COPD (2024)

by Noura Aldosari & Omar Ghazanfar

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.

The image was produced by using ideogram 2.0

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]:

  1. Vital Signs: Pay attention to tachypnea, tachycardia, and hypoxemia.
  2. Respiratory Findings:
    • Air movement and wheezing
    • Be cautious: The absence of wheezing may indicate reduced airflow rather than an absence of obstruction.
  3. Cyanosis: Indicates significant hypoxemia.
  4. Mental Status: Confusion or lethargy suggests worsening respiratory failure.
  5. 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

  1. 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.
  2. 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.
  3. 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

  1. 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.
  2. 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.
  3. 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.
  4. 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

  1. 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.
  2. 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.
  3. 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

  1. DECAF Score (link mdcalc)
    • Includes dyspnea, eosinopenia, consolidation, acidosis, and atrial fibrillation. Higher scores predict in-hospital mortality [26].
  2. 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

  1. 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.
  2. 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].
  3. Circulation
    • Assessment: Assess heart rate, blood pressure, and perfusion.
    • Intervention: Establish IV access and administer fluids judiciously, particularly in hemodynamically unstable patients.
  4. 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].
  5. 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

In the management of acute COPD exacerbations, advanced interventions play a crucial role in stabilizing respiratory function and addressing underlying complications. Non-invasive ventilation (NIV) is a first-line strategy for patients with hypercapnic respiratory failure or persistent hypoxemia, offering improved gas exchange and reducing the likelihood of intubation [15]. For patients who do not respond to NIV or have contraindications, endotracheal intubation with lung-protective ventilation strategies becomes necessary to manage severe respiratory distress while minimizing barotrauma [15]. Additionally, imaging modalities such as chest X-rays or ultrasounds are essential for identifying structural abnormalities like pneumonia or pneumothorax, ensuring comprehensive evaluation and treatment [15].

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

Picture of Noura Aldosari

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.

Picture of Omar Ghazanfar

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

References

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  9. Long B, Rezaie SR. Evaluation and Management of Asthma and Chronic Obstructive Pulmonary Disease Exacerbation in the Emergency Department. Emerg Med Clin North Am. 2022;40(3):539-563. doi:10.1016/j.emc.2022.05.007
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  16. Tan HL, Ong CY, Foo LL, et al. High-flow nasal cannula oxygen therapy versus non-invasive ventilation in acute exacerbations of COPD with moderate hypercapnic respiratory failure: A randomized controlled non-inferiority trial. 2024;165(4):789-798. doi:10.1016/j.chest.2024.02.276.
  17. Schreiber A, Berthelsen PG, Hess D. Monitoring carbon dioxide during acute respiratory failure. 2013;143(3):741-750. doi:10.1378/chest.12-2305.
  18. van Vugt SF, Verheij TJ, de Jong PA, et al. Procalcitonin, CRP levels, and the bacterial etiology of pneumonia. J Clin Microbiol. 2013;51(8):2662-2665. doi:10.1128/JCM.00330-13.
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  34. Lindenauer PK, et al. Association of corticosteroid dose and route of administration with risk of treatment failure in acute exacerbation of chronic obstructive pulmonary disease. JAMA. 2010;303(23):2359-2367. doi:10.1001/jama.2010.796.
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  36. Miravitlles M, et al. COPD exacerbations: management and hospital discharge. Pulmonology. 2018;24(4):204-210. doi:10.1016
  37. Vollenweider DJ, Frei A, Steurer-Stey CA, Garcia-Aymerich J, Puhan MA. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2018;10:CD010257. doi:10.1002/14651858.CD010257.pub2.

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

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.

Spontaneous Pneumothorax (2024)

by Mohd Fazrul Mokhtar & 
Raja Amir Fikri Raja Sulong Ahmad

You have a new patient!

A 24-year-old male with no significant medical history presents to the emergency department for shortness of breath for two days duration. The symptom is associated with left-sided pleuritic chest pain. He denies fever, cough, constitutional symptoms, or trauma. He is an active smoker.

a-photo-of-a-24-year-old-male (the image was produced by using ideogram 2.0)

On assessment, the patient was mildly tachypneic and well-perfused. Auscultation reveals reduced breath sounds over the left lung. There is hyperresonance on percussion over the left lung as well. There is no tracheal deviation. Vital signs are as follows:

Blood pressure – 108/75 mmHg
Pulse rate – 74/minute
Respiratory rate – 24/minute
Oxygen saturation – 98% under room air
Temperature – 36.8o Celcius
Pain score – 4/10

What do you need to know?

Importance

Pneumothorax is defined as the presence of air in the pleural space. Pneumothoraces can be further divided into primary spontaneous pneumothorax (PSP), which occurs in patients spontaneously without any apparent underlying pleural disease, or secondary pneumothorax in patients with underlying diseases such as tuberculosis and lung malignancy [1,2]. Iatrogenic pneumothorax can also occur due to procedures such as thoracocentesis and central venous line insertion [2].

Identifying a pneumothorax is important, as a delay in management can lead to hemodynamic instability. In unstable patients with respiratory and circulatory compromise, the differential diagnosis of tension pneumothorax must be excluded.

Epidemiology

The incidence of primary spontaneous pneumothorax varies significantly between genders. Among the male population, it is reported to occur at a rate of 7.4 to 18 cases per 100,000 individuals annually. In contrast, the incidence in the female population is comparatively lower, ranging from 1.2 to 6 cases per 100,000 individuals per year [1].

Pathophysiology

Under normal circumstances, the pressure in the pleural space is negative compared to atmospheric pressure. This negative pressure is generated due to the opposing forces between the lung’s tendency to collapse because of elastic recoil and the outward expansion of the chest wall [2]. When there is communication between the alveoli and pleural space, the introduction of air alters the gradient until pressure equilibrium is reached, resulting in partial or total lung collapse. Tension pneumothorax occurs when inhaled air accumulates in the pleural space but cannot exit due to a one-way valve mechanism [2].

This condition leads to the clinical presentation of dyspnoea and chest pain. In tension pneumothorax, the increased intrathoracic pressure can decrease venous return and restrict lung function, ultimately leading to shock and hypoxia [2].

Medical History

In patients with a primary spontaneous pneumothorax, mild symptoms may be reported as they often tolerate the consequences of a pneumothorax better compared to those with underlying respiratory problems. The most common symptoms are chest pain and shortness of breath [3].

When inquiring about pain, the SOCRATES mnemonic may be helpful:

  • Site: Pain on the affected side
  • Onset: Usually, sudden onset of pain
  • Character: Typically described as sharp
  • Radiation: Radiation to the ipsilateral shoulder
  • Associated symptoms: Breathlessness
  • Time: Although the onset of pain may be acute, patients may present late if they can tolerate symptoms
  • Exacerbating/relieving factors: Pleurisy (pain worsening on inspiration) is common
  • Severity: Quantify the pain score when possible

Asking about risk factors may also help in strengthening the diagnosis of pneumothorax, including cigarette smoking, male gender, mitral valve prolapse, Marfan’s syndrome, and changes in ambient pressure. It is also important to ask about the history of trauma and recent medical procedures. Family history may be relevant as there may be a genetic predisposition to the condition.

Finally, enquire about the presence of a chronic cough and constitutional symptoms such as weight loss, loss of appetite, and fatigue to help ascertain whether the pneumothorax may be due to an underlying pleural disease.

Physical Examination

When assessing a patient with a potential pneumothorax, examine systematically using the ABC approach to avoid missing potential signs, especially those of a tension pneumothorax, as this condition requires immediate intervention [4].

  • Airway: Tracheal deviation is a late sign of tension pneumothorax, though it is not always indicative.
  • Breathing: Signs include tachypnoea, hypoxia, unequal chest rise, subcutaneous emphysema, hyperresonance, and absent or reduced breath sounds.
  • Circulation: Hypotension (a key sign of tension pneumothorax), tachycardia, and cold peripheries may be present.

Differential Diagnoses

The patients present mostly with shortness of breath (SOB). Therefore, pulmonary, cardiac and other causes of SOB should be considered first.

  • Pulmonary
    • Airway obstruction
    • PE
    • Pulmonary edema
    • Anaphylaxis
    • Asthma
    • Cor pulmonale
    • Aspiration
  • Cardiac
    • MI
    • Tamponade
    • Pericarditis
  • Others
    • Esophageal rupture
    • Toxin ingestion
    • Epiglottitis
    • Anemia

Acing Diagnostic Testing

The diagnosis of spontaneous pneumothorax is confirmed by imaging. After the diagnosis is confirmed, the clinical evaluation, including the history obtained and the patient’s clinical condition, should determine the management strategy.

Chest X-ray

The standard view is the erect PA chest x-ray. However, in a polytrauma patient, when the patient must be kept in the supine position, supine and lateral decubitus views can be performed.

Chest X-ray has been the mainstay diagnostic modality for pneumothorax. Typically, it demonstrates the visceral pleural edge, which appears as a thin, sharp white line. The peripheral space is more radiolucent compared to the adjacent lung (Image 1). A deep sulcus sign can be observed on a supine X-ray (Image 2).

More x-ray images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 1: Left pneumothorax. (Image courtesy of Ian Bickle, Radiopaedia.org, rID: 86926)
Image 2: Right pneumothorax with a deep sulcus sign. (Image courtesy of Mohammad Osama Hussein Yonso, Radiopaedia.org, rID: 18975)

A chest x-ray provides information about the size of the pneumothorax and assists in determining the next steps in management.

In a patient with suspected pneumothorax, a chest x-ray should be performed [5]. However, if clinical assessment suggests features of tension pneumothorax (e.g., hypotension, tracheal deviation, distended neck vein), a needle thoracocentesis must be performed first, as a chest x-ray may delay this life-saving intervention.

CT scan

The presence of bullous lung disease can lead to a misdiagnosis of pneumothorax on a chest x-ray. In patients with chronic lung disease who develop bullae, a chest x-ray may show features similar to pneumothorax. Therefore, if uncertainty exists, a CT scan of the thorax is strongly recommended.

More CT images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 3: CT scan showing right pneumothorax in a diseased lung. (Image courtesy of David Cuete, Radiopaedia.org, rID: 26570)

CT scan is considered the “gold standard” for detecting small pneumothoraces and is the most accurate method to determine the size of a pneumothorax [6]. However, practical drawbacks, such as limited availability, make it unsuitable as the first imaging modality for diagnosing pneumothorax.

Lung Ultrasound

In the emergency department, a lung ultrasound can be performed at the bedside immediately after a physical examination to evaluate undifferentiated respiratory failure. It is part of the point-of-care ultrasound protocol in emergency settings.

In a lung ultrasound, the normal lung interface with pleura shows lung sliding with Z-lines, which appear as vertical comet tails descending from the pleural surface. In pneumothorax, this sliding and the comet tail artifacts from the pleura are absent. Visualizing the intersection between the sliding lung sign and the absence of sliding is referred to as the lung point, which is nearly 100% specific for pneumothorax [7].

Additional ultrasound findings:

  • Absence of B-lines
  • Cessation of lung pulse (lung oscillation in tandem with cardiac contraction)

On M-mode, the following signs are observed:

  • Seashore sign: Indicates normal lung sliding.
  • Barcode/stratosphere sign: Indicates pneumothorax.

More US images can be found in iEM’s Flickr account – https://www.flickr.com/search/?user_id=158045134%40N08&view_all=1&text=pneumothorax

Image 4- Lung ultrasound showing the seashore sign. (Image courtesy of Srikar Adikhari et al. [2014], ResearchGate)
Image 5- Lung ultrasound showing the Barcode:stratosphere sign. (Image courtesy of Maulik S Patel, Radiopaedia.org, rID- 61141)

Laboratory Tests

ABG is indicated when oxygen saturation is below 90% on room air. It is performed to assess the patient’s oxygenation level, as some patients with pneumothorax may present with hypoxemia [8].

Risk Stratification

Pneumothorax is classified into primary spontaneous pneumothorax (PSP) and secondary pneumothorax (SSP). PSP occurs in healthy patients; hence, it is termed “spontaneous,” while SSP is associated with underlying lung diseases such as chronic obstructive pulmonary disease and pulmonary tuberculosis. PSP patients are typically taller than healthy controls [9-11]. Within the first four years, the risk of recurrence of PSP is as high as 54%, with isolated risk factors including smoking, height, and age above 60 years [10, 12,13]. Age, pulmonary fibrosis, and emphysema are risk factors for the recurrence of SSP [11,13].

Since patients with pre-existing lung diseases tolerate a pneumothorax less well, distinguishing between PSP and SSP at the time of diagnosis is critical for determining the next steps in care. Many patients, particularly those with PSP, do not seek medical attention until several days after their symptoms first appear. Meanwhile, the majority of patients with SSP present with more severe clinical symptoms.

Management

General Principle

Airway

The majority of patients with pneumothorax experience breathing issues rather than airway compromise. However, it is essential to assess the airway and breathing simultaneously.

