Adult Chest Surgery

Chapter 49. Surgical Repair of Congenital and Acquired Tracheoesophageal Fistulas 

The term tracheoesophageal fistula (TEF) describes a communication between the gastrointestinal tract and the airway. This defect can present at birth as a congenital TEF or as an acquired pathology secondary to trauma, malignancy, or inflammation. Management of TEF requires expedient diagnosis with thoughtful planning and implementation of tailored single- or multistaged therapy. As in all diseases of the esophagus and trachea, patient outcome depends on a clear understanding of the pathophysiology and anatomy of the disease, expert treatment, and sound surgical technique. This chapter focuses on the management of both congenital and acquired TEF.


Congenital TEF is most frequently associated with esophageal atresia (EA). Thomas Durston first described EA in 1670. Thomas Gibson first described TEF with EA in 1696. However, it was not until 1939 that Thomas Lanman and Logan Leven reported a successful staged repair. This was soon followed by the first report of a primary repair by Cameron Haight in 1941.1

Congenital TEF occurs in about 1 of every 3000–4000 live births.2 The prevalence increases with advancing maternal age and maternal diabetes, and there is a genetic predisposition in children born to affected parents.3 TEF and EA are believed to develop during the fourth week of gestation after the lung bud has begun to separate from the foregut. This is usually followed by separation of the trachea from the esophagus, which begins at the level of the carina and moves cephalad toward the larynx. It is postulated that abnormal endoderm-mesoderm interactions that occur early in development cause incorrect signaling and inappropriate separation and development of the tracheobronchial tree and esophagus.4

Diagnosis and Preoperative Assessment

TEF and EA were first classified by Gross with a lettering system and Ladd with a numbering system. It is now more common to describe the anatomic abnormalities of the esophagus and trachea. The most common variant is EA with distal TEF (85%), followed by EA alone without TEF (7%) and TEF alone without EA (N- or H-type) (4%). Other very rare variants include EA with proximal TEF and EA with proximal and distal TEF1,2 (Fig. 49-1).

Figure 49-1.


EA with distal TEF (85%) is the most common variant, followed by EA alone without TEF (7%) and TEF alone without EA (N- or H-type) (4%). Other very rare variants include EA with proximal TEF and EA with proximal and distal TEF.

With these advances in surgical management of TEF and EA, neonates who undergo successful repair can be expected to live normal lives. However, TEF/EA is associated with other congenital abnormalities in 30–50% of patients that can have a significant impact on long-term outcomes. Associated defects include cardiac, gastrointestinal, neurologic, skeletal, and genitourinary. The most common cardiac defects are atrial and ventricular septal defects, patent ductus arteriosus, tetralogy of Fallot, and aortic arch abnormalities.5 The most common gastrointestinal abnormality is imperforate anus, which occurs in 10% of patients.

These patients also may have multiple congenital defects that have been given the acronym VACTERL (vertebral, anal, cardiac, tracheoesophageal fistula with esophageal atresia, renal, limb). The presence of any three abnormalities determines this designation. The search for additional congenital abnormalities is critical owing to their impact on management strategies and overall survival.1,2


The first sign of possible TEF/EA is typically picked up during prenatal ultrasound with the observation of maternal polyhydramnios and the absence of a fetal stomach bubble. This is especially the case with EA alone, in which the fetus is unable to swallow the amniotic fluid as a consequence of the blind proximal esophageal pouch. In patients with TEF alone without EA or the more common EA with distal TEF, polyhydramnios may be absent owing to the distal fistula.6,7

If not diagnosed prenatally, these patients present soon after birth with excessive drooling and pooling of saliva in the posterior pharynx that is refractory to frequent suctioning. They also have persistent coughing, choking, and cyanosis, especially with the first feeding attempts. In patients with EA with distal TEF, reflux of gastric contents leads to aspiration pneumonitis and respiratory distress with resulting bradycardia, apnea, and sepsis. In patients with TEF without EA, the diagnosis may be delayed. These patients may present later owing to recurrent coughing and choking with feeding, with resulting pneumonia and respiratory infection.

