BRONCHOSCOPIC
VIEWS
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.
