Version May 2024
INTRODUCTION — Most clinicians quickly recognize a variety of abnormal patterns of diffuse parenchymal lung disease on conventional chest radiographs. However, anomalies of the upper respiratory tract, some of which can cause acute respiratory failure, are often overlooked during the initial assessment. Imaging of the trachea will be reviewed here. The radiologic manifestations of diffuse parenchymal lung disease, and the management of central airway obstruction, are discussed separately. (See "Evaluation of diffuse lung disease by conventional chest radiography" and "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults".)
ANATOMY — The trachea extends from the lower border of the larynx (2 cm below the vocal cords) to the carina, where it bifurcates into the mainstem bronchi. The average tracheal length is 10 to 12 cm, and the normal angle of the tracheal bifurcation is 70 ± 20 degrees (image 1A-B). With deep inspiration, the tracheal length increases by as much as 2 cm and the angle of the tracheal bifurcation decreases by up to 10 degrees [1,2].The superior border of the manubrium sterni separates the extrathoracic cervical trachea from the intrathoracic trachea.
The trachea consists of four layers: an inner mucosal layer, a submucosal layer, cartilage, and muscle as well as an outer adventitia. It is supported anteriorly and laterally by 18 to 22 semicircular incomplete rings of cartilage connected by annular ligaments of fibroconnective tissue; this corresponds to two cartilage elements per centimeter of tracheal length. Tracheal cartilages can calcify in older adult patients with a predilection for females and patients on longstanding warfarin therapy. The posterior (membranous) tracheal wall is devoid of cartilage and consists of longitudinally aligned smooth muscle, called trachealis muscle and fibrous connective tissue. The tracheal wall has a thickness of 1 to 3 mm and is delineated by intraluminal gas and mediastinal fatty tissue, as determined on computed tomography (CT) scans.
The normal transverse internal diameter of the trachea ranges between 15 and 25 mm in males and 10 to 21 mm in females, with a cross-sectional area of 250 to 350 mm2 and a volume of 30 to 40 cm3 at total lung capacity (TLC) [1,3]. The transverse diameter of the trachea increases by 10 percent with inspiration and can decrease by 30 percent with coughing. During expiration, CT images display physiologic anterior bowing of the posterior non-cartilaginous membranous wall of the intrathoracic trachea while the anterolateral tracheal wall remains unchanged in its configuration.
The radiographic appearance of the tracheal air column should be assessed routinely when chest radiographs are obtained. If an endotracheal tube is present, proper position must be confirmed and the distance between the endotracheal tube tip and the carina should be measured (figure 1). Aspiration of sand, food, secretions, or other particulates may create a radiopaque outline of the trachea and large bronchi (image 2). Three-dimensional CT imaging and perspective rendering or virtual bronchoscopy are useful additional imaging tools [4].
CONGENITAL ANOMALIES — Some congenital anomalies of the large airways, including tracheal agenesis and tracheoesophageal fistulae, present early in life [5,6]. Other anomalies, including congenital tracheal stenosis (with or without complete tracheal rings), generally cause symptoms later in life. They can be associated with substantial morbidity and coexisting congenital vascular anomalies, such as pulmonary artery slings (the so-called ring-sling syndrome) and right-sided aortic arch anatomy (image 3A-B) [7-9]. (See "Congenital anomalies of the intrathoracic airways and tracheoesophageal fistula".)
Some asymptomatic anomalies are only detected radiographically. As an example, tracheal diverticula (ie, tracheoceles) are occasionally visible on conventional chest radiographs and are increasingly recognized at the thoracic inlet in the right posterolateral region of the trachea, 4 to 5 cm inferior to the vocal cords (image 4 and image 5 and image 6) [10-12]. Tracheal diverticula occur more frequently in males and can be seen in up to 5 percent of individuals. The origin can be a vestigial supernumerary lung bud in abnormally high position. Some of these tracheal diverticula may be acquired due to repeated episodes of increased intratracheal pressure [13,14]. Tracheal cartilages can calcify. This variant is seen more frequently in asymptomatic older adult females, likely the result of senescent changes. On rare occasions these tracheal calcifications can be observed in patients on long-term Warfarin therapy [15]. Rarely, such calcifications have been described in Larsen syndrome, Keutel syndrome [16] and chondrodysplasia punctata [17,18]. In these rare syndromes, associated tracheal stenosis or tracheomalacia can occur as well.
