see also:

• respiratory medicine
• asthma
• chronic bronchitis
• home oxygen

• COPD is the third leading cause of disease burden in Australia
• it is often under-diagnosed and many do not receive optimal medical care
• exacerbations can be caused by:
  • bacterial chest infection (although often over-diagnosed as colonisation by Haemophilus, Strept. pneumoniae is common)
  • viral infection
  • left ventricular failure
  • pulmonary embolism (PE)
  • air pollution
  • chest trauma and inappropriate use of sedatives can lead to sputum retention and hypoventilation

• 2017: regular use of bleach and disinfectants such as with cleaners and health care workers may increase risk by 30% ¹⁾

• Smoking is the most important risk factor in the development of COPD
• Consider COPD in all smokers and ex-smokers over the age of 35 years
• The diagnosis of COPD rests on the demonstration of airflow limitation which is not fully reversible
• If airflow limitation is fully or substantially reversible, the patient should be treated as for asthma
• Consider COPD in patients with other smoking-related diseases

• inhaled bronchodilators provide symptom relief in patients with COPD and may increase exercise capacity
• Long term use of systemic glucocorticoids is not recommended
• Inhaled glucocorticoids should be considered in patients with severe COPD with frequent exacerbations
• Pulmonary rehabilitation reduces dyspnoea, fatigue, anxiety and depression, improves exercise capacity, emotional function and health-related quality of life and enhances patients' sense of control over their condition
• Pulmonary rehabilitation reduces hospitalisation and has been shown to be cost-effective
• Prevent or treat osteoporosis
• Identify and treat hypoxaemia and pulmonary hypertension
• In selected patients, a surgical approach may be considered for symptom relief
• step-wise approach to Rx:
  • short-acting inhaled beta 2 adrenergic agonists (SABA) and/or short-acting anti-muscarinic anticholinergic agents (SAMA) as needed for symptom relief
  • long-acting inhaled beta 2 adrenergic agonists (LABA) and/or long-acting anti-muscarinic anticholinergic agents (LAMA) (with SABA as needed)
    • NB. combining LABA with LAMA is better than increasing doses of either
  • if remain symptomatic (FEV1 < 50% predicted and 2 or more exacerbations in a year) then add inhaled corticosteroid
  • if severe COPD with inadequate response, consider adding theophylline

• Smoking cessation reduces the rate of decline of lung function
• Treatment of nicotine dependence is effective and should be offered to smokers in addition to counselling
• Influenza vaccination reduces the risk of exacerbations, hospitalisation and death
• Mucolytics may reduce the frequency and duration of exacerbations
• Long-term home oxygen therapy (> 15 h/day) prolongs life in hypoxaemic patients (PaO₂ < 55 mmHg, or 7.3 kPa)

• COPD imposes handicaps which affect both patients and carers
• Enhancing quality of life and reducing handicap requires a support team
• Patients and their family/friends should be actively involved in a therapeutic partnership with a range of health professionals
• Multidisciplinary care plans and individual self-management plans may help to prevent or manage crises
  • see self management plans at lungnet.com.au
• Patients who take appropriate responsibility for their own management may have improved outcomes

• see COPDX exacerbations Mx
• Early diagnosis and treatment may prevent admission
• confirm exacerbation and assess severity:

• unless confused or comatose, even the sickest of patients can perform an FEV₁ manoeuvre
• if usual FEV₁ < 1.0L (ie. severe COPD):
  • the most important signs of a severe exacerbation will be worsening hypoxaemia, acute respiratory acidosis (carbon dioxide retention), or both.
• if usual FEV₁ > 1.0L (ie. mild-moderate COPD):
  • check FEV₁ and if < 1.0L or < 40% predicted then usually this can be regarded as a severe exacerbation, and thus perform ABG's in room air if possible:
    • A PaO₂ less than 60 mmHg (8 kPa) indicates respiratory failure, while a PaCO₂ greater than 45 mmHg indicates ventilatory failure.
  • if FEV₁ > 1.0L and > 40% predicted then probably not a severe exacerbation.
    • Multidisciplinary care may assist home management
• CXR and ECG:
  • These help to identify alternative diagnoses and complications, such as pulmonary oedema, pneumothorax, pneumonia, empyema, arrhythmias, and myocardial ischaemia.

