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A 50-year-old man is referred for poorly controlled asthma. Triggers include exercise and exposure to dust, pollen, and fumes. He has allergic rhinitis. He has been treated with several courses of glucocorticoids, but symptoms recurred after he stopped treatment despite regular use of his fluticasone-salmeterol and tiotropium inhalers. His only other medication is albuterol. He has good inhaler technique.
On physical examination, vital signs are normal. BMI is 23. Pulmonary examination reveals few expiratory wheezes. The remainder of the examination is unremarkable.
Laboratory studies reveal a normal total IgE level and complete blood count.
Chest radiograph is normal. Spirometry demonstrates moderate airflow obstruction that improves with bronchodilators.
A. Absolute blood eosinophil count
B. α1-Antitrypsin level
C. Aspergillus-specific IgE level
D. Measurement of common allergen-specific IgE levels
Diagnose allergic asthma phenotype.
The most appropriate diagnostic test for this patient is measurement of the absolute blood eosinophil count (Option A). The patient presents with symptoms suggestive of allergic asthma; establishing this asthma phenotype can help direct therapy. Clinical characteristics suggesting a type 2 asthma phenotype include atopy, seasonal exacerbations, hay fever, and allergen sensitization. Biomarker evaluation in these patients often demonstrates serum or sputum eosinophilia and/or high IgE levels. This patient has a normal IgE level, but this does not preclude type 2 asthma. Obtaining a blood absolute eosinophil count will help establish the phenotype. In patients with severe disease, elevated levels of IgE and eosinophils are therapeutic targets for biologic therapies. Several types of biologic therapies are available that are directed against type 2 inflammation, targeting pathways involved in activation of eosinophils and IgE production. Use of antibody therapies in eligible patients with severe persistent allergic asthma despite standard therapy reduces symptoms, exacerbations, and need for oral glucocorticoids.
An α1-antitrypsin level (Option B) should be obtained once in all patients with chronic obstructive pulmonary disease. A pattern of basilar emphysema, associated liver disease or panniculitis, or a strong family history of emphysema in patients with COPD suggests possible α-1 antitrypsin deficiency, but none of these features is sufficiently sensitive for the condition. Routine testing is not indicated in patients with asthma.
Patients with allergic bronchopulmonary aspergillosis (ABPA) present with difficult-to-control asthma, productive cough, and expectoration of mucus plugs. Commonly accepted diagnostic criteria include elevated IgE levels, positive skin tests to Aspergillus antigens, increased Aspergillus-specific IgE and IgG levels, and either central bronchiectasis or infiltrates. This patient does not have the clinical phenotype of ABPA, radiographic findings, or elevated IgE level suggesting ABPA.
Measuring Aspergillus-specific IgE level (Option C) is not indicated.
Identifying the presence of atopy can identify an allergic asthma phenotype in a patient with respiratory symptoms. Atopic status can be measured by skin prick testing or measurement of allergen-specific IgE testing (Option D). Skin prick testing is rapid, simple, and relatively inexpensive. Measurement of immunoglobulin-specific IgE is more expensive but not more accurate. However, the first management step for this patient is to measure the total blood eosinophil count to determine his asthma phenotype.
Clinical characteristics suggesting a type 2 asthma phenotype include atopy, seasonal exacerbations, hay fever, and allergen sensitization.
For patients with symptoms suggestive of type 2 asthma phenotype, measurement of IgE levels and total eosinophil count can be used to confirm this asthma phenotype and direct therapy.
McGregor MC, Krings JG, Nair P, et al. Role of biologics in asthma. Am J Respir Crit Care Med. 2019;199:433-445. PMID: 30525902 doi:10.1164/rccm.201810-1944CI
Copyright 2019, American College of Physicians.
A 45-year-old woman is evaluated in the ICU for community-acquired pneumonia and septic shock. Appropriate resuscitation efforts are under way.
On physical examination, temperature is 39.2 °C (102.6 °F), blood pressure is 92/50 mm Hg, pulse rate is 120/min, and respiration rate is 25/min. Oxygen saturation is 85% on bilevel positive airway pressure, and FIO2 is 0.60. Auscultation of the lungs reveals decreased breath sounds over the left lung base.
Chest radiograph reveals scattered infiltrates in the lower lungs with dense consolidation in the left lower lobe and a small left pleural effusion.
A. Bedside thoracic ultrasonography
B. Chest CT with contrast
C. Lateral decubitus film
D. Thoracic MRI

Evaluate a pleural effusion in the ICU.
The most appropriate diagnostic test to perform is bedside thoracic ultrasonography (Option A). The patient is presenting with septic shock and hypoxemic respiratory failure. Her presentation is secondary to a multifocal pneumonia with an associated left pleural effusion. Once a pleural effusion is detected on chest radiograph, bedside thoracic ultrasonography can be used to characterize the fluid and the feasibility of drainage. Thoracic point-of-care ultrasonography is a helpful addition particularly in patients who are semirecumbent, such as those who are critically ill, and does not necessitate transporting the patient from the ICU or interrupting resuscitation. Thoracic ultrasonography allows for the easy identification of a free-flowing or loculated pleural effusion and can differentiate between solid masses and loculated effusions. The presence of a loculated pleural effusion in the setting of severe community-acquired pneumonia would be an indication for diagnostic sampling and drainage of the effusion.
Advantages of CT imaging with contrast (Option B) include the ability to detect small amounts of pleural fluid; assessment of coexisting intrathoracic abnormalities such as pulmonary masses and malignant pleural disease; and identification of an empyema, as enhancement of the pleura around the fluid creates a lenticular-shaped opacity. However, CT imaging requires the patient to be removed from the ICU and exposes the patient to irradiation.
A lateral decubitus film (Option C) would also differentiate between a free-flowing and a loculated pleural effusion. However, it is now rarely used in the ICU because bedside ultrasonography is easy to access and to use. In addition, a lateral decubitus film would not demonstrate the feasibility of drainage as ultrasound does.
Finally, a thoracic MRI (Option D) can effectively display pleural tumors, chest wall invasion, spinal cord invasion, and pleural effusions. However, it is not as useful as thoracic ultrasonography and CT for evaluation of parapneumonic effusions, it is expensive, and it requires the patient to be moved from the ICU.
Thoracic ultrasonography allows for the easy identification of a free-flowing or loculated pleural effusion and can differentiate between solid masses and loculated effusions.
Thoracic point-of-care ultrasonography is a helpful addition particularly in patients who are semirecumbent, such as those who are critically ill, and does not necessitate moving the patient from the ICU.
Porcel JM. Chest imaging for the diagnosis of complicated parapneumonic effusions. Curr Opin Pulm Med. 2018;24:398-402. PMID: 29517587 doi:10.1097/MCP.0000000000000485
Copyright 2019, American College of Physicians.