|
|
||||||||
Eur J Cardiothorac Surg 2006;30:833-836
© 2006 Elsevier Science NL
a Birmingham Heartlands Hospital, Bordesley Green East, Birmingham, United Kingdom
b Department of Cardiothoracic Surgery, Government General Hospital and Madras Medical College, Chennai, India
c Department of Gastrointestinal Surgery, Government Royapettah Hospital and Kilpauk Medical College, Chennai, India
Received 17 July 2006; received in revised form 19 September 2006; accepted 25 September 2006.
* Corresponding author. Tel.: +91 44 2642 5414. (Email: smchandra{at}yahoo.com).
| Abstract |
|---|
|
|
|---|
Key Words: Tuberculosis Dysphagia Oesophagus Tracheo-oesophageal fistula
| 1. Introduction |
|---|
|
|
|---|
Tuberculosis can cause dysphagia by many mechanisms; it can be intrinsic oesophageal tuberculosis or it can be extraneous compression. Even in countries with a high prevalence, tuberculous involvement of the oesophagus is rare [1]. Likewise tuberculous adenitis rarely causes dysphagia.
We share our experience with dysphagia due to tuberculous aetiology in this article.
| 2. Aim |
|---|
|
|
|---|
| 3. Methods |
|---|
|
|
|---|
| 4. Findings |
|---|
|
|
|---|
4.2 Presentation
The aetiology of dysphagia was mediastinal and subcarinal lymphadenopathy in seven, tracheo-oesophageal fistula in four, oesophageal ulcer in two and cervical node suppuration in one patient. Two patients had already received medical therapy for pulmonary tuberculosis and one patient who had undergone thoracotomy and drainage for suppurating mediastinal adenopathy now presented with tracheo-oesophageal fistula.
All of them had presented themselves with progressive dysphagia for solids and the patients with tracheo-oesophageal fistula presented with associated aspiration and chest infections. One patient had an oesophageal stent placed in an attempt to close the tracheo oesophageal fistula by the referring unit which was not successful. They also had associated weight loss due to dysphagia and the tuberculous disease process itself.
4.3 Investigations
All the patients underwent routine haematological and biochemical investigations including liver function tests. Investigative workup included oesophagogastroscopy, contrast swallow, fiberoptic bronchoscopy and CT scan of the chest.
Oesophagogastroscopy demonstrated extraneous compression in ten patients and ulcers in two patients. The Chest radiograph demonstrated largely enlarged neck nodes in one patient and loss of the paratracheal stripe in four patients. The CT scan revealed oesophageal and tracheal shift in patients with significantly enlarged cervical and mediastinal nodes (Fig. 1 ). The Barium swallow demonstrated the extrinsic compression in ten patients (Fig. 2 ) and the tracheo-oesophageal fistula in four patients (Fig. 3 ). The bronchoscopy demonstrated tracheal splaying due to enlarged subcarinal nodes. Histological assessment of biopsies produced proof of epithelioid cell granulomas with marginally polygonal Langhans-type giant cells confirming tuberculosis.
|
|
|
Seven patients required surgical procedures, four patients underwent transthoracic repair of tracheo-oesophageal fistula of which three had intercostal muscle flap and one had pleural flap for reinforcement of the repair. Two required drainage of suppurating abscess and one had excision of subcarinal lymph node (Table 1 ).
|
The patient with the caseaous mediastinal node had the abscess opened and drained. The abscess cavity was excised with a sliver adherent to the trachea. The patient with a large subcarinal lymph node mass had the mass excised completely; fortunately the mass was not infiltrating any of the adjacent organs including the oesophagus and was resected without difficulty. All the patients were closed with an apical and basal chest drains. All the patients were extubated on table and were nursed in the high dependency unit.
4.6 Results
There were no mortalities in this series. One patient had air leak till the sixth postoperative day. One patient had a persistent sinus in the neck, which settled down after 2 weeks. All the patients who underwent surgery had relief of their dysphagia immediately after surgery.