Breathing

Provide supplemental oxygen with a high-flow mask. Oxygen treatment accelerates the resolution of pneumothorax by lowering the partial pressure of nitrogen in the alveoli relative to the pleural cavity. This creates a diffusion gradient for nitrogen, which hastens recovery.

The diagram from the British Thoracic Society guideline summarizes the management of pneumothorax [14].

[8] MacDuff A, Arnold A, Harvey J Management of spontaneous pneumothorax: British Thoracic Society pleural disease guideline 2010 Thorax 2010;65:ii18-ii31.
Image 6: Measurement of the apex-to-cupola distance and interpleural distance. (Images courtesy of the British Thoracic Society)

When To Admit This Patient

Patients requiring chest tube thoracostomy insertion must be admitted for monitoring and removal prior to discharge home. Those utilizing a pigtail catheter experience fewer complications, shorter hospital stays, and faster time-to-device removal. While many patients will require hospitalization, some can be discharged after a period of observation, aspiration, or with a Heimlich valve in pigtail catheters [14,15].

Revisiting Your Patient

The patient presented to the Emergency Department in a stable condition, showing no signs of respiratory distress, and was initially seen in the non-critical zone. After a chest X-ray confirmed the diagnosis of pneumothorax, the patient was transferred to the resuscitation zone for management and close monitoring.

Image 7 - Left Pneumothorax (image courtesy of Mohd Mokhtar and Raja Ahmad

A systematic assessment and management plan for patients with pneumothorax should prioritize the identification and stabilization of hemodynamically unstable patients.

Airway
There was no airway compromise in this patient, so no intervention was needed. The examination also revealed no tracheal deviation, which decreases the suspicion of a tension pneumothorax.

Breathing
Although the patient did not appear to be in respiratory distress, high-flow oxygen was administered through a non-rebreather mask to expedite the resorption of the pneumothorax.

Circulation
The patient was not in a tension pneumothorax state, as he remained hemodynamically stable. Therefore, he did not require immediate needle decompression or chest drain insertion.

The next step was to decide on the treatment approach. Following the algorithm set out by the British Thoracic Society, needle aspiration is recommended for this patient with a spontaneous pneumothorax, especially since he was experiencing breathlessness.

Needle aspiration is preferred in cases of spontaneous primary pneumothorax, as it is associated with a higher rate of successful discharges and fewer complications. However, if needle aspiration fails, chest drain insertion and admission will be necessary. The failure rate of needle aspiration in cases of secondary pneumothorax is high, which is why chest drains are typically favored in those instances.

Authors

Picture of Mohd Fazrul Mokhtar

Mohd Fazrul Mokhtar

Dr Mohd Fazrul Mokhtar is a Consultant Emergency Physician at Faculty of Medicine Universiti Teknologi MARA, Malaysia. He obtained his postgraduate training in emergency medicine at Universiti Kebangsaan Malaysia. He has special interest in sepsis, medical simulation; and emergency critical care. He is currently the Coordinator of the Clinical Simulation Centre. His research niche includes CPR educational technologies, cardiac arrest and sepsis. He is the council member of Malaysian Sepsis Association and Malaysian Resuscitation Association.

Picture of Raja Amir Fikri Raja Sulong Ahmad

Raja Amir Fikri Raja Sulong Ahmad

I am currently a second year postgraduate trainee in Emergency Medicine in Malaysia. My interests are point of care ultrasound and critical care.

Listen to the chapter

References

  1. Noppen M. Spontaneous pneumothorax: epidemiology, pathophysiology, and cause. European Respiratory Review. 2010;19(117):217-219. doi:https://doi.org/10.1183/09059180.00005310
  2. McKnight CL, Burns B. Pneumothorax. Nih.gov. Published 2019. https://www.ncbi.nlm.nih.gov/books/NBK441885
  3. Aljehani YM, Almajid FM, Niaz RC, Elghoneimy YF. Management of Primary Spontaneous Pneumothorax: A Single-center Experience. Saudi J Med Med Sci. 2018 May-Aug;6(2):100-103. doi: 10.4103/sjmms.sjmms_163_16. Epub 2018 Apr 16. PMID: 30787829; PMCID: PMC6196700.
  4. Newman MJ. A mistaken case of tension pneumothorax. BMJ Case Rep. 2014 May 16;2014:bcr2013203435. doi: 10.1136/bcr-2013-203435. PMID: 24835806; PMCID: PMC4024963.
  5. Matsumoto, S., Kishikawa, M., Hayakawa, K., Narumi, A., Matsunami, K., & Kitano, M. (2011). A method to detect occult pneumothorax with chest radiography. Annals of emergency medicine57(4), 378–381. https://doi.org/10.1016/j.annemergmed.2010.08.012
  6. Do, S., Salvaggio, K., Gupta, S., Kalra, M., Ali, N. U., & Pien, H. (2012). Automated quantification of pneumothorax in CT. Computational and mathematical methods in medicine2012, 736320. https://doi.org/10.1155/2012/736320
  7. Volpicelli G. (2011). Sonographic diagnosis of pneumothorax. Intensive care medicine37(2), 224–232. https://doi.org/10.1007/s00134-010-2079-y
  8. Inoue S, Egi M, Kotani J, Morita K. Accuracy of blood-glucose measurements using glucose meters and arterial blood gas analyzers in critically ill adult patients: systematic review. Crit Care. 2013 Mar 18;17(2):R48. doi: 10.1186/cc12567. PMID: 23506841; PMCID: PMC3672636.
  9. Withers JN, Fishback ME, Kiehl PV, et al. Spontaneous pneumothorax. Am J Surg 1964;108:772–6.
  10. Sadikot RT, Greene T, Meadows K, et al. Recurrence of primary pneumothorax. Thorax 1997;52:805–9.
  11. Videm V, Pillgram-Larsen J, Ellingsen O, et al. Spontaneous pneumothorax in chronic obstructive pulmonary disease: complications, treatment and recurrences. Eur J Respir Dis 1987;71:365–71.
  12. West JB. Distribution of mechanical stress in the lung, a possible factor in the localisation of pulmonary disease. Lancet 1971;1:839–41.
  13. Lippert HL, Lund O, Blegrad S, et al. Independent risk factors for cumulative recurrence rate after first spontaneous pneumothorax. Eur Respir J 1991;4:324–31.
  14. MacDuff A, Arnold A, Harvey J; BTS Pleural Disease Guideline Group. Management of spontaneous pneumothorax: British Thoracic Society Pleural Disease Guideline 2010. Thorax. 2010 Aug;65 Suppl 2:ii18-31. doi: 10.1136/thx.2010.136986. PMID: 20696690.
  15. Thelle A, Gjerdevik M, SueChu M, Hagen OM, Bakke P. Randomised comparison of needle aspiration and chest tube drainage in spontaneous pneumothorax. European Respiratory Journal. 2017;49(4). doi:https://doi.org/10.1183/13993003.01296-2016

FOAm and Further Reading

  • CDEM curriculum – https://cdemcurriculum.com/pneumothorax/ – link
  • FLIPPED EM Classroom – https://flippedemclassroom.wordpress.com/2013/05/26/pneumothorax/ – link

Reviewed and Edited By

Picture of Erin Simon, DO

Erin Simon, DO

Dr. Erin L. Simon is a Professor of Emergency Medicine at Northeast Ohio Medical University. She is Vice Chair of Research for Cleveland Clinic Emergency Services and Medical Director for the Cleveland Clinic Bath emergency department. Dr. Simon serves as a reviewer for multiple academic emergency medicine journals.

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

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.

Bronchial Foreign Body Aspiration (2024)

by Elhaitham Ahmed & Khalifa Alqaydi

You have a new patients!

Patient 1

A 72-year-old male was brought from an inpatient stroke rehabilitation center to the emergency department for a cough lasting the past ten days. Along with the cough, the patient was noted to have blood-tinged sputum, which is sometimes foul-smelling. His vital signs are as follows: temperature of 38.4°C, blood pressure of 138/78 mmHg, heart rate of 103 bpm, respiratory rate of 26 breaths/min, and oxygen saturation of 93% on room air. On physical examination, the patient exhibits tachypnea, dullness on percussion, bronchial breathing, egophony, and increased vocal fremitus upon examining the right side of his lung.

The image was produced by using ideogram 2.0.

Patient 2

Thirty minutes later, the nurse calls you regarding a 5-year-old boy brought in by his mother, presenting with stridor and an ongoing cough. The mother mentions that she found her child playing with her wallet while she was in the next room and discovered him in this condition. The child is tachypneic, saturating at 90% on room air with subcostal retractions. Examination of the right lung revealed wheezing with decreased air entry.

a-photo-of-a-5-year-old-male-patient-(the image was produced by using ideogram 2.0)

What do you need to know?

Importance

Tracheobronchial foreign body aspiration (FBA) can be a potentially life-threatening event. FBA in children may be suspected based on a choking episode if such an episode is witnessed by an adult or remembered by the child. In contrast, the clinical presentation of unwitnessed FBA may be subtle, requiring careful review of the history, clinical assessment, and judicious use of radiography and bronchoscopy for diagnosis. Flexible and rigid bronchoscopy have become the cornerstone of both diagnosis and treatment in patients with suspected airway foreign bodies, which are most commonly seen in patients with FBA [1].

Epidemiology

FBA is more common in children than in adults. Data from the National Security Council report that approximately 80 percent of cases occur in patients younger than 15 years of age, with the remaining 20 percent presenting in those older than 15 years. Overall, death from FBA is the fourth leading cause of accidental home and community deaths in the United States, with over 5,000 fatal episodes of FBA reported during 2015. Death from FBA peaks in children under 1 year old and in adults over 75 years [2].

Pathophysiology

In children, nuts, seeds, and other organic material account for the majority of foreign bodies. However, in adults, the nature of inhaled objects is highly variable, ranging from organic to inorganic material. The type of foreign body significantly impacts the degree of tissue reaction in the airway. For example, some inorganic materials, such as metal or glass items, may cause little tissue inflammation but can result in direct airway injury if they are sharp. In contrast, some organic materials, such as nuts and a variety of pills, can cause significant inflammation, granulation tissue formation, and airway stenosis. Aspirated organic material can also expand from airway moisture, worsening obstruction. Aspiration of medications in pill form, such as iron tablets, aspirin, and potassium chloride, can also cause severe airway inflammation and ulceration [2].

Medical History

Clinical presentation can range from chronic nonspecific respiratory complaints to acute airway obstruction. In most cases of aspiration, the presence of a foreign body can be suspected after a thorough history. Patients with airway foreign bodies may present with noisy breathing, inspiratory stridor, rhonchi, vomiting, changes in voice, and hemoptysis [3]. Some patients may report a history known as penetration syndrome, which includes a choking sensation accompanied by wheezing and coughing. Coughing may not completely expel the foreign body but may instead cause its impaction in the subglottic region. Therefore, coughing after suspected aspiration should prompt a search for a foreign body, even if symptoms improve [4].

In pediatric patients with suspected foreign body aspiration, the sudden onset of choking or intractable cough associated with wheezing and respiratory distress occurs in more than 63% of cases [5,6]. In addition to coughing and choking, stridor is a frequent symptom. The absence of early coughing and choking is associated with delayed diagnosis and chronic presentations, such as recurrent pneumonia [4]. The sudden onset of dyspnea and odynophagia may indicate an impacted subglottic object. If the object is sharp and thin, the emergency clinician should suspect embedding between the vocal cords or in the subglottic region, resulting in partial obstruction [7].

Other components of the history can assist in diagnosing and characterizing foreign bodies in patients with aspiration of nonfood objects. Many types of items may be aspirated by children exploring their environment. Another at-risk population includes individuals who habitually store small items in their mouths for quick access; examples include construction workers (nails) and seamstresses (pins). The presentation of patients with a retained airway foreign object may involve only infectious complications. A foreign object can lead to a retropharyngeal abscess. Patients with atypical or recurrent pneumonia may have pulmonary infections caused by the persistence of a foreign object serving as a focus of infection [6].

Physical Examination

Physical findings depend on the degree of airway obstruction and the duration of the object’s presence. Depending on the size and location of the foreign body, the examination may reveal a normal patient, one with cyanosis and respiratory arrest, or any condition between these two extremes. Patients may exhibit stridor or hoarseness with upper airway foreign objects, and intercostal or sternal retractions may be observed in patients with high-grade obstruction caused by tracheal foreign bodies [8]. Hypoxemia may be present; however, normoxia does not rule out the presence of a foreign body. Patients with secondary infections may present with fever.

Oropharyngeal examination may reveal a foreign body posteriorly or donor sites of fractured teeth. The examination should also include a search for fractured or missing dental prostheses. Oropharyngeal examination can often be supplemented by indirect or direct laryngoscopy or nasopharyngoscopy, but these procedures should be performed only if the procedural stress does not pose an undue risk of airway compromise.