Tracheal bronchus — Tracheal bronchus is a general term used to describe an abnormal bronchus that usually originates from the distal trachea and is usually directed towards the right upper lobe (figure 2 and image 7) [19-21]. It usually supplies a segment of the right upper lobe as a supernumerary bronchus. It is a common airway malformation that is thought to occur in one out of every 400 normal persons. In one series, a frequency of 0.1 to 5 percent was reported [22,23]. In another series of 35 cases, most tracheal bronchi actually originated from a bronchus (69 percent) rather than the trachea (23 percent) or carinal region (8 percent) [24]. Aberrant bronchi arising from either bronchi or the region of the tracheal bifurcation should not be called tracheal bronchi. An accessory cardiac bronchus arises from the inner wall of the right mainstem bronchus or the bronchus intermedius, opposite to the origin of the right upper lobe bronchus and can be seen in 0.08 percent of the population: it is typically blind-ending and doesn't cause symptoms [25]. The defect in embryogenesis that results in this anomaly includes abnormalities in migration, selection, or reduction of airways during development. (See "Congenital anomalies of the intrathoracic airways and tracheoesophageal fistula", section on 'Tracheal bronchus'.)
A specific malformation in which a single or displaced right upper lobe bronchus arises from the right side of the trachea above the carina and caudad to the azygos vein arch can replace the anatomic right upper lobe bronchus and supply the entire right upper lobe; it is known as bronchus suis (or "pig bronchus") since this is the normal anatomic configuration seen in pigs and other mammals including ruminant animals and dolphins (image 8 and image 9). A tracheal bronchus can be either rudimentary, meaning that it forms a blind-ending pouch, or supernumerary, meaning that its presence is in addition to the normal complement of right upper lobe segmental bronchi. It may also be displaced, replacing either the anatomical right upper lobe bronchus or individual segmental bronchi to the right upper lobe. In patients with a displaced bronchus suis that supplies the entire right upper lobe, a correctly positioned endotracheal tube can lead to lobar collapse of the right upper lobe. (See "Radiologic patterns of lobar atelectasis".)
TRACHEAL DILATION — Dilation of the trachea can be either diffuse or focal. Tracheobronchomegaly (ie, Mounier-Kuhn syndrome) and traction tracheomegaly can cause diffuse tracheal dilation. This pattern can also be seen in rare patients with cutis laxa, Ehlers-Danlos syndrome, Marfan syndrome, and ataxia-telangiectasia, which suggests the possibility of an underlying defect in collagen synthesis [3,26].
Tracheobronchomegaly — Tracheobronchomegaly (also called Mounier-Kuhn syndrome) results from a congenital (genetic) or acquired (epigenetic) atrophy of connective tissue, including elastic fibers and smooth muscle layer of the trachea and bronchi. It occurs more often in males than in females. The average age at presentation is in the sixth decade of life. The entity is characterized by a tracheal width exceeding 3 cm, a right mainstem bronchial diameter of more than 2.5 cm, and a left mainstem bronchial diameter exceeding 2 cm in cross-section [27-33]. The membranous tissue in between the tracheal cartilages can bulge, forming tracheal diverticulosis. This can result in a corrugated appearance of the central airways on imaging. Occasionally, this condition is accompanied by central bronchiectases (image 10 and image 11) and emphysema [34,35]. The airways are very compliant, leading to tracheomalacia and expiratory collapse with a crescent-shaped trachea. The coughing mechanism and the mucociliary escalator are impaired leading to recurrent bronchopulmonary infections. Mixed connective tissue disease can, in rare patients, also lead to tracheomegaly (image 12 and image 13).
