• Retention of air in the lung distal to an airway obstruction

Comment

• Typically visualized on expiratory CT scans as areas of decreased attenuation
• Occurs because obstructed airways prevent normal lung deflation during exhalation
• Leads to a mosaic pattern of varying attenuation
• Can be indicative of small airway disease, asthma, COPD, or endobronchial malignancy
• Clinical presentation ranges from asymptomatic to significant dyspnea

Citation

• Raoof, Chest, 2018

• A mechanism created by a partial airway obstruction that allows air to enter the lung during inspiration but prevents its exit during expiration.

Comment

• This one-way valve mechanism results in the progressive trapping of air and hyperinflation of the lung distal to the obstruction.
• Common causes include endobronchial lesions such as tumors, inhaled foreign bodies, blood clots, or extrinsic compression from enlarged lymph nodes.
• On imaging, this can lead to a hyperlucent, over-expanded lung or lobe, which is often best demonstrated by comparing inspiratory and expiratory CT scans.
• If left untreated, a ball-valve effect can lead to severe complications, including tension pneumothorax and cardiovascular compromise.

• Enlargement of the lymph nodes in the mediastinum, the area in the chest between the lungs.

Comment

• A short-axis diameter of a lymph node greater than 10 mm on CT is a general criterion for enlargement.
• Causes are diverse and include malignancy (like lung cancer or lymphoma), infections (such as tuberculosis), and inflammatory or autoimmune conditions (like sarcoidosis).
• While it can be a sign of cancer, many non-cancerous conditions can also cause mediastinal lymphadenopathy.
• Diagnosis is often made with imaging tests like chest X-rays or CT scans.

• Widening or enlargement of the esophagus, often containing a visible level of trapped fluid and air on imaging.

Comment

• A classic cause is achalasia, a disorder where the lower esophageal sphincter fails to relax, leading to a backup of food and liquids.
• The presence of an air-fluid level is a pathognomonic sign of stasis from obstruction or impaired motility.
• Other causes can include esophageal strictures from acid reflux, tumors, or scarring from radiation.
• On imaging, particularly a barium swallow, it may show a characteristic “bird-beak” tapering at the lower end in achalasia.

• Forward (anterior) bulging of the posterior, non-cartilaginous wall of the trachea during forced expiration.

Comment

• This is a normal finding on expiratory CT scans, as the posterior membrane is flexible.
• However, excessive forward bowing (a reduction of the airway diameter by more than 50%) is a key feature of conditions like tracheomalacia or excessive dynamic airway collapse (EDAC).
• Dynamic expiratory CT is the best imaging modality to assess for pathologic tracheal collapse.

• A central venous catheter (CVC) placed into the right internal jugular (IJ) vein in the neck.

Comment

• The right IJ is a preferred site for central access because it offers a larger diameter and a more direct, straight path to the superior vena cava compared to the left side, reducing complication risks.
• Indications include the need for rapid fluid or medication administration, hemodynamic monitoring, or when peripheral venous access is inadequate.
• Ultrasound guidance is commonly used to reduce complications like arterial puncture or pneumothorax.

• Air trapping is defined as the retention of air in the lung distal to an obstruction, typically partial, which results in an inability to fully exhale.
• This leads to hyperinflation of the lung parenchyma, characterized by areas of decreased attenuation and lack of volume reduction on expiratory CT scans.

• Air trapping is commonly a consequence of small airway disease, leading to increased airway resistance and reduced expiratory flow.
• Conditions contributing to this include inflammation, remodeling of the airways, destruction of peripheral airways and lung parenchyma, and loss of supporting alveolar attachments.
• Common etiologies include asthma and chronic obstructive pulmonary disease (COPD), specifically emphysema and chronic bronchitis.
• Other less common causes may include cystic fibrosis, obliterative bronchiolitis, hypersensitivity pneumonitis, sarcoidosis, and certain post-infectious conditions.