Coughing may result from local irritation caused by bronchial foreign bodies. Localized or apparently generalized wheezing is frequently auscultated in patients with lower respiratory tract foreign bodies [9]. Complete obstruction of a mainstem bronchus may result in absent ipsilateral breath sounds; however, breath sounds can sometimes be transmitted across the thorax, and the only physical abnormality may be asymmetric chest rise. Occasionally, a foreign body acts as a one-way valve, allowing air into the lung during inspiration but preventing its exit during expiration. The affected lung becomes hyperexpanded, which may be detected as hyper-resonance on percussion [6].

Alternative Diagnoses

The selected differential diagnoses for airway foreign bodies include anaphylactic reactions, acute pharyngitis, acute epiglottitis, retropharyngeal abscess, neck tumors, pulmonary carcinomas, pneumonia, bronchitis, bronchiolitis, and tuberculosis.

Acing Diagnostic Testing

Imaging should not delay intervention in cases of suspected acute asphyxiation but is indicated for stable patients [10].

Findings on imaging depend on the type and location of the material aspirated and the time elapsed. In practice, plain films of the neck and chest are often performed simultaneously and can be followed by site-specific CT if suspicion remains. The majority of foreign bodies are radiolucent and not easily identified on plain film. If obstruction of the upper airway (oropharynx and upper trachea) is suspected, initial imaging should include anterior-posterior and lateral soft tissue views of the neck [11]. If these tests are negative and suspicion for FBA persists, further imaging with CT may be indicated. When FBA of the lower airways (below the vocal cords) is suspected, a chest radiograph should be the initial radiographic test to look for an obvious radiopaque airway lesion. Negative scans may prompt further evaluation with CT. The reported sensitivity of chest radiography is approximately 60 to 80 percent in children, and clinical experience suggests similarly poor sensitivity in adults [12].

Given its widespread availability, flexible bronchoscopy is often the diagnostic procedure of choice for non-life-threatening FBA in adults, particularly in cases involving smaller foreign bodies in the lower airway. Flexible bronchoscopy allows precise identification and localization of foreign bodies and facilitates the selection of instruments necessary for retrieval [13]. Additionally, flexible bronchoscopy enables removal of the foreign body during the diagnostic procedure if the operator is skilled in these techniques. Standard diagnostic or therapeutic flexible bronchoscopes are usually adequate for the management of FBA in adults [6].

Risk Stratification

Risk factors in adults include loss of consciousness due to trauma, drug or alcohol intoxication, or anesthesia. Additional risk factors in older adults include age-related slowing of the swallowing mechanism, medication use (impairing cough and swallowing), stroke-related dysphagia, and various degenerative neurologic diseases such as Alzheimer’s or Parkinson’s disease [2].

Management

In a conscious adult, data support the efficacy of chest thrusts, back blows or slaps, blind finger sweeps, and abdominal thrusts in relieving complete foreign body airway obstruction [6, 14]. In cases of life-threatening asphyxiation, initial support should focus on treating airway obstruction and respiratory failure. Once the airway is secured, a laryngoscopic evaluation of the oropharynx should be performed immediately to diagnose and retrieve a supraglottic or glottic foreign body. If a foreign body is not seen, rigid bronchoscopy is generally the procedure of choice for suspected asphyxiating foreign bodies located in the trachea or major bronchi. In patients with non-life-threatening FBA, flexible bronchoscopy is typically performed [15].

When large foreign bodies completely or almost completely obstruct major upper airways (glottis, supraglottis, trachea), it is critical to ensure the patient is oxygenated and the airway is secured [16]. Support measures may include bag-valve-mask ventilation and endotracheal intubation. If ventilation is unsuccessful, an emergent cricothyrotomy or tracheotomy may be required if the foreign body is suspected to be above the vocal cords. Once the airway is secured, immediate inspection of the oropharynx (glottis, supraglottis) is indicated, as one-third of FBA cases presenting as acute asphyxiation are located in the supraglottis. Retrieval of the foreign body with Magill forceps can be safely performed using direct laryngoscopy (glottis, supraglottis) or with smooth or alligator forceps during rigid or flexible bronchoscopy (large central foreign body in the trachea or major bronchus) [17].

The choice of procedure for foreign body removal depends on the type of presentation, characteristics of the inhaled foreign body, its location, the duration it has been in the airway (if known), and local expertise. Anti-inflammatories and antibiotics are not routinely administered to patients with suspected or documented FBA. Antibiotics are indicated only in cases of clinically, radiologically, or microbiologically documented respiratory tract infections. However, their use should not delay foreign body extraction, even if pneumonia or sepsis is suspected [2].

Figure 1 - Approach to Upper Airway Foreign Body. Original Image can be found here: White JJ. Upper Airway Foreign Bodies: Emergency department presentation, Evaluation and Management. emDOCs.net - Emergency Medicine Education. April 12, 2021. Accessed May 9, 2023. http://www.emdocs.net/upper-airway-foreign-bodies-emergency-department-presentation-evaluation-and-management/.

Special Patient Groups

In the pediatric age group, moderate or high suspicion of FBA is suggested by any of the following:

  • Witnessed FBA, regardless of symptoms.
  • History of choking, with any subsequent symptoms or suspicious characteristics on imaging.
  • A young child with suggestive symptoms without another explanation, especially if there are suspicious characteristics on imaging. Suspicious symptoms include cyanotic spells, dyspnea, stridor, sudden onset of cough or wheezing (often focal and monophonic), and/or unilaterally diminished breath sounds.

The tracheobronchial tree should be examined in all cases with moderate or high suspicion of FBA, using rigid bronchoscopy (or, in some cases, computed tomography [CT]). On occasion, the adjunctive use of a flexible bronchoscope may be helpful. Normal chest radiographs are not sufficient to rule out FBA [19], primarily because most foreign bodies are radiolucent. Morbidity and mortality may increase if bronchoscopic evaluation is delayed.

When To Admit This Patient

Most patients improve clinically following FBA removal. Those with imaging abnormalities should undergo follow-up imaging six weeks to three months after extraction to confirm resolution. Patients presenting with a delayed presentation and belonging to high-risk groups should be admitted for management of complications and FBA retrieval and removal.

Revisiting Your Patients

The elderly patient, given his history of a recent stroke and being in a rehabilitation center, is at risk of FBA. His presentation with chronic cough and fever raises suspicion of pneumonia; however, the emergency medicine clinician should maintain a broad differential diagnosis based on further history, including foul-smelling sputum and nursing staff observations of difficulty swallowing and previous admissions for pneumonia. Such delayed presentations of FBA can occur in this age group. The patient’s management began with initial stabilization using oxygen support, along with workup for infection. Imaging modalities started with a chest plain film, which showed right lower lobe opacities but no clear foreign body. With suspicion for FBA still high, a chest CT scan was performed and revealed evidence consistent with FBA. The patient was started on broad-spectrum antibiotics, and bronchoscopy was scheduled as the definitive management for FBA. Follow-up bronchoscopy identified distal fragments of nuts impacted in the right lower lobe bronchus.

In the pediatric patient, the presentation is more acute and requires securing the airway. After placing the patient on a non-rebreather mask with 15L of oxygen, his saturation improved to 100%. Given the history of playing with a wallet, suspicion of coin aspiration was considered. A chest radiograph with posteroanterior and lateral views was performed, showing a rounded radiopaque structure in the right main bronchus. Airway support and supplemental oxygen should be provided until bronchoscopy is performed and the coin is retrieved.

Authors

Picture of Elhaitham Ahmed

Elhaitham Ahmed

Zayed Military Hospital, AbuDhabi

Picture of Khalifa Alqaydi

Khalifa Alqaydi

Zayed Military Hospital, AbuDhabi

Listen to the chapter

References

  1. Ruiz, F.E. (2022) Airway foreign bodies in children, UpToDate. Available at: https://www.uptodate.com/contents/airway-foreign-bodies-in-children?search=airway+foreign+bodies+in+children&source=search_result&selectedTitle=1~83&usage_type=default&display_rank=1 (Accessed: 08 May 2023).
  2. Shepherd, W. (2023) Airway foreign bodies in adults, UpToDate. Available at: https://www.uptodate.com/contents/airway-foreign-bodies-in-adults?search=adult+forign+body+&source=search_result&selectedTitle=3~150&usage_type=default&display_rank=3 (Accessed: 08 May 2023).
  3. Bajaj D, Sachdeva A, Deepak D. Foreign body aspiration. J Thorac Dis. 2021;13(8):5159-5175. doi:10.21037/jtd.2020.03.94
  4. Dabu J, Lindner M, Azzam M, et al. A Case of Chronic Cough and Pneumonia Secondary to a Foreign Body. Case Rep Med. 2017;2017:3092623. doi:10.1155/2017/3092623
  5. Mîndru DE, Păduraru G, Rusu CD, et al. Foreign Body Aspiration in Children-Retrospective Study and Management Novelties. Medicina (Kaunas). 2023;59(6):1113. Published 2023 Jun 9. doi:10.3390/medicina59061113
  6. Goodloe JM, Soulek J. Foreign Bodies . In: Rosen’s Emergency Medicine Concepts and Clinical Practice. 10th ed. Elsevier; 2023:666-681.
  7. Hazra TK, Ghosh AK, Roy P, Roy S, Sur S. An impacted meat bone in the larynx with an unusual presentation. Indian J Otolaryngol Head Neck Surg. 2005;57(2):145-146. doi:10.1007/BF02907672
  8. Swanson KL, Edell ES. Tracheobronchial foreign bodies. Chest Surg Clin N Am. 2001;11(4):861-872.
  9. Kazmerski T, Dedhia K, Maguire R, Aujla S. Chronic Esophageal Foreign Body Presenting as Wheezing and Cough in a Toddler. Pediatr Allergy Immunol Pulmonol. 2014;27(3):151-153. doi:10.1089/ped.2014.0370
  10. White JJ, Cambron JD, Gottlieb M, Long B. Evaluation and Management of Airway Foreign Bodies in the Emergency Department Setting. J Emerg Med. 2023;64(2):145-155. doi:10.1016/j.jemermed.2022.12.008
  11. António P, Raffaella C, Luigia R. Plain Film and MDCT Assessment of Neck Foreign Bodies. 2014;1007/978-88-470-5406-6_1.
  12. Svedström E, Puhakka H, Kero P. How accurate is chest radiography in the diagnosis of tracheobronchial foreign bodies in children?. Pediatr Radiol. 1989;19(8):520-522. doi:10.1007/BF02389562
  13. Turk D, Moslehi MA, Hosseinpour H. Role of Flexible Fiberoptic Bronchoscopy in the Diagnosis and Treatment of Pediatric Airway Foreign Bodies: A 5-Year Experience at a Tertiary Care Hospital in Iran. Tanaffos. 2022;21(3):354-361.
  14. Pavitt MJ, Swanton LL, Hind M, et al. Choking on a foreign body: a physiological study of the effectiveness of abdominal thrust manoeuvres to increase thoracic pressure. Thorax. 2017;72(6):576-578. doi:10.1136/thoraxjnl-2016-209540
  15. Bodart E, Gilbert A, Thimmesch M. Removal of an unusual bronchial foreign body: rigid or flexible bronchoscopy?. Acta Clin Belg. 2014;69(2):125-126. doi:10.1179/2295333714Y.0000000006
  16. Davis RJ, Stewart CM. Complete Glottic Obstruction by an Unusual Foreign Body. Otolaryngol Head Neck Surg. 2019;160(5):935-936. doi:10.1177/0194599818824298
  17. Singh GB, Aggarwal D, Mathur BD, Lahiri TK, Aggarwal MK, Jain RK. Role of magill forcep in retrieval of foreign body coin. Indian J Otolaryngol Head Neck Surg. 2009;61(1):36-38. doi:10.1007/s12070-009-0031-7
  18. White Upper Airway Foreign Bodies: Emergency department presentation, Evaluation and Management. emDOCs.net – Emergency Medicine Education. April 12, 2021. Accessed May 9, 2023. http://www.emdocs.net/upper-airway-foreign-bodies-emergency-department-presentation-evaluation-and-management/.
  19. Pinto A, Scaglione M, Pinto F, et al. Tracheobronchial aspiration of foreign bodies: current indications for emergency plain chest radiography. Radiol Med. 2006;111(4):497-506. doi:10.1007/s11547-006-0045-0

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

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.

Asthma (2024)

by Mohamed Elamin Salama & Ahmed Norain 

You have a new patient!

