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Acute COPD Exacerbation

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Overview

An acute exacerbation of chronic obstructive pulmonary disease (COPD) is a sudden worsening of COPD symptoms beyond normal day-to-day variations.

Epidemiology

  • Acute COPD exacerbations are the second most common cause of emergency hospital admissions

Causes

Bacterial causes

The most common bacterial organisms are:

  • Haemophilus influenzae – most common
  • Streptococcus pneumoniae
  • Moraxella catarrhalis

Other causes

Presentation

In general, patients may have:

  • Increased shortness of breath, cough, and wheezing
  • Increased sputum production which may suggest an infection
  • Purulent (green/pus-filled) sputum is suggestive of a bacterial infection
  • Malaise
  • Signs of respiratory failure:
    • Changes in mental status e.g. confusion
    • Morning headaches and increased daytime sleepiness suggest worsening hypercapnia
    • Accessory muscle use and pursed lip breathing
    • Cyanosis

Differential Diagnoses

Acute exacerbation of asthma

  • An increase in cough may be the first presenting symptom
  • People with asthma tend to have chest tightness
  • Treatment with a short-acting bronchodilator may lead to an improvement, making asthma more likely

Investigations

In hospital

  • Chest x-ray:
    • May show the opacities which can suggest infection
  • Arterial blood gases (ABGs):
    • Used to detect chronic hypercapnia and look for acute respiratory acidosis
    • These results should be compared against a baseline ABG
    • This is used to guide oxygen therapy, see management below
  • Full blood count:
    • To look for additional abnormalities such as infection or anaemia
  • U&Es:
    • To look for additional abnormalities
  • ECGs:
    • To look for additional abnormalities such as a myocardial infarction, right-heart enlargement, or arrhythmia
  • Sputum cultures:
    • May show bacterial infection
  • Blood culture:
    • If pyrexia is present – check for cyanosis

Referral to Hospital

Overview

If the patient has any of the following features, they may need hospital treatment:

  • Significantly worsened dyspnoea
  • Tachypnoea
  • Oxygen saturations <90%
  • Pursed-lip breathing
  • Use of accessory muscles
  • Mental status changes e.g. confusion or impaired levels of consciousness
  • New-onset cyanosis
  • Worsening peripheral oedema
  • Rapid onset
  • Significant reduction in activities of daily living
  • Inability to cope at home
  • Poor or worsening general condition
  • Already receiving home oxygen therapy

Carbon Dioxide Retention

Excessive oxygen administration can lead to type 2 respiratory failure in patients with chronic hypercapnia (CO2 retainers). It was previously thought that over-administering oxygen would cause a loss of hypoxic drive and lead to type 2 respiratory failure. This is not true and patients suffering an acute COPD exacerbation generally have a near-normal respiratory drive, regardless of if they are CO2 retainers or not.

The true reasons for this phenomenon are due to two factors:

  • Ventilation/perfusion (V/Q) mismatches:
    • In patients with COPD, hypoxia leads to vasoconstriction in the lungs leading to changes in alveolar V/Q ratios. This is to optimise their gas exchange.
    • Over-administering oxygen undoes this and increases blood flow to damaged parts of the lung, leading to an increased V/Q mismatch and more dead space (regions of the lung that are not involved in gas exchange)
  • The Haldane Effect
    • Deoxygenated haemoglobin binds to CO2 with greater affinity than oxygenated haemoglobin. Over-oxygenation causes a shift of the CO2 dissociation curve to the right – this is the Haldane effect.
    • Patients with COPD may not be able to increase their respiratory rate to compensate for the increased amounts of dissolved CO2.

Management

In primary care

  • 1st-line: increase dose/frequency of short-acting bronchodilators + 30 mg oral prednisolone for 5 days
  • Give antibiotics if there are clinical signs of pneumonia or the sputum is purulent:
    • Options are: amoxicillin, clarithromycin, or doxycycline

Oxygen

Regarding oxygen, any patient who is acutely critically ill (e.g. anaphylaxis or shock) should initially be treated before ABGs with high-flow oxygen via a reservoir mask at 15 L/min, irrespective of their past medical history. Hypoxia is more likely to kill them than hypercapnic respiratory failure.

  • All patients who are not critically ill with COPD should be given oxygen titrated to reach 88-92% before ABGs are performed
  • Once ABGs have been done, oxygen therapy can be adjusted:
    • If the patient has known to be hypercapnic or the ABG shows a normal pCO2 and raised bicarbonate, their target should be 88-92%
      • This is due to the risk of hypercapnic (type 2) respiratory failure
    • If the pCO2 is normal, aim for 94-98%
    • If the pH is 7.25 – 7.35, non-invasive ventilation (NIV) should be considered in the form of bilevel positive airway pressure (BiPAP).

Medical treatment

  • Salbutamol and ipratropium nebulisers
  • Hydrocortisone (IV) or prednisolone (PO)
  • Antibiotics:
    • If sputum purulent/clinical signs of infection
  • Chest physiotherapy to help sputum
  • IV aminophylline

Ventilatory support

  • Non-invasive ventilation, particularly if the pH is between 7.25-7.35:
    • This is in the form of bilevel positive airway pressure (BiPAP)
  • Intubation and ventilation, particularly if the pH is <7.25

All patients

  • Give prednisolone 30 mg daily for 5 days

Monitoring

  • ABGs should be repeated regularly according to the response to treatment
  • Before discharge:
    • Check oximetry or ABG results are satisfactory
    • Perform spirometry
    • Arrange follow-up and home care

Complications

Prognosis

  • COPD exacerbations generally last for 7-10 days
  • COPD exacerbations requiring hospital admissions are associated with a mortality rate of 4% or higher if they require treatment in an intensive care unit
  • Recurrent exacerbations of COPD can accelerate the decline in lung function

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