• Inhaled bronchodilators are effective treatments for acute exacerbations
  • Inhaled beta-agonist (eg, salbutamol, 400–800 mcg; terbutaline, 500–100 mcg) and anticholinergic agent (ipratropium, 80 mcg) can be given by pressurised metered dose inhaler and spacer, or by jet nebulisation (salbutamol, 2.5–5 mg; terbutaline, 5 mg; ipratropium, 500 mcg). The dose interval is titrated to the response and can range from hourly to six-hourly.
• Systemic glucocorticoids reduce the severity of and shorten recovery from acute exacerbations
  • Oral glucocorticoids hasten resolution and reduce the likelihood of relapse.
  • Up to two weeks' therapy with prednisolone (40–50 mg daily) is adequate. Longer courses add no further benefit and have a higher risk of side effects.
• antibiotics:
  • Exacerbations with clinical signs of infection (increased volume and change in colour of sputum and/or fever, leukocytosis) benefit from antibiotic therapy
  • Antibiotics are given for purulent sputum to cover for typical and atypical organisms.
• Controlled oxygen delivery (28%, or 0.5-2.0L/min) is indicated for hypoxaemia
  • This is indicated in patients with hypoxia, with the aim of improving oxygen saturation to over 90% (PaO2 > 50 mmHg, or 6.7 kPa). Use nasal prongs at 0.5–2.0 L/minute or a venturi mask at 24% or 28%. Minimise excessive oxygen administration, which can worsen hypercapnia.
• Avoid sedatives
  • Narcotic analgesics and sedatives should be avoided, as these may worsen ventilatory failure and hasten the need for positive pressure ventilation
• sputum clearance
  • Patients who regularly expectorate or those with tenacious sputum may benefit from forced expiratory techniques.
  • If patients produce more than 25 mL sputum per day, or if mucus plugging with lobar atelectasis is present, physiotherapy incorporating the use of postural drainage and associated techniques such as percussion and vibration may help
• Non-invasive positive pressure ventilation (noninvasive positive pressure ventilation (NPPV or NIPPV) eg. CPAP or BiPAP) is effective for acute hypercapnic ventilatory failure
  • An improvement in respiratory rate and pH usually occurs within one hour of starting NIPPV
  • Failure to respond or further deterioration would indicate a need to consider intensive care unit admission
  • COPD patients who need intubation and mechanical ventilation have an inpatient mortality of up to 37%
  • The patient's wishes regarding intubation and resuscitation should ideally be documented before an admission for management of respiratory failure
• Involving the patient's general practitioner in a case conference and developing a care plan may facilitate early discharge

• Marked increase in intensity of symptoms
• Patient has acute exacerbation characterised by increased dyspnoea, cough or sputum production, plus one or more of the following:
  • Inadequate response to ambulatory management
  • Inability to walk between rooms when previously mobile
  • Inability to eat or sleep because of dyspnoea
  • Cannot manage at home even with home-care resources
  • High risk comorbidity condition — pulmonary (eg, pneumonia) or non-pulmonary
  • Altered mental status suggestive of hypercapnia
  • Worsening hypoxaemia or cor pulmonale
  • Newly occurring arrhythmia

• Severe dyspnoea that responds inadequately to initial emergency therapy
• Confusion, lethargy or evidence of hypoventilation
• Persistent or worsening hypoxaemia despite supplemental oxygen
• worsening hypercapnia (PaCO2 > 70 mmHg)
• severe or worsening respiratory acidosis (blood pH < 7.3)
• Assisted mechanical ventilation is required.

• unable to protect their airways
• are not spontaneously breathing
• who have severe facial injury or burns

• life-threatening refractory hypoxaemia (PaO2< 60 mmHg, or 8 kPa on 100% inspired oxygen)
• bronchiectasis with copious secretions
• severe pneumonia
• haemodynamic instability

• invasive mechanical ventilation is associated with increased ICU mortality and hospital mortality, although the cause of mortality appears to be related to the severity of the underlying disease and not mechanical ventilation per se, although mechanical ventilation does run risk of muscle atrophy which may impact ability to successfuly wean the patient.
• patients with COPD admitted to an ICU for an acute exacerbation have a substantial hospital mortality (24%). For patients aged 65 years or older, mortality doubles in 1 year from 30% to 59%. Median survival for the patients who died within 1 year was 30.5 days. The need for mechanical ventilation at ICU admission did not influence either short- or long-term outcomes.²⁾
• the decision to institute mechanical ventilation should be based on clinical judgment that integrates many clinical variables including patient's wishes not to be intubated, patient comorbidities and likely short term mortality whether intubated or not.

• A goal of mechanical ventilation is to prevent excessive work of breathing, while maintaining a work of breathing that is sufficient to prevent respiratory muscle atrophy. This can be achieved by using assisted modes of ventilation (ie, modes in which ventilator assisted breaths are triggered by the patient), including Assist-Control Ventilation (ACV), Intermittent Mandatory Ventilation (IMV), and Pressure Support Ventilation (PSV). In addition, IMV is frequently combined with PSV (IMV/PSV).³⁾
• for patients able to maintain an adequate inspiratory flow with Assist-Control Ventilation (ACV), then ACV is generally utilised
• other patients are generally managed with combined Intermittent Mandatory Ventilation (IMV) with Pressure Support Ventilation (PSV) so that the PSV reduces work of breathing during non-mandatory breaths.

• The patient should be in a clinically stable condition and have had no parenteral therapy for 24 hours
• Inhaled bronchodilators are required less than four-hourly
• Oxygen delivery has ceased for 24 hours (unless home oxygen is indicated)
• If previously able, the patient is ambulating safely and independently, and performing activities of daily living
• The patient is able to eat and sleep without significant episodes of dyspnoea
• The patient or caregiver understands and is able to administer medications
• Follow-up and home care arrangements (eg, home oxygen, home-care, Meals on Wheels, community nurse, allied health, GP, specialist) have been completed

• The COPD-X Plan: Australian and New Zealand Guidelines for the management of Chronic Obstructive Pulmonary Disease
• Video podcasts - COPD Exacerbations in the ED by Brian Rowe (54min)
• Aust Presc 2007 - Managing chronic obstructive pulmonary disease