A 40-year-old female with a known case of asthma presents to the emergency department (ED) with complaints of cough, difficulty breathing, chest tightness, and audible wheezing. She has had fever and flu symptoms for three days, which she believes she caught from a colleague at work. She has taken her prescribed home medications with no relief. Her symptoms got worse over the last 2 hours. Her vitals were BP 140/90 mmHg, HR 122 bpm, RR 42 bpm, and SpO2 92% on room air. The physical exam revealed the use of accessory muscles for respiration, expiratory wheezing, and decreased breath sounds with expiratory rhonchi bilaterally. 

a-photo-of-a-40-year-old-female-(image produced by using ideogram2.0)

Nebulized short-acting beta2-agonists (SABA) and systemic corticosteroids were ordered. Peak expiratory flow (PEF) measurements before and after treatment were 125 and 360, respectively. Auscultation after initial treatment revealed much-improved airflow. The patient was discharged following clinical improvement, with a prescription of oral corticosteroids in addition to her current medications.

What do you need to know?

Importance

Asthma is characterized by recurrent symptoms of reversible airway obstruction that range in severity, including bronchial hypersensitivity, hyperresponsiveness, bronchospasm, inflammation, and bronchial hypersensitivity [1,2]. While the exact causes of asthma, a complex chronic disease of the airways, are still not fully understood, researchers continue to study the condition. The high cost of managing and treating asthma is a barrier to effective asthma management. Lack of access, non-compliance with asthma treatment, and excessive reliance on emergency rooms significantly impact asthma morbidity and mortality [1].

Epidemiology

The prevalence of asthma is higher in children than in adults, in women than in men, and in Puerto Ricans and African Americans than in whites or other Hispanics. Adults aged 65 and older have been reported to have the highest death rates, while children 0 to 4 years old have the lowest rates. Asthma deaths were 1.3 times more common in women than in men. The mortality rate from asthma was 2.5–3 times higher among African Americans than among whites [1].

Pathophysiology

Asthma can be divided into allergic and non-allergic based on the presence or absence of immunoglobulin E (IgE) antibodies to common environmental antigens (pollen, dander, mites) and microbiologic antigens (bacteria, viruses). The presence of airway T-helper cells, which release cytokines like interleukin [IL]-4, IL-5, and IL-13 to promote basophil, eosinophil, mast cell, and leukocyte migration to the airways and increase IgE production, is a characteristic of all types of asthma. The outcome is an exacerbation of the inflammatory response in the airways and, over time, irreversible remodeling of the airways. Clinical manifestations of these intricate cellular interactions include bronchospasm, mucus production, airway edema, and airflow restriction [1].

Medical History

Initial history inquiries should include potential triggers, symptom onset, and severity, particularly compared to prior exacerbations. Physicians should also identify comorbidities, particularly those that might be worsened by systemic corticosteroids, like diabetes, peptic ulcer disease, hypertension, and psychosis. All current asthma medications and the times and dosages taken recently should be highlighted. Moreover, any potential asthma aggravators, such as aspirin or nonsteroidal anti-inflammatory drugs (NSAIDs), beta-blockers (including topical agents used for glaucoma), and angiotensin-converting enzyme inhibitors, should also be noted. The use of beta-blockers, both cardioselective and nonselective, increases emergency room visits and hospitalizations. There is a variance in dyspnoea perception among asthmatics with the same degree of airway narrowing. Patients with poor perceptions of their dyspnoea are more likely to require emergency room visits and hospital stays and experience near-fatal and fatal asthma attacks [1].

Physical Examination

Asthma is characterized by classical symptoms such as cough, shortness of breath, and wheezing. Additional clinical features often observed in asthma patients include tachypnea, tachycardia, chest tightness, and cyanosis. In more severe cases, patients may present with the use of accessory muscles for breathing, a “silent chest” (indicative of minimal airflow), altered level of consciousness, or even collapse, highlighting the potential severity of this respiratory condition.

The physical examination findings and some bedside test results for asthma patients vary depending on the severity of the acute asthma attack [3].

For moderate asthma, patients may exhibit increasing symptoms with a peak expiratory flow (PEF) of 50–75% of the predicted value, but they show no physical signs of acute severe asthma.

In acute severe asthma, physical examination may reveal a PEF of 33–50% of the predicted value, a respiratory rate ≥25 breaths per minute, a heart rate ≥110 beats per minute, and an inability to complete sentences in one breath due to shortness of breath.

For life-threatening asthma, physical findings can include altered consciousness, exhaustion, cyanosis (bluish discoloration of the skin), a silent chest (indicative of critically reduced airflow), arrhythmias, and hypotension. Measurements include a PEF of less than 33% of the predicted value, oxygen saturation (SpO₂) below 92%, and normal arterial partial pressure of carbon dioxide (PaCO₂) between 4.6–6.0 kPa, despite the severity of the attack.

In the case of near-fatal asthma, the physical exam may demonstrate poor respiratory effort, and the condition is characterized by elevated PaCO₂ levels or the need for mechanical ventilation with raised inflation pressures, reflecting a critically severe respiratory compromise.

These findings collectively aid in categorizing the severity of asthma attacks and guiding appropriate management.

Alternative Diagnoses

When treating acutely breathless patients, it is imperative to consider aetiologies other than asthma. The differential diagnoses include pneumonia, COPD exacerbation, upper airway obstruction, foreign body aspiration, pulmonary embolism, congestive heart failure, allergic anaphylactic reaction, and gastroesophageal reflux disease. Any of these diagnoses can present concurrently with asthma [1,3].

Acing Diagnostic Testing

In the evaluation and management of acute asthma exacerbations, several diagnostic tools can aid in assessing the severity of the condition and guiding treatment decisions:

Peak Expiratory Flow Rate (PEFR)

Peak Expiratory Flow Rate (PEFR) should be measured in all asthma patients presenting with acute exacerbations as it provides an objective assessment of airway obstruction severity. If a patient is unable to perform the PEFR test, this inability is a critical indicator of severe airway obstruction and necessitates urgent management. PEFR is most valuable when compared to the patient’s previous personal best measurement, as it reflects their baseline respiratory function. In cases where the personal best measurement is unavailable, the predicted PEFR percentage, calculated based on the patient’s age, sex, and height, serves as a practical alternative to estimate the severity of the airway obstruction. Regular monitoring of PEFR can assist in early detection of exacerbations and guide treatment adjustments.

Pulse Oximetry

This non-invasive method is crucial for determining the effectiveness of oxygen supplementation, especially in children or other patients unable to perform PEFR. The target SpO₂ is 94%-98%, with levels below 90% signaling the need for more aggressive therapy.

Capnography

Capnography is valuable for monitoring hypercapnia and respiratory failure in asthma patients. Waveform capnography provides continuous monitoring, showing changes in airway diameter and improvements during acute asthma management.

Blood Gas Analysis

Routine arterial blood gas (ABG) analysis is not typically indicated in acute asthma exacerbations. However, ABG testing should be considered when SpO₂ is below 92% or when PEFR is less than 50% of the patient’s personal best or predicted value, to identify hypercapnia and guide critical care.

Other blood testing

Routine blood testing is not recommended for acute asthma exacerbations. However, in older patients with cardiovascular comorbidities, B-type natriuretic peptide (BNP) levels may be useful to detect unrecognized congestive heart failure.

A chest radiograph (CXR)

Although not routinely required, a chest X-ray may be warranted in cases of suspected complications such as pneumonia, pneumothorax, pneumomediastinum, subcutaneous emphysema, or congestive heart failure.

Electrocardiogram (ECG)

ECG is helpful for assessing patients with chest pain or cardiovascular disease, where the asthma exacerbation may act as a physiologic stressor. In severe asthma, ECG may show a reversible right ventricular strain pattern. Continuous cardiac monitoring is advised for patients with severe hypoxemia.

Point of care ultrasound (POCUS)

Increasingly used in emergency settings, POCUS aids in diagnosing complications like pneumothorax and heart failure in patients with acute dyspnea, offering rapid, bedside insights [4].

Risk Stratification

There are several risk stratification tools for asthma, particularly for the pediatric population. MDCalc offers various tools to evaluate asthma severity and predict future exacerbations. One such tool is the PEFR (Peak Expiratory Flow Rate) estimator, which provides expected PEFR values based on the patient’s age, height, and ethnicity. Additionally, this tool allows clinicians to input the patient’s measured PEFR and offers management suggestions tailored to the patient’s condition. These tools, among others, can assist physicians in managing asthma patients more effectively.

However, in time-sensitive situations, there may not be enough time to use such tools, requiring immediate recognition of risk factors for death from asthma [1,5], which include:

  • History of sudden severe exacerbations
  • Prior intubation for asthma
  • Prior asthma admission to an intensive care unit (ICU)
  • Two or more hospitalizations for asthma in the past year
  • Three or more emergency department (ED) care visits for asthma in the past year
  • Hospitalization or an ED care visit for asthma within the past month
  • Use of more than two MDI short-acting beta-2 agonist canisters per month
  • Current use of or recent withdrawal from systemic corticosteroids
  • Difficulty perceiving severity of airflow obstruction.
  • Comorbidities such as cardiovascular diseases or other systemic problems
  • Serious psychiatric disease or psychosocial problems
  • Illicit drug use, especially inhaled cocaine, and heroin

Management

Effective management of acute asthma exacerbations involves a combination of pharmacological and non-pharmacological interventions tailored to the severity of the patient’s condition. Below is a detailed explanation of these management strategies:

Oxygen Therapy

Oxygen supplementation should be provided to all hypoxemic patients to maintain oxygen saturation (SpO₂) within the target range of 94%-98%. Adequate oxygenation is critical for preventing further respiratory compromise.

Beta-2 Agonist Bronchodilators

Short-acting beta-2 agonists, such as albuterol, are first-line agents for treating acute asthma attacks and should be initiated promptly. Albuterol can be administered via nebulization at a dose of 2.5–5 mg or with a metered-dose inhaler (MDI) delivering 6–12 puffs. The use of an MDI with a spacer provides comparable benefits to nebulization in both adults and children in emergency settings [6]. For patients who cannot use inhaled therapy effectively, intravenous (IV) or subcutaneous beta-2 agonists may be considered, although evidence supporting their use in ventilated or critically ill patients remains limited.

Anticholinergic Agents

Anticholinergic medications, such as ipratropium, are less potent than beta-2 agonists and have a slower onset of action, so they should not be used alone for acute attacks. However, combining a short-acting beta-agonist (SABA) with ipratropium is particularly beneficial in moderate to severe exacerbations, reducing hospitalizations and improving peak expiratory flow rates (PEFR). The initial adult dose of ipratropium is 250–500 mcg.

Corticosteroids

Corticosteroids are essential in the early management of acute asthma exacerbations. Both oral and intravenous (IV) corticosteroids are equally effective, with no additional benefit from adding inhaled corticosteroids to systemic therapy. The recommended oral dose is 50 mg of prednisone, while IV therapy typically involves 125 mg/day of methylprednisolone in one or two divided doses.

Magnesium

Magnesium sulfate is a bronchodilator that relaxes bronchial smooth muscles, making it particularly useful in severe asthma attacks. It is recommended for adults with PEFR <25% of the predicted value, adults and children with persistent hypoxia after initial treatment, and children with PEFR <60% after one hour of care. Magnesium has been shown to reduce hospital admission rates in these patients.

Epinephrine

For asthma patients with concurrent angioedema or anaphylaxis, epinephrine should be administered intramuscularly at a dose of 0.3 mg. This is an adjunct to standard asthma therapies.

Heliox (Helium-Oxygen Therapy)

Heliox reduces airway resistance and enhances the bronchodilatory effects of albuterol [7]. It also reduces respiratory muscle workload and improves ventilation by facilitating carbon dioxide diffusion. Heliox may be considered in severe airflow obstruction (PEFR <30% predicted), rapid onset of symptoms within 24 hours, a history of labile asthma or prior intubation, or in cases where mechanical ventilation is inadequate.

Ketamine

Ketamine, an IV dissociative agent with bronchodilatory properties, is a valuable adjunctive therapy in refractory status asthmaticus when standard treatments are insufficient [8].

High-Flow Nasal Cannula (HFNC)

HFNC delivers high concentrations of oxygen, reduces work of breathing, and provides continuous positive airway pressure. While its role in adults with asthma is not well-defined, small studies suggest it may alleviate respiratory distress in children.

Non-Invasive Ventilation (NIV)

NIV may benefit select patients with severe and resistant asthma. However, it is not a substitute for endotracheal intubation and mechanical ventilation when these are indicated.

Intubation and Mechanical Ventilation

Approximately 2% of all asthma exacerbations, and 10%-30% of cases requiring ICU admission, necessitate intubation. Indications for intubation include altered consciousness, coma, respiratory or cardiac arrest, paradoxical breathing patterns, refractory hypoxemia, and failure of NIV.

Extracorporeal Membrane Oxygenation (ECMO)

In patients with asthma refractory to conventional ventilator management, ECMO may be considered as a last resort to provide oxygenation and ventilation support.

These therapeutic approaches, used in a stepwise manner based on severity, help optimize outcomes for patients experiencing acute asthma exacerbations. Early intervention, combined with evidence-based management, remains critical in preventing complications and reducing mortality.

