Makindo Medical Notes

Related Subjects:Prednisolone |COPD |Asthma |Respiratory failure

COPD is largely a preventable condition. You can significantly reduce your chances of developing it if you avoid smoking. Lack of reversibility measured by FEV 1.0 is key to the diagnosis of COPD. Predictors of a poor prognosis are increasing age and worsening of airflow limitation, i.e. a fall in FEV1.

About

• Almost always a smoker's disease with progressive irreversible airflow limitation
• Heightened inflammatory response of the lung with progressive lung damage.
• Distinct pathologies emphysema and chronic bronchitis merge in degrees to form COPD.

Causes

• Smoking is the main risk factor but only a fraction of smokers develop COPD
• A genetic susceptibility is important
• Alpha-1 anti-trypsin (AAT) deficiency
• Coal workers and Cadmium workers are at increased risk.
• Smoking marijuana

Pathology

• Emphysema (Defined pathologically)
  • Destruction and enlargement of air spaces distal to the terminal bronchiole.
  • Panacinar/Lower lobe destruction - pure AAT deficiency.
  • Centrilobular destruction/upper lobe emphysema is seen in smokers
• Chronic bronchitis (Defined clinically)
  • Defined clinically as a morning productive cough > 3 months per year for 2 consecutive years
• Pathophysiology
  • Increased T lymphocytes / neutrophils release proteases (elastases) damaging local normal elastic walls.
  • Damage heightened in those with antiprotease deficiency
  • Smokers have increased protease activity
  • Increased Bronchial mucus secretion with an increase in size and number of bronchial mucus glands.
  • 'Air trapping' leads to V/Q mismatch and hypoxia.
  • Hypoxia and respiratory acidosis induce pulmonary vasoconstriction and eventually cor pulmonale.
• Pathology
  • Mucous gland hyperplasia, Impaired cilia function,
  • Squamous metaplasia (columnar cells become squamous)
  • Chronic inflammatory process, Localised fibrosis
  • Alveolar wall destruction - centriacinar and panacinar emphysema
  • Large emphysematous spaces > 1cm are called bullae.

Clinical

• Suspect a diagnosis of COPD in people over 35 who smokes and presents with
  • Exertional breathlessness
  • Chronic cough
  • Regular sputum production
  • Frequent winter 'bronchitis'
  • Wheeze
  • Weight loss
  • Reduced exercise tolerance
  • Waking at night with breathlessness
  • Ankle swelling
  • Fatigue
  • Occupational hazards
  • Chest pain and Haemoptysis: exclude malignancy or other diagnoses
• Assess MRC Dyspnoea scale
  • 0 No breathlessness, except with strenuous exercise
  • 1 Breathlessness when hurrying on the level or walking up a slight hill
  • 2 Walks slower than contemporaries on level ground because of breathlessness or has to stop for breath when walking at own pace
  • 3 Stops for breath after walking about 100 m or after a few minutes on level ground
  • 4 Too breathless to leave the house, or breathless when dressing or undressing
• Later changes
  • Prolonged expiration > 5 seconds
  • Nicotine-stained fingers
  • Use of accessory muscles
  • Finger clubbing suggests lung cancer or fibrosis.
  • Hyperinflated Barrel chest, Hyperresonance to percussion
  • Shortened cricoid to notch distance of 3 finger breadths or less
  • Loss of cardiac dullness on percussion.
  • Pursed lip breathing, Central cyanosis
  • Heart sound loudest in epigastrium as heart pushed more vertically by large emphysematous lungs
  • Raised JVP and peripheral oedema with cor pulmonale
  • Hypoventilating Blue bloaters : cyanosis, right heart failure and retain CO₂.
  • Hyperventilating pink puffers: thin, breathless not retaining CO₂

Differentials

• Asthma, Bronchiectasis
• Heart failure

Asthma more likely if

• a large (over 400 ml) response to bronchodilators
• a large (over 400 ml) response to 30 mg oral Prednisolone daily for 2 weeks
• serial peak flow measurements showing 20% or greater diurnal or day-to-day variability.

