Respiratory Flashcards
Dypsnea (ddx and Ix)
Differential diagnosis
• Respiratory
o Acute: pneumothorax, PE, APO, asthma exacerbation, AECOPD
o Subacute: pneumonia, TB, pleural effusion
o Chronic: COPD, malignancy, ILD
• Cardiac: CHF, ACS, arrhythmia
• Metabolic: anaemia, metabolic acidosis, hyperthyroidism
• Neuromuscular: MG, GBS, stroke
• Psychological
Investigations
• Pulse oximetry
• Bloods: CBC, CRP/ESR, cardiac enzymes, D-dimer
• ECG: ST changes, AF, sinus tachycardia
• CXR: HF (cardiomegaly, pulmonary congestion), PTX, consolidation, lung mass
Cough (ddx and Ix)
Differential diagnosis
• Respiratory
o Acute: pneumothorax, PE, APO, asthma exacerbation, AECOPD
o Subacute: pneumonia, TB, pleural effusion
o Chronic: COPD, malignancy, ILD
• Cardiac: CHF, ACS, arrhythmia
• Metabolic: anaemia, metabolic acidosis, hyperthyroidism
• Neuromuscular: MG, GBS, stroke
• Psychological
Investigations
• Pulse oximetry
• Bloods: CBC, CRP/ESR, cardiac enzymes, D-dimer
• ECG: ST changes, AF, sinus tachycardia
• CXR: HF (cardiomegaly, pulmonary congestion), PTX, consolidation, lung mass
Haemoptysis (ddx and Ix)
Differential diagnosis
• Airway disease: CA (lung, NPC), bronchiectasis
• Parenchymal disease: TB, pneumonia, lung abscess
• Vascular disease: PE, LV failure (CHF, MS), vasculitis (Goodpasture’s syndrome, GPA, MPA, HHT)
• Others: bleeding tendency, anticoagulants, pulmonary endometriosis
Important questions
• Severity: volume, blood clot (possible airway obstruction), anaemic symptoms (dizziness, palpitation, SOB, postural hypotension)
Investigations
• Imaging: CXR à CT with contrast à bronchoscopy
• Sputum: staining, culture, cytology
• Bloods: CBC, T&S, ABG, CRP/ESR, clotting, autoimmune markers
Mx of massive haemoptysis
• Definition: arbitrary, expectorated blood > 100ml/day
• Protect airway: ICU care, lie lateral on bleeding side (if can be determined), intubation for suction & ventilation (double lumen ET preferred, single lumen ET if urgent), avoid
cough suppressant & sedation
• Haemostasis: flexible bronchoscopy —> bronchial arterial embolisation (BAE) —> emergency lung resection
• Correct underlying cause: stop anticoagulant, antibiotics if infection
Incidental lung nodules
Definitions
• Nodule: ≤ 3cm (c.f. Mass: > 3cm)
Differential diagnosis
• Extrapulmonary density: nipple shadow, pleural mass, bone lesion, skin lesion, electrodes
• Solitary nodule: primary lung CA, metastatic cancer, benign tumors (e.g. harmatoma), carcinoid, AVM, cyst
• Multiple nodules: abscess, metastasis, granulomatous lung disease (TB, fungal, GPA)
Characteristics of benign & malignant lung nodules
• Caveat: lung nodules are common, most are benign
• Consider other predictors for malignancy: age, smoking, FHx
• Compare with previous film
Malignant (30%) - >2cm, UL more likely, spiculated margin, eccentric calcification, HU >15 for contrast enhancement
Benign (70%) - <2cm, well-defined margin, central or popcorn calcification for haematoma, contrast enhancement is HU<15
Fleischner Society guidelines (2017)
Diffuse pulmonary nodules
- Classify into centrilobular, perilymphatic, or random distribution with different DDx
Screening for lung cancer
• CXR: not useful
• Annual LDCT thorax:
o 55-74y
o Smokers (current or previous)
o Fit for undergoing curative surger
Pulse oximetry
MOA: estimate arterial saturation by absorption of infrared lights (2 wavelengths)
according to Beer-Lambert law
SpO2 90% as critical threshold: sigmoid curve
• But normal oxygenation (SaO2) ≠ normal ventilation
Errors:
• External: dark skin, nail varnish
• Poor peripheral perfusion: discrepancy between HR displayed on pulse oximetry vs HR
measured by ECG
• Abnormal Hb: COHb (falsely high), metHb (falsely high or low), HbA1c (falsely high)
Sputum
Collection:
• Spitted: minimal mouth flora contamination (< 10 squamous cells/ LPF & > 25 PMN/
LPF)
• Induced sputum: after inhalation of nebulised saline (isotonic/ hypertonic)
Microbiology:
• Staining: Gram stain, Ziehl-Neelsen stain
• Culture: bacterial, mycobacterial, fungal
• Rapid testing, e.g. TB PCR
Cytology
Lung function test
** Lung function tests = spirometry + lung volume + DLCO **
Collection: At least 6 seconds to be accurate
Spirometry:
• Upper airway obstruction
• Restrictive pattern (FEV1/FVC >70%, lung volume reduced):
o Intrinsic: ILD
o Extrinsic: pleural thickening, chest wall disease (AS, kyphosis), neuromuscular
diseases (GBS, MG, muscular dystrophy, ALS)
• Obstructive pattern (FEV1/ FVC <70%):
o Asthma, COPD, bronchiectasis, CF, bronchiolitis obliterans
Lung volumes: by helium dilution or plethysmography
• Measure residual volume (RV) after forced maximal expiration
• Total lung capacity (TLC) = RV + VC
Diffusion capacity for CO (DLCO): by inhaling gas mixture containing CO, hold for 10
seconds and then exhaled
• Measure the alveolar membrane permeability
• Decrease due to:
o Thickened alveolar-capillary membrane: ILD, edema, consolidation
o Decrease in surface area for gas exchange: emphysema
o Decrease in blood volume available for O2 uptake: anaemia, pulmonary hypertension
Common patterns
• Obstructive pattern + ↓DLCO: emphysema
• Restrictive pattern + ↓DLCO: ILD
Flow-volume loop
• Restrictive: right-shift (↓lung volumes)
• Obstructive: ↓airflow on y-axis during
expiration
• Fixed airway obstruction (e.g. tracheal stenosis):
flattened loop on both top and bottom
• Dynamic airway obstruction: flattened loop on
either top and bottom
o Inspiration-predominant
o Expiration-predominant
Bronchoscopy
Types: rigid (proximal airway only), flexible (can insert via ET tube)
Diagnostic:
• Histology: brushing, lavage (BAL), biopsy
• Endobronchial USG (EBUS): radial probe (assess depth of tumour invasion) vs linear
probe (real-time sampling of LN for CA staging)
Therapeutic
• Endobronchial valve placement: lung volume reduction surgery (COPD), PAL (PTX)
• Bronchial thermoplasty (asthma)
Contraindications: coagulopathy, risk of bronchospasm (e.g. asthma exacerbation within 6w)
Complications:
• Sedative-related, e.g. hypotension
• Bronchoscopy-related, e.g. bronchospasm, bleeding, pneumothorax
Pleural biopsy
Indications: diagnosis of TB pleuritis, diagnosis of mesothelioma
Methods: percutaneous (Abram’s needle), thoracoscopy
Pleuroscopy/ med
thoracoscopy
Examination of pleural space in a conscious patient (c.f. VATS)
Role: diagnostic (pleural exam, pleural biopsy), therapeutic (drainage, pleurodesis)
Lung biopsy
Bronchoscopy
Transthoracic/ percutaneous
Surgical (VATS): tissue architecture better preserved
Respiratory failure
Types
• Type 1 (hypoxemic): PaO2 ≤ 60 mmHg (8 kPa) with a normal or low PaCO2
• Type 2 (hypercapnic): PaO2 ≤ 60mmHg + PaCO2 ≥ 50 mmHg (6.7kPa)
Approach
- if >20mmHg A-a gradient
a. Only on exertion —> DLCO —> impaired diffusion (lung fibrosis, PJP)
b. Persistent —> give 100%O2
b.1 Hypoxemia not corrected —> Shunt (Alveolar filling, Intracardiac: ASD, VSD, Intrapulmonary: atelectasis, AVM)
b.2 Hypoxemia corrected —> V/Q mismatch (Airway: COPD, asthma; Alveolar filling mild: water(APO), pus(pneumonia), blood(infarction); Pulmonary vessel: PE)
- Normal A-a gradient
a. Normal PaCO2 —> low FiO2
b. Increase PaCO2 —> Hypoventilation (Respiratory centre: drugs like morphine; Nerve: SCI, MND, GBS; NMJ: MG; Chest wall: kyphoscoliosis; Resp muscles: myopathy, fatigue, severe asthma/COPD, lung fibrosis)
• Multiple mechanisms for respiratory failure in ILD: impaired diffusion, shunt, V/Q mismatch
• V/Q mismatch: initially T1RF (compensatory hyperventilation to lower pCO2) à later progress to T2RF
• In Asthma / COPD, T2RF (CO2 retention) indicates decompensation