Special Patient Groups

Pediatrics

For pediatric patients, the recommended initial dose of albuterol is 0.15 mg/kg/dose (0.03 mL/kg/dose), with a maximum dose of 5 mg via nebulization. Alternatively, administering 4–12 puffs of a short-acting beta-agonist (SABA) via a metered-dose inhaler (MDI) with a spacer provides equivalent bronchodilation compared to nebulized therapy. The initial dose of ipratropium bromide depends on the child’s weight: 250 micrograms for children weighing less than 20 kg and 500 micrograms for those over 20 kg.

In terms of corticosteroids, dexamethasone is an effective alternative to prednisone for managing acute asthma in the emergency department, offering comparable efficacy with fewer doses, less vomiting, and improved compliance. For moderately to severely ill children, continuous nebulized albuterol, corticosteroids, magnesium sulfate, and parenteral SABAs form the cornerstone of management.

Admission to the Pediatric Intensive Care Unit (PICU) is indicated for children with continued severe respiratory distress, altered mental status, or the need for advanced interventions such as intravenous SABAs, non-invasive ventilation (e.g., BiPAP), or mechanical ventilation.

Geriatrics

In elderly patients, asthma symptoms may go unreported as they may attribute their shortness of breath to aging, obesity, or comorbid cardiovascular conditions. It is essential for physicians to inquire about all home medications, including eye drops, and carefully consider potential drug interactions to avoid complications.

Pregnancy and Breastfeeding

Asthma exacerbations during pregnancy should be treated in the same manner as in nonpregnant patients. There are no contraindications to using any asthma medication in breastfeeding patients, making treatment decisions more straightforward and ensuring both maternal and infant safety.

When To Admit This Patient

Relapse rates among asthmatic patients discharged from the emergency department (ED) vary significantly, ranging from 11% within 3 days to 45% at 8 weeks.

The Emergency Department Disposition Decision-Making Guidelines assist in determining the appropriate care site for asthmatic patients based on their peak expiratory flow (PEF) percentages and response to treatment [1]. Below are the key details for each category:

Good Response

  • PEF (% predicted/personal best): Approximately 60% or higher.
  • Disposition Site: Patients with a good response are typically discharged home. Hospitalization is not necessary.

Incomplete Response

  • PEF (% predicted/personal best): Between 40% and 60%.
  • Disposition Site: The decision to send patients home or hospitalize them depends on the presence of risk factors outlined in Box 1. A careful evaluation is required to decide the appropriate course of action.

Poor Response

  • PEF (% predicted/personal best): Less than 40%.
  • Disposition Site: Patients in this category are not discharged home and require continued therapy in the emergency department. Hospitalization is necessary if the facility is available and appropriate.

Additional Factors Increasing the Likelihood of Admission

  • Female sex, older age, and non-white race.
  • Use of more than 8 beta-agonist puffs in the past 24 hours.
  • Severity of exacerbation, such as the need for rapid medical intervention upon arrival, respiratory rate >22, oxygen saturation <95%, and final PEF <50% predicted.
  • Past history of intubations or asthma-related hospital admissions.
  • Previous use of oral corticosteroids (OCS).
    These guidelines ensure that patients receive care tailored to the severity of their asthma exacerbation and associated risk factors.

The risk factors for death from asthma can be categorized into asthma history and other factors [1]:

Asthma History:

  • A history of near-fatal asthma that required intubation and mechanical ventilation.
  • Hospitalization or emergency department (ED) visits for asthma in the past year.
  • Current or recent use of oral corticosteroids, which is a marker of event severity.
  • Not currently using inhaled corticosteroids.
  • Overuse of short-acting beta-agonists (SABAs), particularly using more than one canister per month.
  • Poor adherence to asthma medications or a lack of adherence to a written asthma action plan.

Other Factors:

  • Presence of psychosocial problems.
  • Psychiatric diseases.
  • Food allergies in individuals with asthma.

Revisiting Your Patient

The patient in the case presentation is a 40-year-old female with known asthma. She presented with asthma exacerbation due to upper respiratory tract infection with sick contact at work. In the history, asking for any other potential triggers of an acute exacerbation, including potential allergen, onset of symptoms, and severity, is useful. Physical examination should focus on signs that help categorize the disease’s severity and guide a management plan. Like any other emergency, initial evaluation and management should highlight the “ABCDs” assessment (Airway, Breathing, Circulation, and Disability), along with imitation of the appropriate and time-sensitive diagnostic and therapeutic interventions (in our case, initiation of SABA and systemic steroids).
Additionally, Peak Expiratory Flow Rate (PEFR) should be performed for all asthmatics presenting with acute exacerbation who can perform the test. Patients who are unable to perform the test should be considered to have severe airway obstruction. If the patient is fit for discharge, prescription medications and appropriate follow-up appointments should be initiated, with strict return precautions to the emergency department as needed.

Authors

Picture of Mohamed Elamin Salama

Mohamed Elamin Salama

Dr. Salama is currently a Specialty Registrar in Emergency Medicine at the Thames Valley Deanery, Oxford School of Emergency Medicine. He completed his emergency medicine training at Zayed Military Hospital and has obtained both the Arab and Emirati Board certifications in Emergency Medicine. Dr. Salama is dedicated to advancing his clinical practice and actively sharing the most current developments in medical knowledge. His professional interests encompass trauma, resuscitation, sports medicine, and the promotion of public health initiatives.

Picture of Ahmed Norain

Ahmed Norain

Emergency Department, Zayed Military Hospital, Abu Dhabi

Listen to the chapter

References

  1. Walls RM, Hockberger RS, Gausche-Hill M, Erickson TB, Wilcox SR. Rosen’s Emergency Medicine: Concepts and Clinical Practice, 10th edition. Elsevier; 2023.
  2. Gary T Kitching, Jason B Lee. Asthma in Adults. RCEMLearning. Accessed March 8, 2023. https://www.rcemlearning.co.uk/reference/asthma-in-adults/#1568193285479-ef3b01a0-b2ab
  3. Global Initiative for Asthma. GLOBAL STRATEGY for ASTHMA MANAGEMENT and PREVENTION Updated 2022.; 2022. https://ginasthma.org/wp-content/uploads/2022/07/GINA-Main-Report-2022-FINAL-22-07-01-WMS.pdf
  4. Zanobetti M, Scorpiniti M, Gigli C, et al. Point-of-Care Ultrasonography for Evaluation of Acute Dyspnea in the ED. Chest. 2017;151(6):1295-1301. doi:10.1016/j.chest.2017.02.003
  5. D’Amato G, Vitale C, Molino A, et al. Asthma-related deaths. Multidiscip Respir Med. 2016;11:37. Published 2016 Oct 12. doi:10.1186/s40248-016-0073-0
  6. Krylov V, Greuel J. Are bronchodilator nebulizers superior to MDIs for the treatment of acute asthma exacerbations? Evidence-Based Practice. 2018;21(6):3. doi:https://doi.org/10.1097/01.EBP.0000545148.85715.aa
  7. Kress JP, Noth I, Gehlbach BK, et al. The utility of albuterol nebulized with heliox during acute asthma exacerbations. Am J Respir Crit Care Med. 2002;165(9):1317-1321. doi:10.1164/rccm.9907035
  8. Ueoka m, antonette subia g, lai hipp c, tawata w, chung-esaki h. Ketamine infusion for refractory status asthmaticus: a case series. Chest. 2021;160(4):a5. doi:https://doi.org/10.1016/j.chest.2021.07.062

Additional Resources

 

Reviewed and Edited By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

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.

COVID-19 (2024)

by Pei Shan Hoe, Andrew Mariotti, Prem Menon, Alexandra Digenakis

You have a new patient!

A 64-year-old male, Mr Fox, with a history of type II diabetes mellitus, hypertension, congestive heart failure, and cerebrovascular accident with chronic left-sided weakness, presented to the emergency room from a nursing home due to fever, cough, and difficulty in breathing. Per EMS, the patient’s nursing home has had an outbreak of COVID-19 infections. Mr Fox is unvaccinated against COVID-19 and has not been tested for COVID-19 before arrival. The onset of symptoms was 2 days ago, and his symptoms have progressively worsened. At the nursing home, the patient was in acute distress and was tachycardic (130 bpm), tachypneic (30 rpm), and hypoxic (82% on room air). Oxygen saturation improved to 89% on placement of a nonrebreather mask by EMS. He was borderline hypotensive (90/50 mmHg) but improved to 100/60 mmHg after 500cc of IV normal saline. On arrival, the patient appears diaphoretic and tachypneic with O2 saturation of 90% on 15L of O2 via a nonrebreather mask. Mr. Fox is alert but confused and unable to answer questions. He is febrile to 102.3F (39.1oC), remains tachycardic (132 bpm), and his blood pressure is stable at 103/67 mmHg, with delayed capillary refill (2 to 3 seconds). Mr Fox is coughing throughout the examination and has diffuse rales on auscultation of his lungs but has no obvious pitting oedema or JVD.

What do you need to know?

Importance

The COVID-19 pandemic threw the world into a tumultuous few years of fear, death, and isolation as many countries tightened borders and restricted activities. As of March 2023, there have been over 761 million confirmed cases of COVID-19 globally – including almost 7 million deaths – since the virus was first discovered in late 2019, as reported by the World Health Organisation (WHO) [1]. Healthcare institutions bore the brunt of the pandemic’s wrath as wave after wave of case surges drained resources and manpower, overwhelming hospitals and exposing healthcare workers to increased risks. Emergency departments became the frontlines of this battle against a new virus, unprecedented in its worldwide scale and extent of physical and economic disruption. This chapter lays out key information in the assessment and management of the COVID-19 infection, which are important as the virus continues to plague humankind and mutations surface.

Epidemiology

The COVID-19 virus belongs to a family of coronaviruses, which are known to produce respiratory diseases in humans. There have been three major coronavirus outbreaks in recent times, beginning with the severe acute respiratory syndrome coronavirus (SARS) in 2002, followed by the Middle East respiratory syndrome coronavirus (MERS) in 2012, and now the COVID-19 pandemic in 2019 [2].

Reports of COVID-19 cases first emerged from Wuhan, China, at the end of 2019; the virus spread rapidly to other countries worldwide, with cases reported in all continents. On March 11, 2020, WHO declared COVID-19 as a pandemic [3].

Person-to-person spread is the main mode of COVID-19 transmission. The mean or median incubation period ranges from 5 to 6 days. The duration for which a patient with COVID-19 remains infective is unclear. Viral load in the oropharyngeal secretions is highest during the early symptomatic stage of the disease. The patient can continue to shed the virus even after symptom resolution [4,5].

Pathophysiology

The virus is transmitted via respiratory droplets and aerosols from person to person. Once inside the body, the virus binds to host receptors and enters host cells through endocytosis or membrane fusion. After membrane fusion, the virus enters the lungs’ alveolar epithelial cells, and the viral contents are released. The virus undergoes replication within the host’s cells [5].

Medical History

What are the key features that should be interrogated in medical history?

Common symptoms: fever, cough and fatigue.

Other reported symptoms, typically milder and less common, are loss of taste or smell, conjunctivitis, headache, muscle aches and pains, nasal congestion, runny nose, sore throat, diarrhoea, nausea or vomiting, and different types of skin rashes.

Ask also about symptoms of pulmonary embolism, as COVID-19 can be a risk factor. These include sudden and sharp chest pain, dyspnea that worsens on exertion, and coughing that may produce bloody mucus.

There are also some people who become infected but remain asymptomatic and well [6,7,8].

What are the risk factors related to the specific disease in focus that should be picked up in medical history?

Check for any COVID-19 contact, and if the patient is vaccinated against COVID-19 Unvaccinated patients with positive contact are at higher risk of developing infection though vaccinated patients can contract COVID-19 despite vaccination.

What are the red flags that indicate a worse outcome in a patient with this specific disease?

Red flag symptoms that patients should monitor for include difficulty breathing or shortness of breath, confusion, loss of appetite, persistent pain or pressure in the chest [6,8].         

Physical Examination

What are the key features that should be checked during a physical examination?

Check the patient’s following systems:

  • Head, ear, nose and throat
  • Cardiovascular system
  • Respiratory system
  • Gastrointestinal system
  • Skin

What are the findings related to the specific disease in focus that should be picked up during physical examination?

Look out for signs such as [6-10]:

  • Abnormal breath sounds in lungs suggestive of pneumonia, which is the most frequent serious manifestation of infection
  • Abdominal tenderness
  • Conjunctivitis
  • Skin changes, such as maculopapular/morbilliform, urticarial, and vesicular eruptions, transient livedo reticularis, reddish-purple nodules on the distal digits similar in appearance to pernio (chilblains), also known as “COVID toes”
  • Leg swelling, erythema or tenderness on examination

What are the red flags that indicate a worse outcome in a patient with this specific disease?

Red flag signs include [6-10]:

  • Signs of venous thromboembolism, such as deep vein thrombosis — erythema, tenderness and swelling of the lower limbs
  • Arrhythmias
  • EncephalopathyRespiratory distress

Alternative Diagnoses

What other diseases can present with similar clinical features/conditions?

