Esophageal Tuberculosis

Esophageal TB is extremely rare. Denonvilliers (France, 1837) first reported an autopsy-proven case; Torek (1931) reported the first primary esophageal TB, with sporadic reports since. It is divided into primary (M. tuberculosis directly invading esophageal mucosa with no other foci, though some authors deny its existence) and secondary (direct/indirect esophageal wall invasion by peri-esophageal/mediastinal node TB).

Common Symptoms

Back pain; fatigue; lymph node TB; tuberculous toxicity; weight loss; odynophagia; retrosternal pain; dysphagia; night sweats; fatigue

Causes and Pathogenesis

(1) Etiology: Sputum-positive cavitary pulmonary TB rarely complicates esophageal TB despite bacilli being swallowed; this may reflect esophageal mucosal resistance, vertical orientation, rapid transit, and constant food/saliva flow, plus protective stratified squamous epithelium. TB results from host-pathogen interaction; disease requires heavy virulent inoculum plus reduced local resistance. Predisposing factors: reduced resistance (pulmonary TB, diabetes, malignancy, radiotherapy/chemotherapy, late-stage disease); immunocompromise (transplant, long-term immunosuppressants, AIDS); pre-existing esophageal disease (reflux esophagitis, ulcers, stricture). (2) Pathogenesis: Almost all occur in late pulmonary, laryngeal, mediastinal, or bone TB; primary esophageal TB is extremely rare. Routes: (1) swallowing bacillary sputum, especially with malnutrition, stasis esophagitis, candidiasis, or cancer; (2) downward extension from pharyngeal/laryngeal TB; (3) rupture of adjacent node TB or direct spinal TB spread; (4) hematogenous spread from distant foci; (5) retrograde lymphatic spread. It prefers the middle/upper esophagus, mostly above the tracheal bifurcation, at 2-13 cm from incisors; lower-third involvement is only 12%. Pathological types: (1) Ulcerative (most common): submucosal/myocardial granulomas progress to caseation and superficial ulcers with grayish purulent bases; severe ulcers may perforate causing esophagomediastinal, esophagopleural, or esophagotracheal fistulas, or fatal aortic hemorrhage; healing causes fibrosis, stricture, and traction diverticula. (2) Proliferative: stenotic or granulomatous, with tuberculous granulation and fibrous nodules deep in the wall, sometimes pseudotumors. (3) Miliary (rarest): gray-white nodules in severe systemic disease. Pathological course: (1) enlarged nodes compress the esophagus causing dysphagia; (2) nodes adhere to or embed in the wall; (3) caseous nodes liquefy/rupture forming abscesses or fistulas, possibly esophagotracheal; (4) caseous necrosis causes spasm, exudation, ulceration, proliferation, and scarring with irregular, rigid, poorly distensible lumen resembling medullary esophageal cancer.

Treatment

Surgical treatment, drug therapy, supportive therapy

Preventive Measures

Boosting immunity and avoiding contact with TB patients are key; open pulmonary TB patients should avoid swallowing bacillary respiratory secretions to reduce esophageal TB.

Department to Visit

It is recommended to visit the Gastroenterology department; an appointment can be booked on this platform before the visit.

Warm reminder: The above information is for health science reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek medical attention at a regular hospital promptly.