The simplest means of diagnosis is to insert a firm, radiopaque nasogastric tube (8F in preterm and 10F in term infants). This typically passes no further than 10-12 cm in patients with EA, the end of the blind pouch (normal distance to gastric cardia is 17 cm). A chest radiograph and an abdominal radiograph then should be performed to confirm the location of the tube and to estimate the distance of the esophageal gap caused by the atresia. An esophagram can be used cautiously to diagnose TEF without EA, although precautions against aspiration of barium must be taken, with care to suction the airway clear at completion of the procedure. Bronchoscopy and esophagoscopy typically are confirmatory. Recently, CT scanning with sagittal cuts of the thorax has been used to identify the interpouch distance in esophageal atresia. Axial slices may be added when additional information is needed. This noninvasive testing may assist with preoperative planning and can help to identify other associated congenital abnormalities.8

Once the diagnosis of TEF/EA is made, a careful search must be made for additional congenital abnormalities. Physical examination will identify imperforate anus and some limb and cardiac defects. Additional studies include echocardiography, renal ultrasound, and spine and limb radiographs.


Preoperatively, maneuvers to decrease the risk of aspiration should be initiated, including continuous nasogastric suction, maintenance of head elevation, and administration of prophylactic antibiotics (e.g., ampicillin and gentamicin). IV fluids also should be started (e.g., 10% dextrose solution) or parenteral nutrition if surgical correction is to be delayed. In patients with severe pneumonitis and respiratory distress, intubation and mechanical ventilation may be required. Bag mask ventilation should be avoided. In critically ill patients, a gastrostomy tube may be necessary to prevent gastric distention and reflux.

The need to investigate congenital abnormalities cannot be overemphasized. Multiple studies have shown that the two independent predictors of mortality are low birth weight and cardiac abnormalities.9 In some cases, the cardiac defect may need to be corrected first or concurrently with the TEF/EA repair.10

Ligation of the TEF and primary repair constitute the procedures of choice, with staged repair being largely historical.9,11 Unless there is a right-sided aortic arch, the operative approach is via a right posterolateral thoracotomy using an extrapleural approach. The interspace of the thoracotomy varies depending on the location of the atretic esophageal segment. Usually, the fourth intercostal space is preferred. Careful blunt dissection is performed to separate the pleura from the chest wall and the apex of the chest down to the level of the sixth rib. The azygos vein is divided. This usually exposes the distal TEF. It is then encircled and ligated. Bronchoscopy can be used to identify the fistula and rule out any additional fistulas. Esophageal tissue may be left on the trachea to assist with fistula closure and prevent tracheal stenosis.

Next, the upper pouch is dissected off the trachea up to the thoracic inlet. The dissection is facilitated by having the anesthesiologist push on the nasogastric tube, which brings the esophagus into the operative field. The distal pouch then is dissected as necessary to increase length and decrease the interpouch distance. Additionally, transverse circular myotomies can be used to increase esophageal length. Finally, the pouches are opened, and a single-layer end-to-end esophagoesophagostomy is performed. A transanastomotic nasogastric feeding tube should be inserted before completion of the anastomosis. A primary anastomosis should be performed if at all possible. Gastric mobilization may be required. Repair of gaps of up to 6 cm have been reported.12 A chest tube is placed away from the anastomosis in the extrapleural space, and the wound is closed. If repair is impossible despite all efforts, then the esophagus is sewn to the prevertebral fascia and closed. Daily dilations of the upper pouch are performed until the gap is shortened enough for primary anastomosis, usually in 1–2 months. If primary repair is still not possible, esophageal replacement with stomach, colon, and jejunum may be necessary.

