COPD

Definition

COPD (Chronic Obstructive Pulmonary Disease) is a chronic irreversible airflow obstruction and destruction of lung parenchyma by noxious particles or gases.

  • Emphysema = destruction of alveoli with abnormal air space enlargement
  • Chronic bronchitis = chronic cough & phlegm
  • Small airway disease = small bronchioles are narrowed & reduced in number

Epidemiology

Risk Factors

  1. Cigarette smoking
  2. Respiratory infections
  3. Occupational exposures
  4. Air pollution
  5. Passive or second-hand smoking exposure
  6. α1-antitrypsin deficiency

Pathophysiology

  1. Cigarette smoking

    1. Lung parenchyma: lung inflammation → increased number of neutrophil granulocytes → release elastases & proteases (proteolysis)→ damages the alveolar wall → emphysema + hyperinflation
    2. Large airway: persistent irritation → mucous gland hypertrophy → chronic bronchitis
    3. Cell death - cigarette smoke causes oxidant-mediated structural cell death
    4. Ineffective repair - cigarette smoke impairs macrophage uptake of apoptotic cells, limiting repair

  2. α1-antitrypsin deficiency

    1. is a proteinase inhibitor produced in the liver
    2. reduces lung’s ability to prevent damage of the lung tissue

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Signs & Symptoms

Signs Symptoms
1. Wheezing on expiration 1. Chronic productive cough (white sputum)
2. Tachypneic (rapid & shallow breathe) 2. Dyspnea on exertion
3. Reduced chest expansion 3. Fatigue
4. Hoover’s sign during inspiration 4. Susceptible to respiratory infection
5. Use of accessory muscles during respiration 5. Prolonged expiration
6. Pursed-lip during during expiration
7. Barrel chest

*productive cough for at least 3 consecutive months within at least 2 consecutive years

Clinical Findings

  1. Dyspnea
  2. Chronic cough with sputum
  3. Expiratory wheeze
  4. Prolonged expiration
  5. Rapid & shallow breath
  6. Barrel chest
  7. Pursed-lip breathing
  8. Use of accessory muscles (SCM & scalene muscles)
  9. Hoover’s sign (shrinking lower chest during inspiration)
  10. Muscle wasting

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Complications

  1. Acute exacerbation of COPD
  2. Pneumonia
  3. Pulmonary hypertension → cor pulmonale
  4. Pneumothorax - rupture of emphysematous subpleural bullae
  5. Secondary polycythemia
  6. Muscle wastig, atrophy

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Differential Diagnosis

Differential Diagnosis Suggestive Features
1. COPD - onset: mid-life; early adulthood
- alpha-1 antitrypsin def.
- long smoking history
- dyspnea on exertion
- irreversible airflow limitation
2. Asthma - onset: early in life (often childhood)
- symptoms at night/early morning
- allergy, rhinitis, and/or eczema also present
- family history of asthma
- reversible airflow limitation
3. Central airway obstruction - eg, bronchogenic or metastatic cancer, lymphadenopathy, scarring from endotracheal tube
- monophonic wheeze or stridor
- CXR: often normal
- airway narrowing on three dimensional reconstruction of HRCT scan
4. Heart failure - auscultation: fine basilar crackles
- CXR: dilated heart, pulmonary edema
- pulmonary function tests: typically indicate volume restriction, but airflow limitation can sometimes be seen
5. Bronchiectasis - copious purulent sputum
- commonly associated with recurrent or persistent bacterial infection
- clinical findings: coarse crackles, finger clubbing
- CXR/HRCT: bronchial dilation, bronchial wall thickening
6. Tuberculosis - onset all ages
- CXR: upper lung zone scarring and/or calcified granulomata
- positive PPD or IGRA
- high local prevalence of tuberculosis
7. Obliterative bronchiolitis - onset: younger age, nonsmokers
- may have history of rheumatoid arthritis or fume exposure
- HRCT on expiration: shows hypodense areas, mosaic pattern
8. Diffuse panbronchiolitis - most are male and nonsmokers
- highest prevalence in East Asia
- almost all have chronic sinusitis
- CXR & HRCT: diffuse small centrilobular nodular opacities and hyperinflation

Investigations

Non-imaging

  1. ABG - hypoxemia (PaO2 <70), hypercapnia (PaCO2 >45), and ventilation perfusion mismatch (high A-a gradient)
  2. Spirometry - longer total expiration (FEV1/FEV <0.7), hyperinflation (high TLC and VC), reduced diffusion capacity

Imaging

Frontal CXR Lateral CXR
1. Hyperlucent lung field & reduced lung markings (byk air dlm lungs) 1. Increased retrosternal airspace
2. Hyperinflation (>10 post ribs above diaphragm) 2. Increased AP diameter(barrel chest)
3. Hilar enlargement 3. Flat/low hemidiaphragm
4. Bronchial wall thickening(due to airway fibrosis)

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Management

Group Types MOA Treatment effect Side effect
Beta agonists SABA: salbutamol, fenoterol

LABA: salmeterol, formoterol		 - stimulates β2 adrenergic receptors on bronchial sm → bronchodilation

*SABA = reliever, LABA = controller		 Bronchodilation - hypokalemia
- tachycardia
- palpitation
- headache
- tremor
- dry mouth
- hyperglycemia
Muscarinic antagonists SAMA: ipratropium bromide