Traction tracheomegaly — Traction tracheomegaly is a result of severe unilateral or bilateral upper lobe loss of volume due to severe cicatrization atelectasis from post primary tuberculosis, atypical mycobacterial disease, fungal diseases, end-stage sarcoidosis, pneumonectomy, or radiation therapy (image 14A-B). Severe diffuse idiopathic pulmonary fibrosis can also lead to traction tracheomegaly [36].
Focal dilation — Focal, circumferential dilation of the trachea is seen most frequently as a consequence of prior intubation. Endotracheal or tracheostomy tube cuff overdistention can lead to airway wall ischemia and subsequent tracheomalacia with focal bulging of the tracheal wall (image 15A-B) [37,38]. Localized cicatricial retraction due to adjacent lung scarring can similarly result in traction and focal tracheal wall bulging. (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients" and "Tracheostomy: Rationale, indications, and contraindications".)
TRACHEAL NARROWING — Tracheal narrowing can be divided radiographically into long and short segment narrowing (figure 3). Patients may be asymptomatic until the trachea is critically narrowed (<10 mm), regardless of the length of the stenotic lesion. Acute obstruction of the upper airway is a medical emergency, and imaging should not take precedence over rapid therapy [39,40]. (See "Clinical presentation, diagnostic evaluation, and management of malignant central airway obstruction in adults".)
Long segment narrowing — Airway narrowing involving long segments of the trachea is seen with saber sheath trachea, relapsing polychondritis, and tracheobronchopathia osteochondroplastica (image 16 and image 17). Less commonly, amyloidosis, granulomatosis with polyangiitis (GPA), tumors, and airway burns [41] cause long segment narrowing. Inflammatory bowel disease, including Crohn’s disease and ulcerative colitis, can be associated with ulcerative tracheobronchitis. Ulcerative tracheobronchitis can lead to circumferential tracheal wall thickening and eventual stenosis of the trachea, accompanied by bilateral bronchiectases [42-45].
Saber sheath deformity — Saber sheath trachea is an acquired morphologic abnormality of the intrathoracic trachea. The deformity results in marked coronal narrowing and sagittal widening of the intrathoracic tracheal diameter (image 18A-B) [46]. Ossification of tracheal cartilage is frequently noted, and the tracheal index (coronal diameter divided by sagittal diameter) in classic saber-sheath trachea is <0.6 (figure 4 and picture 1) [47,48]. This deformity spares the cervical trachea, which has a normal coronal diameter; the saber sheath trachea is strongly associated with chronic obstructive pulmonary disease (COPD), which is diagnosed on the basis of clinical findings or pulmonary function testing (FEV1/FVC less than 0.7), even if radiologic evidence of emphysema is absent. It is present in 5 percent of older adult males and only rarely seen in females, even those with COPD. Saber sheath trachea is presumably the result of overexpanded upper lobes and repetitive bouts of cough. It should not be mistaken for narrowing due to a mediastinal mass. It is a rigid, fixed abnormality that should not be confused with tracheomalacia [49].
Tracheomalacia — Tracheomalacia is a condition characterized by excessive tracheobronchial compliance and collapsibility. It is usually caused by a flaccid posterior tracheal membranous wall due to hypotonia of the myoelastic elements in tandem with weakness of the supporting tracheal cartilages. The posterior tracheal wall bulges into the tracheal lumen with forced expiration or coughing [50,51]. In patients with normal tracheal cartilages but a floppy membranous wall, excessive dynamic airways collapse can be seen in expiration and with coughing. Obesity has an impact on the shape of the trachea; it can lead to anterior bowing of the posterior membranous tracheal wall with reduced tracheal cross-sectional area as well as excessive expiratory tracheal collapse. Of note, these changes are reversible after successful bariatric surgery with substantial weight loss [52].
Imaging typically shows a hyperexpanded trachea that collapses in expiration and during coughing. CT may reveal a semilunate, discoid, or crescentic trachea when viewed in cross section (image 19 and picture 2 and image 20). A "frown" sign has also been described, which exists when marked anterior bowing of the posterior membranous wall of the trachea occurs (image 21 and image 22) [53,54]. This excessive dynamic airway collapse can be seen in up to 10 percent of chest CT scans as an incidental finding and indicates expiratory phase scanning.
