Respiratory Flashcards

Question

Pleural effusion

Answer 1

Etiology 1. Transudative (usually bilateral) - Failures (heart, liver, renal) - Constricitve pericarditis - Nephrotic syndrome - Protein-losing enteropathy - Pleuroperitoneal fistula in PD 2. Exudative (unilateral) - Infection (parapneumonic effusion, TB) - Malignancy (lung, breast, lymphoma) - Inflammatory (RA, SLE, pancreatitis) - Inflammatory (RA, SLE, pancreatitis) - Trauma (chylothorax, haemothorax) - Iatrogenic (post-thoracic surgery) Investigations • Bloods: CBC, clotting (infection, prep for tapping), CRP/ ESR (inflammation), LRFT, LDH (Light's criteria) • Imaging: o CXR: erect (min 175ml) vs lateral decubitus (min 100ml, identify loculations: no redistribution upon postural drainage) - Findings: blunting of CP angle, meniscus sign, signs of infection/ mass lesion - Amount of fluid: 175ml if obscured CP angle, 1L if lower 1/3, 2L if lower ½ —> >1cm thick on lateral decubitus film: suitable for pleural tapping o USG thorax: content (differentiate from pleural thickening), volume (more sensitive than CXR), echogenicity (exudative if echogenic), loculation, guide drainage & biopsy, • Pleural fluid by pleural tapping: not required if bilateral effusion strongly suggestive of transudative cause • If uncertain diagnosis: o CT thorax with contrast: determine location and size of effusion o Pleural biopsy: esp. TB - Bedside percutaneous (Abram's needle): first line as TB pleuritis common; poor sensitivity in MPE - Imaging-guided (TEMNO needle) - Medical thoracoscopy / pleuroscopy —> Allow drain + biopsy + pleurodesis —> Require IV sedation (c.f. GA in VATS) - VATS thoracoscopy Pleural fluid analysis • Appearance: straw-coloured, turbid (empyema), milky (chylothorax), bloody, brown (old blood) • Biochemistry: Light's criteria (protein, LDH), pH, glucose, adenosine deaminase (ADA > 30 suggests TB) • Cell count with differentials • Microbiology: Gram's stain, AFB smear, bacterial culture, TB culture, MTB-PCR, +/- fungal culture • Cytology (20mL x 3) if suspect malignant effusion **Light’s criteria** Pleural fluid is exudative it any ONE of the following: - Fluid/serum protein >0.5 - Fluid /serum LDH >0.6 - Fluid LDH >2/3 of ULN of serum LDH Note: tend to overdiagnose educative fluid esp if patient on chronic diuretics - Check serum pleural fluid protein <3.1g/dL (exudative) DDx - Low pH/glucose: malignancy, esophageal rupture, empyema, TB, RA/SLE - HIGH LDH>1000: malignancy, empyema, RA, paragonimiasis - Blood: traumatic, malignancy, TB, PE - Cholesterol >4g/dL: chylothorax, lymphatic damage post-surgery, nephrotic Sx, cirrhosis - increase amylase: pancreatitis, malignancy, esophageal rupture Management • Bilateral pleural effusion: treat underlying cause (e.g. frusemide) —> chest drain if failed or respiratory distress • Unilateral pleural effusion: chest drain • Refer to below sections if failed

Answer 2

Risk factors • Poor denture • Aspiration risk • IC state: DM, HIV, malignancy Causative pathogens • Streptococci milleri group • Strep pneumoniae • S aureus • Anaerobes (e.g. Bacteroides) Clinical features • Similar to pneumonia, except • Decreased vocal resonance (c.f. increased in pneumonia) • Complications o Sepsis: pleural “peel” as reservoir for recurrent infections e.g. TB o Trapped lung —> reduced lung function Investigations • Imaging: CXR, USG, CT thorax • Pleural tapping for pleural fluid analysis: determine if chest drain is needed (see below) Management (SAQ!) • Treat underlying infections: o Antibiotics: 1-2 weeks for uncomplicated, 4-6 weeks for empyema o Chest physiotherapy + mobilisation • Chest drain (large-bore): indicated if o Clinical: respiratory distress, sepsis o Radiological: large non-purulent effusion (≥40% hemithorax), loculation on CXR/USG, pleural thickening with contrast enhancement on CT thorax o Pleural fluid shows complicated effusion or empyema: - Appearance: overtly purulent (empyema) - Biochemical: pH < 7.2 or glucose < 2.2 - Microbiology: positive gram stain ± culture • Options if failed chest drain: o Intrapleural tPA + DNase (to dissolve protein) o VATS for surgical drainage and decortication (peel away thickened pleura —> allow lung re-expansion) o Thoracoplasty: e.g. airspace filling procedures with surgical flap (e.g. latissimus dorsi flap) o Open drainage of empyema (Clagget’s procedure)

Answer 3

Pathology • Occur in 50% of all metastatic malignancy (esp. NSCLC) • Mechanism: direct invasion from neighbouring structures, haematogenous spread, lymphatic obstruction Management • Repeated chest drain every few weeks • If persistent / recurrent: consult respiratory team o Chemical pleurodesis (1st line) o Surgical pleurodesis: can be considered if good performance status o Long-term ambulatory indwelling pleural catheter (IPC): consider if short life expectancy / trapped lung o Pleuroperitoneal shunt (e.g. Denver shunt, fig.): consider if short life expectancy / trapped lung