Investigations

• FBC may show polycythaemia especially if continues to smoke
• CRP/ESR raised if infection
• Sputum culture: To identify organisms if sputum is persistently present and purulent
• Serial home peak flow measurements: exclude asthma if diagnostic doubt remains
• CXR can show hyperinflation, flattened diaphragm, bullae, prominent pulmonary vessels and exclude a tumour or consolidation
• CT scan of the thorax: if diagnosis uncertain or to exclude another lung diagnosis (such as fibrosis or bronchiectasis)
• ECG AF, RBBB P pulmonale, RAD.
• BNP and echocardiogram to exclude heart failure and pulmonary hypertension
• Reduced FEV1 < 80%, FEV/FVC < 70% with < 10% reversibility.
• Raised FRC (Functional residual capacity) and total lung volume
• Transfer factor for CO. Reduced gas transfer factor (DLCO) with emphysema
• Serum alpha-1 antitrypsin low in AAT deficiency test in those age < 40 years or with a family history.
• HRCT can show some of the damage and dilatation of the airways and bullae
• Functional tests - BODE index assesses BMI, FEV1, dyspnoea and 6 minute walking tests and predicts mortality

Severity Based on FEV1 (all have FEV/FVC <0.7)

BODE assessment of Prognosis

Approximate 4-year survival rates based on the BODE index point system above is as follows

• 0-2 points: 80%
• 3-4 points: 67%
• 5-6 points: 57%
• 7-10 points: 18%

Management

• Smoking cessation improves prognosis and slows deteriorating FEV.
• Bronchodilators
  • Salbutamol (Albuterol) metered dose inhaler PRN
  • Tiotropium used daily is an inhaled long-acting anticholinergic improves FEV1 and reduces the frequency of exacerbations
  • Long-acting bronchodilators (LABD) e.g salmeterol aid expiration and improve symptoms and exercise tolerance
• Corticosteroid
  • Inhaled steroids may be added to those with FEV < 50% predicted with more than 2 exacerbations a year
  • Oral steroids used for acute flare-ups and then stopped or weaned off slowly
• Oral theophylline may be useful but be wary of interactions
• Surgery - In a small number lung volume reduction surgery is useful - bullectomy and Lung volume reduction may be done thorascopically.
• LTOT (Long term oxygen therapy) - Pulse oximetry to identify patients needing LTOT. Arterial blood gases are measured in clinically stable patients on optimal medical therapy on at least two occasions 3 weeks apart
  • PaO₂ <7.3 kPa irrespective of PaCO₂ and FEV1 <1.5 L
  • PaO₂ 7.3-8 kPa (55-60 mmHg) plus pulmonary hypertension, peripheral oedema or nocturnal hypoxaemia
  • the patient has stopped smoking
  • Agrees to use at least 15 hrs/day at 2-4 L/min to achieve a PaO₂ >8 kPa (60 mmHg) without unacceptable rise in PaCO₂
  • Oxygen concentrators should be used to supply the LTOT at home
  • Assessments usually delayed until 6 weeks post exacerbation
  • Caution as uncontrolled oxygen can lead to drowsiness and CO₂ retention
  • Long term oxygen therapy which can prevent pulmonary hypertension if used for 15+ hrs /day
  • Aim to keep SaO₂ > 90 % and PaO₂ > 8 Kpa.
• Pulmonary rehabilitation improves mobility, quality of life and reduces Symptoms and hospital admissions
• Vaccination against influenza and pneumococcus recommended
• Patients should be supplied with antibiotics and steroids and educated when to take them with exacerbations.
• Involvement of respiratory nurses to educate and support discharges and follow up can prevent admissions and possibly reduce the severity and frequency of exacerbations.

References

• Nice Guidelines on COPD