CT may be helpful in the diagnosis of tracheomalacia because it facilitates the measurement of changes in the diameter of the lumen at end-expiration. During forced expiration, a greater than 50 percent reduction of the luminal diameter can be ascertained. Dynamic expiratory multislice CT tends to reveal a greater degree of airway collapse than static end-expiratory CT and, therefore, is the preferred test [55]. Expiratory gas trapping in the lung of patients with tracheomalacia has been observed more often than in patients without tracheal abnormalities [56]. The diagnostic evaluation of tracheomalacia, including the role of imaging, is discussed separately. (See "Tracheomalacia in adults: Clinical features and diagnostic evaluation".)
Relapsing polychondritis — It is a rare multisystem, noninherited, autoimmune disorder that results in inflammation and destruction of cartilaginous structures throughout the body, including the ears ("cauliflower ears"), nose ("saddle nose deformity"), joints, and laryngotracheobronchial tree. The airways are affected in 50 percent of patients. Airways involvement is slightly more common in female patients between 40 and 60 years of age [57-59]. Manifestations of relapsing polychondritis include auricular and nasal polychondritis, polyarthritis, laryngotracheitis, and aortitis. The latter two complications can be fatal, either due to severe tracheal stenosis or formation of aortic aneurysms with the potential for rupture. On chest radiographs, long segment tracheal stenosis with smooth thickening of the tracheal wall is characteristic (image 19). On CT, the anterolateral tracheal wall is thickened but the posterior tracheal membrane is not involved. The thickened walls demonstrate increased attenuation due to calcifications. Destruction of tracheal cartilages with subsequent stenosis can be seen; if tracheomalacia results, dynamic collapse may be present during expiration (picture 2) [60,61]. (See "Diagnostic evaluation of relapsing polychondritis".)
Tracheobronchopathia osteochondroplastica — Tracheobronchopathia osteochondroplastica (TPO) is a rare entity seen with a frequency of 0.4 percent at bronchoscopy [60,62-68]. It preferentially affects males. Histologically, it is characterized by osseous and cartilaginous submucosal nodules connected to tracheal cartilage (picture 3). The abnormality spares the posterior tracheal membranous wall. In spite of marked radiographic changes, patients are only rarely symptomatic since severe airway obstruction is unusual (image 23). On CT scans, TPO is characterized by 1 to 3 mm calcified nodules arising from the anterior cartilaginous elements of the trachea. These structures protrude into the lumen of the trachea and proximal bronchi with resulting luminal narrowing and tracheal wall thickening. The posterior tracheal wall and the mainstem bronchi are spared. Slow progression can occur. Linear tracheoplasty may be required in patients with symptomatic airway obstruction [69].
Short segment narrowing — Selective diseases cause short, segmental tracheal narrowing that preferentially involves the upper trachea.
Specific granulomatous and inflammatory diseases — Specific diseases in this category include GPA, squamous papillomatosis (caused by the human papilloma virus), rhinoscleroma (caused by Klebsiella rhinoscleromatis), and cicatricial pemphigoid. In general, these diseases cause circumferential tracheal wall thickening, including the posterior tracheal membrane.
●Rhinoscleroma – Rhinoscleroma may demonstrate nodular deformity of the tracheal mucosa or severe circumferential thickening of the tracheal walls and of the central bronchi with marked luminal narrowing [70]. Occasionally, other bacterial infections can lead to similar tracheal wall thickening (image 24).