Answer 4

Indications • Pneumothorax: SSP, PSP (recurrent, synchronous bilateral, PAL, high-risk professions, pregnancy) • Pleural effusion: recurrent malignant pleural effusion, chylothorax with failed conservative treatment • Post-op: persistent output after pericardial window surgery Contraindications: parapneumonic effusion/ empyema (∵difficult drainage and decortication) Surgical pleurodesis • First line in pneumothorax • Techniques: video assisted thoracic surgery (VATS) – more common, or open thoracotomy o Stapling / resection of blebs / bullae o Mechanical abrasion by dry gauze o Pleurectomy • Complications: o Pain: avoid NSAID (inflammatory action essential) o Recurrence 3% Chemical pleurodesis • Preferred in recurrent MPE or surgically unfit patients • Agents: o Talc (5g in 100mL NS) i.e. magnesium silicate o Minocycline (300mg in 100mL NS) o Autologous blood: lower risk of cardiac arrest • Procedure: o Adequate analgesia ± sedation o Connect chest drain, then apply sclerosing agent via drain when lung re-expanded o Clamp chest drain for 1-2h to hold the sclerosant in position, then release o If co-existing PTx / bubbling chest drain, do NOT clamp drain, but hang up drain to ~50cm above patient to drain air but not the sclerosant o Continue drainage until drain output <150mL/day x 2 days + CXR shows lung re-expanded • Complications o Fever o Pain o ARDS (use larger particle talc to prevent systemic absorption) o Cardiac arrest (higher risk in very ill patients with poor GC)

Answer 5

Indications • Pneumothorax: haemodynamically unstable, bilateral PTX, PSP (≥2cm/symptomatic), SSP (≥1cm/symptomatic) • Pleural effusion: unilateral, bilateral effusion failing medical Tx, malignancy, complicated parapneum. effusion / empyema • Post-op: thoracic/ cardiac surgery, thoracoscopy • Haemothorax / Chylothorax • Instillation of agents (e.g. Talc, tPA) Three-bottle chest drain system A. Suction control chamber: limit suction force by the depth of tube inserted into water o Parameters: height of water column indicates amount of negative pressure transmitted to chest B. Underwater seal chamber (2cm H2O): as a one-way valve to prevent back-leak of air during inspiration C. Air leak monitor: blue ball rises on inspiration and drops on expiration o Parameters: swinging, bubbling (see below) D. Collection chamber o Parameters: colour, volume Simplified system • Two-bottle: underwater seal + collection bottle • One-bottle: underwater seal Chest tube insertion • IM pethidine 50mg • Position: supine at 45o, with arm behind head (open up rib spaces) • Locate safety triangle: 5th ICS, lateral border of pectoris major, anterior border of latissimus dorsi • Size of chest tube: smaller for air (24 Fr), larger for blood/ pus (28 Fr) - trocar not recommended • Prepare aseptic field (chlorhexidine) • LA to all layers of thoracic wall including pleura o Aspirate each layer before injection to ensure not in vessel o Aspirate pleural cavity to confirm air or fluid before inserting chest drain • Incise skin just above rib (avoid damaging VAN), up to subcutaneous fat by blade • Blunt dissection through muscles and pleura with artery forceps • Insert chest drain: aim apical for air, basal for fluid • Immediately connect to 2cm underwater seal with bottle at least 1m below patient level. • Ask patient to cough / take deep breaths and check for swinging • Anchor drain to chest wall with suture (purse-string, anchor) • Confirm position with CXR Removal of chest drain • Indications (need to know!) o PTX: no air leak for > 24h - confirm with CXR before removal o Pleural effusion: output < 100ml/day (arbitrary) o Empyema: clinically stable + output < 100ml/day • Switch off suction, prepare aseptic field • Cut anchor suture, keep purse-string stitch (fig.) • Ask patient to inhale deeply, hold his breath, exhale through mouth • At start of exhalation, pull out drain as quickly as possible • Compress wound firmly to allow tissue re-expansion to close "hole" • Tie the purse-string stitch to close the wound firmly • Confirm with CXR Management of chest drain • Regular monitoring: o Swinging, bubbling o Drain output (more frequent at the beginning): clamp for 1h if drain >1L (unless in PTx) o CXR • Encourage mobilization, chest physiotherapy, incentive spirometry (Triflow) • Pain management: prn / regular analgesia 1. Swinging = chest drain in intrapleural space - Normal: Rise & fall with deep breathing & coughing:↑ with inspiration,↓ with expiration (reversed if mechanical ventilation) - Not swinging: • Causes: o System: blocked drain, kinked drain, drain slipped out o Patient: fully re-expanded lung, drain inside loculated pocket • Mx: o Temporarily off suction to assess swinging, ask patient to take deep breath & cough o Rule out system causes: check tubing patency, flush tube, change tube o Check fully expanded lung: CXR, output in past 24h 2. Bubbling = air leak (unless in pneumothorax) - Normal: Air leaks upstream from the seal, Normal if on suction - Abnormal: New/ prolonged bubbling: • Severity: throughout respiratory cycle > expiratory phase only > only upon coughing • System: check connection, drain side holes (slipped out), drain wound (leak through wound) • Patient: persistent air leak (air leak ≥ 5 days due to presence of bronchopleural fistula) o Continue chest drain with low wall suction o CT thorax to localize lesion —> EBV or pleurodesis o NEVER clamp drain (risk of tension pneumothorax) Unexpandable lung after chest drain? • Lung entrapment: lung cannot expand fully because of an active disease, e.g. malignancy; pleural fluid exudative • Trapped lung: lung cannot expand fully because of a remote inflammatory condition that leaves behind a fibrous peel on visceral pleura; pleural fluid transudative • Continuum of the same disease process: the active disease resolves, leaving behind the fibrosis Complications • Failed procedure • Puncture-related: pneumothorax, haemothorax / haemoptysis, surgical emphysema, organ perforation, damage to neurovascular bundle, bronchopleural fistula, segmentation (pockets formed by scar after each puncture) • Drain-related: re-expansion pulmonary oedema (in pleural effusion; avoid drain > 1.5L in 30 min), blockage, dislodgement • Infection (e.g. empyema) Management of surgical emphysema • Look for and treat underlying cause, e.g. tube obstruction • High concentration O2 • Infraclavicular incisions

