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Chronic Obstructive Pulmonary Disease

Author: Katie Manning / Editor: Jason M Kendall / Reviewer: Grace McKay / Codes: CAP6, CAP9 / Published: 29/10/2018 / Review Date: 29/10/2021

 

Introduction

Context

It is estimated that there are 3 million people in the UK with COPD [2].

COPD cases comprise over 1 million hospital bed days every year in England [1]. 1 in 8 medical admissions are secondary to COPD [3]. This group of patients will commonly present to the Emergency Department when they suffer an exacerbation of their disease.

COPD is believed to be the only major cause of death whose incidence is on the rise in the UK and Britain has one of the highest death rates from this condition in Europe [3].

There are approximately 30 000 deaths/ year attributable to COPD [1].

It is therefore vital that the Emergency Physician has a good knowledge of COPD and its management in order to improve its associated morbidity and mortality. It is also important to recognise which patients may be safely treated in the community to avoid unnecessary admissions.

This session aims to outline the management of COPD relevant to the Emergency Department. In particular with reference to the evidence based guidelines published by the National Institute of Clinical Excellence in 2010 [4].

Definition

COPD is a respiratory disease characterised by airflow obstruction that is not fully reversible.

Airflow obstruction is defined as a value of <0.7 when a ratio of the FEV1 (Forced expiratory volume in 1 second) / FVC (Forced vital capacity) is measured.

A diagnosis of COPD should be considered in a patient over the age of 35 who presents with exertional breathlessness, cough, sputum production, wheeze or frequent winter bronchitis in the presence of risk factors [4].

By far the largest risk factor for COPD is smoking, although other risk factors include occupational exposure to fumes or dust, occupational exposure to tobacco smoke or alpha 1 antitrypsin deficiency.

Traditionally within the diagnosis of COPD there were considered to be two main subtypes, namely chronic bronchitis and emphysema. COPD is now the preferred term for all with the disease.

An exacerbation of COPD is defined as a worsening of the patients symptoms beyond their normal day-to-day variability. They will often have worse breathlessness, cough, increased sputum production and change in the nature of their sputum. Additional medication will usually be needed in order to treat the exacerbation.

Learning Bite

COPD is a respiratory disease characterised by airflow obstruction that is not fully reversible.

A diagnosis of COPD should be considered in a patient over the age of 35 who presents with exertional breathlessness, cough, sputum production, wheeze or frequent winter bronchitis in the presence of risk factors [4].

Pathophysiology

Chronicairway inflammation, triggered by the presence of pollution orcigarette smoke in the lungs, is thought to be key in COPD pathogenesis.

During an exacerbation of COPD there is an acute increase of inflammatory mediators which accelerate tissue damage [5].

This chronic versus acute inflammatory pathology may explain why patients experience a gradual decline in lung function over time, and worsen with an increased number of exacerbations

Airway abnormalities include [6]:

  • Chronic inflammation with increased neutrophils, macrophages and T lymphocytes
  • Increased number of goblet cells
  • Mucus gland hyperplasia
  • Fibrosis
  • Narrowing and reduction of small airways
  • Airway collapse

Lung parenchymal abnormalities include [6]:

  • Abnormal dilation or destruction of the respiratory bronchiole or alveolar sac

Pulmonary vasculature [6]:

  • Intimal hyperplasia and smooth muscle hypertrophy secondary to chronic hypoxic vasoconstriction

These changes cause increased airway resistance and expiratory airflow obstruction, which increases the work of breathing and reduces minute ventilation, potentially leading to hypercarbia. Airway destruction results in hypoventilation and ventilation/perfusion mismatch which causes hypoxaemia.

Aetiology of Exacerbations

Most COPD exacerbations are due to viral or bacterial infections of the respiratory tract, however in some cases they are caused by environmental pollution. Up to 30% have an unknown aetiology [5].