Thoracoscopic techniques have been used to avoid thoracotomy. Patients are positioned 45 degrees from prone, three to four ports are placed, and carbon dioxide insufflation is used to develop a working space. The fistula is clipped, and the anastomosis is performed with intra- or extracorporeal knot tying. A multi-institutional study demonstrated comparable results with open techniques, although advanced minimally invasive skills are required.13,14


Early and late postoperative complications are frequent, and careful attention to detail is warranted. Early complications include esophageal leak (20%), missed fistula, and recurrent fistula (10%).2 Anastomotic leak should be suspected in patients with new air leaks, pneumothorax, or salivary drainage from the chest tube. Diagnosis is confirmed by barium esophagram. These leaks can be treated conservatively, especially if an extrapleural approach was used, in which the keys to management are adequate drainage, H2-blockers, and gastric decompression. Large leaks with sepsis may require esophagectomy, cervical esophagostomy, and gastrostomy tube placement with delayed repair several months later after full recovery.

Long-term complications include strictures, gastroesophageal reflux, and respiratory complications. Strictures can occur in up to 40% of patients following repair and are seen mostly in the setting of previous anastomotic leak, recurrent fistula, or ongoing reflux.2 Barium esophagram and esophagoscopy are diagnostic. Management usually requires multiple dilations and aggressive treatment of reflux. Gastroesophageal reflux can be a significant problem for these patients. This is likely because of esophageal dysmotility. Most patients respond to medical management and behavioral modifications, but a significant number require surgical antireflux procedures. Indications include failed medical therapy, failure to thrive, recurrent pneumonias, refractory strictures, and Barrett's esophagus. Nissen fundoplication may not be the best choice of fundoplication because of the esophageal dysmotility. A floppy Nissen or partial fundoplication may be a better choice. These patients require lifelong follow-up. Esophageal cancer can occur in the setting of long-standing reflux.

Respiratory complications are a frequent cause of readmission in patients with TEF/EA. Recurrent pneumonias, chronic cough, wheezing, and aspiration secondary to reflux can be persistent problems that slowly abate over time. In addition, tracheomalacia is a challenging complication that may develop. Early abnormal tracheal development leads to redundant membranous trachea, predisposing to anteroposterior collapse. Bronchodilators may worsen the condition because of relaxation of the tracheal smooth muscle. While most patients improve with time, a few patients may require intervention. Aortopexy of the aorta to the posterior aspect of the sternum via a left thoracotomy allows the trachea to be fixed more anteriorly, preventing airway collapse. Tracheal stent placement has been used, but with mixed results. Tracheostomy may be required in refractory cases.2Overall, the results have been excellent with primary repair of TEF/EA, with survival approaching 100% in children without associated congenital abnormalities. Most children can look forward to essentially normal lives (see also Chap. 48).




The most common cause for benign TEF is a complication of endotracheal intubation or tracheostomy tube placement.15 Symptoms arise secondary to aspiration of gastric contents into the fistulized airway or from insufflation of air into the stomach producing sepsis or hemodynamic collapse. TEF must be diagnosed quickly and managed aggressively. Management is most challenging in the patient who still requires mechanical ventilation.16 The typical patient suffers from chronic illness, is malnourished, has undergone prolonged ventilation with either an endotracheal tube or a tracheostomy, and has a nasogastric tube in place. TEF develops in the ventilated patient secondary to endotracheal cuff pressure that causes necrosis and erosion of the airway into the esophagus.17 The nasogastric tube serves as a second foreign body against which the tracheal cuff rides and chafes. The advent of high-volume, low-pressure endotracheal cuffs has made tracheal stenosis and TEF less common but has not eliminated the problem.

Diagnosis of TEF in the ventilated patient is usually straightforward. It should be suspected in a patient who becomes acutely distended and difficult to ventilate with a significant loss of return of ventilated breaths and accompanying bilious secretions. A presumptive clinical diagnosis of TEF is then made. A plain chest radiograph should be performed but is usually noncontributory. Mediastinal air is present occasionally. However, mediastinal inflammation and adhesions usually prevent frank pneumomediastinum and mediastinitis. Bronchoscopy and esophagoscopy are the cornerstones of diagnosis and management.