Answer 6

Definition • A chronic inflammation of airway causing airway hypersensitivity • Can potentially lead to irreversible airway remodelling —> progressive loss of lung function Common phenotypes • Atopic (Extrinsic): Type I HSR (↑serum IgE), eosinophilic (responsive to ICS), most common phenotype in children, better prognosis with newer treatment (e.g. biologics) • Non-atopic (Intrinsic): normal IgE, mostly eosinophilic, usually adult-onset Clinical features Asthma is a CLINICAL diagnosis from history and physical examination ± spirometry • Characteristic respiratory symptoms: wheeze, dry cough, SOB, decreased ET, chest tightness o Diurnal pattern: Worse at night or on waking o Triggers: URTI (rhinovirus), exercise, allergens (bed sheets, pets, dust/pollen), cold air, drugs (e.g. aspirin, beta-blockers), smoking • Evidence of variable expiratory airflow limitation, e.g. o Obstructive pattern: Reduced FEV1/ FVC ratio < 0.7 o Excessive bronchodilator reversibility: increased FEV1 ≥12% AND 200ml after bronchodilator - Stop SABA 6h before testing - Administer salbutamol 4 puffs, then spirometry after 15min o Daily diurnal PEF variability > 10% o Significant increase in FEV1 or PEF after 4 weeks of controller (ICS or oral steroid) • Personal or family history of atopy • Co-morbidities: chronic sinusitis (Samter’s triad), OSA, obesity, GERD Investigations • Spirometry with bronchodilator response • CXR: rule out other DDx • Bloods: CBC D/C (eosinophil count), ESR/CRP (infection) • Phenotypic assessment (features of type 2 inflammation) for add-on therapy: o Skin-prick test, total serum IgE, allergen-specific IgE (ELISA) o Blood eosinophils, FeNO o Sputum eosinophils (n/a in HA)

Answer 7

Non-pharmacological treatments • Avoid / Control triggers: change bed sheets and wash ≥ 60°C, regular vacuuming of floors • Smoking cessation • Regular physical activity • Seasonal influenza vaccination • Patient education: self-monitor PEFR, inhaler techniques Pharmacotherapy (GINA 2022) Personalized asthma management: “assess-adjust-review” cycle Reliever —> Low dose ICS-formoterol PRN* /SABA PRN Step 1: Sx < 2x/month —> Low dose ICS-formoterol PRN / ICS whenever SABA taken Step 2: Sx ≥ 2x/month —> Low dose ICS-formoterol PRN / Low dose ICS Step 3: Sx most days / night waking ≥1x/week —> Low dose ICS-formoterol / Low dose ICS-LABA Step 4: above + poor lung function —> Medium dose ICS-formoterol / Medium-to-high dose ICS-LABA Step 5: —> Above + add-on LAMA (tiotropium) Non-phenotypic treatment: • Montelukast (LTRA): for aspirin-exacerbated asthma • Low dose oral steroid Phenotypic treatment (refer above for Ix before initiating): • Anti-IgE (SC omalizumab) - if high serum IgE • Anti-IL5: (SC mepolizumab / IV reslizumab) – if blood eosinophil >300 • Anti-IL5R (benralizumab) / Anti-IL4 / Anti-TSLP (tezepelumab) Allergen-specific SLIT: consider in those with concomitant AR Bronchial thermoplasty: bronchoscopic radiofrequency energy to shrink airway smooth muscle, mainly for non-eosinophilic asthma *Rationale of using Vannair (budesonide-formoterol) as first-line reliever: • Early use of anti-inflammatory drug: reduces risk of asthma exacerbations compared to SABA reliever • Formoterol as LABA with fast onset (c.f. salmeterol) Inhaled corticosteroids (ICS) – brown/red • Beclomethasone (Becloforte) • Budesonide (Pulmicort) • Fluticasone (Flixotide) Local side effects: oral candidiasis, HOV, contact hypersensitivity • Rinse mouth & spacers • Spit out after inhalation • Switch to ciclesonide Long-acting b2 agonist (LABA) • Salmeterol (Serevent) • Formoterol (Oxis) Tachycardia, headache, cramps Leukotriene receptor antagonist (LTRA) • Montelukast (Singulair) Neuropsychiatric S/E, e.g. agitation, anxiety, psychosis, suicidal ideation Systemic corticosteroids • Prednisolone PO 5-10mg daily Short term: sleep disturbance, reflux, increased appetite, hyperglycaemia Long term: central obesity, metabolic (HT, DM, osteoporosis), infection ICS-LABA: e.g. salmeterol-fluticasone (Seretide) - purple Short-acting beta2 agonist (SABA) - blue • Salbutamol (Ventolin) • Terbutaline (Bricanyl) Tremor, tachycardia, arrhythmia (hypokalaemia) Short-acting anticholinergics (SAMA) • Ipratropium (Atrovent) Few (poor BA), dry mouth, bitter metallic taste Stepping down asthma treatment • Good asthma control for 3 months + low risk for exacerbations: reduce ICS dose by 25-50% at 3 month interval • ICS should never be completely stopped o Confirm diagnosis of asthma: half ICS dose and assess lung function after 2 week Stepping up asthma treatment • Based on asthma control test (ACT) (SAQ!) o Symptom control over past 4 weeks (⽇夜藥動): Partly controlled if 1-2, poorly controlled if 3-4 - Daytime asthma symptoms >2/week - Night waking - Reliever use > 2/week - Activity limitation • Must review compliance and inhaler technique, correct modifiable risk factors, and treat comorbidities (e.g.allergic rhinitis) • Regimen: o Sustained step-up (≥2-3 months) o Short-term step-up (1-2 weeks): for acute exacerbation, e.g. viral infection