Clinical assessment
• Severity:
o Tissue hypoxia: cyanosis, altered mental status
o Increased respiratory effort: tachypnoea, use of accessory muscles, nasal flaring, intercostal/ suprasternal/
supraclavicular retraction, see-saw breathing
o Sympathetic stimulation: sweating, tachycardia, hypertension (bradycardia & hypotension are late signs)
o Hypercapnia (T2RF): flapping tremor, bounding pulse, flushed skin (peripheral vasodilation)
• Cause: consider speed of onset (e.g. minutes if PE, days if pleural effusion)
• Pulse oximetry: SpO2 90% as critical threshold
• ABG (serial): A-a gradient, PaCO2 (determine type of respiratory failure)
Treatment
• Posture: sitting position can improve SaO2
• Correct underlying cause e.g. bronchodilator for asthma, relieve airway obstruction
• Oxygen supplementation: step up or down according to SaO2
o Target: > 90%
o COPD: 90-94% by Venturi mask, change to NIPPV if progressive
• NIPPV: reduce shunt by recruiting collapsed alveoli
• Mechanical ventilation
Non-invasive ventilation (NIV)
Definitions: oxygen delivery via positive pressure, pressure preset (vs volume preset)
Types
• BiPAP (bi-level positive airway pressure)
o IPAP (usually start at 10cmH2O): reduce CO2
o EPAP (usually start at 4cmH2O): prevent UAO
o Modes: spontaneous (S), spontaneous/timed (ST)
• CPAP (constant fixed positive pressure): maintain airway patency, but
inadequate for supporting ventilation
Common settings:
• APO: CPAP at 8-12 cmH2O
• COPD: BiPAP with IPAP at 8-
15 cmH2O and EPAP at 4-5
cmH2O,
Indications
• BiPAP
o T2RF, e.g. COPD with respiratory acidosis pH < 7.35, secondary to neuromuscular disease
o Weaning from tracheal intubation
o Post-op hypoxaemia (except UGI surgery)
• CPAP: despite optimal medical treatment, T1RF
o Airway disease: OSA, chest wall trauma
o Alveolar: APO
• Less efficacious: acute severe asthma, ARDS, pneumonia with copious secretions
Contraindications
Consider intubation in these cases
• Unable to protect airway, e.g. unconscious, confusion
• Haemodynamic instability e.g. respiratory arrest
• High aspiration risk, e.g. vomiting, excessive secretions
• Recent facial/ upper GI/ upper airway surgery/ trauma / burns
Complications
• Mask: air leak, eye irritation, facial skin necrosis (MC)
• Hypotension (reduced VR)
• Vomiting, aspiration (gastric distension)
• Breathing discomfort: too high IPAP or EPAP
Points to note
• Monitor Vitals: BP, RR, SpO2
• Monitor ABG within 1-2 hours to determine success —> repeat at 4-6h if little improvement —> consider intubation
• Remove mask for short periods every few hours for meals, sputum clearance or bronchodilator inhalation
• Infection control
Acute respiratory distress syndrome (ARDS)
Definition: any acute conditions that lead to acute onset of pulmonary oedema without heart failure
Pathogenesis: neutrophilic infiltration of lung—> diffuse alveolar damage with increased permeability of alveolar-capillary membrane —> alveolar and interstitial oedema
Clinical course: exudative phase (<7 days) —> fibroproliferative phase (>7 days)
Aetiology
• Direct lung injury
o Airway: aspiration, pneumonia, inhalation injury
o Circulation: embolism, reperfusion injury
• Indirect lung injury
o Neurogenic: HI, ICH, drug overdose (e.g. narcotics)
o Circulation: sepsis, shock, pancreatitis
Diagnosis: Berlin criteria
All of the following must be met
• Acute onset: ≤ 7 days of worsening respiratory symptoms
• Pulmonary oedema: CXR shows bilateral opacities not explained by pleural effusion / collapse / nodules
• Non-cardiogenic cause: not fully explained by cardiac failure / fluid overload; no evidence of elevated LA pressure (PCWP < 18mmHg)
• PaO2/FiO2: ALI / mild ARDS (200-300 mmHg), moderate ARDS (100-200 mmHg), severe ARDS (<100 mmHg)
Management
• Treat underlying cause
