Chronic Obstructive Pulmonary Disease

last authored: Sept 2009, David LaPierre

 

Introduction

Chronic Obstructive Pulmonary Disease (COPD) is the only major killer on the rise in Canada, and is currently the fourth leading cause of death in adults. It accounts for 10% of bed occupancy in most hospitals.

 

COPD is characterized progressive dyspnea and is caused by irreversible or poorly reversible airflow limitation, lung hyperinflation, and systemic manifestations due to a combination of emphysema, chronic bronchitis, and chronic bronchiolitis within the same person. This is contrasted with asthma, a chronic inflammatory disorder characterized by airway hyperactivity and reversible airway obstruction, as well as cystic fibrosis or bronciectasis.

 

An acute exacerbation of COPD (AE-COPD) is defined as at least two of: worsening SOB, increased sputum production, or increased sputum purulence.

 

 

The Case of...

clinical presentation and diagnosis

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Causes and Risk Factors

 

Smoking

Smoking is the cause of COPD in over 90% of cases, although only 20% of smokers develop clinically significant COPD, suggesting genetic involvement as well.

but can also result from exposure to air pollution, occupational hazards, infections, and immunological reactions (check this last one). Women who smoke are more susceptible to disease than are men.

 

Prevalence is associated with increasing age, lower SES, and smoking.

 

Most nonsmokers show a decline in FEV1 of 35-40 ml/year. This rate is increased to 45-60 ml/year in smokers, and up to 70-120 ml/year in people apparently genetically susceptible.

 

Alpha-1 antitrypsin deficiency accounts for less than 1% of all cases.

 

Globally, the most important risk factors are indoor air pollution, especially biomass used as fuel, and tobacco use. Outdoor air pollution is less important.

 

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Pathophysiology

COPD is characterized by mild chronic inflammation of the airways, parenchyma, and vasculature.

 

Macrophages, CD8+ lymphocytes, and neutrophils are all involved, and a variety of mediators, including leukotriene B4, IL-8, TNF, and others, damage lung structures and sustain inflammation.

 

An imbalance between proteases and antiproteases appears involved, as evidenced by α1-AT deficiency. An imbalance in oxidant-antioxidant levels is also important.

Tobacco smoke recruits neutrophils and macrophages, both which release elastase. Smoke also leads to the inactivation of alpha-1 antitrypsin.

With advanced disease, large abnormal airspaces can lead to blebs or bullae. Their rupture can lead to pneumothorax.

 

Decreased elastic recoil leads to hyperinflation, increased residual volumes and FRC, and total lung capacity. Diaphragmatic flattening reduces contractile efficiency.

 

Emphysema

Emphysema describes the rupture or fragmentation of alveolar walls, without obvious fibrosis, leading to airspace enlargement.

It is classified according to its lobular distribution.

Centriacinar emphysema is the most common form, affecting the central or proximal acini located on respiratory bronchioles while sparing the distal sacs. It is more common in the upper lobes. Centriacinar emphysema is associated with heavy smoking, and walls often contain a large amount of black pigment. Smoke particles predominantly impact the bronchiole bifurcations.

Panacinar (panlobular) emphysema affects the entire acinus, more commonly in the lower zones of the lung. It is associated with α1-antitrypsin deficiency.

Paraseptal diease usually occurs in upper lobes, often caused by spontaneous pneumothorax.

 

 

Chronic bronchitis

In chronic bronchitis, mucus hypersecretion and goblet cell hyperplasia follow chronic irritation by tobacco smoke or other factors such as grain, cotton, or silica dust. Many of these changes appear to be mediated by EGFR. Increases in mucus gland size can be estimated by the Reed index, or the proportion of the wall thickness taken up by the mucous layer. Above 0.4 is considered pathologic.

Small airways can become obstructed by mucus, inflammation, and fibrosis.

Infection can be caused by decreased performance of the ciliary elevator and decreased clearing of bacteria by leukocytes, both mediated by smoking.

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Signs and Symptoms

We want to be able to diagnose people early.

Chronic bronchitis is defined as persistent cough with sputum for at least three months in at least 2 consecutive years, in the absence of any other identifiable cause.

 

  • history
  • physical exam

History

Emphysema symptoms do not appear until at least one third of lung parenchyma is damaged.

 

Dyspnea is usually the first symptom, with a slow but steady progression. To imagine COPD dyspnea, take a deep breath in, breath out a little bit, and don't breathe below that anymore.

Dysnpea is increased with upper arm exercise as people lose the use of their accessory breathing muscles.

 

  • cough and wheezing
  • sputum production, depending on extent of associated bronchitis
  • recurrent chest infections
  • weight loss can be common and severe.

 

MRC Categorization of Dyspnea

5 grades

Assess actual exercise capacity; ask I could you walk up a hill?

Physical Exam

Physical exam is not diagnostic of COPD, and may underestimate severity. As disease progresses, lungs may appear hyperresonant to percussion. Auscultation can show few ronchi, wheezes, or faint crackles.

 

During late stages, patients can show evidence of increased work, sitting forward in a hunched position, using accessory muscles, and breathing through pursed lips.

People with COPD can develop barrel chests.

 

If pulmonary hypertension develops, cor pulmonale can follow. Heart gallop, distended neck veins, hepatojugluar reflux, and leg edema can all be present.