Answer 8

Definition: acute/subacute worsening in symptoms and lung function from patient’s usual status Initial assessment • Airway, breathing, circulation • Look for life-threatening features (any +ve = consult ICU) o Drowsiness, Confusion, Silent chest • Prepare for intubation Acute management Stratify according to worst feature identified 1. Mild-moderate - Clinical features: talk in phrases, prefer sitting to lying, calm, RR increased, no use of accessory muscle - Findings: HR 100-120, SpO2 90-95 on RA, PEF >50% predicted, PaCO2 normal/los - Mx: O2 by nasal cannulae/face mask (aim SpO2 93-95), Salbutamol 4 puff Q4H + prn with spacer (titrate up if needed), prednisolone PO 1mg/kg 2. Severe (refer ICU) - Clinical features: talk in words, sit hunched forwards, agitated, RR >30, Use of accessory muscle - Findings: HR>120, SpO2<90 on RA, PEFR<50% predicted, PaCO2 normal/low - Mx: above + Ipratropium bromide 4 puff with spacer, IV steroid, IV MgSO4 2g over 20min, Mechanical ventilation: support fatigued resp muscle 3. Life-threatening (immediate ICU) - Clinical features: cannot speak, confused drowsy, slight chest, no use of accessory muscle(fatigued) - Findings: HR>160 or bradycardia, SaO2<90 on O2 15L/min via reservoir face mask, REF<33% predicted, PaCO2 increased - Mx: same as 2 Further management • Close monitoring of vitals, SpO2, PEF / FEV1, +/- ABG, electrolytes, CXR • Reassess S/S and PEF/FEV1 for response 1 hour after initial treatment —> wean O2 and titrate bronchodilators accordingly • Treat bacterial infection if suspected • Suspect (tension) pneumothorax if sudden deterioration in haemodynamics • Discharge: if no S/S and PEF > 60% predicted • Avoid known allergens/ triggers o Prednisolone up to 50mg daily x 5-7 days o Early OPD follow up for long-term Tx plan and inhaler technique **PEF = peak expiratory flow** Indications of ICU admission • Life-threatening features: drowsiness, confusion, silent chest • Deterioration in PEF / FEV1 • Worsening / Persistent hypoxia or hypercapnia • Respiratory failure requiring IPPV • Cardiorespiratory arrest

Answer 9

Definitions COPD 慢性阻塞性肺病: progressive and irreversible* airway obstruction due to: 1. Chronic bronchitis - Definition: Clinical diagnosis: productive cough on most days for ≥3 months in 2 consecutive years - Pathogenesis: Narrowing of small airways Due to fibrosis of bronchiolar walls by inflammation - Appearance: Blue bloaters - Cyanosis: prominent - Hyperinflation: + - Dypsnea: + - Corpulmonale: ++ - Inspiratory drive: reduced 2. Emphysema - Definition: Pathological diagnosis: Permanent enlargement of air spaces distal to terminal bronchioles, accompanied with wall destruction but no obvious fibrosis - Pathogenesis: Protease-antiprotease imbalance —> loss of elastic recoil —> enlarged air spaces - Appearance: Pink puffers - Cyanosis: absent - Hyperinflation: ++ - Dypsnea: ++ - Corpulmonale: + - Inspiratory drive: present Risk factors • Host factors: low birth weight, AAT deficiency, genetics • Environmental factors: o Smoking: - Induce macrophages to release neutrophil chemotactic factors elastases (—> protease-anti-protease imbalance) - Goblet cell hyperplasia (mucus overproduction) - Damage ciliated epithelial cells (mucus retention) o Pollutants (air pollution, chemical agents, cooking fume) Clinical features • Symptoms: productive cough, SOB, wheeze • Signs o Respiratory distress: pursed lips on expiration, tachypnoea, prolonged expiration with wheezing, use of accessory muscles o Hyperinflated lungs: reduced chest expansion, barrel chest, reduced cricoid-notch distance, tracheal tug, loss of cardiac & liver dullness, Hoover’s sign (inward movement of lower ribs during inspiration) • Complications: o Polycythaemia (2o to hypoxemia) o Cor pulmonale (2o to pulmonary vasoconstriction o Pneumothorax (2o to rupture of emphysematous bullae) Mechanisms of respiratory failure in COPD • V/Q mismatch (MC) • Alveolar hypoventilation • Shunting (if complicated by pneumonia / CHF)