Differential diagnoses of COVID-19 include [11]:

  • Community acquired pneumonia, and other forms of pneumonia (e.g. aspiration pneumonia, pneumocystis jirovecii pneumonia)
  • Influenza
  • Middle East respiratory syndrome (MERS)
  • Avian influenza virus infection
  • Pulmonary tuberculosis

Which risk factors make COVID-19 more probable than alternative differentials?

Risk factors for COVID-19 include:

  • Close contact with COVID-19 patients
  • Lack of COVID-19 vaccinations

Acing Diagnostic Testing

Diagnosing COVID-19 infections may involve the use of multiple modes of testing and evaluation. In this section, we will discuss the role that bedside tests, lab studies, and imaging play in diagnosing and treating COVID-19.

Bedside Tests

Testing for COVID-19 that can be done at the bedside falls into one of two categories: antigen testing or nucleic acid amplification testing (NAAT), sometimes known as PCR testing due to the use of polymerase chain reaction (PCR) methods to amplify the DNA samples in question. Both have a place in testing for COVID but indications for use and the subsequent results should be approached thoughtfully.

Antigen Testing

With antigen testing, a nasal or oropharyngeal swab – or even a blood sample – is used to collect mucosal secretions and saliva from the patient with a suspected COVID infection. The sample is placed in a lateral flow assay that contains antibodies to COVID antigen with a detector molecule attached. If the sample contains COVID antigen, the antibodies will bind and read as a positive test. Rapid testing can yield results in under a half-hour with 99.4% specificity and 68.4% sensitivity, is conducive for self and at-home administration, and has been an effective method for increasing access to testing [12]. Due to its high specificity, rapid testing is reliable when positive, however, one of the major drawbacks is its low sensitivity. It is important to understand that patients who test negative for COVID via an antigen test cannot be reliably ruled out for the disease until it has been verified with NAAT testing.

NAAT Testing

This form of testing – while still utilizing swabbed samples of mucosal secretions and saliva as in antigen testing – relies on a different method of disease verification using PCR and COVID specific RNA primers to amplify any viral DNA present in the sample. Results yield similar levels of specificity (98.9 – 99.2%) but have a markedly higher sensitivity of 83.2 – 84.8% making this a much more reliable testing option [13]. The major drawback to this method of testing is that it cannot be administered at home and must be done where there is a lab present that has a technician with the knowledge to perform the testing using the PCR machine.

Laboratory Tests

If both antigen and NAAT testing returns negative – or if NAAT results are pending after a negative antigen test – clinicians will often opt to send for a respiratory viral panel to determine if there is an underlying primary or comorbid infection. A respiratory viral panel uses PCR to test for a standard slate of viruses that usually includes influenza, respiratory syncytial virus (RSV), adenovirus, parainfluenza virus, adenovirus, rhinovirus, enterovirus, and human metapneumovirus.

While no specific set of labs is directly indicative of a COVID-19 infection, a specific constellation of lab findings has been found to be suggestive of potential COVID infection when pretest probability is high. These lab findings include lymphopenia, transaminitis – specifically elevations in AST – and an elevated c-reactive protein [14]. While not diagnostic, this constellation of laboratory results can lend support to a future diagnosis and help guide early treatment.

Imaging

Neither Magnetic Resonance Imaging (MRI), Computed Tomography (CT), nor X-ray can provide a conclusive diagnosis of COVID-19. Ground glass opacities seen on CT are a typical finding in COVID-19 infection and have been proven effective at differentiating COVID-19 and non-COVID-19 viral illnesses in certain retrospective analyses [15]. Despite this, the presence of ground glass opacities alone does not provide definitive diagnosis and would only be indicated for diagnostic purposes if COVID pre-test probability was already high due to known community presence or recent exposures [16].

Figure 1: ground glass opacities on chest CT[16]

Imaging becomes far more important when diagnosing two major sequelae of COVID-19: pneumonia and acute respiratory distress syndrome (ARDS). The prolonged, severe pulmonary inflammation of COVID-19 causes damage to capillaries and leakage of fluid into the alveoli leading to ARDS. This should be suspected in those who develop acute onset shortness of breath, hypoxemia, and/or rattling breath sounds. A chest x-ray showing a classic “white out” appearance can greatly aid in diagnosis of ARDS.

Figure 2: A chest x-ray showing classic ARDS findings[17]

Similarly, opportunistic bacterial infections can take root in damaged lung tissue secondary to COVID infection, leading to bacterial pneumonia. This should be a major consideration in patients who rapidly develop shortness of breath or pleuritic chest pain. A chest x-ray showing lung field consolidations can greatly aid in the diagnosis of pneumonia.

Figure 3: A chest x-ray showing classic consolidated findings of pneumonia[18].

Risk Stratification

When stratifying the potential risk of severity of COVID-19, the two major considerations are age and the number and type of comorbidities. Global data evaluating age in relation to COVID mortality during the early stages of the pandemic demonstrated a less than a 1.1% mortality rate in those younger than 50 years but an overall mortality rate of 12.1% among those greater than 80 years old, with each subsequent decade in between demonstrating increased mortality rates from the prior decade [19].

Furthermore, the presence of comorbid conditions increased morbidity and mortality compared to the general population, with cardiovascular disease and diabetes respectively acting as significant predictors for future intensive care requirements and lower survival rates [20]. Though individual comorbidities present a lesser risk than age alone, patients with multiple comorbidities are at greater risk of mortality than those who present with one comorbid condition. Studies have shown 10 or greater comorbidities result in a 3.8-fold increase in RR as compared to those with 1 comorbidity [21].

Risk Stratification Tools

Many tools exist to stratify patients into risk categories based on covid infection based on the setting and presentation of the patient. The notable tools with a description of their intended use are described below.

  • 4C Mortality Score – This tool was developed by the International Severe Acute Respiratory and emerging Infection Consortium (ISARIC) to predict in-hospital mortality of COVID based on age, oxygenation, renal function, and other statistical measures.
  • ACEP ED COVID-19 Management Tool – Developed by emergency physicians from around the world, this tool walks the clinician through the steps of managing a patient with COVID in an emergent setting from severity classification to treatment.
  • Pediatric COVID Risk Assessment Tool – Physicians at the University of California San Francisco created this tool to assess the risk of children with asymptomatic infection.

Management

Management options in unstable patients begin with determining the severity of disease. Mild disease presents with symptoms characteristic of upper respiratory infections such as fever, cough, malaise, and rhinorrhea. Acute, life-threatening airway, breathing and circulation concerns are absent in mild disease.

In moderate to severe disease, one of the initial signs is dyspnea. Severe disease specifically is defined by hypoxemia (oxygen saturation at or below 94% on room air) which may or may not require supplemental oxygen or even intubation. In the case of severe disease initial stabilization is followed by medical management and even certain procedures. These are described below.

Initial Stabilization

The steps to initial stabilization for severe COVID-19 infection are described below in terms of the ABCs of emergency medicine.

  • Airway – The patient should be evaluated for the ability to protect and maintain the airway. Signs that a patient may require or soon require intubation include worsening hypoxia despite maximized oxygen supplementation, increased work of breathing, and signs of distress.
  • Breathing & Circulation—Assuming patients can maintain their airway but their oxygen saturation is still below 94% on room air, they will require supplemental oxygen. Low-flow supplemental oxygen with the nasal cannula at 1-2 liters/minute can be used initially, but high-flow supplementation via non-rebreather and even non-invasive ventilation, such as a high-flow nasal cannula or BiPap, should be considered depending on patient needs.

Once the patient is stabilized per their needed oxygen and ventilation requirements, pharmaceutical and bedside management can begin with the goal of ultimately weaning the patient from their oxygen requirements.

Medical Management

The ensuing table outlines the major pharmaceutical agents used in the treatment of COVID-19. They are described based on class, indication, contraindications and adverse effects, and dosing.

Drug

Class

Indication

Contraindications (CI) &

Adverse Effects (AE)

Dosing

Nirmatrelvir/

Ritonavir (Paxlovid)

Anti-viral

Mild to moderate COVID-19 infection for patients at risk for increased severity

CI: <12 years old or eGFR <30ml/min as well as many medications interactions

AE: dysgeusia, diarrhea, hypertension, and myalgia

eGFR > 60ml/min: 300/100mg twice daily for 5 days

 

eGFR 30-60ml/min: 150/100mg twice daily for 5 days

Dexamethasone

Glucocorticoid

Severe disease in patients requiring oxygen or ventilatory support

AE: Hyperglycemia, increased secondary infection risk

6mg/day for up to 10 days

Baricitinib

JAK Inhibitor

Severe disease in patients requiring high-flow oxygen supplementation but not intubation.

CI: Already on IL-6 inhibitors, lymphopenia, neutropenia, CKD

Max 4mg/day oral

Tocilizumab

IL-6 Inhibitor

Markedly elevated inflammatory markers (D-dimer, CRP, etc.)

CI: must already be taking dexamethasone

AE: secondary infection risk

Single dose at 8mg/kg IV

Anakinra

IL-1 Inhibitor

Severe disease in patients who are at high risk of progressing to ventilatory support

AE: anaphylaxis, stomach pain, headache, nausea

100mg/day for 10 days, subcutaneous

Remdesivir

Antiviral

Severe disease in patients who are not intubated or in need of ventilatory support. Benefits uncertain in non-severe cases.

CI: under 12 years of age

AE: nausea, vomiting, fever, hyperglycemia, transaminitis

Loading dose: 200mg IV

Maintenance Dose: 100mg/day IV for up to 10 days

Monoclonal Antibodies

Antibody Based Therapy

No longer indicated due to decreased benefit from increased circulating variants

N/A

N/A

Convalescent Plasma

Antibody Based Therapy

Patients with impaired humoral immunity who have severe disease

AE: serum sickness, anaphylaxis

1 unit of high titer convalescent plasma

Ivermectin

Anthelmintic

Patients with latent Strongyloides infection undergoing glucocorticoid therapy for COVID

CI: no studies to prove efficacy against COVID-19 itself as a primary therapeutic

AE: GI upset, neurological disturbances

200ug/kg for 1-2 days

Procedures

There are few COVID specific procedures though intubation and mechanical ventilation are common requirements in severe cases. Some patients will even progress in severity to a point that extracorporeal membrane oxygenation (ECMO) will be required.

Patients who develop ARDS, independent of COVID, may benefit from proning – a technique by which the patient is rolled onto their abdomen to increase ventilation/perfusion matching of the lungs [22].  It should be noted that any procedure which must be done that involves aerosolization (bronchoscopy, intubation and extubation, suctioning, etc.) should be done under extreme caution and only after all who are present have the appropriate personal protective equipment, as these procedures increase the risk of spreading the virus to non-infected individuals. 

Complications: Long COVID

The United States Department of Health defines Long COVID as “signs, symptoms, and conditions that continue or develop after initial COVID-19 or SARS-CoV-2 infection.” These are typically present four weeks or more after the initial phase of infection and may be multisystemic [23]. Some patients may have a “relapsing-remitting pattern and progression or worsening over time, with the possibility of severe and life-threatening events even months or years after infection.”

Those who are at higher risk of developing Long COVID include patients with more severe COVID-19 illness, or with underlying health conditions, without the COVID-19 vaccine, or who experienced multisystem inflammatory syndrome (MIS) during or after COVID-19 illness.

Special Patient Groups

This chapter has already touched on the severity of this disease from the standpoint of age and comorbidities; however, this section seeks to expand on that topic by presenting special considerations for other demographics who may be infected with COVID-19.

Pediatric Populations

Pediatric populations generally have far fewer severe outcomes and are more likely to present asymptomatically when infected with COVID-19 [24]. However, it is important to be aware of a rare but potentially life-threatening complication known as multi-system inflammatory syndrome in children (MIS-C). If a patient develops MIS-C, signs and symptoms begin to present within 2-6 weeks of infection and include ongoing fever accompanied by any of the following: stomach pain, bloodshot eyes, diarrhea, lightheadedness, rash, and vomiting. If the child’s condition continues to worsen and they develop difficulties breathing, medical attention should be sought immediately. Physicians can provide supportive care as well as treatment of the underlying infection or co-occurring infections. With timely and appropriate care, MIS-C rarely leads to death or long-term complications [24].

Geriatric Populations

Geriatric populations are those defined as over the age of 65 years and represent an extremely high-risk category even in the absence of comorbidities. Because of this, geriatric patients who contract COVID-19 infections should be watched closely and receive antiviral treatments – such as Paxlovid – as soon as possible to stem the progression of disease. Other considerations for geriatric populations that may not be immediately apparent are concerns with access. Elderly patients often require assistance walking, driving, or navigating to clinic appointments due to a higher prevalence of comorbid conditions (dementia, osteoporosis, wasting, etc.) and making care more accessible to these populations is the first step in ensuring they can get the treatment they need. This position is notably called out by the World Health Organization in their considerations for caring for elderly with COVID-19.

