Pneumonia Lecture Notes PDF

Lec 5: Pneumonia and bronciectasis Lung infection sites: Upper respiratory tract infection Lower respiratory tract infection ○ Bronchitis: infection over the bronchial tree ○ Pneumonia: infection over the lung parenchyma Pneumonia Definition: Acute infection that...

Lec 5: Pneumonia and bronciectasis Lung infection sites: Upper respiratory tract infection Lower respiratory tract infection ○ Bronchitis: infection over the bronchial tree ○ Pneumonia: infection over the lung parenchyma Pneumonia Definition: Acute infection that inflames the air sacs in one or both lungs, caused by bacterial, viral, fungal parasites or infection //Non-infectious pneumonia (Idiopathic interstitial pneumonia) Content in the air sac: fluid, pus Trend: less cases, more deaths, death: M>F Types of pneumonia– based on the origin 1. Community-acquired (CAP): developed in the community 2. Healthcare-associated (HCAP): developed in long-term facilities such as nursing home, outpatient, or extended-stay clinics 3. Healthcare-acquired (HAP): during/ following a stay in healthcare setting 4. Ventilator associated (VAP): after being on a ventilator, a machine that support breathing 5. Aspiration pneumonia: Aspiration of food, saliva or gastric contents into airways CAP vs HAP CAP HAP Causative organisms SCM 3 pneumoniae + MRSA haemophilus influenzae Multiply-resistant Streptococcus staphylococcus pneumoniae aureus (most often) Haemophilus Enteric influenzae gram-negative (e.g. Mycoplasma E coli, proteus, pneumoniae enterobacter, Chlamydia klebsiella, serratia pneumoniae spp.) Chlamydia pneumonia Pseudomonas aeruginosa Anaerobic bateria  Fungi * According to QEH, 2011-2013 1st: E coli 2nd: Klebsiella 3rd: Pseudomonas aeruginosa Risk factor Habits: Hospitalisation for Smoking more than 5 days Alcoholism Previous infection Other comorbidities: with resistant COPD organisms Congestive heart Surgery failure (CHF) Pleural effusion Immuno-compromise Chemotherapy Seizure Dialysis Dementia Prolonged wound care Residence in a nursing home Types of pneumonia– based on the affected sites 1. Bronchopneumonia: descending infection started around bronchi and bronchioles → spread to the lung 2. Lobar pneumonia: Acute exudative inflammation of the entire lobe 3. Interstitial pneumonia: Inflammation in the structural spaces between the alveoli. Causes of pneumonia – based on different age Infants (6) ○ Normal: Respiratory syncytial virus (RSV), Adenovirus and bacterial ○ Sick infants: staphylococcus, Ecoli and gram-negative bacteria and virus Children (4) : Viruses, Staphylococcus, mycoplasma, haemophilus influenzae (leading to bronchitis) Adult (8) : Viruses, Staphylococcus, mycoplasma, haemophilus influenzae,+ 4 pneumococcus, chlamydia psittaci from bird/ farm animals, legionella from contaminated water system and HIV (leading to pneumocystis pneumonia) Elderly/ previous resp. Illness (10, 3 from children, 3 from adult +4): Staphylococcus, mycoplasma, haemophilus influenzae, Pneumococcus, Legionella, HIV, Klebsiella and gram-negative organisms, Aspiration pneumonia, TB, Carcinoma General risk factors of pneumonia: Advanced age Smoking history Alcohol consumption Malnutrition Loss of consciousness (LOC) Underlying lung disease (ex: COPD, cystic fibrosis, bronchiectasis) Impaired swallowing and endotracheal intubation Post-operation especially with poor pain control Immobilization Cardiac and/or liver disease Medications that decrease gastric pH (ex: H2 receptor blockers) Immunocompromise (ex: HIV/AIDS, chemo) Symptoms of Pneumonia 1. High fever (up to 40 deg celsius)/ swinging fever (=fever with large daily conciliation) 2. Fatigue 3. Loss of appetite 4. Confusion or altered mental state 5. Cough with yellow, green or bloody mucus 6. SOB 7. Chest pain esp with coughing and deep breathing 8. Tachypnoea 9. Tachycardia 10. Sweating or chills 11. Cyanosis (due to hypoxia) Pathophysiology of pneumonia Multiplication of pathogen: Bacterial pathogen has escaped the respiratory defenses and begins to multiply within the alveoli and airways Intense immune and inflammatory response: Macrophages in the lower airways and alveoli recognize pathogens Consolidation: Inflammatory cytokines,white blood cells and edema flood the alveoli and bronchi Hypoemia: V/Q mismatch Spreading: The infection may spread to the bloodstream (bacteremia and sepsis), pleura (empyema) or other organs (e.g meningitis) Diagnosis: Physical sign + abnormal CXR Vital signs, esp fever, tachycardia, low BP, desaturation and ↑ RR ○ Low BP + ↑ RR → indicate sepsis ↑ WBC count in CBP/ CBC ↑ CRP (normal: 0.25 ng/mL → indicate infection Sputum culture and sensitivity test (C/ST) FOB fuberoptic bronchoscopy *Rule out pulmonary embolism and other → CT thorax *Rule out DVT → well’s score Aspiration and test with bronchoscopy and bronchoalveloar lavage (BAL) Viral pneumonia Route of infection: droplet Frequent site of infection: ciliated cells of respiratory tract Pathophysiology: Some ciliated cells become paralyzed and degenerate → necrosis and desquamation 剝落 → a thin layer of non-ciliated basal replacement cells in the mucociliary blanket → inflammatory responses leading to exudation of fluid and erythrocytes in both alveolar space and airways → Formation of intra-alveolar hyaline membrane leading to congestion (alveoli filled with blood) and oedema → involved lung are susceptible to superimposed bacterial infections Clinical presentation: ○ Fever ○ Dyspnoea ○ Persistent and non-productive cough ○ Auscultation: with scattered insp. crackles ○ CXR: from minor infiltrates to severe bilateral involvement and less frequent consolidations and pleural effusion ○ Often occur secondary bacterial infections → productive cough Medical management ○ Rest and sleep ○ High fluid intake and good nutrition ○ Reduced stress ○ Prevention: receive vaccine Bacterial pneumonia Primary infection & Secondary infection: ○ pneumococcal origin & when patient's defence system is ineffective Present of pleural fluid = thoracentesis Four stages of bacterial infection of lung tissues Timeline Engorgement First few days of Vascular engorgement stage 塞 infection Serious exudation bacterial colonisation Red within 2-4 days Diapedesis of RBC (moving out hepatisation from blood vessel) stage Alveoli full of polymorphonuclear leukocytes, fibrin and RBC Fluid exudate and organism continue to multiply within it Areas of consolidation become evident Gray within 4-8 days Abdundant fibrin, ↓ hepatisation polymorphonuclear leukocytes stage and dead bacteria consolidation continues Resolution after 8 days area of consolidation begins to stage resolve Macrophages and enzymatic digestion of exudate is present affected tissue with large amount of grayish-red fluid within the alveoli → Chest physio -remove of secretion Continues 2-3 weeks → lung with more normal appearance Clinical presentation: ○ Fever ○ Dyspnoea ○ Tachypnea and tachycardia ○ Hypoxemia ○ Cough with purulent sputum ○ Pleuritic chest pain over affected lung field ○ Physical examination: ↓ chest expansion over the affected area and muscle splinting  ○ Auscultation: ↓/ absence breath sound, wheeze or crackles ○ CXR: atelectasis, infiltrates and consolidation *Causes of atelectasis: Airway obstruction (absorption ateletasis): compressed by tumour/ abnormal tissues/ foreign body// secretion Hypoventilation, usually post-op Fibrosis and chronic inflammation (chronic pneumonia) Medical management ○ Antibiotics (tablet/ IV) ○ Medication ○ ↑ fluid intake ○ Ultrasonic nebulisation → help to breathe better ○ Supplementary O2 if severe Physiotherapy management (goals) (6) Reversing alveolar hypoventilation Increasing ventilation/ perfusion matching Minimizing effects of impaired mucociliary transport Augmenting mucocilliary clearance Minimizing effects of increased mucous production Reducing sputum retention Optimizing lymphatic drainage of lungs Promoting lung expansion CXR RUL | LtUL&lingula Complication of pneumonia (6) Lung fibrosis Cavitary lesion with lung abscess → postural drainage  Pleural effusion Empyema = pus (infection) in the pleural spaces Septicemia Respiratory failure, may require mechanical ventilation Differentiating pneumonia and lung fibrosis By auscultation Pneumonia Lung fibrosis Insp. crackles Quality of crackles can be altered by cough Quality X be altered by cough Prevention of pneumonia Improve body resistance Improve personal hygiene Avoid crowded area Wear masks if suffering from respiratory symptoms Wash hands VAP Ventilator associated pneumonia Definition CDC: Pneumonia occur at the time of intubated and ventilated or within 48 hours ATS (American thoracic society) and IDSA: arises > 48-72 hours after intubation Importance? Common in mechanically ventilated patients  2nd most common of infection in ICU, ↑stay in ICU It is preventable Risk factor for nosocomial (inside the hospital) pneumonia Major: Improper handling by healthcare professional Enhancing colonisation of oropharynx /or stomach ○ Mechanical intubation ○ Administration of antibiotics ○ Underlying chronic lung disease Favoring aspiration into the respiratory tract/ reflux from GI tract ○ Supine ○ Nasogastric tube placement ○ Immobilisation ○ Surgery of head/ neck/ thorax/ upper abdomen ○ Coma Pathogenesis Pooling of secretion → thru microchannels to the lung under suction ETT Tracheostomy Aspiration → thru microchannels to the lung Biofilm formation Intubation procedures Contaminated respiratory equipment  VAP prevention bundle (6) 1. Elevation of the Head of the Bed 30°-45° *avoid supine 2. Daily sedative interruption and daily assessment of readiness to extubate 3. Daily oral care with chlorhexidine 4. Maintain airway pressure a. maintenance of PEEP and minimise MHI (manual lung hyperinflation) b. Avoid routine suction and keep lowest suction pressure and shortes suction duration 5. Peptic ulcer disease and deep venous thrombosis prophylaxis 6. Promote early mobilisation PT aspect to prevent VAP! Minimise the chance of disconnecting the ventilator Replace MHI by performing ventilator hyperinflation Minimise saline instillation Strictly follow the suction pressure and keep suction duration 2mm), resulted from destruction of the muscular and elastic components of the bronchial wall due to chronic airway inflammation and/ or infection Changes of the affected areas: scarring, edema, ulceration and transmural inflammation + distal lung parenchyma may also be damaged Etiology: Idiopathic (etiology not identifiable at time of diagnosis) Post infections (after pneumonia/ TB/ childhood infections e.g. whooping cough百日 咳, measles) Primary cililary dyskinesia (PCD) Presence of other lung diseases Chronic obsrtuctive pulmonary diseases Asthma Chronic aspiration  Pathophysiology Infection → mucocillary response + microorganism trigger release of toxins and inflammatory response (release of neutrophils, lymphocytes and macrophages within the bronchial lumen) → Neutrophils alter the function of cilial epithelium → changes in cilial beat freq and mucous gland hypersecretion → compromise mucociliary clearance → Neutrophil allows bacterial adherence to the lung epithelium → colonisation → intense chronic inflammatory response (further release of inflammatory mediators) → neutrophils migrate to the bronchial lumen and mucosa → destroy bronchial elastin and other supporting structure → permanent dilation of the bronchi Common pathogens Types of bronchiectasis Cylindrical (tram track sign): Dilated airways seen in a horizontal orientation Cystic or saccular: a cluster of thin walled cystic spaces Varicose: Non-uniform bronchial dilation Signet-ring: the dilated airway lies adjacent to a pulmonary artery branch giving the appearance of a ring Symptoms Mild case → asymptotic Cough and daily mucopurulent sputum production, often lasting months to years Blood-streaked sputum or hemoptysis from airway (permanent ditation → tear of blood vessels) Dyspnea, pleuritic chest pain, wheezing, fever, weakness, fatigue, and weight loss Episodic hemoptysis Physical examination Auscultation: crackles, rhonchi, scattered wheezing and insp. Squeaks Digital clubbing in advanced pulmonary cases Cyanosis and plethora with polycythemia (increased red blood cell mass) from chronic hypoxia  ○ Hypoxia → Pulmonary vasoconstriction + redistribution of blood to optimally ventilated lung segment (an adaptive vasomotor response) ○ Polycythemia → Check hematocrit (ratio of RBC to total V of blood) >55% * & hemoglobin level F: >16.5g/ dL and M: >18.5g/dL Wasting and weight loss Nasal polyps and signs of chronic sinusitis Physical stigmata of cor-pulmonale (right heart failure) in advanced disease ○ ↑ viscosity (polycythemia) and ↑resistance (hypoxia) → extra work to pump blood thru the lung →Bulk of right ventricle of the heart → ↑pressure → dilate and bulge CT findings Consequences of bronchiectasis Recurrent chest infection Pneumonia Lung abscess Empyema Septicemia Chronic hypoxemia → cor-pulmonale Respiratory failure Management Antibiotics- e.g. azithromycin Mucolytic agent → lossen sputum- e.g. N-acetylcysteine (NAC), ambroxol, sobrerol,and carbocysteine  Trasmine for case with active bleeding Bronchial artery embolisation for massive haemorrhage Hypoxemia → oxygen therapy Chest physio ○ Airway clearance techniques + home management – home postural drainage and percussion ○ Prescription of adjuncts e.g. flutter, acapella for self-management ○ Breathing retraining ○ Dyspnea management ○ O2 therapy ○ Physical reconditioning Patient education ○ Self management skills ○ When to take transmine/ antibiotics for prophylaxis ○ When to increase freq of home chest physio ○ When to visit doc – acute exacerbation and uncontrolled haemoptysis ○ Appropriate physical training