2403AHS_Wk11_Lecture_Pathology of Respiratory Diseases_1pp-46-94.pdf

Pneumonia: 4 stages (Macroscopic) • Congestion: oedema, bacteria accumulation • Red Hepatisation: vasodilation → RBCs + WBCs • Grey Hepatisation: → macrophages r/o RBCs • Resolution: alveolar exudate r/o, sputum production Parenchymal partial consolidation Parenchymal consolidation Red-brown (from...

Pneumonia: 4 stages (Macroscopic) • Congestion: oedema, bacteria accumulation • Red Hepatisation: vasodilation → RBCs + WBCs • Grey Hepatisation: → macrophages r/o RBCs • Resolution: alveolar exudate r/o, sputum production Parenchymal partial consolidation Parenchymal consolidation Red-brown (from RBCs) Liver-like consistency Uniformly grey Liver-like consistency Gradual aeration Healing • Failure protective pulmonary Community-acquired pneumonia mechanisms • Infiltration of pulmonary parenchyma by pathogen • Impaired alveolar ventilation • Hypoxia (Ramirez, 2022) Pneumonia stages (Microscopic) Pneumonia: Signs and symptoms • Fever (Pyrexia) → ?confusion • mild to marked lethargy Pneumonia • Dyspnoea (SOB) • V/Q mismatch • ↑ resp effort (WOB) • Chest pain • Cough → sputum (green / yellow / haemoptysis) Infection Impaired gas exchange Sputum production Pneumonia: Complications • Pleural effusion • Empyema • Lung abscess Pneumonia: Physiotherapy Physiotherapy implications: • Minimal role in early phases → Mobilisation • +/- Airway clearance techniques (?) → Resolution phase • Particularly if underlying respiratory condition Medical Mx: • Analgesics (pain relief) • Antibiotics (if bacterial) • Oxygen COVID-19 (pneumonia) COVID-19 Acute respiratory illness caused by droplet-borne severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) • Viral infection • Immune response COVID-19 prevalence • Worldwide pandemic • Elderly more vulnerable (70+ yrs) • Immuno-compromised • Co-morbidities (Respiratory compromise) • ATSI • Disability (Health.gov.au, May 2022) COVID-19 Aetiology • SARS-CoV-2 • Highly contagious • Droplet • Coughing / sneezing / rhinorrhoea • +/- Airborne • Aerosol airborne infected particles CoV binds to ACE2 receptors, primarily on type II alveolar cells. Virus releases RNA → proliferates (Thomas, 2020) Severe acute respiratory syndrome coronavirus 2 COVID-19 Mild URTI Asymptomatic 80% Home – self-care Severe Viral Pneumonia 15% Hosp:02 5% ICU (Thomas, 2020) Severity Primary features Asymptomatic No clinical Sx Positive nasal swab test Normal chest XRay Mild Fever, sore throat, dry cough, malaise, body aches Nausea, vomiting, abdominal pain, loose stools Moderate Symptoms of pneumonia (persistent fever and cough) without hypoxemia Significant lesions on HRCT chest Severe Pneumonia with hypoxemia (SpO2 < 92%) Critical ARDS, shock, coagulation defects, encephalopathy, heart failure, acute kidney injury (Parasher 2021) COVID-19 (Mild) Most patients (80-85%) • Immune response • Inflammation in lungs • Alveolar oedema (Thomas, 2020) COVID-19 symptoms • Dry cough • Fatigue+ • Pyrexia (Fever) (WHO, 2022) COVID-19 (Mod-Severe) Less common (15-20%) Immune response++ • Inflammation in lungs • Macrophages recruited • Release cytokines • Vasodilation • Alveolar oedema (Thomas, 2020) azuravesta.com/covid-19-pandemic COVID-19 Severe: Impaired gas exchange • Alveolar oedema++ • • • Excessive release cytokines Immune system attacks healthy cells ↓ Type II cells • ↓ surfactant • Alveolar collapse ↓ Type I cells • ↓ O2 • → Acute Respiratory Distress Syndrome (ARDS) → Systemic inflammatory response syndrome (SIRS) →Septic shock (Thomas, 2020) COVID-19 symptoms • Dry / moist cough • Dyspnoea • Chest pain • Fatigue • Pyrexia (Fever) (WHO, 2022) COVID-19 Symptom COVID-19 Pa02/Fi02 Low