COPD is a progressive airway disease characterized by airway limitation and chronic inflammation to noxious particles or gases. Exacerbations and comorbidities contribute to disease severity.

Related diagnoses

  • Emphysema, chronic bronchitis, asthma
  • Asthma and COPD overlap can be found

Associated comorbid conditions;

  • Metabolic syndrome
  • Osteoporosis
  • Cardiovascular disease
  • Cerebrovascular disease
  • Lung cancer
  • Depression

Risk factors;

1. Environmental factors;

  • Cigarette smoking- >95% of cases. Both amount and duration are important
  • Indoor pollution- firewood smoke
  • Exposure to coal dust, silica, and cadmium
  • Childhood infections and maternal smoking
  • Low birth weight
  • Recurrent respiratory infections
  • Cannabis smoking
  • Low socioeconomic status

2. Host factors

  • Alpha 1 antitrypsin deficiency
  • Airway hyper reactivity
  • Primary ciliary dyskinesia

Pathophysiology

The airflow limitation and early airway closure lead to air trapping and hyperinflation, thus affecting compliance. Pulmonary hyperinflation causes flattening of diaphragmatic muscles and horizontal alignment of intercostal muscles. The work of breathing thus increases as the disease advances. an impaired gaseous exchange may occur and lead to respiratory failure, as occurs in exacerbations

Clinical presentation

  • Three cardinal symptoms- are dyspnoea, chronic cough, and sputum production.
  • Exertional dyspnoea is the earliest symptom. Dyspnoea should be graded
  • Hemoptysis can complicate COPD exacerbations but should be investigated first
  • Symptoms of right-sided heart failure- e.g., pedal oedema, abdominal distension. However, pedal oedema may also occur in the absence of heart failure, and this is due to salt and water retention due to renal hypoxia and hypercapnia.
  • Weight loss in advanced disease- associated with poor prognosis
  • Symptoms may be worse in the morning
  • Depression and anxiety are common

Physical examination;

  • The physical examination may be unremarkable in early disease
  • Cyanosis may be present
  • Nicotine staining of palms and fingers
  • Barrel-shaped chest- a sign of severe disease
  • Depressed diaphragm with limited movement- on percussion
  • Increased resonance to percussion
  • Breath sounds are typically quiet. Wheeze may be present
  • Crackles- may accompany infection. Bronchiectasis must be ruled out
  • Distant heart sounds
  • *Finger clubbing is not typical

Two classical types;

1. Pink puffers- are usually breathless and thin. They can maintain a normocapnia until late disease

2. Blue bloaters- develop hypercapnia early in the disease and may develop secondary polycythemia and oedema

Investigations

1. Chest Xray features;

  • Increased anteroposterior diameter on a lateral view
  • Rapidly tapering vascular shadows
  • Bullae
  • Prominent vascular shadows and encroachment of the heart shadow in Cor pulmonale ane pulmonary hypertension. There may be cardiomegaly

2. Complete blood count- anaemia; leukocytosis in infection; polycythemia

3. Brain natriuretic peptide (BNP) or NT-proBNP – suspected heart failure

4. Urea, creatinine, electrolytes, and calcium

5. TSH- rule out other diagnoses

6. Elevated bicarbonate- chronic hypercapnia

7. Testing for alpha one antitrypsin

8. Pulmonary function tests- obstructive picture

9. Helium dilution technique- for lung volume measurement

10. HRCT- enables characterization and quantification of emphysema

11. Pulse oximetry and arterial blood gases

Assessing the severity

  • Traditionally based on FEV% predicted- the spirometric classification

Differential diagnosis

  • Chronic bronchitis
  • Chronic asthma
  • Bronchiectasis
  • Central airway obstruction
  • Tuberculosis
  • Constrictive bronchiolitis
  • Heart failure

Management

Goals;

  • reduce frequency and severity of exacerbations
  • Improve breathlessness
  • Improve health status and prognosis

1. Reducing exposure to noxious agents

  • Cessation of smoking
  • Use of nonsmoking cooking devices

2. Bronchodilators

  • Mild disease- short-acting
  • Moderate to severe disease- long-acting
  • Oral bronchodilators, e.g., theophylline, in those who can’t use inhaled- although monitoring is required

3. Oral glucocorticoids

  • Useful during exacerbations. Maintenance therapy causes osteoporosis and impaired muscle function and should be avoided

4. Combined inhaled glucocorticoids and bronchodilators

  • Improves lung function, reduces exacerbations, and improves the quality of life
  • However, it may increase the risk of pneumonia in the elderly

5. Exercise- should be encouraged at all stages.

  • Accompanied by improvement in exercise tolerance and health status

6. Oxygen therapy-

  • improves survival in those with severe hypoxemia. More significant benefits are observed in those who use it for more than 20 hours in a day
  • Ambulatory oxygen should be considered Olin those who desaturate on exercise.

7. Surgery-

  • lung volume reduction surgery where peripheral emphysematous tissue is removed to reduce hyperinflation and work of breathing
  • Bullectomy- when large bullae compress surrounding normal lung tissue

8. Others- influenza and pneumococcal vaccination, nutritional care, management of depression and social isolation, and palliative care

Acute COPD exacerbation

  • Triggered by bacteria, viruses, or a change in air quality
  • It May be accompanied by respiratory failure and fluid retention
  • Many patients can be managed at home with antibiotics, increased bronchodilator therapy, and oral glucocorticoids
  • Referral to hospital- the presence of cyanosis, altered consciousness, or peripheral edema

Management

1. Oxygen therapy- controlled oxygen at 24 or 28% should be used. A high concentration of oxygen leads to respiratory depression. The aim is to maintain a PaO2 of more than 60mmHg

2. Bronchodilators

  • Nebulised short-acting beta two agonist plus an anticholinergic
  • Maybe driven together with oxygen

3. Glucocorticoids

  • Oral Prednisone 30mg for ten days

4. Antibiotics

  • Recommended for those with increased sputum amount and purulence or breathlessness
  • Aminopenicilli, a macrolide or tetracycline
  • Co-amoxiclav in areas of beta-lactamase production

5. Noninvasive ventilation

  • For patients whose exacerbation is complicated by acidosis
  • Should be considered early in respiratory failure

6. Additional therapy

  • Diuretics for peripheral oedema
  • Use of respiratory stimulants, e.g., doxapram

7. Discharge

  • When stable and on their usual maintenance medication
  • Follow up

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