The main known causes [7] are as follows:

Viruses

  • Rhinovirus
  • Influenza
  • Para-influenza
  • Coronavirus
  • Adenovirus
  • Respiratory syncytial virus
  • Chlamydia pneumoniae

Bacteria

  • Haemophilus influenza
  • Streptococcus pneumoniae
  • Moraxella catarrhalis
  • Staphylococcus aureus
  • Pseudomonas aeruginosa

Pollutants

  • Nitrogen dioxide
  • Particulates
  • Sulphur dioxide
  • Ozone

While infection is by far the commonest case of an acute exacerbation of COPD it is important to consider other causes such as:

  • Pneumothorax
  • Pulmonary embolism
  • Intra-abdominal pathology
  • Cardiac failure
  • Metabolic disturbance

Learning Bite

Most COPD exacerbations are due to viral or bacterial infections of the respiratory tract, however environmental pollution may also trigger an exacerbation. Up to 30% of exacerbations have an unknown trigger.

 

Clinical assessment

History

Common presenting symptoms to the Emergency Department for patients with an exacerbation of COPD may be:

  • Breathlessness
  • Cough
  • Wheeze
  • Chest tightness
  • Increased or change in sputum production
  • Inability to cope at home
  • Reduced exercise tolerance
  • Fatigue
  • Confusion
  • Ankle swelling

Patients will often have an established diagnosis of COPD but there will be a proportion who have not been formally diagnosed so it is important to consider the diagnosis in those >35 years with risk factors for the disease.

Other important aspects of the history to consider are:

  • Past medical history especially any previous respiratory disease
  • Medication history including recent use of corticosteroids
  • Home oxygen use
  • Nebuliser use
  • Previous hospital admissions
  • Use of any invasive or non-invasive ventilation
  • Exercise tolerance normal and current
  • Social history especially housing, stairs, mobility, care support
  • Smoking history ideally the number of pack years should be determined
  • Previous ITU admissions

Exacerbations of COPD are more likely in winter and in those with previous exacerbations of their disease [8].

Examination

Important aspects of the clinical examination to note:

  • Vital signs including oxygen saturations, HR, BP, RR, temperature:
    • In severe exacerbations patients will be more likely to be tachycardic and tachypneic
    • However a tiring patient may have a reduced respiratory rate
  • Peripheral signs of respiratory disease such as:
    • Tar staining
    • Palmar erythema
    • Cyanosis
    • Asterixis
  • Increased work of breathing:
    • Use of accessory muscles
    • The patient may be holding themselves in the tripod posture
    • Pursed lip breathing
  • Reduced ability to speak in full sentences
  • The presence or absence of cyanosis
  • Presence of chest wall deformity or barrel shaped chest secondary to hyperinflation
  • Reduced chest wall movement
  • Chest percussion may show signs of hyper-resonance
  • Chest auscultation may show reduced air entry, wheeze, a prolonged expiratory phase +/- crepitations
  • Consciousness level may be normal or reduced
  • Signs of right heart failure such as raised JVP, peripheral oedema, hepatomegaly
  • Body mass index may be low secondary to reduced intake and increased calorie expenditure on work of breathing
  • Sputum assessment

 

Differential Diagnosis

Diagnosis of COPD

There is no one single test that can confirm a diagnosis of COPD.

In addition to a relevant clinical history and spirometry, at the time of initial diagnosis the patient should undergo the following investigations [4]:

  • Chest X-ray to exclude other pathology
  • Full blood count to identify anaemia and polycythaemia
  • Calculation of body mass index

Additional investigations to consider depending on individual factors may be [4]:

  • Serial home peak flow measurements to exclude asthma if diagnostic doubt
  • Alpha 1 antitrypsin if early onset of symptoms, minimal smoking history or a relevant family history
  • CT Chest to investigate CXR abnormality and/or exclude pulmonary embolism
  • Echocardiogram and ECG to assess for cor pulmonale
  • Sputum culture in cases of chronic productive cough.

Table 1: NICE Guideline 2010. Clinical factors that may help differentiate asthma and COPD [4]:

COPD_diagnosis

 

Investigation Strategies

Investigations

Investigations that should be performed in the ED when a patient is presenting with an exacerbation of COPD include:

  • Arterial blood gas analysis: to evaluate evidence of acidosis, hypercapnia, hypoxaemia and chronic metabolic compensation
  • CXR: to look for evidence of consolidation, exclude pneumothorax and exclude other pathologies which may cause increased breathlessness
  • ECG: to exclude other or concurrent causes of breathlessness such as ischaemic heart disease or signs of pulmonary embolism. In severe disease there may be signs of pulmonary hypertension such as peaked p waves or right ventricular hypertrophy
  • Full blood count: This may identify anaemia as a cause of breathlessness or show evidence of secondary polycythaemia.
  • Urea and electrolytes
  • Theophylline level if the patient is already on theophylline therapy
  • Sputum analysis: if sputum is purulent a sample should be sent for microscopy, culture and sensitivity
  • Blood cultures if pyrexia present

Learning Bite

Arterial blood gas analysis should be performed on arrival in patients who are breathless with acute exacerbations of COPD.