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Investigations

  • pulmonary function testing
  • diagnostic imaging

Pulmonary function testing

 

Decreased airflow can be detected with pulmonary function testing. Loss of elastic driving force reduces FEV1, the best indicator of disease. Decrease in FEV1 predominates over that of FVC, and the FEV1 / FVC is less than 70% in COPD.

 

Destruction of alveoli can lead to ventilation/perfusion (V/Q) mismatch, leading to hypoxemia.

It is essential to diagnose COPD early. The Canadian lung health test suggests current or ex-smokers over 40 years of age, who answer 'yes' to any of the following questions, should have spirometry done:

  • do you cough regularly?
  • do you cough up phlegm regularly?
  • do simple chores make you short of breath?
  • do you wheeze when you exert yourself or at night?
  • do you get frequent colds, lasting longer than other people you know?

 

Vital capacity decreases while FRC and RV increases and TLC increases or stays the same.

Obstruction leads to expiratory airflow limitation.

 

 

Classification by impairment of lung function: FEV1 value (GOLD guidelines)

  • >80%: mild
  • 50-80%: moderate
  • 30-50%: severe
  • <30%: very severe

 

PFT volumes are necessary for diagnosis of COPD.

Diagnostic Imaging

Chest X-rays do not often show early signs of COPD, but can later show hyperinflation, hyperlucency, diaphragmatic flattening, and bullous formation. If pleural abnormalities, lymphadenopathy, or mediastinal widening are seen, lung cancer should be suspected.

 

CT allows for detailed evaluation of lung tissue.

 

ECG can show evidence of right ventricular strain.

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Differential Diagnosis

Other conditions to rule out include:

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Management of COPD

Patients need to be self-managers, requiring education and collaboration with the health care team.

  • preventing progression
  • medications used
  • oxygen
  • AE-COPD
  • emergency treatment

Preventing Progression

Quitting smoking is the single most effective intervention to reduce the risk of developing COPD and the only intervention shown to slow its progression. (Fletcher and Peto, BMJ, 1977) has a good figure showing slowed decline of FEV1 in people who have quit smoking.

 

regular physical exercise could be considered a medical intervention with COPD.

  • ideally set up in rehab programs to ensure exercise is done effectively and safely
  • in Nova Scotia, there are exercise training programs in many DHAs
  • reduce dyspnea, increase exercise endurance, improved QoL, other

close follow-up and disease monitoring

bronchodilator therapy

Bronchodilators reduce dyspnea and air trapping while improving quality of life, though this may not be accompanied by improvement in spirometry. A combination of agents and/or long-acting medications is generally preferred. Bronchodilators can be delivered in metered-dose inhalers (MDIs) or nebulizers.

 

β-adrenoreceptor agonists

  • salbutamol 200 mcg QID prn
  • salmedrol

anticholinergic drugs

  • ipratropium bromide 40 mcg QID prn
  • tiotropium bromide 18 mcg once daily (+ Salbutamol prn)

methylxanthine medications are weak systemic sympathomimetic agents. Not first-line due to potential toxicity, though can be used in people who do not respond to inhaled agents.

  • theophylline

 

Anti-Inflammatory Agents

 

Chronic inhaled cortocisteroids appears to improve symptoms, decrease exacerbations, and increase survival.

  • fluticasone
  • budesonide

Systemic or IV corticosteroids can be used in acute settings, including AECOPD.

Oxygen

Oxygen is one of the only interventions shown to improve survival in COPD. It is recommended once saturation decreases to 88%, though can be used if end-organ damage becomes apparent.

Oxygen is frequently necessary in AE-COPD.

 

AE-COPD

 

prevention of exacerbations

vaccinations

  • annual influenza vaccination is the single-most effective intervention at reducing morbidity and mortality
  • pneumovax (not evidence-based), repeated every 5-10 years

 

AECOPDs: if sputum is purulent, treat with antibiotics. Emperic antibiotics should be used.

corticosteroids, typically 30-50 mg daily prednisone or equivalent for 7-14 days.

long term systemic steroids should not be used.

Emergency Treatment

Oxygen, inhaled β2 agonist, and consider anticholinergic, oral or IV corticosteroids

inhaled anticholinergic

admit to hospital

RF: consider aminophylline

  • heliox
  • IV magnesium
  • intubation and ventilation

 

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Consequences and Course

Severe disease can lead to pulmonary hypertension and cor pulmonale, respiratory acidosis, or massive pneumothorax.

 

AE-COPD

Most of the health care costs are associated with acute exacerbations of COPD (AECOPD). Most common pathogens include S. pneumoniae, H. influenzae, and Moraxella catarrhalis.

AECOPDs are sustained worsening of dysnpea, cough, or sputum production leading to an increase in the use of maintenance medications and/or supplementation with additional medication.

AECOPDs have a 2x mortality risk of acute MI patients.

patients can be taught to measure the colour of their sputum.

 

End-of-Life Care

People at increased risk of death include:

It is critical to ensure to have discussions surrounding end-of-life care.

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The Case of...

case #2, leading students to reflect on diagnosis and management

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Additional Resources

www.respiratoryguidelines.ca

Can Resp.J 2008 15(Suppl A)1A-8A.

 

Bourbeau et al, Arch Int Medicine 2003

Living Well with COPD (password: copd)

 

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Topic Development

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