You Have A New Patient!
A 67-year-old male arrives at the emergency department with increasing shortness of breath over the past 2 days. He has a 50-pack-year smoking history and a prior diagnosis of chronic obstructive pulmonary disease (COPD). On arrival, he appears fatigued and slightly cyanotic. Vitals: HR 110 bpm, BP 145/85 mmHg, RR 30 breaths/min, SpO2 84% on room air, and temperature 37.3°C. He uses accessory muscles to breathe, and auscultation reveals diffuse expiratory wheezes.
What Do You Need To Know?
Importance
It is important to learn about Chronic Obstructive Pulmonary Disease (COPD) in the emergency department because COPD exacerbations are a common and potentially life-threatening presentation that requires prompt recognition and management. Emergency providers must quickly identify signs of respiratory distress, understand the appropriate interventions, such as oxygen therapy, bronchodilators, and steroids, and be able to differentiate COPD from other respiratory conditions. Effective and timely treatment can prevent further deterioration, reduce hospital admissions, and improve patient outcomes. Additionally, understanding COPD allows for better patient education on prevention and follow-up care, ultimately reducing the risk of recurrent exacerbations.
Epidemiology
COPD affects approximately 390 million individuals globally and is the third leading cause of death worldwide [1]. In the United States alone, COPD impacts over 16 million individuals, and many cases remain undiagnosed [2]. The prevalence of COPD is strongly associated with smoking, environmental exposures, and aging. However, occupational hazards and indoor air pollution, such as biomass fuel exposure, are significant risk factors in low and middle-income countries. COPD prevalence increases with age, with the highest incidence among individuals over 65 years. A meta-analysis was done and showed that 12.64% of people aged 40 and older had COPD with similar prevalence between males and females [3].
Pathophysiology
COPD is characterized by persistent respiratory symptoms and airflow limitation caused by airway and/or alveolar abnormalities due to chronic exposure to noxious particles or gases [4]. Inhaled irritants, such as cigarette smoke or biomass fuel, trigger exaggerated airway inflammation, mucus hypersecretion, and structural remodeling. Neutrophils, macrophages, and CD8+ T lymphocytes release proteases and cytokines that cause tissue damage [5]. Protease activity, particularly from neutrophil elastase, destroys elastic fibers in alveolar walls, resulting in emphysema and airflow limitation.
Repeated inflammation also induces goblet cell hyperplasia, fibrosis, and smooth muscle hypertrophy, narrowing airways and increasing resistance to airflow [6]. These processes clinically manifest as chronic cough, sputum production, and dyspnea. Spirometry measures expiratory airflow limitation, with reductions in forced expiratory volume in 1 second (FEV1) and the FEV1/forced vital capacity (FVC) ratio.
Medical History
A thorough medical history is important when evaluating a patient with COPD, especially during an exacerbation. Symptoms include dyspnea, which often worsens over hours to days, increased sputum production, and changes in sputum color that may suggest infection.1 Other symptoms include wheezing, chest tightness, fatigue, and reduced tolerance to exercise. It is important to ask about the onset, timing, exacerbating factors (infections, exposure to pollutants, medication non-adherence), and relieving factors (use of bronchodilators).
Ask about risk factors such as smoking history, occupational/environmental exposures, and previous exacerbations requiring hospitalizations. Also, ask about medications, including prior use of short-acting beta-agonists (SABAs), inhaled corticosteroids, long-acting bronchodilators, and home oxygen therapy.
Allergies should also be noted. Red flags that indicate worse outcomes include severe baseline dyspnea, frequent exacerbations, altered mental status, and signs of respiratory fatigue, such as inability to complete sentences or accessory muscle use. Ask about the patient’s medical history, including cardiovascular disease, diabetes, or pulmonary infections [7,8].
Physical Examination
Physical Examination The physical exam should prioritize a thorough assessment of the patient’s cardiorespiratory status [9]:
- Vital Signs: Pay attention to tachypnea, tachycardia, and hypoxemia.
- Respiratory Findings:
- Air movement and wheezing
- Be cautious: The absence of wheezing may indicate reduced airflow rather than an absence of obstruction.
- Cyanosis: Indicates significant hypoxemia.
- Mental Status: Confusion or lethargy suggests worsening respiratory failure.