Answer 10

Diagnosis Require all three criteria • Risk factors e.g. chronic smoker • Symptoms: dyspnea, cough, sputum production • Spirometry (mandatory - PEFR cannot be used as replacement): Post- bronchodilator FEV1/FVC < 0.7 Other investigations • CXR: hyperinflated chest/ flattened diaphragm, long narrow heart shadow, hyperlucency of lung fields • Bloods: CBC (2o polycythaemia), ABG (T1RF à T2RF if decompensated), ESR/CRP • ECG ± Echo: P pulmonale (tall P waves), RVH +/- RV strain, RBBB • Sputum C/ST Assessment of severity • Assessment of airflow limitation: GOLD criteria (FEV1 post-bronchodilator) - GOLD 1 (mild): FEV1 ≥ 80% predicted - GOLD 2 (moderate): 50% ≤ FEV1 < 80% predicted - GOLD 3 (severe): 30% ≤ FEV1 < 50% predicted - GOLD 4 (very severe): FEV1 < 30% predicted • Assessment of symptoms / risk of exacerbations: o Modified MRC dyspnoea scale (mMRC): - Grade 0: SOB during strenuous exercise - Grade 1: SOB when walking up hill 斜 - Grade 2: walk slower because of SOB 慢 - Grade 3: stop for breath after walking for a few minutes 分 - Grade 4: too breathless to leave the house 街 o COPD Assessment Test (CAT): include QoL & impact on life, full score = 40, cut-off at 10 • Long-term outcomes: BODE index - BMI, obstruction (FEV1/FVC), dyspnea (mMRC), exercise (walking distance) ABE assessment tool - >/= 2 moderate exacerbation or >1 leading to hospitalisation = Group E —> LABA + LAMA +/- ICS(only if blood eos>300) - 0 or 1 moderate exacerbation (not leading to hospitalisation) + mMRC 0-1/CAT<10 = Group A: bronchodilator - 0 or 1 moderate exacerbation (not leading to hospitalisation) + mMRC 2-4/CAT>10 = Group B —> LABA+LAMA *Moderate exacerbation: require SABD / oral steroid

Answer 11

Non-pharmacological treatment (SAQ!) • Smoking cessation: non-pharm (nicotine gum / nasal spray patch), pharm (bupropion, varenicline) • Vaccination (flu, pneumococcal), weight reduction, encourage exercise, inhaler technique, compliance • Pulmonary rehabilitation (see separate section) Pharmacological treatment - Reduce symptoms, reduce frequency & severity of exacerbation, improve lung function, improve ET - No drugs modify the long-term decline in lung function • Initial treatment by ABE class o Relievers: SABA / SAMA prn (e.g. Ventolin, Bricanyl, Atrovent) to all patients for symptomatic relief • Other add-on medications: all reduce exacerbations 1. ICS: Beclomethasone / Budesonide / Fluticasone - preferred in Blood eosinophil ≥ 300 / Hx of or concomitant asthma - Avoid regular use: increases risk of pneumonia - Stop if AECOPD 2. PDE4 inhibitor - Roflumilast - preferred in FEV1 < 50% & chronic bronchitis - S/E: reduced appetite, diarrhoea, weight loss, sleep disturbance 3. Mucolytics - Acetylcysteine - All patients 4. Antibiotics - Azithromycin - Former smokers - Issues: increasing resistance, QT prolongation, impaired hearing 5. Anti-IL5 Mepolizumab Anti-IL5R Benralizumab - Currently under clinical trial Note: Triple therapy (LABA/LAMA/ICS): e.g. Trelegy Ellipta (vilanterol-umeclidinium-fluticasone Long-term O2 therapy (LTOT) (SAQ!) Continuous LTOT: Improve 3-year survival by 50%, prevent progression of complications • Start only when patient is stable with ABG x2 at least 3-4 weeks apart, and after optimization of medical therapy • Indications: stopped smoking + o Resting hypoxaemia (SaO2 ≤ 88% / PaO2 ≤ 7.3 kPa) – note: NO survival benefit if moderate (SaO2 89-92%) o SaO2 ≥ 89% / PaO2 7.4-7.9 kPa with complications (3Ps) - Peripheral oedema suggestive of cor pulmonale - Pulmonary hypertension: P pulmonale on ECG (P wave >3mm in leads II, III, or aVF) - Polycythaemia (Hct > 56%) • Duration: ≥15h/day • Target: SaO2 ≥ 90% Non-continuous LTOT: during exercise / sleep Surgical options • Bullectomy • Lung volume reduction surgery: reduce hyperinflation + improve lung recoil (resection of inelastic portions) o Approaches: thoracotomy, VATS, endobronchial valve (EBV) • Lung transplant: definitive treatment