Dyspnoea Mild HPV (Hypoxic Pulmonary Vasoconstriction) Absent V/Q mismatch Severe Pulmonary hypertension Mild Pulmonary Capillary Pressure Low Reduced Lung Compliance Mild Pneumonia: Physiotherapy Physiotherapy role: • Not indicated in mild Sx / dry cough (incl. pneumonitis – no exudative consolidation) • Indicated in severe Sx (pneumonia – exudative consolidation / mucous hypersecretion / poor clearance) Physiotherapy Mx: • Mobilisation +/- ACT • Analgesics (pain relief) • Oxygen therapy Bronchiectasis What is Bronchiectasis? “Permanent airway dilatation from recurrent infection / inflammation” • Abnormal, permanent dilation of bronchi / bronchioles • Caused by chronic inflammation • → progressive destruction bronchial walls & lung tissue • Characterised by persistent cough with excess sputum, airflow obstruction & episodes of worsening symptoms Bronchiectasis - Prevalence • Unknown • Estimated 1400/100,000 Indigenous Australians • F:M 2:1 hospitalisations • Increase rural, low SES (AIHW 2011) Bronchiectasis - Aetiology 1. Idiopathic (50%) 2. Post-infectious (20%) 3. Chronic infectious (15%) • ABPA, mycoplasma, mycobacteria, MAC, HIV/AIDS 4. Systemic (10%) • CF, Primary Cilia Dyskinesia, Immunodeficient, Autoimmune (RA) 5. Anatomic (5%) • Aspiration/GORD, RML Syndrome, Foreign body Inflammation Neutrophil-derived proteases Infection Bacterial colonisation Permanent airway dilatation, loss of cilia Airway remodelling Mucus accumulation Maselli, 2017 BE: Airway dilatation • Irreversible dilatation and destruction Easily collapsible airways Chronic bronchial infection and inflammation Irreversibly dilated bronchi Defect in immunity and/or mucus clearance Infection Persistent bacteria in airway Tissue damage Mucociliary escalator (BE) • Airway dilatation – Damaged wall • Destruction of basal membrane • Stretched columnar epithelium • Loss of cilia • Pooling of mucosal layer →↑ secretions Risk of infection: influenza / pneumonia Pathophysiology Further impairment of bacterial clearance AS → crackles > wheeze Structural damage to bronchial walls Haemoptysis Irreversibly dilated bronchi Tissue damage Chronic bronchial infection and inflammation Defect in immunity and/or mucus clearance Easily collapsible airways Epithelial destruction of airways VQ mismatch and ↓ gas exchange Chest pain Dysponea Fatigue ↓ oxygenation Persistent bacteria in airway Inflammatory response Chronic cough (Mucopurulent) Digital clubbing Fever Cyanosis Rhinosinusitis 1. Initial infection 2. Irreversible dilatation and destruction 3. Accumulation of secretion (due to increased goblet cell activity and decreased mucociliary transport) 4. Bacteria growth (increased inflammation CSLD and Bronchiectasis Gold standard imaging: CT Scan Specialist referral recommended when: • Persistent wet cough not responding to 4 wks of antibiotics • Recurrent (3+) episodes chronic wet cough which (> 4 wks) per year responding to antibiotics • Persistent CXR abnormalities >6 wks after Rx 4 Normal 4 Wu, 2019 3.2 e.g. 4 / 4 = 1 Adult: Bronchioalveolar ratio >1 4 e.g. 3.2 / 4 = 0.8 Child: Bronchioalveolar ratio > 0.8 Bronchiectasis - Symptoms • Chronic productive cough • Dyspnoea • Recurrent pneumonia • Haemoptysis* Bronchiectasis - Progression • Recurrent exacerbations (average 1.5 / year) • Progressive decrease in FEV1 • PsA colonisation → Worsening of disease PsA = Pseudomonas Aeruginosa (bacteria) Bronchiectasis - Management Physiotherapy Management • Exercise • Airway clearance techniques Medical Management • Treat underlying cause if known • Antibiotics • Inhaled bronchodilators Cystic Fibrosis Cystic Fibrosis • Chromosome 7 defect → abnormal expression CFTR protein • 100s of mutations, genotype ∆F508 most common • Defective epithelial Chloride ion transport • Sustained pulmonary inflammation CFTR: Cytsic Fibrosis Transmembrane conductance Regulator Cystic Fibrosis - Prevalence • Common inherited genetic disorder • Autosomal recessive inheritance (1: 25 carriers) • 1: 3600 live births • 1 in 2500 Australians • Life expectancy rising (~47yo) Has CF Cystic Fibrosis - Diagnosis ▪ Heel prick screen @ birth ▪ blood test measures pancreatic enzyme levels ▪ if levels abnormal → genetic testing CFTR mutation ▪ Definitive diagnosis: Chloride levels from a sweat test (2-6 weeks old) CF Unlikely ≤ 29 mmol/L CF Possible 30-59 mmol/L CF Likely ≥ 60 mmol/L CFTR: Cytsic Fibrosis Transmembrane conductance Regulator Multi-system disorder affecting exocrine glands • • • • • • Lungs Liver Intestines Pancreas Heart Reproductive Respiratory = cause morbidity & mortality • 80-90% mortality from lung disease Pathophysiology of CF CFTR Mutation Abnormal Chloride ion transport ↑ Mucous viscosity • Mutation in Cystic Fibrosis Transmembrane Regulator (CFTR) gene on chromosome 7 inflammation Chronic infection • Dysfunction of the CFTR protein (Transmembrane chloride ion channel Lung injury Respiratory failure found in exocrine tissue) Brown, 2017 Pathophysiology of CF CFTR Mutation Abnormal Chloride ion transport ↑ Mucous viscosity inflammation Chronic infection Lung injury Respiratory failure • Exocrine glands • CFTR proteins facilitate diffusion of Clinto secretions ↓ Cl- diffusion into periciliary fluid → ↓ water composition of peri-ciliary fluid ↓ clearance of mucociliary secretions CF: CFTR protein • Defective / Absent CFTR protein • Cl- unable to cross into Sol layer CF Normal Cl- H2O H2O • ↑ [Cl-] within cell • H2O moves via Osmosis from Sol layer → cell • Cilia damage • Thick mucous layer Cl- Cl- Cl- Mucociliary escalator (CF) • Impaired CFTR protein • Reduced Sol layer • → Thick Viscous mucous • Shortened / damaged cilia • ↑ pathogen (e.g. PsA.) May also have BE / pneumonia Pathophysiology of CF: Vicious cycle of: • Abnormal mucus • Obstruction • Inflammation & repeated infections → Lung damage → Cysts → Lung scarring → Fibrosis • Chronic colonisation with Ps aeruginosa. Explanted lungs of 32 yrs man with CF CF: Symptoms • Chronic wet, productive cough (sputum) • Thick, sticky mucous • SOB • Hypoxia • Fatigue • Ausc: Crackles, +/- Wheeze • Exercise intolerance • Fever • Pulmonary HTN Complications in CF • Airways irritability; asthma • Paroxysmal cough • Haemoptysis • Pneumothorax • Urinary Incontinence • ENT problems • Musculoskeletal problems clubbing Cystic Fibrosis - Management Physiotherapy Management • Bi-daily Airway Clearance Techniques • Exercise • ↑ if unwell • Musculoskeletal (incl. pelvic floor) Medical Management • MDT: Nursing, Dietetic, Social Work, Psychology, ENT, OT, Gastroenterology, Psychiatry…..etc • Respiratory failure → Lung transplant Cystic Fibrosis - Management Medical Management • Pulmozyme (Mucolytics-thin sputum) • Salbutamol (bronchodilator) • Prednisolone (Corticosteroid → reduce inflammation) • Antibiotics (if bacterial infection) • Trikafta® (Chloride channel opener) • Pancreatic enzyme therapy (most) • Fat-soluble vitamins Diagnosis or Clinical Reasoning? ◙ Asthma, Bronchiolitis, Empyema, Pneumonia: x NO active chest Rx in acute phase; ?post-acute airway clearance; ?exercise advice in asthma. Review baseline vs acute state ◙ Bronchitis: ?ACT during acute episode / exacerbation if productive / wet cough. Review baseline vs acute state. ◙ CF, Bronchiectasis : ongoing, every day: exercise and ACT based on pathophysiology and severity of disorder (mild / mod / severe lung disease). Review baseline vs acute state Thank you