• The pathophysiology of air trapping involves a combination of factors that impede expiratory airflow.
• These include luminal narrowing of small airways due to inflammation and remodeling, leading to increased resistance; small airway collapse due to loss of supporting alveolar attachments; destruction of peripheral airways and parenchyma, reducing elastic recoil; and expiratory flow limitation during tidal breathing.
• In COPD, this results in increased compliance of the lungs and progressive airflow obstruction.
• In asthma, air trapping can be associated with disease severity and may persist even after bronchodilator treatment.

• The structural consequence of air trapping is lung hyperinflation, where the affected lung portions may become larger than normal.
• This is characterized on imaging by areas of decreased attenuation on expiratory CT scans, reflecting the retained air that prevents normal lung deflation.
• In severe cases, this can lead to dynamic and static hyperinflation.

• Functionally, air trapping contributes to dyspnea, particularly during exertion, as the reduced expiratory time during hyperventilation exacerbates gas trapping.
• It results in increased residual volume (RV) and an increased RV to total lung capacity (TLC) ratio, which is associated with a decline in lung function and increased mortality risk in patients with COPD.
• Air trapping can also increase the work of breathing, create a cycle of activity avoidance and deconditioning, and potentially contribute to the development of comorbidities.

• Diagnosis typically involves pulmonary function tests and imaging.
• Pulmonary function tests may show a decreased forced expiratory volume in 1 second to forced vital capacity ratio (FEV1/FVC) and an increased residual volume.
• Computed tomography (CT) is the primary imaging modality for visualizing air trapping.
• Inspiratory and expiratory phase CT scans are crucial for accurate diagnosis, as air trapping appears as geographic areas of differing attenuation on expiratory images that fail to increase in attenuation or decrease in volume compared to inspiratory images.
• Chest radiography may reveal lung hyperinflation and hyperlucent areas.

• Specific laboratory tests for air trapping itself are not typically performed.
• However, laboratory investigations may be conducted to assess for underlying conditions that cause air trapping, such as complete blood counts (CBC) or allergy testing.

• Treatment strategies for air trapping focus on managing the underlying cause and improving airflow.
• This includes bronchodilators to relax airway muscles, inhaled steroids to reduce airway inflammation, and potentially oxygen therapy.
• Breathing techniques, such as pursed-lip breathing and diaphragmatic breathing, can help regulate breathing patterns and improve exhalation.
• In severe cases, interventions like bronchoscopic lung volume reduction (BLVR) or surgical lung volume reduction (LVRS) may be considered to decrease lung volume.

• The prognosis associated with air trapping is largely dependent on the underlying etiology and severity of the condition.
• In COPD, air trapping is a predictive index for decline in lung function and mortality, and it is associated with an increased risk of exacerbations.
• However, effective management of the underlying condition and adherence to treatment can help alleviate symptoms and improve outcomes.

• Complete airway obstruction would lead to atelectasis, not air trapping.

• The “ball valve” effect describes a scenario where an object or lesion allows air to enter an airway during inspiration but obstructs its egress during expiration. This leads to air trapping distal to the obstruction and can cause hyperinflation and a mosaic pattern of attenuation on CT.
• Part B, Basic Science Explanations, Q1.

• Alveolar collapse (atelectasis) is the opposite of what occurs with air trapping.

• Vascular occlusion causes infarction and decreased attenuation, but not the dynamic air trapping characteristic of a ball valve mechanism.

• Small airway disease, such as constrictive bronchiolitis, is a common cause of mosaic attenuation due to air trapping.

• Pulmonary vascular disease, like chronic thromboembolic pulmonary hypertension, can cause heterogeneous attenuation due to differential perfusion.

• Mosaic attenuation typically results from disorders affecting the airways (e.g., constrictive bronchiolitis, asthma), pulmonary vasculature (e.g., chronic thromboembolic disease), or interstitium. Alveolar proteinosis primarily affects the alveoli, leading to diffuse opacification, not typically a mosaic pattern of differential attenuation.
• Part B, Basic Science Explanations, Q2.

• Interstitial lung diseases can present with mosaic attenuation due to various mechanisms, including airway involvement or inflammatory processes.

