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Developmental anomalies of the trachea and bronchi: causes, symptoms, diagnosis, treatment
Last reviewed: 06.07.2025
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Acquired deviations of the trachea and bronchi occur without significant changes in their lumen. Most often, bronchial deviations occur due to external pressure from a tumor or cyst located in the lung parenchyma. Tracheal deviations are usually caused by pressure from volumetric formations or traction by scars that arise in the upper mediastinum. Deviations can be temporary or permanent.
Temporary deviations of the trachea and bronchi are caused by the difference in pressure in the mediastinum, which occurs on both sides of the organ, for example, with partial or total atelectasis of one of the lungs. Radiography reveals a shift of the trachea and bronchi toward atelectasis, and fluoroscopy reveals the Holzknecht-Jacobson phenomenon, which consists of oscillations of the trachea and bronchi in time with respiratory movements. Endoscopically, this phenomenon manifests itself in atypical excursions of the tracheal carina, which shifts during inhalation toward the affected lung with insufficient air filling (Mounier-Kuhn symptom). With rapid filling of the pleural cavity with effusion or air, the mediastinum initially shifts toward the healthy side, taking the trachea and bronchi with it. These signs are less pronounced in mediastinal tumors.
If the above factors causing secondary displacement of the trachea and bronchi quickly pass, then the mediastinal organs take their normal position.
Permanent or chronic deviations of the trachea and bronchi manifest themselves with the same external signs as temporary deviations, they differ only in their long course and the occurrence of secondary inflammatory reactions. Usually, chronic deviations of the trachea and bronchi occur as a result of cicatricial processes in the pleural cavity, lung tissue and mediastinum, caused by the corresponding purulent-inflammatory banal or specific diseases. The main sign of such deviations is respiratory failure during physical exertion. The diagnosis is easily established using fluoroscopy or radiography with contrast.
Narrowing of the trachea and bronchi lumen, which occurs as a result of their external compression, regardless of the cause, causes a disruption in the circulation of the air flow and the phenomena of chronic hypoxic hypoxia. The initial signs of these phenomena occur when the area of the trachea lumen decreases by 3/4 and progressively increase with further narrowing of its lumen. Narrowing of the bronchial lumen causes respiratory function depending on the caliber of the bronchus.
Of the mediastinal neoplasms that cause tracheal compression, the first to be mentioned are those that grow into the trachea and narrow its lumen with their volume. Bronchial compressions owe their origin primarily to adenopathy, neoplasms, and pulmonary atelectasis, including that artificially induced by the collapse therapy method. Of the adenopathy that most often causes compression of the trachea and bronchi, these are banal microbial adenopathy, metastatic adenopathy, adenopathy in lymphogranulomatosis, etc. Compression of the middle part of the trachea can be caused by damage to the thyroid gland, hyperplastic lymph nodes, embryonic tumors, diverticula and foreign bodies of the esophagus, aortic aneurysm, pleurisy, tumors of the pleura and lungs, abscesses and phlegmons of the mediastinum, etc.
The main symptoms are cough and dyspnea, which increase in intensity and duration. If the recurrent nerve is involved in the process, there is a violation of voice formation, manifested by a bitonal voice sound. The general condition of the patient depends on the cause that caused the compression of the respiratory tract and on the degree of respiratory failure.
The diagnosis is established by means of X-ray examination. Tracheobronchoscopy with a rigid instrument is contraindicated.
Tracheobronchial fistulas. Tracheobronchial fistulas are communications between the trachea and bronchi with surrounding organs and tissues that arise as a result of a number of destructive processes both in the lower respiratory tract itself and outside of it.
Lymph node fistulas. In the vast majority of cases, these fistulas develop as a result of tuberculous lesions of the lymph nodes directly adjacent to the trachea or bronchus. With such an arrangement of the lymph nodes, the caseous-necrotic process occurring in it passes to the wall of the trachea or bronchus, destroys it, resulting in the formation of a tracheobronchial-lymphatic fistula. The formation of such a fistula can occur in two forms - acute and protracted.
The acute form is characterized by a sudden and massive breakthrough of caseous masses into the trachea or main bronchus, which causes rapidly increasing suffocation: the patient becomes very anxious, becomes pale, then cyanotic, loses consciousness, and only emergency tracheal intubation or tracheotomy with suction of the detritus and purulent masses that have blocked the airways can save him from death.