- Other Signs: Fever may point to an infectious cause
Indicators of Severe Exacerbation
- Use of accessory muscles during breathing.
- Inability to lie flat or in a tripod position to optimize breathing.
- Speaking only one or two words between breaths due to dyspnea.
Red Flags: Impending Respiratory Failure Be alert for these critical signs requiring immediate intervention:
- Bradycardia or other dysrhythmias.
- Cyanosis indicates severe hypoxemia.
- Marked reduction in mental status, such as confusion or drowsiness.
- Loss of respiratory effort is a concerning sign that indicates a possible pre-arrest state [9].
Alternative Diagnoses
It is crucial for an emergency physician to consider the broad differentials to dyspnea during the initial and ongoing evaluation, including bedside treatments and the plans that follow [10-14]. It is important to acknowledge that patients with COPD can have concurrent comorbid conditions, including other cardiopulmonary diseases.
The emergency physician should suspect COPD in patients with symptoms including shortness of breath, wheezing, and chronic cough with sputum production. In addition, COPD patients have known risk factors, including smoking and environmental exposures that include working in areas with smoke production, and that is when it is important to have adequate history-taking skills. History-taking will give us a better understanding of the patient’s chronic dyspnea with declining pulmonary function, especially on exertion.
When a patient presents with acute dyspnea, one can classify the etiologies based on the organ systems. HEENT causes include angioedema, anaphylaxis, foreign body, and deep neck infections. If a patient presents with acute dyspnea after a motor vehicle accident, then it is plausible to consider rib fractures and lung contusion. Since our chapter focuses on COPD, we can consider cardiopulmonary cases of acute dyspnea. Pulmonary causes are asthma exacerbation, pulmonary embolism, pneumothorax, pulmonary infections, ARDS, and hemorrhage. Cardiac causes consist of acute coronary syndrome, acute decompensated heart failure, flash pulmonary edema, cardiomyopathies, arrhythmia, valvular pathologies, and cardiac tamponade.
Patients with COPD can often present with wheezing, which should not be confused with other causes. When a patient presents to you with wheezing, this suggests that there is an obstruction below the tracheal level. This obstruction occurs in asthma, foreign body, anaphylaxis, and pulmonary edema, also known as a cardiac wheeze [10-14].
The emergency physician should also be mindful of the severity of COPD exacerbation. In some cases, patients deteriorate rapidly, and urgent intervention is warranted. COPD patients can present with other conditions, as mentioned above.
Acing Diagnostic Testing
There are bedside, laboratory, and imaging tests that aid in the evaluation and management of patients with respiratory distress, particularly those with suspected or known COPD exacerbations.
Bedside Tests
- Pulse Oximetry [15]
- Assesses oxygenation status in real-time.
- Indicated in patients presenting with dyspnea or suspected hypoxemia.
- SpO₂ <88% indicates the need for supplemental oxygen. However, hyperoxia (SpO₂ >92%) should be avoided in COPD to prevent worsening hypercapnia.
- Arterial Blood Gas (ABG) [16]
- Evaluates ventilation (PaCO₂), oxygenation (PaO₂), and acid-base status.
- Indicated in severe dyspnea, altered mental status, or suspected respiratory failure.
- Acidosis (pH <7.35) and hypercapnia (PaCO₂ >45 mmHg) confirm significant respiratory compromise.
- Capnography [17]
- Provides continuous monitoring of end-tidal CO₂ levels.
- This is for patients on mechanical ventilation or receiving non-invasive ventilation (NIV).
- High end-tidal CO₂ suggests hypoventilation, while decreasing levels may indicate respiratory improvement.
Laboratory Tests
- Complete Blood Count (CBC)
- This is for patients with fever, purulent sputum, or systemic symptoms.
- An elevated white blood cell (WBC) count may suggest bacterial infection, a common trigger for exacerbations.
- C-Reactive Protein (CRP) and Procalcitonin [18]
- Indications: Differentiating bacterial vs. viral triggers.
- Interpretation: Elevated CRP and procalcitonin levels support bacterial infection as the underlying cause of exacerbation.
- B-Type Natriuretic Peptide (BNP) [19]
- Differentiates COPD exacerbation from acute decompensated heart failure.
- For patients presenting with dyspnea and peripheral edema.