• Pericardial effusion is a cardiac complication, not a direct pulmonary manifestation of cervical cancer spread.

• Superior vena cava syndrome is typically caused by extrinsic compression of the SVC by mediastinal masses or lymphadenopathy, often related to lung cancer or lymphoma, and presents with upper extremity and facial swelling, though it can cause dyspnea.

• Lymphangitic carcinomatosis represents the spread of cancer through the lymphatic channels of the lungs. In patients with advanced cervical cancer, particularly stage III or IV, lymphatic spread to the thoracic lymphatics can cause dyspnea, cough, and characteristic reticular or reticulonodular opacities on imaging, mimicking interstitial lung disease or infection.
• Part B, Clinical Explanations, Q1.

• Diaphragmatic paralysis can occur due to phrenic nerve involvement by malignancy or treatment effects, but it is a less common direct manifestation of metastatic cervical cancer compared to lymphangitic spread.

• Pulmonary embolism can cause mosaic attenuation due to perfusion defects, but bronchial compression by lymphadenopathy is a more direct explanation for air trapping in the context of malignancy.

• Pneumocystis pneumonia would present with diffuse ground-glass opacities and typically in an immunocompromised host, not primarily as air trapping and mosaic attenuation from obstruction.

• In patients with a history of cervical carcinoma, metastatic involvement of mediastinal and hilar lymph nodes can lead to extrinsic compression of the bronchi. This compression can create a ball valve effect, leading to air trapping, mosaic attenuation, and dyspnea. While pulmonary embolism (a) can cause mosaic attenuation, the history of malignancy makes lymphadenopathy a strong consideration. Pneumocystis pneumonia (b) is an opportunistic infection typically seen in immunocompromised individuals, and congestive heart failure (d) would usually present with other findings like pulmonary edema.
• Part B, Clinical Explanations, Q2.

• Congestive heart failure usually manifests with cardiomegaly, pleural effusions, and interstitial edema, rather than focal air trapping.

• Inspiratory CT shows normal lung inflation and is less sensitive for detecting air trapping.

• Air trapping, a key feature in conditions like the ball valve phenomenon or small airway disease, is best visualized on expiratory CT scans. During expiration, normally inflated lung segments deflate and become more attenuated (whiter) on CT. Areas with persistent air trapping remain low in attenuation (darker), highlighting the obstruction.
• Part B, Imaging Explanations, Q1.

• Intravenous contrast is useful for evaluating vascular structures and perfusion but does not directly improve the detection of air trapping.

• Low-dose CT may reduce radiation but is not optimized for subtle findings like air trapping compared to dedicated thin-section expiratory protocols.

• Dilated pulmonary arteries would suggest pulmonary hypertension, which can cause mosaic attenuation but through a different primary mechanism than small airway disease.

• In small airway disease causing mosaic attenuation, the affected lung regions are hypoperfused due to hypoxic vasoconstriction and/or compression of pulmonary vessels by the trapped air and surrounding inflammation. This results in smaller or absent-appearing pulmonary arteries within the underperfused areas, contrasting with the normally perfused regions.
• Part B, Imaging Explanations, Q2.

• Thickened interlobular septa are more characteristic of interstitial lung disease or edema.

• Ground-glass opacities suggest alveolar or interstitial filling, not typically the primary finding in small airway disease causing air trapping and mosaic attenuation.

• Para-aortic lymph nodes are located retroperitoneally and are unlikely to cause bronchial compression.

• Pelvic lymph nodes are in the lower abdomen and pelvis and have no role in bronchial obstruction.

• Enlargement of lymph nodes in the hilar and mediastinal regions can directly compress the major bronchi and their bifurcations. This compression can lead to partial or complete obstruction, creating a ball valve effect and subsequent air trapping, which manifests as mosaic attenuation and dyspnea.
• Part B, Imaging Explanations, Q3.

• Inguinal lymph nodes are in the groin and are not related to intrathoracic airway obstruction.