COPD exacerbation

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Background

  • Persistent airflow limitation (FEV1:FVC < 0.70) that is progressive and not fully reversible
    • The new definition from the GOLD initiative avoids either chronic bronchitis (85%) and emphysema (15%); most patients have mixture of both
  • Although smoking is a major risk factor for developing COPD, only 15% of smokers actually develop COPD[1]
  • Characterized by a combination of parenchymal destruction and small airway disease with failure of gas exchange
  • Acute exacerbations due to increased V/Q mismatch, not expiratory airflow limitation
  • Relative chronic hypoxia present in many

Precipitants

Pseudomonas Risk Factors

  • Recent hospitalization (>2 days within previous 3 months)
  • Frequent antibiotic treatment (>4 courses within past year)
  • Severe underlying COPD (FEV1 < 50% predicted)
  • Previous isolation of pseudomonas

Clinical Features

Differential Diagnosis

Bronchoconstriction

Acute dyspnea

Emergent

Non-Emergent

Evaluation

CXR with hyperinflated lungs consistent with broncoconstriction.
  • VBG/ABG
    • Perform if SpO2 <90% or concerned about symptomatic hypercapnia, however its routine use is not recommended
    • Monitoring the patient's clinical status and pulse oximetry is often sufficient
    • The decision to start noninvasive ventilation or to intubate should be guided to by the clinical state of the patient, presence of fatigue and response to therapy
    • For every increase in PaC02 of 10 mmHg, the pH should change by 0.08
  • Peak flow
    • <100 L/min indicates severe exacerbation
  • CXR
    • Consider if concerned for alternative/additional diagnoses (e.g. pneumonia, CHF, pneumothorax, effusions)
  • Sputum culture
    • Usually not indicated except for patient with recent antibiotic failure
  • ECG
  • Blood tests add little to the treatment of a COPD exacerbation
  • GOLD Grading (based on post-bronchodilator FEV1/FVC less than 70%):
    • I (mild COPD) -> FEV1 ≥ 80% of predicted
    • II (moderate COPD) -> 50% ≤ FEV1 < 80% predicted
    • III (severe COPD) -> 30% ≤ FEV1 < 50% predicted
    • IV (very severe COPD) -> FEV1 < 30% of predicted

Management

Oxygen

  • Some COPD patients accustomed to relative hypoxia, thus higher oxygen levels may--> loss of hypoxic vasoconstriction-->increased shunt + increased alveolar dead space + haldane effect --> suppression of respiratory drive cause high levels of oxygen may cause loss of hypoxic vasoconstriction causing areas of increased shunt and increased alveolar dead space along with the Haldane effect and suppression of the respiratory drive.
    • Do not withhold O2 if SpO2 <88%
  • Maintain PaO2 above 60 mmHg or SpO2 88-92%
    • SpO2 >93% associated with higher inpatient mortality
  • If unable to correct hypoxemia with a low FiO2 consider alternative diagnosis
  • Adequate oxygenation is essential, even if it leads to hypercapnia
  • If hypercapnia leads to altered mental status, dysrhythmias, or acidemia consider Intubation

Albuterol/ipratropium

  • Improves airflow obstruction and treatment should involve rapid administration upon recognition of COPD exacerbation. [2]

Steroids[3]

Similar efficacy between oral and intravenous. Treatment options include:

  • Hydrocortisone 100-125mg Q6H x 5 days
  • Methylprednisolone 1-2mg/kg IV daily (usual adult dose 125mg)[4]
  • Prednisone 60mg x 1, then 40mg PO daily x 5 days
    • For outpatients a 5 day dose appears equally effective as longer doses and a taper is not required.[5]

Magnesium

  • Mechanism: bronchial smooth muscle relaxation
  • Studies have found that while helpful in asthma, results are mixed for COPD[6]

Antibiotics

Indicated for patients with purulent sputum, increased sputum production, or requiring Non Invasive Positive Pressure Ventilation[7] (NNT = 3 to prevent treatment failure and 8 to prevent death)[8]

  • Antibiotics for COPD exacerbations have an NNT of[9]:
    • 3:1 to prevent conservative treatment failure
    • 8:1 to prevent short-term mortality
    • 20:1 to cause diarrhea

Outpatient Healthy

Outpatient Unhealthy

Inpatient

Noninvasive ventilation (CPAP or BiPaP)

  • CPAP: start at low level and titrate up to max 15
  • BiPAP: Start IPAP 8 (max 20), EPAP 4 (max 15)

Outcomes

  • Improves acidosis and ease respiratory distress

Contraindications:

  • Uncooperative or obtunded patient
  • Inability to clear secretions, high aspiration risk
  • Hemodynamic instability
  • Upper airway obstruction, craniofacial trauma, recent craniofacial surgery

Mechanical ventilation

Indications:

  • Severe dyspnea with use of accessory muscles and paradoxical breathing
  • RR>35 bpm with anticipated clinical course for respiratory failure
  • Respiratory arrest
  • PaO2 <50 or PaO2/FiO2 <200
  • pH <7.25 and PaCO2 >60
  • Altered mental status
  • Cardiovascular complications (hypotension, shock, CHF)
  • Noninvasive ventilation failure


Consider ketamine for sedation for intubation (in combination with paralytic) as ketamine has bronchodilatory effect


General principles for ventilator settings

  • Consider pressure control to prevent markedly elevated peak pressures
  • Maximize expiratory time by modifying I:E ratio
  • If patient with worsening hypercarbia, may benefit from paradoxically decreasing respiratory rate to improve expiratory time and improve gas exchange

Disposition

Consider hospitalization for:

  • Marked increase in intensity of symptoms (e.g. sudden development of resting dyspnea)
  • Background of severe COPD
  • Worsening hypoxia or hypercarbia (from baseline)
  • Onset of new physical signs (e.g., cyanosis, peripheral edema)
  • Failure of exacerbation to respond to initial medical management
  • Significant comorbidities
  • Newly occurring arrhythmias
  • Diagnostic uncertainty
  • Older age
  • Insufficient home support

See Also

EBQ:NIPPV in COPD

References

  1. ↑ Bates C, et al. Chapter 73: Chronic Obstructive Pulmonary Disease. In: Tintinalli J. Tintinalli's Emergency Medicine. A comprehensive study guide. 7th ed. 2011: 511.
  2. ↑ Celli BR. Update on the management of COPD. Chest. Jun 2008;133(6):1451-62.
  3. ↑ Do systemic corticosteriods improve outcomes in COPD exacerbations? Feb 2016. Annals of EM. 67(2):258-259
  4. ↑ Eisner MD, et al: An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2010; 182:693-718
  5. ↑ Eisner MD, et al: An official American Thoracic Society public policy statement: Novel risk factors and the global burden of chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2010; 182:693-718
  6. ↑ Shivanthan MC, Rajapakse S. Magnesium for acute exacerbation of chronic obstructive pulmonary disease: A systematic review of randomised trials. Ann Thorac Med. 2014 Apr;9(2):77-80.
  7. ↑ GOLD collaborators
  8. ↑ Ram FS, Rodriguez-Roisin R, Granados-Navarrete A, et al. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006; 19(2):CD004403.
  9. ↑ Ram FS, et al. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006.19(2).
  10. ↑ Rothberg MB, et al: Antibiotic therapy and treatment failure in patients hospitalized for acute exacerbations of chronic obstructive pulmonary disease. JAMA 2010; 303:2035-2042
  11. ↑ Anzueto A, Miravitlles M: Short-course fluoroquinolone therapy in exacerbations of chronic bronchitis and COPD. Respir Med 2010; 104:1396-1403
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