●Granulomatosis with polyangiitis – In GPA, the upper airways are frequently affected in up to 55 percent of patients [71,72]. Diffuse circumferential tracheal thickening and bronchial wall thickening may be present on CT scans. Approximately 25 percent of patients develop circumferential, subglottic, laryngeal, and tracheal stenosis, and 10 percent may present with bronchial stenosis with smooth or nodular wall thickening [71]. Additional lung findings on CT scanning may show pulmonary masses, cavities, or consolidation and ground-glass opacities due to pulmonary hemorrhage [73]. Magnetic resonance imaging can be useful in evaluating active inflammation with thickening of the subglottic larynx and tracheal narrowing; T1-weighted spin-echo imaging demonstrates the pathologic anatomy of the airway, whereas short inversion recovery spin-echo imaging shows increased signal intensity in the presence of edema [74].
●Amyloidosis – Amyloidosis is a rare disorder characterized by deposition of abnormal proteinaceous material in various tissues, including the tracheobronchial tree. Diffuse nodular thickening of the trachea and mainstem bronchi or short segment stenosis can be demonstrated on thoracic CT scans. The subglottic larynx and adjacent cervical trachea are most commonly involved. The nodules can calcify and ossify and resemble tracheopathia osteochondroplastica yet amyloidosis involves also the posterior tracheal wall, whereas in TPO the posterior wall is spared [75].
Short segment tracheal narrowing of the lower trachea is also seen in tuberculosis [76], inflammatory bowel disease, histoplasmosis, and sarcoidosis [42,60]:
●Tuberculosis – In tuberculosis, between 10 and 40 percent of patients exhibit features of endobronchial infection. Stenoses are not restricted to the trachea but also involve the proximal bronchi. In the active phase of the disease the stenotic regions exhibit a thick, irregular wall, whereas after treatment the stenosis is smooth and the tracheal wall is thin.
●Inflammatory bowel disease – Inflammatory bowel disease can lead to tracheal stenosis late in the course of the disease. CT scans can demonstrate focal or diffuse circumferential airways narrowing with either smooth or irregular wall thickening. Additional findings are bronchiectases, bronchitis, and obliterative bronchiolitis.
●Sarcoidosis – In sarcoidosis, tracheobronchial involvement is rare, affecting up to 3 percent of patients. The lower trachea as well as the upper trachea can be involved. Granulomatous infiltration of the tracheal wall or extrinsic compression by enlarged mediastinal lymph nodes may precipitate the stenosis.
Short segment tracheal narrowing can be caused by extrinsic compression from cervical or mediastinal mass lesions at any level (image 25). Thyroid masses are most likely to influence the position and dimensions of the trachea due to the proximity of the gland to the tracheal wall and owing to the thyroid capsule being intertwined with the connective tissue of the trachea (image 26 and image 27 and image 28) [77].
Enlarged lymph nodes from lymphoma [78], metastatic lung tumors, or, particularly in children, granulomatous disease, can lead to tracheal narrowing. Sinus histiocytosis (Rosai-Dorfman disease) is a rare nonmalignant proliferation of histiocytes seen in children. It is most likely due to an infection with the Epstein-Barr virus or the Human Herpes Virus 6. In the airways, solitary or multiple polypoid masses can be found with subsequent lumen narrowing [79]. Imaging may show additional mediastinal lymph node enlargement [80]. The disease can resolve spontaneously [81,82].
Primary lung tumors (image 29) and esophageal tumors, aortic aneurysms, or vascular rings can lead to extrinsic tracheal compression. In rare cases of severe osteophytic changes of the cervical spine or with flowing hyperostosis seen in diffuse idiopathic skeletal hyperostosis (Forestier disease), posterior narrowing of the cervical trachea can occur with clinical stridor. Cross-sectional imaging is the preferred method of diagnosis and quantification of the stenosis [83].
Granulomatous short-segment tracheal stenoses can be treated with temporary insertion of silicone stents and CT scanning can optimize the time of silicone stent removal [76]. Primary tracheal tumors can cause short segment narrowing in the upper and lower trachea.
Malignant tumors — Malignant tumors account for 90 percent of primary tracheal neoplasms [84]. Most occur in adults. They are responsible for 0.1 percent of all cancer deaths and are 180 times less common than bronchogenic carcinoma and 75 times less frequent than laryngeal carcinoma. (See "Malignant tracheal tumors".)