Pregnant Populations

Individuals who are pregnant are at increased risk of complications from COVID-19 for themselves and their child. One of the best ways to help these patients is to provide timely vaccination to either prevent or reduce the severity of initial infection. Despite controversy, a myriad of clinical trials has proven that mRNA vaccines for COVID-19 are safe and without adverse outcomes for either the mother or baby during pregnancy [25]. If a mother and her unborn child do contract COVID-19 and require hospitalization, these patients should be taken care of in facilities that have the capability to monitor the status of the fetus and uterine contractions to ensure the health and safety of mom and baby. 

When To Admit This Patient

Admission criteria for COVID-19 is very specific to the individual patient and institution practices and guidelines. In general, however, admission should be considered for patients presenting with severe COVID-19 infection. This includes but is not limited to patients that are in respiratory distress, patients requiring oxygen therapy to maintain oxygen saturations >90%, or patients unable to tolerate food, fluid, or meds by mouth. Abnormal lab work can also warrant hospital admission including patients with significant electrolyte abnormalities, kidney injury, ischemic changes on EKG or elevation in cardiac markers. Persistent vital sign abnormalities could also warrant admission, including COVID-19 patients that are persistently tachycardic even after IV fluid resuscitation and fever reduction. Age can also contribute to the threshold for admission. For example, a patient over 65 with COVID-19 infection and pneumonia on X-ray could warrant admission.

Patients that are presenting with mild COVID-19 disease, have access to follow-up, have normal vital signs and with no significant abnormalities on lab and imaging studies may be safely discharged with primary care follow-up.

It is important to provide patients with COVID-19 strict return precautions should their symptoms worsen. Particularly, these patients should be told to return if they experience any worsening shortness of breath, difficulty in breathing or abnormal home oxygen saturation readings. Patients should be warned that they may lose their sense of taste and/or smell and this is a common symptom of the disease. If patients are unable to tolerate food and/or fluid, they should be instructed to return back to the emergency department. Any new altered mental status, confusion, chest pain, focal weakness or seizures should also prompt patients to return immediately to the emergency department.

Revisiting Your Patient

Let’s return to Mr. Fox, who presented to the emergency department in respiratory distress from his nursing home. The providers have high clinical suspicion for COVID-19 infection given his exposure to COVID-19 at the nursing home, and are concerned considering his risk factors for severe disease. He is placed on contact and droplet precautions and COVID-19 tests are collected. Given his severe presentation there is concern for sepsis, a lactic acid level and blood cultures to be obtained. He is started on high-flow nasal cannula oxygenation to improve his oxygen saturation, and IV fluid resuscitation is initiated to improve his hemodynamic status. He is given acetaminophen for his fever. A chest x-ray is obtained, which demonstrates bilateral patchy infiltrates. Per discussion with Mr. Fox’s nursing home, he has not been hospitalized recently or been on any antibiotic treatment. He receives cefepime and vancomycin to treat possible hospital-acquired pneumonia given he is a nursing home resident – please refer to your institution’s antibiotics guidelines – while awaiting his COVID-19 test results. Given the high concern for COVID-19 infection and Mr. Fox’s severe hypoxia, he is also started on Dexamethasone, as this has been shown to improve mortality in patients with severe COVID-19 infections.

Despite these interventions, Mr. Fox continues to have increased work of breathing and is becoming fatigued. An arterial blood gas is obtained, which demonstrates worsening respiratory acidosis. Mr. Fox is confirmed to be full code by the nursing home, and thus the decision is made to proceed with intubation. He is placed on a ventilator and started on lung-protective ventilation settings. His COVID-19 test comes back positive. He remains persistently tachycardic despite appropriate IV fluid resuscitation and correction of his fever. His providers are concerned that he may have developed a pulmonary embolism in the setting of possible hypercoagulability associated with his COVID-19 infection. A CT scan of his chest with contrast is obtained, which demonstrates multiple right-sided pulmonary emboli without evidence of right heart strain. Mr. Fox is started on a heparin drip. He is admitted to the medical intensive care unit with the diagnoses of acute hypoxic respiratory failure secondary to COVID-19 infection and right-sided pulmonary emboli.

Authors

Picture of Pei Shan Hoe

Pei Shan Hoe

Medical Officer, Ministry of Health Holdings, Singapore.

Pei Shan Hoe is a former journalist-turned junior doctor currently working at Singapore General Hospital. She studied comparative literature as an undergrad at New York University, obtained a Masters in investigative journalism from Columbia University, and then an MD from Duke-NUS Medical School. She is an ACEP/EMRA Global EM Student Leadership Program mentee (‘22-23) and co-author of published articles related to Covid-19 and ED design. Her interests lie in global health, acute care, medical education, healthcare systems and services research. She is certified for overseas disaster deployment under Singapore Red Cross and has also participated in peacetime medical missions.

Picture of Andrew Mariotti

Andrew Mariotti

Resident Physician, University of Colorado Department of Anesthesiology

Andrew Mariotti, M.H.A, has been caring for patients since 2015 as both an emergency medical technician and administrator. In 2020, Mr. Mariotti worked as an administrative fellow under the executive board of the University of Colorado Hospital where he directly aided the coordination of the hospital’s emergency response to the COVID-19 pandemic in Denver and Aurora, Colorado. He is currently a medical student at the University of Colorado, where he serves as Vice President of the student body and his research in quality improvement has led to abstract publications with the Society of Hospital Medicine and American Society of Anesthesiologists.

Picture of Prem Menon

Prem Menon

Global Emergency Medicine Fellow, Brigham and Women’s Hospital

Prem Menon is a chief resident at Emory University’s Emergency Medicine residency program in Atlanta, Georgia. Prem began his training during the height of the COVID-19 pandemic and has managed many critically ill COVID-19 patients. His interests within Emergency Medicine include Refugee, Immigrant and Asylee health and Global Emergency Medicine. During his residency training he worked to improve emergency care globally, specifically in the country of Liberia. He is originally from Austin, Texas and obtained his medical degree at the University of Texas Health San Antonio – Long School of Medicine. He will be starting fellowship in Global Emergency Medicine at Brigham and Women’s Hospital/Harvard in the Fall of 2023.

Picture of Alexandra Digenakis

Alexandra Digenakis

Clinical Assistant Professor, East Carolina University Emergency Medicine

Alexandra Digenakis, D.O., completed her undergraduate degree at Penn State University. She completed her medical school training at the Philadelphia College of Osteopathic Medicine in 2019. She completed her emergency medicine residency at the University of North Carolina in 2022. She is currently a clinical assistant professor of emergency medicine at East Carolina University. She has a strong interest in providing education, opportunities and exposure to global health to medical students and resident physicians. She has participated in the EMRA/ACEP Global Emergency Medicine Student Leadership Program as a medical student mentee, resident co-director, faculty advisor and faculty co-director.

Listen to the chapter

References

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  14. Brinati, D., Campagner, A., Ferrari, D., Locatelli, M., Banfi, G., & Cabitza, F. (2020). Detection of covid-19 infection from routine blood exams with Machine Learning: A feasibility study. Journal of Medical Systems, 44(8). https://doi.org/10.1007/s10916-020-01597-4
  15. Elmokadem, A. H., Bayoumi, D., Abo-Hedibah, S. A., & El-Morsy, A. (2021). Diagnostic performance of chest CT in differentiating COVID-19 from other causes of ground-glass opacities. Egyptian Journal of Radiology and Nuclear Medicine, 52(1). https://doi.org/10.1186/s43055-020-00398-6
  16. Parekh, M., Donuru, A., Balasubramanya, R., & Kapur, S. (2020). Review of the chest CT differential diagnosis of ground-glass opacities in the covid era. Radiology, 297(3). https://doi.org/10.1148/radiol.2020202504
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  21. Kompaniyets L, Pennington AF, Goodman AB, et al. Underlying Medical Conditions and Severe Illness Among 540,667 Adults Hospitalized With COVID-19, March 2020-March 2021. Prev Chronic Dis. Jul 1 2021;18:E66. doi:10.5888/pcd18.210123
  22. Hadaya, J., & Benharash, P. (2020). Prone positioning for acute respiratory distress syndrome (ARDS). JAMA, 324(13), 1361. https://doi.org/10.1001/jama.2020.14901
  23. Long Covid or post-covid conditions. Centers for Disease Control and Prevention. https://www.cdc.gov/coronavirus/2019-ncov/long-term-effects/index.html. Accessed April 14, 2023.
  24. Acevedo L, Pineres-Olave BE, Nino-Serna LF, et al. Mortality and clinical characteristics of multisystem inflammatory syndrome in children (MIS-C) associated with covid-19 in critically ill patients: an observational multicenter study (MISCO study). BMC Pediatr. Nov 18 2021;21(1):516. doi:10.1186/s12887-021-02974-9
  25. Ciapponi, A., Berrueta, M., P.K. Parker, E., Bardach, A., Mazzoni, A., Anderson, S. A., Argento, F. J., Ballivian, J., Bok, K., Comandé, D., Goucher, E., Kampmann, B., Munoz, F. M., Rodriguez Cairoli, F., Santa María, V., Stergachis, A. S., Voss, G., Xiong, X., Zamora, N., … Buekens, P. M. (2023). Safety of covid-19 vaccines during pregnancy: A systematic review and meta-analysis. Vaccine, 41(25), 3688–3700. https://doi.org/10.1016/j.vaccine.2023.03.038

Reviewed By

Picture of Arif Alper Cevik, MD, FEMAT, FIFEM

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.

Question Of The Day #90

question of the day
366 - pneumonia-middle lobe

Which of the following is the most likely cause of this patient’s condition?

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with shortness of breath, productive cough, and fever for 5 days.  On exam, the patient is febrile, tachycardic, and has a low SpO2 on room air.  The lung exam demonstrates focal rhonchi at the right base.  The chest X-ray demonstrates a consolidation at the right middle lobe that obscures the right heart boarder.  The consolidation is highlighted with a red star in the patient’s X-ray below.

Lung consolidations have multiple causes, including pneumonia, malignancy, heart failure, pulmonary emboli, and septic emboli from endocarditis.  Septic pulmonary emboli (Choice A) can present with cough, fever, and difficulty breathing, but often have multiple foci of consolidations on chest X-ray.  This patient has a single area of consolidation.  This patient also lacks the typical risk factors for septic emboli, like IV drug use, recent dental procedures, structural heart disease, or prosthetic heart valves.  An infected pleural effusion (Choice B), also known as an empyema, is shown as a blunted or hazy right costo-diaphragmatic angle.  This patient’s X-ray shows no fluid in both costo-diaphragmatic recesses to indicate the presence of a pleural effusion.  A pulmonary embolism (Choice D) often presents with clear lungs on auscultation and a normal chest X-ray.  However, if the pulmonary embolism progresses to a pulmonary infarct, a wedge-shaped opacity can be seen on the X-ray.  This patient’s X-ray lacks this finding.  The most likely cause for this patient’s symptoms is a right middle lobe pneumonia (Choice C).  She should receive IV fluids, antipyretics, supplemental oxygen, and IV antibiotics.

References

[cite]

Question Of The Day #89

question of the day

Which of the following is the most appropriate next step in management?

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with acute shortness of breath, an urticarial rash, hypotension, tachycardia, swelling of the lips and tongue, and wheezing on lung exam.  This patient is in anaphylactic shock and requires prompt treatment with epinephrine.  Anaphylaxis is an IgE-mediated life-threatening allergic reaction that by definition affects two or more body systems (i.e., skin/mucosa, pulmonary, cardiovascular, gastrointestinal, etc.).  This patient has involvement of the skin (urticarial rash, mucosal swelling), cardiovascular system (hypotension and tachycardia), and pulmonary system (wheezing).  Symptoms of anaphylaxis may include urticaria, shortness of breath, wheezing, facial or airway swelling, vomiting or diarrhea, and abdominal pain.  Anaphylaxis is a clinical diagnosis and does not require vital signs to be unstable in order to be diagnosed.  Once diagnosed, the most time sensitive and lifesaving treatment is epinephrine.  The recommended initial dose for epinephrine is 0.3-0.5mg intramuscularly in the thigh for adults.  Epinephrine doses can be repeated every 5-15 minutes if there is no improvement after the initial dose. Antihistamines, like Diphenhydramine (Choice D) or famotidine may be helpful as adjunctive treatments, but they are not lifesaving.  Steroids, like Dexamethasone (Choice C), are also routinely given in anaphylaxis with the theory that they can prevent “rebound” allergic reactions.  Again, steroids are not acutely lifesaving and should be given after IM epinephrine.  IV epinephrine can be given in a patient unresponsive to IM epinephrine at a dose of 1-5mcg/min.  A dose of IV Epinephrine 1mg (1000mcg) (Choice A) is the dose of Epinephrine used during cardiac arrest and is too high of a dose to use in anaphylaxis.  The best initial step in management is IM Epinephrine 0.3mg (Choice B).  