- High BNP levels (>400 pg/mL) may indicate heart failure, while normal levels mainly suggest pulmonary etiology.
- Electrolytes
- Identifies metabolic disturbances, such as hypercapnic acidosis.
- For all patients with severe COPD exacerbations or on chronic diuretics.
- Low bicarbonate (HCO₃⁻) levels can reflect chronic compensation in hypercapnia.
Imaging
- Chest X-Ray (CXR) [20]
- Rules out alternative or concurrent diagnoses, such as pneumonia, pneumothorax, or pulmonary edema.
- This is for patients with fever, chest pain, or unilateral lung findings on auscultation.
- Consolidation suggests pneumonia; hyperinflation and flattened diaphragms are consistent with COPD. A visible pleural line indicates pneumothorax.
- Computed Tomography (CT) Scan [21]
- Identifies pulmonary embolism (PE) or atypical infections.
- Consider CT for patients with high clinical suspicion of PE (e.g., sudden dyspnea, pleuritic chest pain) or non-resolving symptoms after standard treatment.
- Pulmonary artery filling defects confirm PE. CT also provides detailed imaging for complex pneumonic infiltrates.
- Ultrasound [22]
- Bedside evaluation for pleural effusions or cardiac function.
- It is helpful in patients with dyspnea with suspected heart failure or pleural pathology.
- Positive B-lines indicate pulmonary edema; pleural effusions appear as anechoic regions.
Risk Stratification
Frequent exacerbations (>2/year) and prior ICU admissions are associated with a higher mortality risk in patients, particularly those with comorbidities like cardiovascular disease and diabetes, which further worsen prognosis [23,24]. On physical examination, signs such as tachypnea (>30 breaths/min), accessory muscle use, cyanosis, and altered mental status strongly indicate severe respiratory distress [15]. Diagnostic testing, including arterial blood gas (ABG) analysis, reveals that acidosis (pH <7.35) and hypercapnia (PaCO₂ >45 mmHg) are predictive of ventilatory failure [25]. Imaging studies, such as chest X-rays, play a critical role by identifying conditions like pneumonia or pneumothorax that necessitate urgent medical intervention [20].
Risk Stratification Tools
- DECAF Score (link mdcalc)
- Includes dyspnea, eosinopenia, consolidation, acidosis, and atrial fibrillation. Higher scores predict in-hospital mortality [26].
- BAP-65 Score (link mdcalc)
- Evaluates hypotension, acidosis, pulse >110 bpm, and age ≥65 years to predict ICU need and mortality [27].
Management
Initial Stabilization: The ABCDE Approach
- Airway
- Assessment: Evaluate airway patency and signs of obstruction.
- Intervention: Patients with severe respiratory distress may require endotracheal intubation if non-invasive ventilation (NIV) fails or they are unable to protect their airway.
- Breathing
- Assessment: Check respiratory rate, oxygen saturation, and work of breathing.
- Intervention: Provide supplemental oxygen targeting SpO₂ levels between 88% and 92%. Non-invasive ventilation (e.g., BiPAP) is the preferred first-line treatment for hypercapnic respiratory failure or severe dyspnea. NIV reduces intubation rates and mortality [9].
- Circulation
- Assessment: Assess heart rate, blood pressure, and perfusion.
- Intervention: Establish IV access and administer fluids judiciously, particularly in hemodynamically unstable patients.
- Disability
- Assessment: Monitor neurological status for signs of hypoxia or hypercapnia (e.g., confusion, agitation).
- Intervention: Correct hypoxemia and hypercapnia promptly to prevent further deterioration [9].
- Exposure
- Assessment: Perform a thorough examination to identify underlying triggers (e.g., infections, pneumothorax).
- Intervention: Obtain chest imaging to evaluate for pneumonia, pneumothorax, or other contributing factors [9].
Medications
The management of COPD exacerbations often includes a combination of pharmacological treatments tailored to address airway obstruction, inflammation, and potential infections. Key medications include bronchodilators like albuterol and ipratropium to relieve bronchospasm, corticosteroids such as prednisone to reduce inflammation, and magnesium sulfate for severe bronchospasm. Antibiotics are considered when infection is suspected. Each drug requires careful dosing and monitoring, with specific precautions based on patient factors and pregnancy category [15].