LAMA: tiotropium, glycopirronium bromide		 - inhibits M3 (muscarinic acetylcholine) receptors in airway muscles
- ⬇️ activation of IP3 pathway
- ⬇️ Ca2+ release → bronchodilation

*SAMA = reliever, LAMA = controller		 Bronchodilation - dry mouth
- sore throat
- tachycardia
Corticosteroids Inhaled: budesonide

Systemic: prednisone, hydrocortisone, prednisolone,		 - steroid binds to nuclear receptor within cells
- ⬇️ synthesis of cytokines

*Inhaler = controller, Systemic = exacerbation		 - reduce airway mucous
- reduce mucosal edema		 - ⬆️ susceptibility to infection
- oral thrush
- hoarseness of voice
Phosphodiesterase inhibitor Ex: roflumilast (oral) - inhibit phosphodiesterase-4 from breaking down cAMP → ⬆️ cAMP conc.
- cAMP activates intracellular signalling cascade in bronchial sm
- ⬇️ Ca2+ release → bronchodilation

*controller		 Bronchodilation - nausea
- abdominal pain
- weight loss
- sleep disturbances
- anxiety

Reliever: used as needed to ⬇️ symptoms during attacks
Controller: used daily to ⬇️ freq. & severity of attacks
Exacerbation: used emergently in acute exacerbation (used together with relievers)

Acute Exacerbation of COPD

  • it is important to identify severe/life threatening exacerbation

Clinical Features of Severe Exacerbation

  1. Altered mental status: drowsy, confused, agitated
  2. Speaks in word
  3. Use of accessory muscles
  4. Very rapid breathing/poor breathing effort
  5. Assoc. symptoms: cough, fever, noisy breathing

Causes of Exacerbation

  1. Respiratory infection
  2. Non-compliance to medication
  3. Wrong inhaler technique
  4. Exposure to allergen
  5. Smoking

History Taking

  • Diff. from asthma: “When the diagnosis is made?” “Atopy & fam. hist. of asthma?”
  • Ask regarding the risk factors: smoking, occupational exposure
  • Control of the disease:
    • Freq. of exacerbation
    • Summary of all admissions
    • Reasons of poor control: non-compliance, wrong technique, still smoking
  • Severity of the disease:
    • HDU/ICU admission, hist. of intubation
    • Need of long term O2 therapy (LTOT)
  • Complications from the disease:
    • Cor pulmonale
    • Pneumothorax
    • Lung cancer

Full diagnosis: Acute exacerbation of COPD secondary to ………

Physical Examination

  • Vital signs: tachypnoea, SpO2, temp., tachycardia
  • General inspection:
    • Signs of resp. distress: tachypnoea, use of accessory resp. muscles, intercostal and subcostal recessions, pursed-lip breathing
    • Cachexia, malnourished
  • General examination:
    • Hands: flapping tremor, tar stain
    • Face: polycythemia
  • Resp. examination:
    • Scar: bullectomy, chest tube insertion
    • ⬇️ chest expansion
    • Hyperinflated chest
    • Auscultation: prolonged expiratory, rhonchi, crepitation (in early inspiratory phase)
    • Peak flow meter
  • CVS examination:
    • Raised JVP
    • Deviation of apex beat to the right
    • Parasternal heave
    • Loud P2
    • Signs of right-sided heart failure: lower limb edema, hepatomegaly

Investigations

During exacerbation

  1. FBC: evidence of infection, polycythemia
  2. ABG: resp. acidosis and type-2 resp. failure
  3. Sputum culture & sensitivity
  4. CXR: hyperinflated lungs, hyperlucent lung fields, consolidation (infection)

To diagnose COPD

  • Lung function test:
    • FEV1/FVC <70%
    • Obstructive pattern
    • Not reversible on post-bronchodilator test

Management

For acute exacerbation

  1. Oxygen: maintain SpO2 >90% using Venturi mask (24-28% O2)

  2. Bronchodilator: nebulized SABA or Combivent (salbutamol + ipratropium bromide) for more exacerbation every 6 hourly

  3. Antibiotics: empirial abx (augmentin, azithromycin)

  4. Corticosteroid: oral prednisolone 40mg for 5-7 days

  5. Mechanical ventilation support in: resp. acidosis, severe dyspnea, persistent hypoxemia despite treatment

  6. Intubation in: depressed concious level, hemodynamic unstable

  7. Hospital admission:

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For stable COPD

  1. Pharmacological: SABA/LABA + SAMA/LAMA + ICS
  2. Non-pharmacological: smoking cessation, pulmonary rehab
  3. Prevention: vaccination against influenza & pneumococcal

COPD vs Asthma

Asthma COPD
Diagnose Childhood or teen age Usually around 50y/o and above
Onset Sudden Gradual
Clinical features Episodic symptoms with interspersed symptom-free period Chronic & progressive symptoms
Risk factors - Fam. hist. of asthma & atopy
- Personal hist. of atopy		 - Smoking
- Occupational exposure
Pattern of obstruction Reversible Irreversible
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Table Of Contents
COPD
Definition
Epidemiology
Risk Factors
Pathophysiology
Cigarette smoking
α1-antitrypsin deficiency
Signs & Symptoms
Clinical Findings
Complications
Differential Diagnosis
Investigations
Non-imaging
Imaging
Management
Acute Exacerbation of COPD
Clinical Features of Severe Exacerbation
Causes of Exacerbation
History Taking
Physical Examination
Investigations
During exacerbation
To diagnose COPD
Management
For acute exacerbation
For stable COPD
COPD vs Asthma