References

[cite]

Question Of The Day #88

question of the day
Which of the following is the most appropriate next step in management?

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with shortness of breath and abdominal discomfort for 1 day.  On exam, she is hypotensive, tachycardic, and tachypneic.  Her lungs are clear, the abdomen is tender and distended, and the pregnancy test is positive.  This patient has a ruptured ectopic pregnancy until proven otherwise and requires prompt surgical management.  Once diagnosed by the Emergency clinician, ectopic pregnancy can be managed medically or surgically.  See the chart below for more details.

Treatment options for ectopic pregnancy

 

Medical Management (Methotrexate) Indicated:

Surgical Management

Indicated:

Patient hemodynamically stable

Patient hemodynamically unstable

HCG <5,000

HCG >5,000

Able to comply with Methotrexate treatment and follow up

Unable to comply with Methotrexate treatment and/or follow up

No fetal cardiac activity on ultrasound

Fetal cardiac activity present on ultrasound

   

This patient has an assumed ectopic pregnancy due to the positive pregnancy test and presence of hemodynamic instability.  A transvaginal ultrasound (Choice C) would help definitively diagnose the patient with a ruptured ectopic pregnancy, but this should not delay consultation with the OBGYN team for definitive surgical management.  Methotrexate (Choice A) is a medical treatment for ectopic pregnancy, but Methotrexate is contraindicated in ruptured ectopic due to the need for surgical treatment and intra-abdominal hemorrhage control.  IV antibiotics (Choice B) are often given preoperatively for infection prophylaxis (prevention), but this is not a crucial next step.  This patient is in shock and needs operative management. The best next step is OBGYN consultation for operative management (Choice D).

References

[cite]

Question Of The Day #87

question of the day

 

Test Value

Reference Range

BUN

14

6 – 24 mg/dL

Creatinine

0.87

0.59 – 1.04 mg/dL

Hemoglobin

5.5

12.0 – 15.0 g/dL

WBC count

5.2

4.5 to 11.0 × 109/L

HCG quantitative

0

<5 mIU/mL

Which of the following is the most like cause for this patient’s condition?

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with shortness of breath with deceased exercise tolerance or 5 days.  Her vital signs are normal and lungs are clear, but she appears pale.  The laboratory test provided shows normal kidney function, a negative serum pregnancy test, and a markedly low hemoglobin level.  A ruptured ectopic pregnancy (Choice B) can cause shortness of breath due to anemia and hemorrhagic shock, but this patient has a negative pregnancy test.  Asthma (Choice A) is unlikely given the patient’s normal lung exam without wheezing and no mention of cough.  A pulmonary embolism (Choice D) is possible due to the tachycardia, but the patient lacks other risk factors as stated in the question stem.  A D-Dimer test could help further evaluate if this patient has a pulmonary embolism, but the low hemoglobin likely explains the patient’s symptoms.  The patient’s history of menorrhagia, also known as heavy menses (Choice C), is a common cause of anemia in women of childbearing age.  Even though this patient is not currently menstruating, her heavy menses are the most likely cause for her shortness of breath.  Choice C is the best answer.

References

[cite]

Question Of The Day #86

question of the day
420 - right pneumothorax1
Which of the following is the most appropriate next step in management for this patient’s condition?

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient arrives to the Emergency department with acute onset shortness of breath with pleuritic right sided chest pain.  On exam, there is mild tachypnea and a borderline low SpO2 of 95% on room air.  The chest X-ray demonstrates a small right sided pneumothorax (see location of red stars below).

Needle decompression to the right chest (Choice C) would be the right choice if the patient had a right sided tension pneumothorax.  Signs of a tension pneumothorax are hypotension, tachycardia, tracheal deviation, and mediastinal shift on Chest X-ray.  Tension pneumothorax should be diagnosed clinically without a chest X-ray and promptly treated with needle decompression with a 14-16 gauge needle at the 2nd intercostal space in the mid clavicular line.  Needle decompression can also be performed at the 4th or 5th intercostal space in the anterior axillary line. Needle decompression is always followed by placement of a formal chest tube.  This patient does not have the hemodynamic instability or chest X-ray findings of a classic tension pneumothorax. IV Azithromycin (Choice D) would be appropriate for a COPD exacerbation or for community-acquired pneumonia.  This patient does have a cough, but lacks fever, sputum production, and also has a pneumothorax on X-ray that can explain his symptoms.  An IV Heparin bolus and infusion (Choice A) would be the ideal treatment for a pulmonary embolism or acute coronary syndrome.  Again, the Chest X-ray provided shows support for an alternative cause for the patient’s symptoms.  The best next step is supplemental oxygen (Choice B).  100% supplemental oxygen helps decrease the time to lung expansion in patients with pneumothoraces.   A nonrebreather mask at 15L/min is the ideal method to providing this level of oxygen.

This patient has a small pneumothorax (<3cm between lung margin and chest wall).  Small primary pneumothoraces have two treatment options.  The first option is to administer 100% oxygen and place a pigtail catheter for rapid lung re-expansion.  The second option is to only administer 100% oxygen administration for a period of 4-6 hours followed by a repeat chest X-ray to evaluate for improvement of the pneumothorax.   If the pneumothorax is improving and symptoms are improving (less shortness of breath and chest pain), the patient can be discharged home with close outpatient follow up and no chest tube placement.  Deciding which treatment option is best should depend on the patient’s ability to follow up with a doctor, patient reliability, and resource availability.  This patient does have a small pneumothorax by measurement, but he likely has a secondary pneumothorax from his COPD.  Secondary pneumothoraces have a higher rate of recurrence and almost always require chest tube placement.  Regardless, the best initial step in treatment is supplemental oxygen (Choice B).

References

[cite]

Question Of The Day #85

question of the day
SS Video 3  Pericardial Tamponade
Which of the following is the most likely cause for this patient’s condition?

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

This patient presented to the Emergency department with 2 days of shortness of breath without chest pain, cough, or fevers.  The exam shows tachycardia, hypotension, mild tachypnea, clear lungs, and distant heart sounds.  Tension pneumothorax (Choice B) can cause hypotension and tachycardia and COPD is a risk factor for pulmonary bleb formation and rupture.  However, the lungs are equal and clear bilaterally, so this diagnosis is not likely.  Septic shock due to pneumonia (Choice C) is also less likely as there is no fever, the lungs are clear, and the patient lacks a cough.  The ultrasound image given also provides a clear explanation for the patient’s symptoms.  This patient is at risk for pulmonary embolism (Choice A) given his cancer history which can cause a hypercoagulable state and predispose him to clot formation.  Again, an understanding of the ultrasound image will provide the diagnosis.

The ultrasound image is a subxiphoid view of the heart demonstrating a pericardial effusion (red stars) with compression of the right ventricle (yellow arrow). 

This presentation is consistent with cardiac tamponade (Choice D).  Cardiac tamponade is a condition defined by the accumulation of fluid in the pericardial sac to the point of right ventricular collapse and obstructive shock.  Common presenting symptoms of cardiac tamponade include shortness of breath, chest pain, or nonspecific symptoms.  Risk factors for this diagnosis are penetrating chest trauma (hemopericardium), cancer (malignant effusion), lupus, end stage renal disease, uremia, HIV, Tuberculosis, or history of chest radiation.  The presence of hemodynamic instability (hypotension and tachycardia) is a hallmark of this condition, although early stages of tamponade can be seen on cardiac ultrasound before vital signs decompensate.  The patient may have Beck’s triad of muffled distant heart sounds, jugular venous distension, and hypotension, although the majority of patients with cardiac tamponade do not have all three of these signs together.  Treatment involves IV fluids, bedside pericardiocentesis (ultrasound guided preferred), and surgical pericardiotomy (“pericardial window”).

References

[cite]

Question Of The Day #84

question of the day
475.3 xray abdomen series normal chest
Which of the following is the most appropriate next step in management for this patient’s condition?

Shortness of breath, also known as dyspnea, is a common reason for patients to visit the Emergency Department.  Dyspnea is often caused by a pulmonary or cardiovascular condition, but it is important to remember that dyspnea can be due to endocrine conditions, toxicologic conditions, neurologic conditions, hematologic conditions, musculoskeletal conditions, and psychiatric conditions. 

The initial approach to all patients with shortness of breath involves the primary survey, or “ABCs” (Airway, Breathing, Circulation).  This first involves checking the patient for a patent airway.  A simple method to assess the airway is to ask the patient to speak and listen for the voice.  A muffled voice, the presence of stridor, hematemesis, or a lethargic patient are clues that a patent airway may not be present.  Problems with the airway, such as an obstructing foreign body, inflammation (i.e., epiglottitis, anaphylactic shock), or vocal cord dysfunction can certainly cause shortness of breath.  Endotracheal intubation may need to be performed before moving forward.  Breathing is assessed by evaluating the function of the lungs.  Steps include looking at how the patient is breathing (fast or slow), measurement of an SpO2 level, and auscultation of both lungs for wheezing, crackles, rhonchi, or distant or absent sounds.  A low oxygen level should be immediately addressed with supplemental oxygen before moving forward.  The patient’s breathing rate and lung sounds can be very helpful in discovering the diagnosis and guiding treatment.  Lastly, circulation should be assessed.  Check the heart rate, blood pressure, peripheral pulses, skin color and temperature, and evaluate for any sites of hemorrhage.  The presence of hypotension or tachycardia should be addressed appropriately based on the presumed cause.  After the primary assessment (“ABCs”) and initial treatment actions, a more detailed history and physical exam should be conducted. 

Pertinent causes of shortness of breath for the emergency practitioner to know are outlined in the chart below. 

 

 

Select Causes of Shortness of Breath (Dyspnea)

Pulmonary

 

Tension pneumothorax, pneumonia, empyema, pleural effusion, pulmonary edema, asthma, COPD

Cardiovascular

 

Acute coronary syndrome (i.e., STEMI), pulmonary embolism, cardiac tamponade, Decompensated Congestive Heart Failure (acute pulmonary edema)

Endocrine

 

Diabetic ketoacidosis (Kussmaul breathing)

Toxicologic

 

Salicylate overdose, or any ingestion that causes a severe metabolic acidosis

Neurologic

 

Intracranial hemorrhage, Stroke, Spinal cord injury, Guillain-Barre syndrome, Myasthenia Gravis crisis (myasthenic crisis)

Hematologic

 

Severe anemia (i.e., GI bleeding, trauma, miscarriage, post-partum hemorrhage, ruptured ectopic pregnancy)

Musculoskeletal

 

Rib fracture, flail chest

Psychiatric

 

Anxiety, Panic attack

Airway Problem

Foreign body, epiglottitis, anaphylactic shock (laryngeal swelling), expanding neck hematoma

 

This patient arrives to the Emergency Department with shortness of breath and generalized weakness or 3 days.  On physical exam, there is tachycardia, tachypnea, normal oxygen saturation, and a markedly elevated glucose.  The Chest X-ray provided is normal; there are no lung infiltrates or pleural effusions. 

This patient has diabetic ketoacidosis (DKA).  DKA is a serious condition of insulin deficiency characterized by hyperglycemia, metabolic acidosis, and ketosis.  Presenting symptoms include weakness, increased thirst (polydipsia), increased hunger (polyphagia), increased urination (polyuria), abdominal pain, or vomiting.  Shortness of breath can also be seen in DKA as the metabolic ketoacidosis triggers an increased respiratory rate to drive more exhaled carbon dioxide out of the body.  This deep rapid breathing seen in severe DKA is known as Kussmaul breathing.  The treatment of DKA involves IV fluids for hydration, insulin infusion, and close monitoring for electrolyte derangements (potassium abnormalities are common).  DKA patients are severely dehydrated due to osmotic diuresis from their hyperglycemic state.  For this reason, IV fluid resuscitation is the first step to DKA management.  Either normal saline or lactated ringers (Choice B) can be used, although large volumes of normal saline can worsen the acidotic state by causing a hyperchloremic metabolic acidosis.  Intravenous fluids should be started with a 20-30cc/kg bolus.  IV insulin infusion (Choice A) should never be started without a potassium level, and no potassium level is provided in the question stem.  Insulin lowers potassium, and administration of insulin without a potassium level can result in hypokalemia, arrythmia, and death.  Endotracheal intubation (Choice D) should be avoided in DKA whenever possible as the patient’s respiratory status serves as a compensation for the metabolic acidosis.  This patient is tachypneic and mildly confused, but he is not somnolent and does not require immediate intubation.  Intubated DKA patients need carefully monitored ventilator settings in combination with blood gas measurements to avoid worsening acidosis and cardiac arrest.  Nebulized beta-2 agonist (i.e., albuterol, salbutamol) is helpful in asthma, however this patient has DKA and not an asthma exacerbation.  IV lactated ringers solution (Choice B) is the best next step.

References

[cite]