All patients had complete remission of their dysphagia following the course of treatment and were followed up between 6 months and 2 years and discharged back to the care of referring clinician.
| 5. Discussion |
|---|
|
|
|---|
Tuberculosis though a systemic disease rarely causes dysphagia. Tuberculous dysphagia can be due to intrinsic oesophageal ulcers, tracheo-oesophageal fistulae and extrinsic compression due to mediastinal or cervical lymph nodes.
Tuberculosis has been known to involve the oesophagus, either as a primary infection or as a secondary manifestation of reactivated disease. The exposure of the oesophagus to the organism is limited by the rapid clearance of infected sputum by means of coordinated peristalsis, combined with upright posture and an intact lower oesophageal sphincter [3]. Oesophageal tuberculosis is almost always associated with mediastinal lymphadenopathy with or without a tracheo-oesophageal fistula [4]. The two most common differential diagnoses are carcinoma of the oesophagus and Crohn's disease of the oesophagus [5,6].
The primary complaint is chronic dysphagia in almost 75% of the patients and other symptoms included weight loss, haematemesis and productive cough suggestive of tracheoesophageal fistula formation [7].
Most of the reported cases of oesophageal tuberculosis are secondary to tuberculosis elsewhere in the body, most commonly pulmonary tuberculosis [8]. Oesophageal tuberculosis can present as ulcers, strictures or fistulae [9]. Endoscopic features of oesophageal tuberculosis are deep and large oesophageal ulcers, tracheoesophageal fistula, and chronic nonhealing ulcer [10]. Histological assessment of biopsies produce proof of epithelioid cell granulomas with marginally polygonal giant cells of Langhans-type and the presence of acid-fast bacilli confirms the diagnosis. In difficult scenarios, oesophageal tuberculosis has been diagnosed by identification of mycobacteria in paraffin-embedded oesophageal biopsy specimens by polymerase chain reaction [11]. Mediastinal tuberculous lymphadenitis is rare in adults, and it is even rare to present as dysphagia. This may lead to oesophageal ulceration, mucosal or submucosal mass with ulceration, fistula or sinus formation, extrinsic compression, or displacement of the oesophagus [1216].
Acquired, nonmalignant tracheoesophageal fistulae usually result from erosion of the tracheal and oesophageal walls by endotracheal or tracheostomy tube cuffs [17]. However, tuberculous mediastinal lymphadenitis can also lead to tracheo-oesophageal fistula. These patients usually present with dysphagia and recurrent aspiration and chest infections [18].
Bronchoscopy, possibly with the application of methylene blue dye into the oesophagus, or oesophagography with a water-soluble agent will exactly define even a small fistula. Oesophagoscopy may reveal the fistula, however, the fistula can be overlooked in the mucosal folds of the oesophagus [19].
Tracheo-oesophageal fistulae caused by Mycobacterium tuberculosis usually require a combination of both surgical treatment and medical treatment with anti-tuberculosis drugs.
It can be managed by simple division and closure of the fistula or tracheal resection and reconstruction. Primary reconstruction definitely corrects the fistula and removes concurrent tracheal disease and is preferred to simple division and closure of the fistula [17,20]. The oesophageal defect is closed in two layers and a viable strap muscle interposed between the two suture lines [20]. However, there are case reports with complete healing of the fistula with medical therapy alone [4,21].
Medical therapy is the mainstay of management of these patients. The standard drug regimen incorporating Izoniazid, Rifampicin, Pyrazinamide and Ethambutal usually lead to complete cure. Maintenance of a good nutritional state is imperative especially considering the altered liver metabolism and vitamin deficiencies associated with it.
| 6. Conclusion |
|---|
|
|
|---|
| References |
|---|
|
|
|---|
This article has been cited by other articles:
![]() |
T. F. Molnar, F. Detterbeck, and Z. Baliko Another perspective of the dysphagia due to tuberculosis Eur. J. Cardiothorac. Surg., July 1, 2007; 32(1): 184 - 184. [Full Text] [PDF] |
||||
![]() |
S. Rathinam and S. M. Chandramohan Reply to Molnar et al. Eur. J. Cardiothorac. Surg., July 1, 2007; 32(1): 184 - 184. [Full Text] [PDF] |
||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |