EM@3AM: Acute COPD Exacerbation

Author: Brit Long, MD (@long_brit, EM Attending Physician, San Antonio, TX) // Edited by: Alex Koyfman, MD (@EMHighAK, EM Attending Physician, UTSW / Parkland Memorial Hospital)

Welcome to EM@3AM, an emDocs series designed to foster your working knowledge by providing an expedited review of clinical basics. We’ll keep it short, while you keep that EM brain sharp.

A 58-year-old male presents with severe shortness of breath, productive cough with purulent sputum, and decreased ability to ambulate at home. He has COPD and is on oxygen at home. Several days ago he noted worsening congestion, myalgias, and cough. He tried to use his nebulizer at home, but his cough worsened. He is now severely short of breath and unable to complete his activities of daily living. He has a 40 pack year history of tobacco use, and his only other known medical issue is hypertension.

Triage vital signs (VS): BP 153/81, HR 107, T 99.9 Oral, RR 28, SpO2 81% on 2L.

Physical exam reveals a patient who appears older than stated age in respiratory distress. The oral mucosa is dry, his heart is normal except for tachycardia, and you hear decreased air movement bilaterally and distal wheezes. EKG: sinus tachycardia at 110 beats per minute, but otherwise unactionable.

What is the diagnosis, and what are your next steps?

Answer: Acute COPD Exacerbation

  • Background: Pathophysiology consists of persistent airflow obstruction, usually progressive and associated with abnormal inflammation.
    • Two primary forms: chronic bronchitis (85%) and emphysema (15%).
    • Chronic bronchitis: chronic productive cough for 3 months in each of 2 successive years.
    • Emphysema: destruction of alveoli and bronchioles, resulting in alveolar hypoventilation.
    • Both result in chronic lower airway obstruction and decreased expiratory airflow, reducing total minute ventilation and increasing respiratory work.
    • Though smoking is the predominant risk factor for COPD, only approximately 15% of smokers develop COPD.
    • Tobacco smoke, chemical exposure, occupational dust, pollution, alpha1-antitrypsin deficiency are risk factors.
    • Epidemiology: over 700,000 hospitalizations per year. Increasing prevalence in women, who account for over half of COPD deaths.
  • Acute Exacerbation:
    • Primarily due to increased V/Q mismatch rather than expiratory airflow limitation.
    • Precipitants: infection (75% of cases), cold weather, pollution, opioid/sedative agents, PE, pneumothorax, pollution, medication non-compliance, poor nutrition.
    • Features: increase in cough, sputum, dyspnea; hypoxemia, tachypnea, hypertension, confusion/altered mental status, cyanosis, hypercapnia (resulting in respiratory acidemia).
    • Criteria typically include 2 of 3 cardinal symptoms: increased dyspnea, increased sputum volume, increased sputum purulence.
    • Patients may try to relieve dyspnea with accessory muscle use, tripod position, pursed-lip exhalation. These signs and patients with confusion, diaphoresis, and poor air movement are evidence of impending respiratory failure.
    • Risks for Pseudomonas: recent hospitalization, severe COPD (FEV1 < 50%), > 4 antibiotic courses in past year, previous Pseudomonas infection.
  • ED Evaluation for Acute Exacerbation:
    • Assess hemodynamic and respiratory status and intervene if necessary (ie NIPPV, IVs, monitors).
    • History: COPD exacerbation symptoms, smoking, daily function/tolerance, home oxygen use, prior hospitalizations/intubations/ICU, comorbidities (CHF, HTN), steroid use, medication compliance.
    • Exam: VS, circulation, respiratory status, air movement, plethora/cyanosis. Signs of severity discussed above. Evaluate closely for inciting event for exacerbation.
    • VBG: May identify hypercapnia and acidemia. Can trend values.
    • Pulse oximetry can demonstrate hypoxemia. If possible, assess patient’s baseline level (often 88%-92%).
    • Capnography may be useful for hypercarbia and monitoring.
    • ECG should be obtained: evaluate for ischemia, acute MI, right heart strain, RV hypertrophy, RAD, RBBB, P pulmonale.
    • CBC: may find polycythemia.
    • Chest X-ray: hyperinflation, flattened diaphragm, decreased lung markings. Evaluate closely for enlarged proximal lung markings (suggestive of pulmonary hypertension) and inciting event (pneumothorax, pneumonia, effusion).
  • Management:
    • Oxygen: Target patient’s baseline if known or 88%-92%. Targeting 88%-92% reduces risk of death from respiratory failure. Higher saturations with high flow oxygen demonstrates number needed to harm (NNH) of 14.
      • If unable to correct hypoxemia with oxygen supplementation, consider other inciting agents rather than just acute COPD (PE).
    • Albuterol/Ipratropium: Improves airflow obstruction. If in distress, provide one hour continuous nebulizer. Provides improved clinical outcomes and shorter ED length of stay if albuterol and ipratropium are used together.
    • IV Fluids: Patients may require fluid bolus to address fluid loss from respiratory distress or decreased PO intake. Be wary of over-resuscitation.
    • Corticosteroids: Oral and IV equivalent (similar time to onset, trend to shorter hospital stay with oral). If in distress, provide IV form.
      • Methylprednisolone 125 mg IV, prednisone 40-60 mg PO, hydrocortisone 100 mg IV.
    • Antibiotics: Recommended in patients with purulent sputum, increased sputum production, fevers, pneumonia, severe exacerbation, or if patient requires NIPPV. NNT 3 to prevent treatment failure and 8 to prevent death.
      • Macrolide (azithromycin), doxycycline, fluoroquinolone, or amoxicillin with clavulanic acid.
    • Magnesium: May relax bronchial smooth muscles. Controversial benefit in COPD. More study needed.
    • NIPPV: Significantly decreases morbidity, mortality, length of stay, need for intubation.
      • BiPAP may assist with correcting hypercapnia and improving work of breathing. Either CPAP or BiPAP can be used.
      • Can provide duoneb therapy within circuit.
      • Regular monitoring needed to evaluate for improvement/worsening.
      • Contraindicated in respiratory arrest, uncooperative patient, high aspiration risk, copious secretions, craniofacial trauma/surgery, burns.
    • Intubation: Try to avoid intubation due to high risk of barotrauma and air trapping. Indicated if respiratory failure, worsening respiratory acidemia, worsening mental status, worsening hypoxemia, failure of NIPPV.
      • Keep patient upright prior to intubating. Provide small fluid bolus to avoid post intubation hypotension.
      • Ketamine can be used for delayed sequence intubation if necessary.
      • Use large ETT (8 or greater) to reduce airway resistance, assist with suctioning.
      • When intubated, avoid dynamic hyperinflation and barotrauma. Support spontaneous breathing. Provide low RR, low I:E (1:4), low PEEP.
  • Disposition:
    • Hospitalization: marked symptom increase, severe COPD background, failure to respond to treatment, major comorbidities, new arrhythmia, poor social situation/unable to obtain medications, severe respiratory symptoms/distress/failure.
    • Discharge may be appropriate if patient responds and improves with therapy and did not present in respiratory distress/failure. “Walk of life” may assist in determining discharge capability.
      • Provide bronchodilator therapy, short course of steroids (5 days), follow up, and antibiotics (if indicated).


For a nice summary from Dr. Katelyn Hanson:


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