 

Management

Risk Stratification

The National Institute of Health and Clinical Excellence has published guidance on factors that should be considered when determining the most appropriate place for the treatment of patients with exacerbations of COPD (see Table 2).

Table 2: NICE 2010 Guideline. Factors to consider when deciding where to treat the patient [4]:

COPD_treatment_factors

NICE have also classified severity of airflow obstruction related to spirometry measurements (see Table 3).

Table 3: NICE guideline 2010. Severity of COPD airflow obstruction post bronchodilator [4]:

COPD_severity

Management

Bronchodilators and oxygen therapy:

  • Increased dose of short acting bronchodilators which can be inhalers or nebulisers as indicated [4]
  • The most commonly used bronchodilators in the ED are Beta 2 agonists such as salbutamol and terbutaline, and anticholinergics such as ipratropium bromide
  • Bronchodilators improve FEV and symptoms; there is thought to be no difference between the classes of short acting bronchodilators [9]
  • The recommendation is to increase the dose and frequency of a patients existing medication regime [9]
  • If a patient is acidotic or hypercapnic nebulisers should be driven by air not oxygen [4]
  • Oxygen should be given to maintain saturations in a targeted range which should normally be 88-92% [4]

Steroids:

  • Oral corticosteroids should be used in all patients admitted to hospital or in the community if their breathlessness interferes with their activities of daily living, unless there is a significant contraindication [4]
  • Steroids improve symptoms, FEV and PaO2 in moderate to severe exacerbation [9]
  • Steroid use reduces treatment failure, relapse and length of hospital stay [9]
  • Prednisolone 30mg should be given for 7 to 14 days [4]

Learning Bite

Corticosteroids should be given to all those admitted with an exacerbation of COPD and to those being treated at home where their symptoms are affecting their activity of daily living.

Antibiotics:

Antibiotics should be given to patients with an increase in purulent sputum, consolidation on CXR or clinical signs of pneumonia [4]
Empirical antibiotic therapy should be with aminopenicillin, macrolide or tetracycline unless local microbiological policy states otherwise [4]

Learning Bite

Antibiotics should be given to those with purulent sputum or those with clinical signs of pneumonia or CXR changes.

Theophylline / aminophylline:

  • Intravenous aminophylline should be considered only if there is an inadequate response to nebulised bronchodilators [4]. The loading dose of aminophylline should be omitted in patients taking oral theophylline
  • The dose of oral theophylline should be reduced at the time of an exacerbation if the patient needs concurrent macrolide or fluroquinolone antibiotics

Non-invasive ventilation:

  • Non invasive ventilation should be used as the treatment of choice for hypercapnic respiratory failure if optimal medical therapy has not been successful [4]
  • The Royal College of Physicians guideline [10] states that maximum medical treatment includes:
    • Controlled oxygen therapy to maintain SaO2 88-92%
    • Nebulised salbutamol 2.5-5 mg
    • Nebulised Ipratropium 500 micrograms
    • Prednisolone 30 mg
    • Antibiotic agent when indicated
  • NIV should be considered within 60 minutes of arrival to hospital in all patients with an exacerbation of COPD and a persistent respiratory acidosis (pH <7.35 7.26 andPaCO2 >6kPa) in whom the above treatment has been unsuccessful [10]
  • Non invasive ventilation used as an adjunct to standard care has been found to be associated with lower mortality, lower need for intubation, lower likelihood of treatment failure and shorter duration of stay in hospital [11]

Learning Bite

Those patients who are hypercapnic despite optimal medical therapy should be considered for non-invasive ventilation.

