Article Update

Thursday, May 7, 2020


While the bronchoscope is being passed through the oro or nasopharynx, the larynx, and the tracheobronchial tree, careful attention should be paid to the mucosa, the size of the lumen, and any difference from expected anatomy. Normal bronchial mucosa is pale pink, but its color varies with the intensity of the light source. The surface follows the contours of tracheal and bronchial walls and becomes paler where it overlies cartilaginous rings. A small amount of mucus and a thin layer of surface lining fluid reflect the light from the bronchoscope. In the trachea and main bronchi, the shape of the lumen is an incomplete circle or arch with a membranous posterior portion; this portion disappears distally as the airways become surrounded first by irregular cartilaginous plates and eventually by concentric muscle and elastic tissue.

Inflammation may be diffuse or localized. The endobronchial changes seen are erythema, increased vascularity, edema, mucosal irregularity, augmented secretion production, and occasionally ulceration. Edema may lead to loss of the cartilaginous prominences, the normal mucosal pattern, and narrowing of bronchial orifices. Excess secretions may be mucoid or purulent and range from thin and watery to thick and viscid. Localized inflammation accompanies carcinomas, tuberculosis, foreign bodies, pneumonia, bronchiectasis, and abscess formation. Healing of endobronchial inflammation may lead to scar formation and permanent stenosis or tracheobronchomalacia or excessive dynamic airways collapse. Newer imaging technologies such as autofluorescence, narrow-band, optical coherence tomography, and confocal microendoscopy each allow visualization of subepithelial changes such as neo- vascularization. Some of these modalities may allow for visualization of intracellular organelles and provide an “optical biopsy” (i.e., the ability to identify pathology without removing a specimen for external visualization under a microscope).
Extrinsic compression is most commonly caused by malignancy, lymphadenopathy, thyroid goiter, aspirated foreign bodies, and vascular abnormalities. Endobronchial ultrasonography has been shown to be more sensitive than chest computed tomography for differentiating airway compression from invasion. Extrinsic compression from any cause may reduce the airway lumen enough to cause distal atelectasis.
Tissue involved by tumor growth may be firm and fibrous or soft and hypervascular. The mucosa may appear inflamed or pale and yellow. There may be concentric narrowing of the lumen or an irregular mass that at times is polypoid and occludes the bronchus entirely. Engorgement of superficial vessels is common and may result in hemoptysis. The majority of endobronchial tumors are bronchogenic carcinomas, but other neoplasms, such as renal cell, breast, thyroid, colon, and melanoma, can also metastasize to the airway.
Nonmalignant airway obstruction may result from extrinsic disease as listed above or from disease confined to within the airway itself. Inflammatory conditions, including amyloidosis, Wegener granulomatosis, and relapsing polychondritis, may cause significant endoluminal obstruction. Infectious causes of nonmalignant airway obstruction include tuberculosis, fungal disease such as aspergillosis, and papillomatosis caused by human papilloma virus. Granulation tissue resulting from endotracheal or tracheostomy tubes and airway stents is also increasing in prevalence as a form of iatrogenic airway obstruction.

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