The protracted form is characterized by less rapid clinical development of tracheal and bronchial obstruction, which depends on the degree of evacuation of caseous masses penetrating into the lumen of the respiratory tract. In this form, repeated tracheobronchoscopy with removal of purulent sputum, lavage of the tracheal cavity and bronchi, and introduction of complex antibiotic drugs into them are effective.
Melting of the affected lymph node that formed the fistula and its drainage through the fistula or its scarring with subsequent calcification leads to healing of the fistula with the possible formation of stenosis of the affected bronchus or trachea.
Tracheoesophageal fistulas occur more frequently than those described above and are caused mainly by damage to the esophagus. Most often, these fistulas occur at the points of contact between the trachea and the left main bronchus and the esophagus, which facilitates the transition of the inflammatory-destructive process from one organ to another. Indirect transition of the pathological process is also possible, through the affected lymph node.
Among the causes of tracheoesophageal fistulas, cancer and purulent inflammation of the lymph node are in the first place. During endoscopy of the trachea or bronchus, such a fistula looks like a granuloma or rosette formed from granulation tissue, partially blocking the lumen of the air-bearing formation. When swallowing water, water can leak into the trachea or bronchus; during esophagoscopy, during exhalation, especially with straining, air bubbles enter the esophagus.
In case of respiratory dysfunction, these formations are coagulated by diathermy or cauterized with chemicals.
Other causes of tracheobronchial fistulas may include deep chemical burns of the esophagus, penetrating foreign bodies, especially if they are recognized late, tuberculous and syphilitic granulomas, purulent esophagitis, etc. Spontaneous aeroesophageal fistulas have been described, occurring in the late period of inflammatory lesions of the walls of the esophagus and trachea or bronchus, as a result of their cicatricial degeneration and thinning. Such fistulas usually occur with strong straining (constipation, lifting significant weights, sudden sneezing or strong coughing).
Often the subject of diagnosis and treatment of pulmonologists, phthisiologists and thoracic surgeons are bronchopleural perforations, postoperative bronchial fistulas, most often occurring with partial lobeectomy, tracheal fistulas, arising as a complication of mediastinal phlegmon.
Developmental abnormalities of the trachea and bronchi. These abnormalities may remain unrecognized for a long time and are discovered during routine examination of the lower respiratory tract.
Congenital esophageal-tracheal fistulas are usually small, breaking off behind a fold of the esophageal mucosa that acts as a protective valve, which explains the scanty symptoms of this defect (periodic cough with sputum).
Congenital dilatation of the trachea and bronchi is an extremely rare malformation of the lower respiratory tract; sometimes caused by congenital syphilis. Clinical manifestations include frequent colds, tracheobronchitis, a tendency to bronchiectasis, and increased sensitivity to respiratory infections.
Kartagener syndrome is a complex of autosomal recessive hereditary anomalies:
- bronchiectasis with chronic bronchitis, recurrent pneumonia and bronchorrhea;
- chronic sinusitis with nasal polyposis and rhinorrhea;
- situs viscerum inversus.
Radiologically, the lungs show saccular areas of enlightenment, shadowing of the paranasal sinuses, fused ribs, cervical ribs, spina bifida, congenital heart defects, infantilism, plurigenital insufficiency, dementia, and clubbing of the fingers.
Tracheal (accessory) bronchi: the accessory bronchus branches off directly from the trachea, above the bifurcation.
Anomalies of bronchial branching and distribution. Most often occur in the lower lobe of the lung, do not impair respiratory function.
Absence of half of the lower respiratory tract, combined with the absence of the corresponding lung.
Tracheomalacia is a rare phenomenon, which, like laryngomalacia, consists of thinning and weakness of the tracheal cartilages, which are distinguished by significant compliance during tracheoscopy. Areas of tracheomalacia may occur in the area of the carina, in the area of the entrances to the bronchi, or on any part of the tracheal wall. As a rule, tracheomalacia is combined with the same anomaly in the development of the bronchi. Clinically, this defect of the lower respiratory tract is manifested by constant dyspnea, often with crises of hypoxic hypoxia, up to asphyxia with a fatal outcome.
Treatment of the above-described anomalies of the lower respiratory tract is exclusively palliative and symptomatic, with the exception of congenital esophageal-tracheal fistulas, which can be eliminated by endoesophageal microsurgical intervention.
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