• Appearance of tubular opacities within dilated bronchi.
• Resembles fingers within a glove.
• Results from mucoid impaction.

Comment

• Bronchi become dilated and filled with mucus or other secretions.
• CT imaging is particularly useful for differentiating mucoid impaction from other conditions.
• Can be associated with congenital and acquired conditions.
• Congenital causes include bronchial atresia and cystic fibrosis.
• Acquired causes encompass inflammatory and infectious diseases like allergic bronchopulmonary aspergillosis (ABPA), broncholithiasis, and foreign body aspiration.
• Can also be seen in benign neoplastic processes such as bronchial hamartoma, lipoma, and papillomatosis, as well as malignancies including bronchogenic carcinoma, carcinoid tumor, and metastases.
• In patients with a smoking history, a bronchoscopy may be advised to rule out malignancy.
• Clinical history, symptoms, and predisposing factors are crucial for accurate diagnosis.

Citation

• Lee, Radiology, 2019

• An imaging finding describing an abnormal increase in the thickness of bronchial walls.
• It is also referred to as peribronchial thickening or bronchial cuffing.

Comment

• Considered a common response of the airways to various irritants that cause inflammation and swelling.
• It can be caused by a wide range of conditions, including infections (like bronchitis or aspergillosis), inflammatory diseases (such as asthma, COPD, and cystic fibrosis), and infiltrative processes.
• On CT scans, the normal bronchial wall thickness is typically in the range of 0.8-1.4 mm.
• High-resolution CT (HRCT) is effective in detecting bronchial wall thickening and associated abnormalities.

Citation

• Marom EM, et al. AJR Am J Roentgenol, 2001.

• Small nodules (1-3 mm) located in the central portion of the secondary pulmonary lobule.
• They are found in the small airways 

Comment

• This finding can result from a wide variety of conditions affecting the bronchioles and less commonly adjacent arterioles.
• Causes include infectious processes (like endobronchial spread of tuberculosis), inflammatory conditions (such as hypersensitivity pneumonitis and respiratory bronchiolitis), aspiration, and pulmonary edema.
• When connected by branching lines, they can create a “tree-in-bud” appearance, which often suggests bronchiolitis.
• The appearance can be well-defined or ill-defined (ground-glass).

Citation

• Murata K, et al. Radiology, 1986.

• Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction of the immune system, specifically a Type I and Type III response, directed against antigens of the fungus Aspergillus species, most commonly Aspergillus fumigatus.
• ABPA is a complex pulmonary disorder that primarily affects individuals with pre-existing airway diseases, notably asthma and cystic fibrosis (CF).
• It is characterized by an exaggerated immune response, leading to airway inflammation and damage.

• ABPA is caused by colonization of the airways by Aspergillus species, typically Aspergillus fumigatus.
• The spores of Aspergillus are ubiquitous in the environment, found in soil, dust, and decaying vegetation.
• While most individuals can effectively clear these spores, individuals with asthma or CF possess compromised mucociliary clearance and excessive mucus production, which facilitates fungal colonization.
• This colonization then triggers a vigorous allergic inflammatory response in susceptible individuals.

• The pathophysiology of ABPA involves a Type I (immediate hypersensitivity) and Type III (immune complex-mediated) hypersensitivity response to Aspergillus antigens.
• Inhalation of Aspergillus spores leads to colonization of the bronchial mucus.
• In atopic individuals, particularly those with asthma or CF, this colonization elicits an IgE-mediated response, resulting in mast cell degranulation, bronchoconstriction, and increased capillary permeability.
• Concurrently, immune complexes form, attracting inflammatory cells, including eosinophils, into the airway walls.
• This inflammatory process leads to bronchial wall edema, eosinophilic infiltration, and mucus hypersecretion.
• Over time, this chronic inflammation can result in airway remodeling, including loss of bronchial smooth muscle and cartilage, leading to bronchiectasis.
• Th2 immune responses and activation of innate lymphoid cells (ILC2) producing cytokines like IL-5 and IL-13 play a significant role in driving eosinophilic inflammation and IgE production.

• The chronic inflammatory process in ABPA leads to structural changes in the airways and lung parenchyma.
• These include bronchial wall thickening, mucoid impaction within dilated bronchi (often described as “finger-in-glove” appearance), and central bronchiectasis, predominantly in the upper lobes.
• Bronchiectasis, a condition characterized by abnormal and irreversible dilation of the bronchi, can be saccular and contribute to mucus pooling.
• In advanced stages, fibrosis and scarring of the lung tissue can occur, potentially leading to irreversible lung damage.

• ABPA significantly impacts lung function, primarily by causing airway obstruction and inflammation.
• Symptoms include wheezing, coughing (often with thick, brown mucus plugs or even hemoptysis), dyspnea, and exercise intolerance.
• The bronchospasm and mucus plugging contribute to airflow limitation.
• The development of bronchiectasis further compromises lung function by impairing mucociliary clearance and increasing the risk of recurrent infections.
• In patients with cystic fibrosis, ABPA can exacerbate the already compromised lung function, leading to a more rapid decline.
• Chronic inflammation and remodeling can lead to a progressive loss of lung function over time.

• Imaging plays a crucial role in the diagnosis and staging of ABPA.
• Chest radiography may reveal transient, patchy pulmonary infiltrates, atelectasis due to mucoid plugging, and, in later stages, central bronchiectasis, often predominantly in the upper lobes.
• High-resolution computed tomography (HRCT) is more sensitive and demonstrates findings such as central bronchiectasis, bronchial wall thickening, centrilobular nodules, and mucoid impaction (which can appear as high-attenuation mucus).
• The “finger-in-glove” sign is a classic radiographic finding of mucoid impaction in dilated bronchi.
• In some cases, HRCT may be normal, leading to the classification of serologic ABPA (ABPA-S).
• Advanced disease may show signs of pulmonary fibrosis.

• Laboratory findings indicative of ABPA include peripheral blood eosinophilia, an elevated total serum IgE level (often >1000 IU/mL), and positive Aspergillus-specific IgE antibodies.
• Precipitating antibodies (IgG) against Aspergillus species also support the diagnosis.
• Sputum cultures may reveal Aspergillus hyphae, particularly within mucus plugs, which can be considered pathognomonic in some contexts, though fungal elements in sputum are not consistently diagnostic.
• Charcot-Leyden crystals, derived from eosinophils, may also be found in sputum.

• The primary therapeutic approach for ABPA involves systemic corticosteroids, such as prednisolone, to dampen the inflammatory and immune response.
• Antifungal agents, particularly itraconazole, are often used adjunctively, especially in patients who are steroid-dependent, have frequent relapses, or where benefits outweigh risks.
• The goals of treatment are to reduce symptoms, decrease airflow obstruction, lower IgE levels, resolve pulmonary infiltrates, and prevent irreversible lung damage and fibrosis.
• Monitoring of clinical symptoms, IgE levels, and imaging findings is essential for guiding treatment and assessing response.
• Other treatment modalities, such as omalizumab, may be considered in specific cases.

• The prognosis for ABPA is variable, with a generally good response to treatment, leading to symptom stabilization and remission in many patients.
• However, relapses are common, and repeat treatment may be necessary.
• Early diagnosis and prompt treatment are crucial to prevent progression to irreversible lung damage, such as pulmonary fibrosis and advanced bronchiectasis.
• Without adequate treatment, ABPA can lead to progressive lung function decline and increased morbidity.
• While long-term prognosis can be good with effective management, complete cure is not always achievable, and close monitoring is often required.
• The presence of comorbidities, such as COPD, can negatively impact survival rates.