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Chronic obstructive pulmonary disease


Essentials

  • 1

    Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation that is not fully reversible.

  • 2

    The majority of exacerbations of COPD are due to infection, but other important precipitants must be excluded.

  • 3

    It is prudent to control oxygen flow rate to achieve an arterial oxygen saturation of approximately 88% to 92% to ensure correction of hypoxia while avoiding the complication of hyperoxic hypercapnia.

  • 4

    The use of non-invasive ventilation in acute respiratory failure is associated with reduced mortality, reduced rates of intubation and reduction in treatment failure.

  • 5

    Bronchodilators and systemic steroids are recommended for acute exacerbations.

Introduction

Chronic obstructive pulmonary disease (COPD) is a major public health problem causing chronic morbidity and mortality throughout the world. It is characterized by airflow limitation that is not fully reversible, is usually progressive and is associated with an abnormal inflammatory response of the lung to noxious particles or gases. An acute exacerbation of COPD is a heterogeneous event believed to be caused by complex interactions between the host, respiratory viruses, airway bacteria and environmental pollution. It is clinically characterized by an increase in the patient’s baseline dyspnoea, cough and/or sputum that is beyond normal day-to-day variations, is acute in onset and may warrant a change in regular medication. COPD is a complex chronic systemic inflammatory disorder with multiple extrapulmonary manifestations and acute exacerbations that may include life-threatening respiratory failure.

Aetiology, genetics, pathogenesis and pathology

The most important factor leading to the development of COPD is cigarette smoking. Less common factors include genetic disorders, such as α 1 -antitrypsin deficiency, occupational exposures and exposure to air pollution. Only 30% of smokers develop clinically significant COPD.

The airflow limitation seen in COPD is due to a combination of luminal obstruction with hypersecretion of mucus, disruption of alveolar attachments and mucosal and peribronchial inflammation and fibrosis (obliterative bronchiolitis).

COPD causes chronic and increasing dyspnoea with a reduction in exercise tolerance. It is characterized by intermittent acute exacerbations (usually due to intercurrent infection). Chronic complications include pulmonary hypertension, cor pulmonale, secondary polycythaemia, bullous lung disease, medication-related complications (e.g. osteoporosis), weight loss and increasingly poor quality of life.

There is a high incidence of comorbid bronchiectasis in COPD patients, which is associated with a poorer prognosis. These patients are more likely to be male, have longer smoking histories, produce greater daily sputum and have more frequent exacerbations. They are more likely to be colonized by potentially pathogenic micro-organisms, including Pseudomonas aeruginosa (requiring broader antibiotic therapy during exacerbations).

Epidemiology

Projections from the Global Burden of Disease Study suggest that COPD will be the fifth leading cause of disability-adjusted life years lost worldwide by the year 2020. COPD is found in 7.5% of Australians aged 40 years or over and ranks sixth among the causes of death in Australian men and women. In the New Zealand population, it ranks fifth.

Clinical features

History

Most patients with COPD experience a slow, steady deterioration in their respiratory function. Most emergency department (ED) presentations are the result of a superimposed acute exacerbation. As the disease becomes more severe, the frequency of exacerbations also increases. It is important to have a good understanding of the patient’s baseline function. Questioning to determine this should include the following :

  • Questions to establish diagnosis:

    • Has the patient been diagnosed with COPD, and if so, when?

    • When did symptoms first develop?

    • If pulmonary function tests were undertaken, what were their most recent results?

    • Is the patient a smoker (past or present) and what are the total pack-years?

    • Are there any other risk factors, such as family history of COPD or α 1 -antitrypsin deficiency?

    • Who is the physician managing this?

  • Questions to establish severity:

    • Current medications: short- and long-acting bronchodilators, antimuscarinic agents, steroids (inhaled or oral), home oxygen and any other medications.

    • When the patient is well, what is his or her usual level of exercise tolerance?

    • Does the patient limit his or her physical activity to avoid breathlessness?

    • What is the patient’s baseline peak expiratory flow rate?

    • What is the patient’s incidence, frequency and severity of hospital admissions over the last few years (specifically including non-invasive ventilation [NIV] or intubation).

    • What is the patient’s current body mass index (BMI)?

    • Has the patient experienced a recent weight loss?

  • Nature of acute deterioration (seeking baseline and current features):

    • Fever

    • Cough

    • Sputum quantity and colour

    • Chest pain

    • Ability to walk between rooms

    • Ability to eat and sleep with current dyspnoea

    • Current increase in out-patient therapy and duration of escalation

    • High-risk comorbid conditions making out-patient therapy challenging (ischaemic heart disease, morbid obesity, congestive cardiac failure, diabetes)

    • Inhaler technique and compliance with medications

    • Presence of medications that may exacerbate COPD (e.g. β-blockers, sedatives)

    • Is there an advanced care plan and has the patient considered goals-of-care/end-of-life issues?

  • Questions regarding complications should also be asked.

Examination

Exacerbations of COPD can be immediately life-threatening for some individuals and require immediate management of the airway and breathing with concurrent assessment. Clinical features of severe respiratory compromise or failure include the following:

  • Work of breathing

    • Tachypnoea

    • Posture (pursed-lip breathing, tripoding)

    • Ability to speak (sentences, phrases, words)

    • Intercostal recession or poor respiratory effort

  • Hypercapnia

    • Altered conscious state, somnolence, exhaustion

    • Miosis/smaller pupils

  • Auscultation

    • Silent chest

    • Poor air-entry in lower lung zones

  • Clinical evidence of tension pneumothorax

    • Tracheal deviation

    • Unilateral absence of breath sounds

    • Distension of neck veins

  • Profound hypoxia

    • Central cyanosis

    • Hypoxia confirmed with either blood gas sampling or good trace oximetry

Once critical issues have been managed, assessment focuses on acute and chronic features of COPD. Acute examination findings may include non-specific features (tachypnea, tachycardia, hypotension, atrial fibrillation or multifocal atrial tachycardia), infection (fever, focal crepitations, coloured/blood-stained sputum) and bronchospasm. Chronic examination findings are varied due to the heterogeneity of the disease. Patients may be thin and barrel-chested through to oedematous with cor pulmonale.

Important precipitants and complications to search for include infection, sputum retention, bronchospasm, air pollution, reduction in respiratory drive (e.g. sedatives), chest injuries, reduced respiratory muscle strength (e.g. metabolic or neuromuscular cause, other unrelated illness that increase metabolic demand). Important differential diagnoses include decompensated left ventricular failure, acute coronary syndromes, pulmonary embolism, pneumothoraces and bullae.

Classification of severity and typical stepwise management for each phase of COPD

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