Malignant tracheal tumors include squamous cell carcinoma, adenoid cystic carcinoma, mucoepidermoid carcinoma, and carcinoid tumors, all of which arise from the surface epithelium or salivary glands [85,86]. Chondrosarcoma originating from the tracheal cartilages occurs in the trachea as well. Hematogenous tracheal metastases have been described in patients with carcinoma of the breast, colon, and kidney, as well as those with melanoma. Direct invasion of the trachea is a potential consequence of carcinoma of the lung, esophagus, larynx, or thyroid gland [87-90]. This direct invasion of the trachea by adjacent neoplastic processes is more commonly encountered than primary tracheal tumors. Esophageal carcinoma can lead to the formation of a tracheoesophageal fistula (image 30). Primary lymphoma of the trachea originates from mucosa-associated lymphoid tissue (MALT) and is rarely seen [78]. Secondary involvement originating from mediastinal lymph node disease is more common.
Squamous cell carcinoma is the most common histopathologic type of tracheal malignancy, comprising about one-third of primary malignant tracheal tumors. It is seen primarily in smokers. Up to 10 percent can be multifocal. The peak incidence is in the sixth to seventh decade of life, with a five-year survival rate of only 10 percent. Tumors progress from an intraluminal nodule or mass to stenosis, mediastinal extension, lymph node metastases, tracheoesophageal fistula, and/or distant metastases (image 31). CT may reveal polypoid lesions, focal stenosis, eccentric narrowing, or circumferential wall thickening. Positron emission tomography using (18)F-2-deoxy-2-fluoro-D-glucose (FDG-PET) typically demonstrates high uptake of radioactively labeled glucose tracer [85].
Tracheal adenoid cystic carcinoma, previously called cylindroma, is a well-differentiated, slow-growing neoplasm of minor salivary gland origin. It is the second-most common malignant tracheal tumor and has the histologic features of salivary gland neoplasms [91,92]. It accounts for slightly less than one-third of malignant tracheal tumors and has a better prognosis than squamous cell carcinoma: 75 percent of patients are alive at five years. The peak incidence occurs in the fourth and fifth decade of life. It affects males and females equally and usually afflicts non-smokers. Late tumor recurrence after 10 to 15 years is possible since early perineural infiltration can occur.
Characteristic features of this lesion include an intraluminal and an even larger extraluminal component, so called iceberg lesions. The tumor has a predilection for the posterolateral wall of the trachea where an agglomeration of salivary-gland-like structures is present (image 32A-B) [93]. Mucoepidermoid carcinomas can involve the trachea, and are also of minor salivary gland origin (picture 4) [94]. The tumor can present on CT scans as an enhancing lesion with smooth or scalloped borders and with occasional punctate internal calcifications. Cavitation and diffuse tracheal wall thickening have rarely been described [95,96].
Pleomorphic adenoma, while representing the most common neoplasm of the major salivary glands can on rare occasions affect the trachea as well [97]. Adenoid cystic carcinoma and mucoepidermoid carcinoma show variable glucose avidity on the FDG-PET scan [85]. The magnitude of uptake depends on the degree of differentiation (ie, high-grade malignancies show high, homogeneous uptake of radiotracer).
Tracheal carcinoid tumors are relatively unusual; carcinoid tumors occur preferentially in the bronchi [98]. Most are typical carcinoids histologically. Internal calcifications or ossifications can occur in up to one-third of cases [99]. Carcinoids show intense enhancement with intravenous contrast material on CT scanning, but usually have lower radiotracer uptake on the FDG-PET scan, than would be expected from a high-grade malignant tumor [85].
Tracheal lymphoma — Both primary and secondary types of lymphoma can manifest as soft-tissue nodular or polypoid intraluminal masses and rarely present as diffuse mural thickening [78]. Endotracheal post-transplantation lymphoproliferative polyclonal disease or monoclonal lymphoma triggered by the Ebstein-Barr virus (Herpes virus Type 4) can, in rare instances, present as an FDG-avid tracheal mass [100].
