Chronic Obstructive Pulmonary Disease

Background and Epidemiology

• COPD is a preventable, treatable but not curable disease characterised by persisten airflow limitation that is usually progressive.  It is a combination of airway disease (obstructive bronchiolitis) and parenchymal disease (emphysema) and is mainly due to an inflammatory response of the lungs, usually to noxious chemicals/particles.
• It is estimated that about 3-5% of the population have COPD.  Around 1 in 8 emergency hospital admissions are due to COPD.  It also contributes towards 5% of all deaths globally.
• More common in men and with age

Aetiology/Risk factors

• Tobacco smoking (up to 95% of cases can be due to smoking in the UK)
• Other risk factors include indoor air pollution, occupational exposure to harmful chemicals e.g. coal dust; poor lung development (can, again, be due to smoking but can also be due to repeated chest infections
• Lower socioeconomic status

Pathophysiology

•  Chronic inflammation of the lungs is usually a result of inhalation of toxic chemicals (usually as a result of smoking)
  • In patients who get COPD, there is a heightened immune response to these toxins
  • Neutrophils, macrophages and T lymphocytes (CD8>CD4) are recruited to the lungs.  The result is a release of a number of inflammatory mediators e.g. leukotriene B4, IL8, TNF and IL1β and IL6, which cause inflammation and tissue fibrosis and destruction
• There is also often an imbalance of protease activity and production of free oxygen radicals (and oxidative damage)
• This results in
  • Mucous hypersecretion and ciliary dysfunction (squamous metaplasia, increased goblet cell number and activity)
  • Airflow obstruction and hyperinflation/air trapping
    • Airflow obstruction mainly occurs in the small airways (<2mm) and is due to inflammation and airway remodelling/narrowing (other contributing factors include loss of lung’s elastic recoil due to destruction of the alveolar walls and alveolar support/attachments)
    • Because expiration is a passive process, the small airways can close and trap in inspired air, causing hyperinflation at rest and dynamic hyperinflation during exertion, limiting lung function on exertion and causing breathlessness.
  • These structural changes can also cause gas exchange abnormalities – due to abnormal ventilation-perfusion ratio – usually resulting in arterial hypoxaemia +/- hypercapnia
• In severe disease, pulmonary hypertension and right ventricular failure (cor pulmonale) can develop and severely impair gas exchange

Presentation

• Suspect in patients >35 who presents who has risk factors (namely smoking) and who present with
  • Exertional breathlessness
    • Important to try and grade the severity e.g. how much can you do?
  • Chronic cough
  • Regular sputum production
  • Frequent episodes of bronchitis/chronic bronchitis
  • Wheezing
• Signs on examination may include
  • Weight loss (cachexia may be present late on in the disease)
  • Cyanosis (‘blue bloaters’ – or ‘pink puffer’)
  • Raised JVP
  • Hyperinflated chest (+/- reduced cricosternal distance), pursed lip breathing, use of accessory muscles
  • Wheeze/quiet breath sounds.  There may also be some crackles (either infection or bronchiectasis)
  • Also ask about waking at night, ankle swelling and fatigue; chest pain and haemoptysis

Investigations

• CXR (exclude alternative/concomitant diagnosis) +/- high-resolution chest CT (used increasingly more to identify any emphysema)
• FBC (exclude any anaemia/polycythaemia) +/- ABGs (hypoxia)
• Measure BMI
• Spirometry (Diagnostic)- Perform post-bronchodilator tests (reversibility is not a feature of COPD)
  • FEV1/FVC <0.7 must be present for diagnosis
  • Severity can be graded by FEV1 predictions (vs patient)
    • ≥80% + presence of symptoms is mild
    • 50-79%- Moderate
    • 30-49% – Severe
    • <30% (or FEV1 <50% but with respiratory failure)- Very severe
  • Other lung function tests, e.g. lung volumes, gas exchange (gas transfer factor for CO) can also be performed to assess hyperinflation and emphysema (respectively)
• Other tests may be appropriate e.g.
  • In particularly young patients with minimal smoking history + family history, genetic testing for Alpha-1-antitrypsin deficiency
  • ECG/Echo to assess cardiac function
  • Pulse oximetry to assess degree of desaturation
    • If <92%, consider oxygen therapy
  • Sputum culture

Management

• Smoking cessation – Recommend smoking cessation to all patients who smoke.  Do this and offer help/support at every opportunity.
• Inhaled therapy
  • Short-acting β-2 agonists (e.g. salbutamol) (or a short-acting muscarinic antagonist e.g. ipratropium, although SABA is often preferred as this can be continued at other stages of treatment) should be offered for initial treatment for PRN relief of breathlessness.
  • If there are continuing exacerbations or persistent breathlessness (using SAMA/SABA >4x/day)-
    • If the FEV1 ≥ 50%
      • Add a long acting β2-agonist e.g. salmeterol, or a long-acting muscarinic antagonist e.g. tiotropium
    • If the FEV1 <50%
      • Add a LABA + inhaled corticosteroid (combination inhaler) or a LABA + LAMA or (if BAs are not appropriate) LAMA only
  • If symptoms are still problematic
    • Consider LABA + ICS + LAMA
• Oral therapy
  • Not routinely recommended
  • Theophyllines can be trialled (after short- and long-acting inhaled therapy or in those in whom inhaled therapy is not possible)
  • Mucolytics e.g. carbocysteine can be used for patients with chronic productive cough but should not be used to prevent exacerbations
  • Corticosteroids are not routinely recommended, but can be used low-dose and ideally short-term following an acute exacerbation
• Oxygen therapy (Long-term)
  • Consider in people with
    • Very severe COPD (FEV1 <30% predicted)
    • Cyanosis
    • Polycythaemia
    • Peripheral Oedema
    • Raised JVP (Pulmonary hypertension)
    • Saturating at <92% on air
  • Assess the need by measuring ABGs for hypoxia on two occasions at least 3 weeks apart in patients receiving optimum treatment
    • If pO2<7.3 kPa when stable, offer oxygen therapy
    • If 7.3kPa < pO2 < 8 kPa when stable and one of
      • secondary polycythaemia, nocturnal hypoxaemia, peripheral oedema or pulmonary hypertension
      • .. offer therapy
  • Patients should be breathing using the oxygen for ideally a minimum of 15 hours/day.
  • AVOID if possible in patients who smoke.

Management of an Acute Exacerbation of COPD

• Treat acutely unwell patients with ABCDE approach
  • NB If there is a clinical diagnosis of COPD- aim for oxygen saturations of 88-92%
    • NOTE: This, however, IS NOT and indication to withhold high-flow oxygen if the patient needs this.  If a diagnosis is not known- aim for 98-100%.
  • ABGs should be taken early (if type II resp failure- continue to maintain sats at 88-92%)
• Manage breathlessness with
  • Nebulised salbutamol (2.5mg)
  • Prednisolone 50mg oral for up to 7 days (or IV Hydrocortisone 100mg TDS)
  • If severely ill (and/or PaCO2 >8kPa and/or pH <7.35)- consider also starting IV aminophyllin infusion 5mg/kg in 100ml normal saline over 20 mins then 500 micrograms/kg/hr
  • Consider BiPAP and escalation of care if not improving
• Manage exacerbation with antibiotics if there are signs of infection (increased purulent sputum, fever, dyspnoea)
  • Amoxicillin 500mg TDS (5 days) or doxycycline 200mg loading dose then 100mg OD (5 days) if penicillin allergic
    • NB If CXR shows new infiltrates/consolidation- treat as per pneumonia

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