• Circulatory support: fluid, inotrope
• Mechanical ventilation: low tidal volume to avoid barotrauma
• ECMO if necessary
Lung collapse
S/S: Displaced mediastinum towards lesion, dull on percussion, reduced BS & vocal resonance
Causes:
1. Obstructive
• Intraluminal: mucus plug,
sputum, FB, ET tube
• Mural: malignancy, strictures,
tuberculoma
• Extramural: hilar LN, goitre,
enlarged atrium
2. Non-obstructive
• Compression atelectasis (air squeezed out of alveoli): malignancy, pleural effusion,
• Relaxation atelectasis (loss of contact between 2 layers of pleura —> elastic recoil of lungs): pleural effusion, pneumothorax
• Adhesive atelectasis (surfactant deficiency): ARDS, post-RT
• Cicatrisation atelectasis (parenchymal scarring): ILD, necrotising pneumonia, granulomatous lung diseases
Investigations
• CXR to confirm diagnosis, HRCT for structural lesion
• Early morning sputum x3: Gram stain C/ST, AFB smear + TB culture, cytology
Lobectomy / Pneumonectomy
S/S: trachea grossly deviated to affected side, reduced/absent chest expansion, absent BS,
VATS / thoracotomy scars
Indications: malignancy, bronchiectasis, tuberculosis, lung nodule / abscess (lobectomy), COPD lung volume reduction (lobectomy)
Venous thromboembolism
Types
• Superficial thrombophlebitis: pain, tenderness, erythema along superficial vein
• Deep vein thrombosis (DVT): distal embolism lower risk of PE than proximal
• Pulmonary embolism (PE)
Cause of death in massive PE: ↑RV
afterload —> RV enlargement —>
Septum deviates to left —> ↓LV
volume & ↓cardiac output
Risk factors
• Virchow’s triad:
o Stasis: inactivity, long travel > 8h
o Endothelial injury: trauma/ surgery, central catheter, smoking / HT / DM / HL
o Hypercoagulability: inherited thrombophilia, drugs (OCP/ HRT, tamoxifen), malignancy, APLS, pregnancy, nephrotic syndrome
• History of thrombosis
• PMH: obesity, smoking, acute infection, postpartum
Clinical features:
DVT
- Calf pain & swelling > 3cm than unaffected side; Homan’s sign (5%): calf pain on dorsiflexion
PE:
Acute onset of SOB
Pleuritic chest pain, palpitations
Hemoptysis
Dizziness / syncope
P/E: right heart strain (JVP, loud P2), pleural effusion
Investigations
Initial workup
• Bloods:
o Clotting profile: baseline for thrombolysis
o Cardiac enzymes: for risk stratification
o ABG: T1RF, A-a gradient, met. acidosis if shock
o D-dimer: sensitive (r/o PE in low-risk individuals) but non-specific (DDx: sepsis, malignancy, ACS)
• CXR: usually normal, may show pleural effusion
o Fleischner sign: enlarged pulmonary artery
o Westermark sign: focal oligemia
o Hampton hump: peripheral wedge-shaped infarct
• ECG: sinus tachycardia (MC), S1Q3T3 (15%), R heart strain (RBBB, RAD, P pulmonale, inverted T V1-4), r/o MI
Risk stratification by Well’s score for PE “MarcoPolo Has NO STD”
Malignancy +1
Previous PE/DVT +2
Hemoptysis +1
No other DDx +3
Surgery/immobilization +2
Tachycardia +2
DVT sign +2
Interpretation
• High risk (≥7): proceed to CTPA (1st line), V/Q scan or TTE
• Moderate risk (2-6): D-dimer —> CTPA if positive
• Low risk (0-1): D-dimer to r/o PE
Further tests if indicated (Note: if hemodynamically unstable, can give empirical tPA without diagnostic tests)
• CT pulmonary angiogram: gold standard (Sn 91%, Sp 78%) - look for filling defects in pulmonary artery
o Must inform radiologists to look for PE: contrast timed to highlight PA
• V/Q scan: for patients C/I for CTPA (e.g. renal impairment, contrast allergy) (Sn 41%, Sp 97%)
o Inhalation + injection of radioisotope —> perform CXR to detect areas of lung ventilated but not perfused
• Echocardiogram (TTE / TEE): assess RV failure in massive PE
• Lower limb venous duplex: Up to 50% negative in PE
Management
• General: leg elevation, compression stockings, O2, analgesics