Benign tumors — Benign tumors of the trachea occur predominantly in children and account for only 10 percent of tracheal neoplasms. They include squamous papilloma, hemangioma, chondroma, hamartoma (image 33), lipoma, neurogenic tumors, and fibroma [101,102].
Laryngotracheal papillomatosis results from perinatal infection with human papilloma virus (HPV-6 and HPV-11), which leads to papillomatous growth of the tracheobronchial epithelium [103-105]. It is the most common pediatric laryngeal tumor (image 34) and is likely contracted via vertical transmission from an infected mother during childbirth. Adult-onset manifestations of the disease occur less frequently but overall occur more commonly in males. Distal spread of papillomas into the trachea can occur after five years in 2 percent of cases with laryngeal involvement. Bronchoalveolar dissemination can occur after 10 years and is seen in 0.1 percent of patients with laryngeal papillomatosis [106]. Malignant degeneration of squamous papillomas occurs in at least 3 to 10 percent of surviving adults, particularly after recurrence [60,106-108]. The CT images show multiple intraluminal nodules of varying size and number that involve the entire tracheal circumference, including the posterior membranous wall [103-105]. The disease process can spread distally and can lead to the formation of cavitary lung nodules as well as consolidation and atelectasis of the lung parenchyma [109,110].
Hemangiomas, chondromas, hamartomas, lipomas, neurogenic tumors, and fibromas arise from mesenchymal tissue. They usually display little or no radiotracer uptake on FDG-PET scanning, which allows differentiation from malignant tumors [85].
Pseudotumors — Pseudotumors produce intraluminal space-occupying lesions and mimic a neoplastic process. They include mucus plugs (image 35 and image 36), foreign bodies including aspirated food, (image 37 and image 38), amyloidomas, tuberculosis (image 39A-B), coccidioidomycosis, rhinoscleroma, GPA (image 40), inflammatory pseudotumor (image 41), and plasmacytomas [111]. If an unexpected tracheal mass represents a mucus plug, a repeat study after coughing may demonstrate the transient nature of the intraluminal lesion. On CT scans, mucus plugs have a low attenuation of less than 22 Hounsfield Units with occasional interspersed gas bubbles, which also facilitates their differentiation from endoluminal neoplastic lesions [112].
Necrotizing tracheobronchitis due to Herpes simplex infections (HSV) Type 1 can lead to tracheal ulcerations with secondary pseudomembrane formations that can form pseudotumors and result in upper airways obstruction [113]. Occasionally, extraneous artifacts can mimic intratracheal foreign bodies on chest radiographs. (See "Airway foreign bodies in adults".)
TRACHEAL TRAUMA — The most common causes of tracheal trauma are intubation and tracheostomy with cuff overdistention, which can result in focal stenosis (image 42A-B and picture 5), granuloma formation (picture 6), focal tracheomalacia (image 20) [114-117], or tracheo-esophageal fistula.
The most common site of stenosis is at the level of the inflated cuff in the upper thoracic trachea (image 43). The mucosal injury occurs when the cuff pressure exceeds the capillary pressure with subsequent ischemic injury, granulomatous reaction, and eventual fibrosis within three months post extubation. Use of low-pressure high-volume cuffs has reduced but not eliminated the incidence of these injuries. CT demonstrates circumferential cervical tracheal wall thickening and short-segment stenosis at the cuff about 3 to 6 cm above the tracheal carina. In post-tracheostomy patients the site of stenosis is typically at the prior stoma site or at the site of the balloon cuff.