Answer 12

Definition: acute worsening of respiratory symptoms that results in additional therapy: • Increased dyspnoea • Increased sputum volume • Increased sputum purulence Triggers • Infection: bacterial (Strep pneumoniae, Hib, Moraxella catarrhalis), viral (rhinovirus) • Environmental pollution Differential diagnosis of SOB in COPD patients • AECOPD • Pneumothorax/ rupture of bullae: chest pain • Pneumonia: fever, chest pain • PE: chronic hypoxia —> secondary polycythaemia -> hyperviscosity • CA lung (smoking as common risk factor) Management • Pulse oximetry, ABG (look for T2RF), CXR (to rule out pneumothorax), ECG, CBC RFT CRP/ESR, sputum, NPA 1. Hypoxia - Mx: O2 - Start with 1-2L/min by nasal cannula (or Venturi mask: not used in PWH) Target SpO2 88-92%, monitor ABG 30-60mins after initiation of O2 therapy and modify flow rate according to PaO2 and pH 2. Respiratory acidosis - Mx: Mechanical ventilation (NIPVV/ invasive) - NIPPV: ↓work of breathing, improve respiratory acidosis Usual setting: EPAP 4, IPAP 14, aim TV 6-8mL/kg, RR ≤ 25 • Respiratory acidosis (i.e. T2RF with pH ≤ 7.35 / PaCO2 > 6.0kPa) • SOB with signs of respiratory fatigue (e.g. use of accessory muscles, paradoxical abdominal motion, RR > 25) Check ABG at 30-60mins (consider intubation if fail to improve) Invasive mechanical ventilation: Refer ICU Indications: • Unable to tolerate/ fail NIPPV • Unable to protect airway, e.g. impaired consciousness (GCS < 10), aspiration risk (UGIB, severe gastric distension) • Severe hemodynamic instability / ventricular arrhythmia / arrest 3. Expiratory obstruction - Bronchodilator —> SABA (salbutamol) +/- SAMA (ipratropium) with spacer S/E: tachycardia, hypokalemia (check blood K Q6h) - Corticosteroid —> PO Prednisolone 40mg for 5-10 days & discontinue after acute ep. (S/E: hyperglycemia, fluid retention, hypertension) 4. Underlying cause - Antibiotics - Indications (need to know!) • ≥2 cardinal symptoms (inc. ↑sputum purulence) • Need of mechanical ventilation / intubation Choice: Augmentin / cefotaxime x 5-7 days

Answer 13

Definition: secondary permanent dilation of bronchi & bronchiole Pathophysiology • Destruction of bronchial wall causes abnormal dilation of proximal medium-sized bronchi (>2mm) • Transmural inflammation causes impaired clearance of secretions, leading to colonisation & infection which exacerbates bronchial damage - vicious cycle • 4 morphological subtypes: cylindrical (MC), varicose, cystic, mixed Aetiology • Congenital: o Primary ciliary dyskinesia : dynein mutation (AR); sinusitis, otitis media, male infertility o Kartagener's syndrome: PCK + situs inversus o Cystic fibrosis: AR mutation in CFTR; respiratory (nasal polyps, recurrent AOM & pneumonia), pancreatic insufficiency (steatorrhoea, gallstones), male infertility o Young syndrome: male infertility, rhinosinusitis, bronchiectasis o Yellow nail syndrome: sinusitis, lymphatic hypoplasia (yellow nails, lymphedema, exudative pleural effusion) • Acquired: o Post-infection: TB (MC), recurrent pneumonia, pertussis, measles, ABPA o Obstruction: luminal (FB), mural (tumour, e.g. carcinoid; severe asthma/ COPD), extramural (LN) o Autoimmune: RA (rheumatoid lung), Sjogren's, IBD (UC > CD) o Immune: AIDS, primary immunodeficiency (e.g. CVID, CGD) o Fibrosis (e.g. IPF, post-RT) —> traction bronchiectasis Clinical features • Chronic cough with copious sputum production & haemoptysis, clubbing • Constitutional symptoms: weight loss, low grade fever • Inspiratory coarse crackles that clear after coughing • Acute exacerbation: similar to AECOPD o Pathogens: Strep pneumoniae, H influenzae, Pseudomonas aeruginosa, S. aureus o S/S: increase in sputum volume, purulence, dyspnoea, haemoptysis, fatigue Investigations For diagnosis • Spirometry: obstructive (can be reversible pattern) or restrictive (severe disease with scarring & atelectasis) • CXR (not sensitive): tram-track opacities, ring shadows, air-fluid level, segmental collapse • High-resolution CT thorax (HRCT) o Signet ring sign (bronchial diameter > adjacent PA diameter - normally similar) (fig.) o Tram-track sign (thickened non-tapering wall) (fig.) o Visible airway within 1cm of pleural surface o Tree-in-bud appearance: endobronchial mucus plug (non-specific) For underlying causes • Sputum for gram stain, C/ST, AFB smear, TB culture (post-infective cause) • Bronchoscopy: look for obstruction, BAL if high suspicion but sputum negative • IgE & aspergillus serology (ABPA) • Autoimmune markers, CLN (if suspect inflammatory causes) Management 1. Treat underlying causes - Only some causes are treatable, e.g. • GERD: PPI, fundoplication • ABPA: steroid + antifungal (itraconazole) 2. Treat acute exacerbation - Sputum x C/ST - Empirical treatment: IV Tazocin x 10-14 days - NTM: triple therapy (macrolide + rifampicin + ethambutol) 3. Prevent recurrence General: smoking cessation, adequate nutritional intake, vaccination Airway clearance • Pulmonary rehab: deep breathing, postural drainage, chest percussion • Nebulised hypertonic saline • Mucolytics / expectorants Antibiotic prophylaxis • Consider if ≥3 exacerbations/ year • Oral macrolides e.g. azithromycin (extra immunomodulatory effect) • If still frequent exacerbations, consider adding long-term inhaled anti- pseudomonal Abx or regular IV antibiotics every 2-3months Other adjuncts: bronchodilators / steroids (concomitant asthma/COPD) Surgery • Indications: recurrent exacerbation, haemoptysis, resistant NTM • Approach: lobectomy, bronchial artery embolization, lung transplant Complications • Recurrent infections à Repeated antibiotics à Antimicrobial resistance • Pulmonary hypertension à Cor pulmonale • Respiratory failure