Albuterol (Nebulizer):
- Dose: 2.5 mg
- Frequency: Every 20 minutes as needed
- Maximum Dose: 10 mg/hour
- Pregnancy Category: C
- Cautions/Comments: Monitor for tachycardia and tremors.
Ipratropium (Nebulizer):
- Dose: 500 mcg
- Frequency: Every 6 hours
- Maximum Dose: Not applicable
- Pregnancy Category: B
- Cautions/Comments: Use in combination with albuterol for synergistic effects.
Prednisone (Oral):
- Dose: 40-60 mg
- Frequency: Once daily
- Maximum Dose: Not applicable
- Pregnancy Category: C
- Cautions/Comments: Use cautiously in diabetic patients.
Magnesium Sulfate (IV):
- Dose: 2 g
- Frequency: Single dose
- Maximum Dose: 2 g
- Pregnancy Category: C
- Cautions/Comments: Consider in severe cases with bronchospasm.
Antibiotics:
- Dose: Based on local guidelines
- Frequency: Per protocol
- Maximum Dose: Not applicable
- Pregnancy Category: Varies
- Cautions/Comments: Initiate if infection is suspected.
Procedural Interventions
Special Patient Groups
Pediatrics
Although COPD is primarily an adult disease, children with chronic respiratory conditions, such as bronchopulmonary dysplasia or severe asthma, may exhibit symptoms resembling COPD exacerbations.
- Clinical Differences:
- Symptoms may mimic asthma exacerbations, presenting as wheezing and breathlessness.
- Pulmonary function tests are often challenging to interpret in younger children.
- A history of prematurity or recurrent lower respiratory tract infections may predispose children to COPD-like symptoms.
- Management Implications:
- Employ pediatric-specific dosing for bronchodilators and corticosteroids.
- Avoid overuse of systemic steroids due to potential risks, such as growth suppression and adrenal insufficiency [15].
Geriatrics
The elderly population often presents unique challenges in COPD exacerbations due to comorbidities and altered physiological responses.
- Clinical Differences:
- Exacerbations may manifest atypically, such as confusion or lethargy, rather than standard respiratory symptoms.
- Comorbidities, including heart failure and frailty, complicate diagnosis and treatment.
- There is an increased risk of medication side effects, including corticosteroid-induced hyperglycemia and osteoporosis.
- Management Implications:
- Emphasize non-pharmacological interventions, such as pulmonary rehabilitation.
- Closely monitor for potential drug interactions and side effects [28].
Pregnant Patients
Pregnant individuals with COPD exacerbations face unique clinical challenges stemming from physiological changes and fetal considerations.
- Clinical Differences:
- Increased respiratory rate and reduced functional residual capacity may exacerbate symptoms.
- Exacerbations pose risks to maternal and fetal health, including preterm labor and fetal growth restriction.
- Management Implications:
- Prioritize non-teratogenic medications, such as inhaled corticosteroids and short-acting beta-agonists.
- Monitor maternal oxygen saturation to ensure adequate fetal oxygenation [29].
When To Admit This Patient
Indications for Hospital Admission
Hospitalization is indicated for patients with any of the following:
Severe Symptoms:
- Marked dyspnea interfering with daily activities.
- Respiratory rate >30 breaths/min, use of accessory muscles.
- Cyanosis or signs of hypoxemia (oxygen saturation <90% despite supplemental oxygen) [15,30].
Hemodynamic Instability:
- Hypotension or signs of poor perfusion (e.g., confusion, altered mental status) [31].
Failure of Outpatient Management:
- Lack of improvement or worsening symptoms despite appropriate outpatient therapy, including bronchodilators, corticosteroids, and antibiotics [32].
Comorbidities:
- Exacerbations complicated by comorbid conditions such as congestive heart failure, diabetes mellitus, or arrhythmias [33].
Acute Respiratory Failure:
- Arterial blood gases (ABGs) showing PaO2 <60 mmHg or PaCO2 >50 mmHg with pH <7.35 [16].
High-Risk Features:
- Frequent exacerbations (e.g., ≥2/year) [11, 23].
- Recent hospitalizations for COPD exacerbation [11, 23],
- Advanced COPD with significant functional limitations (e.g., home oxygen use) [15].