Blunt or penetrating trauma (image 44), burns (image 45), and foreign bodies can also contribute to tracheal stenosis [118] (see "Inhalation injury from heat, smoke, or chemical irritants"). Transmediastinal injuries of the trachea due to firearms or knives are rarely imaged. Tracheal injuries from penetrating trauma usually affect the anterior extrathoracic trachea in the lower neck, unlike blunt trauma, in which injuries are most commonly found in the posterior membranous trachea and mainstem bronchi within 2 cm of the tracheal carina with preferential tear of the right mainstem bronchus [119]. Radiographic signs of tracheal rupture include rapidly progressing pneumomediastinum and deep cervical emphysema. Pneumothorax may occur as well. An abnormally positioned endotracheal tube or an overinflated endotracheal tube balloon cuff to over 28 mm in diameter may also indicate tracheal rupture. On CT scans, transtracheal herniation of the balloon cuff through the defect in the posterior tracheal membrane causes a dumbbell shape and a "Mickey Mouse" shape with anterior tracheal ruptures. The tracheal wall injury can be directly visualized in 71 percent of patients as a defect of the cartilaginous elements, a gas-filled tract between the tracheal lumen and the paratracheal gas or tracheal deformity [120].
Both intubation and tracheostomy can be complicated by posterior tracheal wall perforation (image 46), pneumomediastinum, mediastinitis, and the development of tracheoesophageal fistulae [121,122]. Posttraumatic tracheoesophageal fistulae usually occur after penetrating trauma or as a result of compression by a tracheal cuff and a concurrent enteric tube (picture 7). They can also result as a complication of laryngectomy or to facilitate esophageal speech as well as after esophagectomy [123] (image 47). These fistulae have to be differentiated from congenital, postinfectious, or neoplastic lesions (image 48A-B). (See "Complications of the endotracheal tube following initial placement: Prevention and management in adult intensive care unit patients" and "Tracheostomy: Rationale, indications, and contraindications".)
Tracheal stents are increasingly used to treat symptomatic patients with tracheal obstruction who are not amenable to surgical resection, like primary lung cancer and metastatic disease. Stents can also be used to treat patients with airways stenosis due to benign disease like tracheomalacia, relapsing polychondritis, postintubation tracheal stenosis, postoperative anastomotic stenosis, and granulomatous disease. Stents can also be used as a barrier method in the management of esophagorespiratory fistulae. (See "Airway stents".)
Tracheal stents are classified as silicone, covered and uncovered metal and hybrid stents which are made of silicone with reinforced metal rings. Multidetector CT scanning plays an important role in determining the cause, location, and extent of tracheal obstruction. It can depict complications that ensue after stent insertion [124].
SUMMARY AND RECOMMENDATIONS
●The trachea should be visualized and scrutinized on every chest radiograph. (See 'Anatomy' above.)
●Some congenital anomalies of the large airways present early in life. Other anomalies generally cause symptoms later in life and can be associated with substantial morbidity and coexisting congenital vascular anomalies. (See 'Congenital anomalies' above.)
●Dilation of the trachea can be either diffuse or focal. Causes of diffuse tracheal dilation include tracheobronchomegaly (ie, Mounier-Kuhn syndrome) and traction tracheomegaly. (See 'Tracheal dilation' above.)
●Tracheal narrowing can be divided radiographically into long and short segment narrowing. Patients may be asymptomatic until the trachea is critically narrowed (<10 mm), regardless of the length of the stenotic lesion. Acute obstruction of the upper airway is a medical emergency. (See 'Tracheal narrowing' above.)
•Airway narrowing involving long segments of the trachea is seen with saber sheath trachea, relapsing polychondritis, and tracheobronchopathia osteochondroplastica. Less commonly, amyloidosis, granulomatosis with polyangiitis, tumors, inflammatory bowel disease, and airway burns cause long segment narrowing. A saber sheath trachea should not be mistaken for extrinsic tracheal compression. (See 'Long segment narrowing' above.)
•Airway narrowing involving short segments of the trachea is seen with malignant tumors, benign tumors, pseudotumors, extrinsic compression, granulomatous processes, and other select diseases. (See 'Short segment narrowing' above.)
●Imaging findings associated with tracheal trauma vary with the type of traumatic event ranging from circumferential subglottic tracheal wall thickening and short-segment stenosis due to endotracheal cuff-induced tracheal stenosis, to pneumomediastinum, mediastinitis, and the visualization of tracheoesophageal fistulae resulting from penetrating tracheal injuries. (See 'Tracheal trauma' above.)
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