• Risk stratification: parameters include hemodynamic stability, RV dilation, cardiac Tn level, PE severity index
• If haemodynamically stable:
o Anticoagulation
- Duration: 3-6 months (1st unprovoked episode) or indefinite (2nd episode / malignancy)
Initial antcoagulation:
LMWH / UFH
• Dosage: SC enoxaparin 1mg/kg Q12h or IV UFH 5000U bolus then 500-1500 U/hr infusion
to keep APTT 1.5-2.5x control
• UFH preferred if: renal failure (CrCl < 30), pregnancy, morbid obesity (poor SC
absorption), thrombolytic use considered (acute reversal by protamine is needed)
Subsequent anticoagulation
- Warfarin / DOAC
o IVC filter: indicated if C/I for anticoagulation, recurrent DVT/PE despite anticoagulated
• If haemodynamically unstable: thrombolysis / embolectomy
o Book ICU / CCU
o Rule out contraindications of tPA
o Thrombolysis (tPA) 100mg IV over 2 hours (only for onset < 14 days) —> Anticoagulate with UFH 500-1500 units/hr infusion to keep APTT 1.5-2.5x control
o Embolectomy (catheter-directed or surgical; when tPA C/I or fails)
- Surgical first, mechanical if C/I
• Workup for idiopathic VTE (after acute phase)
- Malignancy —> blood test, CXR
- Thrombophilia
• Follow up at 3-6 months: Echocardiogram for CTEPH
Pulmonary hypertension
Definition
• Mean pulmonary artery pressure (mPAP) > 25mmHg at age > 3mo
• Cor pulmonale: chronic lung disease —> pulmonary hypertension —> right heart failure
WHO classification
- Right heart catheterization: classify into pre-capillary (1/3/4/5) & post-capillary (2/5)
- All treat with O2 and diuretics
Class 1- Pulmonary arterial hypertension (PAH)
- Cause:
—> idiopathic
—> Collagen vascular disease e.g. scleroderma, SLE, RA, PPHN, Eisenmenger syndrome
- Treatment options:
Vasodilators:
—> CCB: nifedipine/diltiazem
—> PDE5 inhibitor (NO pathway), e.g. sildenafil
- Endothelin receptor antagonist, e.g. bosentan. Ambrisentan
—> Prostacyclin analogue (PGI pathway), e.g. epoprostenol (Flolan), treprostinil (Remodulin)
Class 2 - PH due to left heart disease
- Cause:
—> Left-sided valvular heart disease, e.g. AS, MS
—> Congenital left heart outflow tract obstruction, e.g. HOCM
- Treat underlying cause
Class 3 - PH due to hypoxic lung disease
- Casue:
—> Obstructive: COPD, asthma
—> Restrictive: ILD
—> Others: OSA
- Treat underlying cause
Class 4- - Chronic thromboembolic PH
- Cause: Recurrent PE
- Treatment: anticoagulation, thromboendarterectomy
Class 5 - PH with unclear multifactorial mechanism
- Cause: Chronic haemolytic anemia, Myeloproliferative disorders
- treat underlying cause
End-stage disease: surgical management
• Atrial septostomy: create a right-to-left shunt
• Lung transplant
Clinical features
• Symptoms: dyspnoea, fatigue, retrosternal chest pain, syncope,
• Signs: RV gallop rhythm with loud P2, signs of RV failure (elevated JVP, peripheral oedema, TR, parasternal heave), Graham-Steell murmur (PR)
• Pulmonary oedema: not associated with class I (proximal to capillary bed), most commonly associated with class II
Investigations
• CXR: enlarged central pulmonary arteries, attenuation of peripheral vessels, oligemic lung fields, signs of underlying causes (e.g. cardiomegaly, hyperinflated chest & bullae, honeycomb lung)
• ECG: RVH, RV strain pattern, LAH (mitral valve disease), LVH +/- strain (aortic valve disease / HT)
• ECHO: RA & RV enlargement, TR, PA systolic pressure
• ABG: Type 1 / Type 2 respiratory failure
• Right heart catheterisation (RHC): gold standard for diagnosis and quantification of pulmonary hypertension
**Precapillary vs Post-capillary: pre has PCWP<15mmhg and PVR >3 woods units, post has PCWP>15 mmHg and PVR normal
Idiopathic pulmonary hypertension
• Disease of children and young adults
(F:M = 2:1) – median survival 3 years
• Associated with connective tissue
disorder, HIV, vasculitis
Pneumothorax
Aetiology (need to know!)