Answer 14

Definitions: tailored therapies to improve overall physical and psychological conditions Components: • Physical training o Breathing training (e.g. pursed lip breathing, diaphragmatic breathing) o Inspiratory muscles training o Energy conservation technique: work ergometry & work flow o Limbs aerobic and resistive training: increase mitochondrial density à prevent de-conditioning, improve ADL o Neuromuscular electrical stimulation • Nutrition: maintain muscle mass • Behavioural: coping strategies • Psychological counselling • Education: use of inhalers/ LTOT, smoking cessation

Answer 15

Overview • Definition: a group of lung diseases (>200 types), characterised by o Chronic lung inflammation (predominantly macrophages & lymphocytes) o Varying degrees of lung fibrosis • Pathophysiology: 2 main types o Predominant inflammation & fibrosis: distortion and destruction of normal alveoli & microvasculature o Predominant granulomatous reaction Etiology: • Primary: idiopathic pulmonary fibrosis • Secondary: o Autoimmune: systemic sclerosis > RA > Sjogren > polymyositis/ dermatomyositis > SLE (more commonly pleuritis) o Infection: TB, ABPA o Occupation-associated/ pneumoconiosis (inorganic dusts): - Coal worker's pneumoconiosis - Silicosis: rock mining; more common in upper lobe, increase risk of TB but not CA - Asbestosis: construction site, shipyard; more common in lower lobe, increase risk of CA lung and mesothelioma o Environment-associated/ hypersensitivity pneumonitis (organic dusts): farmer's lung, bird fancier's lung, malt worker’s lung o Drug-related: amiodarone, methotrexate, bleomycin, nitrofurantoin o Radiation o Pulmonary vasculitis: GPA, Goodpasture's syndrome By location Upper lobe predominant: BREASTS CLAP • Berylliosis, Radiation, Extrinsic allergic alveolitis (hypersensitivity pneumonitis), Allergic bronchopulmonary aspergillosis (ABPA), Sarcoidosis, Tuberculosis, Silicosis, Coal worker’s pneumoconiosis, Langerhans cell histiocytosis, Ankylosing spondylitis, Psoriasis Lower lobe predominant: RASIO • Rheumatoid arthritis, Asbestosis, Systemic sclerosis, Idiopathic pulmonary fibrosis, Other drugs (e.g. amiodarone, methotrexate, nitrofurantoin) Clinical features • Age of onset (typically >50y in IPF) • Chronic dry cough, SOBOE • Signs: clubbing, fine inspiratory crackles that do not clear with coughing, Cushingoid features (steroid), signs of underlying systemic diseases Investigations • Blood tests o Initial: CBC, LRFT (baseline for drugs), CRP/ESR, ANA, RF (routine) o Specific for underlying cause: CK/ LDH, myositis-specific Ab (PM/DM), anti-CCP (RA), anti-dsDNA (SLE), anti-Scl70 (SSc), anti-Ro/La (Sjogren), c-ANCA (GPA), anti-GBM (Goodpasture's) • ABG: T1RF (± respiratory alkalosis) • CXR: small lungs, reticulonodular pattern (signs of fibrosis), honeycomb appearance, pleural plaques (asbestosis) • HRCT: distribution of ground-glass opacities (GGO) & consolidation (signs of inflammation): upper lobe vs lower lobe, peripheral vs central o IPF (= UIP pattern): volume loss, ground-glass opacities, traction bronchiectasis, subpleural and basal reticular shadowing & honeycombing (enlarged cystic airspaces with thick fibrotic walls) • Lung function test: restrictive pattern, reduced DLCO (↓total surface area for gas exchange) • Lung biopsy (definitive): uncertain Dx (i.e. no rheumatological disease & HRCT not consistent with UIP o Approaches: bronchoscopy, VATS, open Diagnosis of IPF Exclusion of other causes + HRCT ± lung biopsy Management • Education: smoking cessation, vaccination • Supportive: O2, pulmonary rehab • Immunosuppressants: indicated for most types except IPF & pneumoconiosis (increased mortality) o Steroids: oral prednisolone 40mg BD x 6 weeks o Steroid-sparing agents: azathioprine, cyclophosphamide, MMF • Management of IPF: o Antifibrotic agents: For moderate disease (FVC ≥50%), do NOT relieve symptoms 1. Nintedanib 150mg BD oral - INPULSIS trial - MoA: Small-molecule TKI that targets VEGF-R, FGF-R, PDGF-R - S/E: Liver impairment, GI upset (n/v/d) - C/I: Child’s B/C cirrhosis, on full anticoagulation 2. Pirfenidone 40mg/kg/day oral - ASCEND trial - MoA: TGFβ inhibitor: block fibroblast proliferation - S/E: photosensitive rash, GI upset, dLFT • Lung transplant: based on decline in DLCO, FVC, ET (6-minute walk test), etc. Prognosis • Median survival 5 years (but prolonged by anti-fibrotic agents) • Causes of death o Pneumonia o Cor pulmonale o Lung malignancy

