COPD Exacerbation Flashcards
1
Q
How is COPD defined?
A
- COPD: non-reversible airway obstruction with a combination of chronic bronchitis and emphysema.
- Airway obstruction: FEV1/FVC <0.7.
- Chronic bronchitis: chronic excess mucus secretion in the bronchial tree. Presents as a non-productive cough lasting >3 months for 2 consecutive years (‘smoker’s cough’).
- Emphysema: increase in air spaces beyond terminal bronchioles and destruction of alveolar walls without obvious fibrosis.
2
Q
What are the causes of COPD?
A
- 5% are due to smoking, and it occurs in 15% of smokers.
- 10-15% are occupational. Due to many of the same dusts that cause interstitial lung disease.
- 2-3% are due to α1-antitrypsin deficiency.
3
Q
What are the signs and symptoms of COPD?
A
- Symptoms:
- Cough with sputum.
- SOB
- Signs:
- ↑RR
- Wheeze
- Accessory respiratory muscle use.
- Hyperinflation
- Pulsus paradoxus.
4
Q
How can COPD be differentiated from asthma?
A
- Suggest COPD: smoker, older (>35 years old), chronic productive cough, progressive SOB.
- Suggest asthma: nocturnal symptoms, significant diurnal or day-to-day variability in symptoms.
5
Q
How is COPD diagnosed/classified?
A
- Diagnosis is based on history and spirometry.
Pulmonary function testing:
- Spirometry: FEV1/FVC <0.7, ↓FEV1, ↑TLC.
- Should be measured post-bronchodilator for diagnosis. However, full reversibility testing – quantifying change in response to therapy – is only needed if uncertainty re. asthma vs. COPD as diagnosis. Asthma suggested by large (>400 ml) response to bronchodilators or prednisolone, or 20% diurnal or day-to-day variability in peak flow readings.
- ↓DLCO (diffusing capacity of lung for CO, aka TLCO): normal in asthma, so helps distinguish, though not essential in practice.
- Classification by % FEV1 predicted:
- Mild: ≥80%. Symptoms must be present for diagnosis.
- Moderate: 50-79%.
- Severe: 30-49%.
- Very severe: <30%.
6
Q
Which other investigations should be performed in COPD?
A
- ABG: ↓O2, ↑CO2.
- CXR may show hyperinflation: >6 anterior ribs and flat/tented diaphragm. Other findings include large pulmonary arteries, bullae, loss of lung markings (emphysema), and cardiomegaly (cor pulmonale).
- CT not needed for diagnosis, but emphysema may be incidental finding which prompts consideration of COPD.
- ECG: RVH.
7
Q
How is COPD managed?
A
- Lifestyle and preventative
- Intense smoking cessation support. The only disease-modifying treatment: slows FEV1/FVC decline and increases survival. Also reduces SOB, exacerbations, and hospitalisations, and increases quality of life and exercise tolerance.
- Vaccines: one-off pneumococcal and annual flu.
- Pulmonary rehab: offer if there are exacerbations or disability. Helps many variables, including anxiety and depression; these may also respond to CBT. Not suitable if immobile or has severe IHD.
- Stepwise medical treatment
1. SOB or exercise limitation → PRN inhalers, either one of:
- Short acting β2 agonist (SABA) e.g. salbutamol, which is continued at all stages.
- Short acting muscarinic antagonist (SAMA) e.g. ipratropium.
- Persistent SOB or exacerbations → regular inhalers, either one of:
* Combination long-acting muscarinic antagonist (LAMA e.g. tiotropium, an M3 antagonist) plus long-acting β2 agonist (LABA e.g. salmeterol, formoterol). First line for most.
* Combination LABA plus inhaled corticosteroid (ICS) e.g. Seretide (salmeterol + beclometasone), Symbicort (formoterol + budesonide). Consider if there are asthmatic features such as prior diagnosis of asthma or atopy, eosinophilia, or substantial FEV1 or peak flow variability. ICS increases the risk of pneumonia in COPD, but does not affect (or even reduces) mortality risk.
- Persistent SOB or exacerbations → regular inhalers, either one of:
- Still persistent:
* Triple therapy: LAMA+LABA+ICS.
- Still persistent:
- Further options in severe disease:
* Home nebulizers.
* Oral immunomodulators: prednisolone, roflumilast (PDE-4 inhibitor).