ICU Admission Criteria [30,34,35]
Intensive care unit (ICU) management is required if:
- Non-invasive ventilation (NIV) fails, or mechanical ventilation is necessary.
- Life-threatening hypoxemia or severe hypercapnia.
- Persistent hemodynamic instability.
Criteria for Safe Discharge [32,33,36]
Patients can be discharged or managed on an outpatient basis if:
- Symptoms are mild and improving with therapy [15,30]
- No significant hypoxemia or hypercapnia (oxygen saturation ≥90%, stable ABGs).
- No significant comorbidities or recent hospitalizations.
- The patient has a reliable social support system and access to follow-up care.
Follow-Up Recommendations [8,15,37]
Patients managed as outpatients should have the following:
- Clear instructions for medication use (e.g., short-acting bronchodilators, oral corticosteroids, antibiotics if indicated).
- A follow-up appointment within 2 weeks.
- Education on recognizing warning signs of worsening symptoms.
Discharge Information [15,34,35]
Before sending a patient home, provide:
- A detailed medication plan, including proper inhaler technique.
- Instructions on the duration of oral corticosteroid and antibiotic therapy.
- Education on lifestyle modifications (e.g., smoking cessation, pulmonary rehabilitation).
Safety-Netting Measures [30,33]
- Clear guidance on when to seek medical attention (e.g., worsening dyspnea, fever, confusion).
- Contact information for emergency services and primary care provider.
Closing Loops [31,32,36]
- Arrangements for follow-up appointments and pulmonary function testing.
- Discuss long-term COPD management strategies, such as home oxygen therapy or vaccinations (influenza, pneumococcal).
- Confirm that the patient understands the discharge instructions and can to prescribed medications.
Revisiting Your Patient
The management of the patient who presented with a COPD exacerbation followed a structured approach. Oxygen therapy was initiated, targeting SpO₂ levels of 88–92% using a nasal cannula or a Venturi mask, with BiPAP considered for cases of persistent hypoxemia or hypercapnic respiratory failure. Medications included nebulized bronchodilators, such as albuterol (2.5 mg) combined with ipratropium (0.5 mg), which were administered every 20 minutes for the first hour. Systemic steroids, like oral prednisone (40 mg) or IV methylprednisolone, were given as needed. Empiric antibiotics, such as doxycycline or amoxicillin-clavulanate, were started when an infection was suspected. Diagnostics involved chest X-rays, arterial blood gas analysis, a complete blood count (CBC), and electrolyte evaluation, with an ECG performed due to concerns about potential cardiac involvement. Continuous monitoring of SpO₂, respiratory rate, and ABG was conducted to track the patient’s progress. Regarding disposition, the patient was admitted due to severe hypoxemia and hypercapnia, with plans for outpatient follow-up scheduled within 1–2 weeks after discharge. Finally, the patient received education, including smoking cessation support and instructions on proper inhaler use, to reduce the risk of future exacerbations.
Authors
Noura Aldosari
Emergency medicine resident at Cleveland Clinic Abudhabi. Interested in neurocritical and trauma resuscitation. Rotated in the neurocritical ICU department of Brigham and Women's Hospital (Harvard University) and worked in a research lab to detect genes involved in the pathophysiology of glioblastoma in Virginia University. Outside of medicine, I am a musician where I play the guitar and I cook.
Omar Ghazanfar
Dr Omar Ghazanfar is the Medical Director HIMS and Emergency Physician Cleveland Abu Dhabi.Dr Ghazanfar has a keen interest in research and is part of the IFEM research committee as well as the scientific committee for ESEM. He is triple board certified with boards in Emergency and Disaster Medicine as well as Medical Quality. He has also completed an MBA.
Listen to the chapter
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Reviewed and Edited By
Arif Alper Cevik, MD, FEMAT, FIFEM
Prof Cevik is an Emergency Medicine academician at United Arab Emirates University, interested in international emergency medicine, emergency medicine education, medical education, point of care ultrasound and trauma. He is the founder and director of the International Emergency Medicine Education Project – iem-student.org, chair of the International Federation for Emergency Medicine (IFEM) core curriculum and education committee and board member of the Asian Society for Emergency Medicine and Emirati Board of Emergency Medicine.