Answer 16

Terminology • Apnoea: complete cessation of oronasal airflow in sleep ≥ 10s • Hypopnoea: ≥30% reduction in oronasal flow for ≥ 10s each episode + ≥ 3% oxygen desaturation or associated with EEG/clinical arousal • Obstructive sleep apnoea syndrome (OSAS): require o AHI ≥ 15 o Or AHI ≥ 5 + at least one OSA-related symptoms or medical conditions • Central sleep apnoea (CSA): apnoea without ventilatory effort (no arousal) • Mixed sleep apnoea: features of OSA + CSA Risk factors • OSA: o Male (or postmenopausal women) o Obese, alcohol, smoking o Craniofacial factors (e.g. mandibular retroposition, micrognathia, macroglossia, adenotonsillar hypertrophy, nasal obstruction) o Endocrine diseases (e.g. acromegaly, hypothyroidism) o Familial / Genetic diseases (e.g. Down’s syndrome) • CSA: brainstem lesions, CHF Diagnosis • Night-time / daytime symptoms (r/o sleep deprivation): o Night-time symptoms: loud persistent snoring, witnessed pause in breathing, choking/ gasping for air, restless sleep, nocturia (hypoxia-induced atrial natriuretic peptide ANP) o Daytime symptoms: excessive daytime sleepiness (EDS), early morning headache (CO2 retention), poor concentration, irritability, GERD • AND AHI ≥ 5 in sleep study Complications • Biological: o Cardiovascular: HT, DM, HF, arrhythmia, stroke o Hypoxia: polycythaemia, pulmonary hypertension, glaucoma (increased vascular resistance) • Psychological: excessive daytime sleepiness, poor concentration • Sleepiness-related accidents Physical examination • BP, BMI, H&N exam (Mallampati score) • Features of acromegaly / hypothyroidism • CVS: AF, heart failure (cor pulmonale), pulmonary hypertension • Neuro: stroke Investigations: sleep study • Refer to sleep study if: o Pre-op STOP-Bang ≥ 5 o Epworth Sleepiness Scale (ESS: measure of daytime sleepiness) ≥10 • Types o Home sleep study: only SpO2 ± video o Hospital-based polysomnography (gold standard): + electrophysiology (EEG/ ECG/ EMG/ EOG), airflow (nasal & oral), movement (chest and abdominal walls, video), blood gas (etCO2), etc. o Drug-induced sleep endoscopy (DISE): VOTE classification (velum, oropharynx, tongue base, epiglottis) • Interpretations: o Apnoea-hypopnoea Index (AHI) = (apnea + hypopnea) / total sleep time - Severity of OSA depends on AHI (fig.) o Respiratory disturbance index (RDI) = (apnea + hypopnea + RERA) / total sleep time - RERA (respiratory effort-related arousals): increased respiratory efforts ≥ 10s STOP-BANG questionnaire • Snoring loudly • Tired often • Observed apnea/choking • BP high • BMI ≥ 35 • Age > 50 • Neck circumference >40cm • Gender (M) Management • Conservative management o Weight control o Sleep hygiene / Positional therapy (sleep in lateral position) o Avoid alcohol and sedatives before bedtime o Nasal decongestion o Treat underlying systemic disease • CPAP: maintain upper airway patency through positive pressure —> improve symptoms and reduce stroke risk o Indications (important!) - Moderate or severe OSA - Mild OSA with risk factors (e.g. occupational drivers) or complications (e.g. malignant arrhythmias, cor pulmonale) o Poor compliance due to complications: sleep disruption, dry nose / mouth, face irritation o Note that BiPAP is NOT indicated in OSA (c.f. OHS) • Other non-operative managements o Refer dental for appliances e.g. mandibular advancement device (MAD) - Less effective than CPAP - Complications: dental pain, dislodgement, sleep disruption o Myofunctional therapy • Surgery: o Adenotonsillectomy (first-line for children) o Upper airway surgery depends on level of obstruction: refer ENT - Nasal cavity: e.g. septoplasty, turbinate reduction - Oral cavity / oropharynx: tonsillectomy, uvulopalatopharyngoplasty (UPPP) - Retrolingual obstruction: e.g. tongue suspension suture - Skeletal surgery: e.g. maxillo-mandibular advancement (MMA) - Hypoglossal nerve stimulation via implantable neurostimulator device o Bariatric surgery if morbid obese

Answer 17

• Awake hypoventilation due to gross obesity o Different from OSA: high daytime pCO2 • Clinical features: gross obesity, EDS, nocturia • Treatment: o Lifestyle modifications o Non-invasive ventilation: CPAP —> BiPAP (effective in OHS) o Weight reduction: consider Orlistat / bariatric surgery

Answer 18

Presentation: -Pulmonary TB: fever, cough, haemoptysis, unexplained weight loss, night sweats, fatigue, chest pain, lymphadenopathy -Extrapulmonary TB: leukocytosis, anaemia, SIADH-induced hypoNa -Genitourinary TB: flank pain, dysuria, urinary frequency. (M) scrotal mass, prostatitis, orchitis, epidyditmitis. (F) PID -TB meningitis: persistent headache, altered mental status -GI TB: pain, non-healing ulcers, diarrhea, malabsorption -Skeletal TB [Pott’s disease]: spine pain/stiffness Mx: - Rifampicin – orange bodily fluids, thrombocytopenia, HUS, hepatitis, drug rash - Isoniazid – peripheral pure sensory neuropathy, hepatitis - Ethambutol – optic neuritis, drug rash - Pyrazinamide – gout, hepatitis, drug rash - (Streptomycin) – nephrotoxic, ototoxic, vertigo

Respiratory Flashcards

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