• Spontaneous:
o Primary (PSP = no underlying lung disease): predominantly tall, thin, young males
o Secondary (SSP = underlying lung disease): COPD (bullae + smoking as a risk factor), CA lung, PCP infection, Langerhan’s cell histiocytosis (young M), lymphangioleiomyomatosis (LAM, young F)
• Traumatic: penetrating, blunt, barotrauma
• Iatrogenic: CVC, mechanical ventilation (barotrauma)
CXR features
• Diagnostic: erect CXR (rim of hyperlucency without lung marking) —> lateral decubitus film (suspected side up c.f. pleural effusion)
• Severity:
o Size: small (<2cm) or large (≥2cm, i.e. ↓50% lung volume)
- % pneumothorax = (1-average lung diameter3/ average hemithorax diameter3) x 100%
- 1cm on PA CXR ≈ 27% hemithorax
o Bleeding from torn pleural vessels: blunted CP angle (haemopneumothorax) à consult CTS if profuse bleeding
Management
To remove air from the pleural space
• O2 therapy
o Mechanism: to promote absorption of air (O2 easier to absorb than N2)
o Avoid high-flow nasal cannula (HFNC) & NIPPV: positive pressure may worsen PTX
• Needle aspiration (thoracocentesis): considered if >15% lung volume
o 14G/16G needle, 2nd anterior ICS
• Chest drain: indications
o Bilateral PTX
o Haemodynamically unstable
o PSP: size ≥2cm or symptomatic
o SSP: size ≥1cm or symptomatic
To decrease likelihood of recurrence (risk: 20-30%)
• Smoking cessation (risk factor)
• Pleurodesis
o Indications (SAQ!)
- SSP
- PSP: recurrent (i.e. first contralateral, second ipsilateral), synchronous bilateral PTX, PAL, high-risk professions (e.g. drivers), pregnancy
o Modality:
- Surgical: pleural abrasion with dry gauze, laser abrasion, talc
- Chemical (if surgically unfit): talc, autologous blood, Tetracycline
S/E: ARDS
Persistent air leak (PAL)/ bronchopulmonary fistula
• Definition: air leak ≥ 5 days
• Management:
o Conservative: continued chest drain with low wall suction
o If failed, CT thorax to localise lesion, then
- Bronchoscopy: endobronchial valve (EBV)
(fig.) - one-way valve to intentionally collapse
the lung lobe —> remove 6 weeks after recovery (foreign body)
- Pleurodesis: surgical/ chemical (see below)
Tension pneumothorax
• Pathophysiology: build up of pressure —> compress IVC —> decrease VR —> obstructive shock & V/Q mismatch
• Clinical diagnosis
o Severe respiratory distress
o Obstructive shock: hypotension, elevated JVP
o Tracheal deviation to contralateral side
• Management: DO NOT wait for CXR
o High-flow O2
o Urgent needle thoracotomy: large bore needle (12G) at 2nd ICS mid-clavicular line
o Chest drain: after stabilisation
Pleural effusion
Etiology
1. Transudative (usually bilateral)
- Failures (heart, liver, renal)
- Constricitve pericarditis
- Nephrotic syndrome
- Protein-losing enteropathy
- Pleuroperitoneal fistula in PD
- 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
Parapneumonic effusion
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)
Malignant pleural effusion
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
Pleurodesis
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)
Chest drain
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
- 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 - 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
Asthma definition, S/S, Ix
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)
Asthma treatment
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
Asthma exacerbation
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
- 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 - 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 - 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
Chronic obstructive pulmonary disease (COPD) (definition and S/S)
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)
COPD (Ix, severity
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
Mx of COPD
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
- ICS: Beclomethasone / Budesonide / Fluticasone
- preferred in Blood eosinophil ≥ 300 / Hx of or concomitant asthma
- Avoid regular use: increases risk of pneumonia
- Stop if AECOPD - PDE4 inhibitor
- Roflumilast
- preferred in FEV1 < 50% & chronic
bronchitis
- S/E: reduced appetite, diarrhoea, weight loss, sleep disturbance - Mucolytics
- Acetylcysteine
- All patients - Antibiotics
- Azithromycin
- Former smokers
- Issues: increasing resistance, QT prolongation,
impaired hearing - 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
Acute exacerbation of COPD
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
Bronchiectasis
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
Pulmonary rehabilitation
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
Interstitial lung disease
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
Obstructive sleep apnoea
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
Obesity hypoventilation syndrome (Pickwickian syndrome)
• 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
TB
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