Inclusion / exclusion criteria for NIV:

  • Inclusion criteria for NIV are [10]:
    • Primary diagnosis of COPD exacerbation
    • Able to protect airway
    • Conscious and cooperative
    • Patients wishes considered
    • Potential for recovery of quality of life that will be acceptable to the patient
    • NIV can be considered in the unconscious if within a critical care setting or intubation is inappropriate
  • Exclusion criteria for NIV are [10]:
    • Life threatening hypoxaemia
    • Severe co-morbidity
    • Confusion/agitation
    • Facial burns/trauma/recent facial or upper airway surgery
    • Vomiting
    • Fixed upper airway obstruction
    • Undrained pneumothorax
    • Upper gastrointestinal surgery
    • Inability to protect the airway
    • Copious respiratory secretions
    • Patient moribund
    • Bowel obstruction
    • Intubation and ventilation is possible and would be in patients best interests
    • Patient declines treatment

Commencing NIV:

  • Before commencing NIV there should be a clear plan of escalation and ceilings of treatment [4]. This should be documented in the patient notes
  • NIV should be clearly prescribed, a full facemask should be used for the first 24 hours, an initial Inspiratory positive airway pressure (IPAP) of 10 cm H20 and Expiratory positive airway pressure (EPAP) of 4-5 cm of water should be used. This should be increased rapidly at a rate of approximately 5 cm of water every 10 minutes to a target of 20 cm H2O, or patient unable to tolerate further, or therapeutic response achieved [10].
  • Arterial blood gas (ABG) analysis should be performed at baseline, 1 hour after commencing NIV and 1 hour after changing settings
  • All patients should be on continuous pulse oximetry and ECG monitoring for the first 12 hours [10].
  • The decision to commence NIV should be made by a doctor of ST2 level or above or other competent designated health care professional, locally agreed

Indications for invasive mechanical ventilation:

  • A decision to intubate and proceed with mechanical ventilation should normally be made within 4 hours of starting NIV, as improvements should usually be apparent during this time [10]
  • Patients with COPD should be considered for ITU treatment when necessary [4], especially if they are more unwell i.e. pH < 7.26 [10]
  • The Global Initiative for Chronic Obstructive Lung Disease 2013 guideline [12] states the following may be indications for invasive mechanical ventilation:
    • NIV failure
    • Inability to tolerate NIV
    • Respiratory or cardiac arrest
    • Respiratory pauses with loss of consciousness or gasping for air
    • Reduced consciousness or uncontrolled agitation
    • Massive aspiration
    • Persistent inability to remove respiratory secretion
    • Heart rate <50 with loss of alertness
    • Haemodynamic instability unresponsive to fluid and vasopressors
    • Life threatening hypoxaemia
  • Mortality amongst ventilated COPD patients is lower than patients ventilated for non-COPD causes [12,13]. However the decision to admit to the intensive care unit will lie with a senior anaesthetist or intensive care consultant

Other therapy:

  • Hospital at home and assisted discharge schemes are safe, effective and should be considered in patients who would otherwise require hospital admission [4]
  • Patients should be advised and assisted with smoking cessation [4]

Learning Bite

Hospital at home and assisted discharge schemes are safe and effective and should be considered for whose who would otherwise require admission.

 

Prognosis & Followup strategies

Prognosis

One cohort study [14] has shown that predictors of increased mortality in COPD include:

  • Increasing age
  • Significant co-morbidity
  • Decreasing post bronchodilator FEV1
  • Those patients already on long term oxygen therapy
  • Increased number of COPD exacerbations, particularly those with 3 or more episodes
  • Increased number of hospital admissions

A further UK audit [15] has shown death in 14% of patients admitted to hospital within 3 months of admission. The most important prognosticators for death in this group were:

  • Poor performance status*
  • Low arterial pH on admission*
  • Presence of bilateral leg oedema*
  • Age >70
  • Home circumstances, particularly if the patient is in a nursing home
  • Unrecordable peak flow on admission
  • Pulse oximetry showing oxygen saturation under 86%
  • Intervention with assisted ventilation

The 3 marked with * were the 3 major independent predictors of mortality.

 

Safety pearls and Pitfalls

Pitfalls

  • Failure to consider a diagnosis of COPD in the presence of relevant symptoms and risk factors, even if the patient has not previously been formally diagnosed
  • Not all patients presenting with an exacerbation of COPD require admission to hospital. In addition to a specific clinical history, it is important to take a good social and functional history, as many of these factors will determine the need for admission. It is safe to treat many patients at home with the relevant local resources and support
  • While infection is common many patients do not have bacterial infection and will not have any benefit from receiving antibiotic therapy
  • Be aware of other causes of clinical deterioration of the patient with COPD such as pneumothorax and venous thromboembolism, especially if other risk factors are present

 

MedicoLegal and other considerations

Key Learning Points

  • A diagnosis of COPD should be considered in patients over 35 years with a history of breathlessness, wheeze, cough, sputum production, frequent winter bronchitis, in the presence of risk factors for disease (LEVEL D EVIDENCE)
  • Hospital at home and assisted discharge schemes are safe and effective and should be considered for whose who would otherwise require admission (LEVEL A EVIDENCE)
  • Corticosteroids should be given to all those admitted with an exacerbation of COPD (LEVEL A EVIDENCE) and to those being treated at home where their symptoms are affecting their activity of daily living (LEVEL B EVIDENCE)
  • Antibiotics should be given to those with purulent sputum (LEVEL A EVIDENCE) or those with clinical signs of pneumonia or CXR changes (LEVEL B EVIDENCE)
  • Arterial blood gas analysis should be performed on arrival (LEVEL D EVIDENCE)
  • Those patients who are hypercapnic and acidotic despite optimal medical therapy should be considered for non-invasive ventilation (LEVEL A EVIDENCE)

 

References

  1. British Thoracic Society. The burden of lung disease: a statistical report from the British Thoracic Society. 2nd edn. London: British Thoracic Society, 2006.
  2. Stang P, Lydick E, Silberman C et al. The prevalence of COPD. Using smoking rates to estimate disease frequency in the general population. Chest 2000;117:354S- 359S.
  3. British Lung Foundation. Lost in translation: bridging the communication gap in COPD. London. British Lung Foundation: 2006.
  4. National Institute for Health and Clinical Excellence 2010. Chronic obstructive pulmonary disease. Management of chronic obstructive pulmonary disease in adults in primary and secondary care. Clinical Guideline 101. London: NICE.
  5. Sapey E, Stockley R. Review Series. COPD Exacerbations 2: Aetiology. Thorax 2006;61:250-258.
  6. Rennard S. Chronic obstructive pulmonary disease: definition, clinical manifestations, diagnosis and staging. In: UpToDate, Stoller JK (Ed), UpToDate,Waltham, MA, 2014.
  7. Wedzicha J. Exacerbations. Etiology and pathophysiological mechanisms. Chest 2002;121:123S- 141S.
  8. Donaldson G, Wedzicha J. Review Series. COPD Exacerbations 1: Epidemiology. Thorax 2006;61;1:164-168.
  9. Rodriguez-Roisin R. Review Series. COPD Exacerbations 5: Management. Thorax 2006;61:535-544.
  10. Royal College of Physicians, British Thoracic Society, Intensive Care Society. Chronic obstructive pulmonary disease: non-invasive ventilation with biphasic positive airways pressure in the management of patients with acute type 2 respiratory failure. Concise Guidance to Good Practice Series, No 11. London: RCP, 2008.
  11. Lightowler J, Wedzicha J, Elliott M et al. Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis. BMJ 2003;326:185-187.
  12. Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2014. Available from: http://www.goldcopd.org
  13. Esteban A, Anzueto A, Frutos F et al. Characteristics and outcomes in adult patients receiving mechanical ventilation, a 28 day international study. JAMA 2002;287:345-355.
  14. Soler-Cataluna J, Martinez-Garcia M, Roman Sanchez P et al. Severe acute exacerbations and mortality in patients with chronic obstructive pulmonary disease. Thorax 2005;60:925-931.
  15. Roberts C, Lowe D, Bucknall C et al. Clinical audit indicators of outcome following admission to hospital with acute exacerbations of chronic obstructive pulmonary disease. Thorax 2002;57:137-141.

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1 Comments

  1. Thomas Parish says:

    Excellent summary of ways to differentiate COPD and Asthma

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