucus to the upper airways (trap microbes within it) What are the characteristics of LRTI? Serious Morbidity/ Mortality - complicate PTs suffering from other conditions. Bacteria, viruses, atypical organisms, fungi Secondary to irritants Pneumonia - infection of alveolar spaces - broncho & lobar Host reaction: alveolar exudates polymorphs, fibrin, oedema fluid resulting in consolidation (whitish appearance on CXR) Classification: Morphology - bronchopneumonia, lobar pneumonia Aetiology (cause) Clinical setting Types: Pulmonary Sepsis 4  Bronchopneumonia - Strep pneumoniae, Haem influenzae, Moraxella catarrhalis, Staph pneumonia, Klebsiella, Pseudomonas aeruginosa Characteristics: Starts in bronchi → secondarily affect the alveoli polymorphs, fibrin patchy foci coalesce consolidation frequently widespread and bilateral rarely heals with fibrosis Lobar pneumonia - 90-95% Strep pneumoniae Characteristics: Starts in alveoli → spreads luminally - exudate flows to bronchioles & alveoli Virulent organism Host vulnerability polymorphs, fibrin, oedema fluid in alveoli most / all lobe consolidation resolution in majority Pulmonary Sepsis 5  Causes: Bacterial ‘Atypical’ - mycoplasma, legionella, chlamydia, coxiella, term not used anymore Streptococcus pneumoniae – in smokers, often follows viral infection, gram +ve diplococci Haemophilus influenzae - smokers, COPD Moraxella cartarrhalis - smokers, COPD, gram -ve diplococci Staphylococcus aureus - IV drug addicts, infancy, gram +ve cocci (usually seen in skin infections) Klebsiella - aspiration pneumonia, hospitalised ill patients, gram -ve rods, capsule Pseudomonas aeruginosa - aspiration pneumonia, hospitalised ill patients, gram -ve rods, mucoid type Coliform bacteria - hospitalised ill patients Chlamydia Legionella pneumophilia - from infected water systems TB – to be discussed separately Mycobacterium avium-intracellulare - immunosuppression Fungal Pulmonary Sepsis 6  Pneumocystis jirovecii/ Pneumocystis carinii - immunosuppression, major cause of death in HIV PTs Aspergillus fumigatus - immunosuppression Viral Aspiration Radiation Allergic mechanisms Community-acquired acute pneumonia Strep. Pneumoniae, H. influenzae (esp if smoker), Moraxella catarrhalis, Staphylococcus aureus, Legionella, Klebsiella, Pseudomonas Characteristics either morphological pattern is possible - lobar/bronchopneumonia lower lobes or right middle lobe due to aspiration of pharyngeal flora sputum - Gram-positive diplococci, numerous neutrophils blood cultures - may be positive in 20-30% responsive to penicillin but increasing resistance Pneumococcal infections are more common in PTs w splenectomies, chronic diseases etc Community-acquired atypical pneumonia mycoplasma, chlamydia, coxiella, viruses Hospital-acquired (nosocomial) pneumonia Gram negative rods (Klebsiella, E. coli, Pseudomonas) Staphylococcus aureus (usually MRSA) Aspiration pneumonia - anaerobes Pneumonia in immunocompromised host Pulmonary Sepsis 7  CMV, Pneumocystis carinii, mycobacterium avium-intracellulare, aspergillosis, candidiasis, “usual” organisms What is the pathogenesis of pneumonia? impaired defence mechanisms suppression of cough reflex - coma, anaesthesia, drugs - aspiration possible impaired ciliary function - cigarette smoke, hot gases, corrosives, viruses impaired phagocytic activity - alcohol, tobacco, smoke, excess oxygen pulmonary oedema and congestion - heart failure secretions - cystic fibrosis, bronchial obstruction low host resistance, low CMI - chronic disease, immune deficiency, immunosuppression, leucopenia, chemotherapy virulent infections - influenza What are the complications of pneumonia? Complete resolution if correct antibiotic Complications are commoner with lobar pneumonia Pleurisy & pleural adhesions - inflammatory infiltrate → formation of bands of fibrin (painful) Lung abscesses - localised suppurative area with a central necrotic cavity surrounded by granulated tissue Presentation: swinging fever Causes: Aspiration of infected material, gastric contents - most common Necrotizing or suppurative pneumonia anaerobic bacteria, commensals in mouth or mixed with S. aureus, b haemolytic streptococci, Klebsiella, Pseudomonas Pulmonary Sepsis 8  Bronchiectasis Bronchial obstruction via carcinoma Septic emboli - endocarditis Blood spread - Staphylococcal bacteraemia Treatment: drainage + antibiotics bacteraemia - metastatic abscesses cause endocarditis, meningitis, arthritis Rare complications: alveolar fibrosis, empyema Viral pneumonia - influenza type A & B, RSV, adenoviruses, rhinoviruses, SARS (coronavirus) Characteristics: interstitial pneumonia → no alveolar exudate interstitial infiltrate - histiocytes, lymphocytes initially atypical pneumonia generally mild severe LRTI if debility, alcoholism, immunocompromised low mortality unless epidemic/secondary bacterial infection ⚠️ Bacterial pneumonia → inflammation concentrated to the centre Viral pneumonia → inflammation in the interstitium Bronchiectasis What are the characteristics of bronchiectasis? abnormal permanent dilatation Pulmonary Sepsis 9  lower lobe distal bronchi, bronchioles associated chronic infection What is the pathogenesis of bronchiectasis? Obstruction → air reabsorbed from distal airways → atelectasis → loss of elastic tissue in interstitium → fibrosis attaches to lung pleura → dilation of the airways (due to pressure of inspired air) → reversible → become irreversible Irreversible if obstruction persists especially during growth persistent infection - bronchial wall ulceration, inflammation and further dilatation Causes: localised obstruction tumours, foreign bodies, mucus, chronic bronchitis congenital - lobe / lung Cystic fibrosis, immunodeficiency, immotile cilia necrotizing or suppurative pneumonia virulent organisms – Staph. aureus, Klebsiella, tuberculosis Symptoms precipitated by URTI or new pathogens What are the complications of bronchiectasis? lung abscess cor pulmonale metastatic brain abscesses distinguish from emphysema Pulmonary Sepsis 10