* Prophylactic azithromycin three times per week if frequent/prolonged exacerbations with sputum.
* O2 therapy: short-burst for those who desaturate on exertion, long-term (LTOT) if chronically hypoxic.
* Non-invasive ventilation: consider long-term if hypercapnic or acidotic on LTOT.
- Further options in severe disease:
- Adjuncts and alternatives:
- Theophylline PO if inhaled therapy not possible.
- Carbocisteine, a mucolytic, if there is a chronic productive cough.
- Surgical treatment
- Lung volume reduction surgery (LVRS), namely upper lobe resection. Offer if SOB and severe COPD, but well enough for surgery (6-minute walk test >140 m).
- Bullectomy, like LVRS, removes areas of dead air space, but is more limited. Offer if SOB and bulla >⅓ of hemithorax.
- Transplant if nothing else works in severe disease.
8
Q
What complications can occur in COPD patients?
A
- Complications
- Exacerbations
- Chronic type 2 respiratory failure. Respiratory acidosis is compensated for with raised HCO3- and hence normal pH, but this can decompensate in exacerbations.
- Pulmonary hypertension and right heart failure (cor pulmonale).
- Anxiety and depression.
- Bullae: dilated air spaces in lung which may require surgical excision due to compression of surrounding lung.
9
Q
What are the pros and cons of long term oxygen therapy and in which patients might it be indicated?
A
- Home nebulizers for COPD
- Pros: easy, fast onset, and maximal dose uptake.
- Cons: worse side effects (↑dose), expensive, requires maintenance, patient may delay seeking help, and not portable.
- So only give it if nothing else works.
- Long-term oxygen therapy (LTOT) for COPD
Benefits
- ↓Mortality
- ↑Quality of life.
- Slows progression of cor pulmonale.
- Risks
- Respiratory depression if target sats too high.
- Burns from ignition: continued smoking is a contraindication.
- Indications
Consider LTOT if they have any one of:
- Very severe disease (FEV1 <30% expected).
- Signs of hypoxia: cyanosis, polycythaemia, O2 sats <92%.
- RHF signs: ↑JVP, peripheral oedema.
- Assess need with 2 ABGs, 3 weeks apart, and give LTOT if:
- pO2 <7.3kPa or…
- pO2 <8kPa plus any one of polycythaemia, peripheral oedema, or pulmonary HTN.
- Management
- Target O2 sats: 88-92%.
- Must be used for ≥15 hours per day.
- Can also have ambulatory O2 prescribed if they want to use outside the home and they have exercise desaturation.
10
Q
What may cause an acute exacerbation of COPD?
A
- Causes
- Upper or lower respiratory tract infections, due to viruses or bacteria such as Strep. pneumo, H. influenzae, or Moraxella catarrhalis.
- Pollution
- Drug changes.
- Co-morbidities: HF, PE.
11
Q
How can an acute exacerbation of COPD be managed from home?
A
- IPAD:
- Increase frequency or double dose of their short-acting bronchodilators.
- Prednisolone PO 1-2 weeks.
- Antibiotics only if there is purulent sputum. Amoxicillin or Doxycycline PO 5 days. Culture only necessary if initial antibiotic ineffective.
- Give those at risk a back-up course of steroids PO and antibiotics so they can self-manage.
12
Q
What are the indications for admitting a patient with an acute exacerbation of COPD into hospital? How is acute COPD exacerbation managed in hospital?
A
- Indications:
- Severe SOB.
- SaO2 <90%.
- Cyanosis
- Generally unwell, reduced activity, or altered mental status.
- Not coping, especially if living alone.
- Worsening oedema.
- On LTOT.
- Investigate fully:
- Bedside: ABG, ECG.
- Bloods: FBC, U+E.
- Imaging: CXR, and consider echo.
- Micro: sputum culture, and blood culture if fever.
- Treatment, VENTS:
- Give 24-28% O2 through a Venturi mask if sats <90%. Target O2 sats 88-92%.
- Nebulized SABA ± SAMA. Stop LAMA while using SAMA.
- Theophylline IV if there is a poor response.
- Steroids, ideally prednisolone PO 1-2 weeks.
- Consider non-invasive ventilation (NIV) with BIPAP (if pH 7.25-7.35), or even invasive ventilation if required (if pH <7.25).
- At discharge, arrange 6 week follow up.