As initial management, the patient must be stabilized and the airway protected from further contamination. In addition, the stomach must be decompressed. The nasogastric tube must be kept continuously sumping to evacuate air from the stomach. Ventilatory pressures should be lowered to the lowest levels that will support oxygenation and ventilation. This may require pharmacologic sedation and paralysis. The anesthesiologist carefully controls the airway from the head of the bed while the surgeon removes the tracheostomy. With the tracheostomy out, a bronchoscopy should be carried out through the stoma. The fistula typically is evident a few centimeters distal to the stoma on the membranous wall where the opposing balloon of the tracheostomy was located. The nasogastric tube frequently will be visible through the fistula, making the diagnosis obvious. Alternative modalities for diagnosing TEF include esophagoscopy and CT scan of the neck and chest. However, bronchoscopy is the simplest and fastest way to obtain a diagnosis and also can be employed to aid in its treatment.

Once the diagnosis of TEF is made, the next step in its management is to ventilate the patient distal to the fistula. This is simple in principle but frequently difficult in practice. The location of the fistula in the midtrachea leaves little room between the carina and the fistula to place the cuff of the endotracheal tube. A tracheostomy must have a distal arm that is long enough to traverse the fistula but not so long that it produces a main stem intubation. This is often difficult to find and may need to be custom made. Careful bronchoscopic measurements of the distance of the fistula from the carina must be made as well as measurements of the endotracheal tube and its balloon to ensure correct placement. The tip of the endotracheal tube should be positioned at the carina or directed just down the left main stem bronchus, with the Murphy eye of the endotracheal tube directed to the right main stem bronchus to prevent atelectasis. Confirmatory bronchoscopy must be performed regularly to check position and clear secretions. Sedation or paralysis may be required to prevent the patient from dislodging the endotracheal tube. Once stabilized, the patient should be taken to the OR for placement of a formal drainage gastrostomy tube and a feeding jejunostomy tube. The nasogastric tube then should be removed to prevent enlargement of the TEF. However, spontaneous closure of the TEF is unlikely to occur.

After initial stabilization and management, the next more difficult step is definitive management of the fistula. The principal surgical objective is closure of the fistula with prevention of breakdown of the airway and esophageal closure. While the primary objective of closure of the fistula frequently can be met, the prevention of breakdown of the closure is far more difficult to achieve in this debilitated, ventilated group of patients.18Attempts at closure of the fistula while the patient still requires positive-pressure ventilation are almost always doomed to failure, and every attempt should be made to wean the patient from the ventilator with the focus on nutrition and the prevention and treatment of airway contamination and nosocomial infection.

Esophageal diversion should be avoided because of its high morbidity and mortality. However, this may be required if aspiration cannot be controlled. In this setting, the gastroesophageal junction must be divided and an end-cervical esophagostomy performed. Tracheal stenting while the patient is still intubated is technically difficult and not recommended. Esophageal stenting has been performed with some limited success in this difficult group of patients. One report describes bedside deployment of a flexible stent to cover the fistula in a series of 12 ventilated patients, with successful fistula occlusion in all patients.19 While no stent migration or failure was reported, nine patients died after prolonged hospital courses, with only three surviving to repair. Presently, we do not recommend esophageal stenting in this setting given the limited experience in the literature of ventilated patients with TEF and generally poor outcomes.

If the patient can be weaned successfully from the ventilator, definitive surgical repair then can be performed. Surgical approach depends on the location of the fistula. Small fistulas can be addressed through a lateral cervical approach with mobilization of the trachea and direct suture closure of the membranous trachea and esophagus with interposition of strap muscle. However, most fistulas are large and require tracheal resection with concomitant repair of the esophagus. The most frequently applied approach is an anterior cervical approach with a low collar incision. An upper sternal split can be performed if more distal exposure to the trachea is necessary. Fistulas close to the carina should be approached through a right posterolateral thoracotomy.

Standard techniques of tracheal resection apply. The trachea is dissected with care circumferentially to preserve the lateral-segmental blood supply and avoid the recurrent laryngeal nerves. Proximal and distal mobilization should be performed only as far as absolutely necessary to bring the trachea together with minimal tension. The airway is transected distally and secured with traction sutures. An armored, flexible endotracheal tube is brought into the field and used to intermittently ventilate the distal trachea. Alternatively, jet ventilation can be used, but this technique is seldom required. With the airway divided, the esophagus is exposed. After carefully defining the mucosal edges, the esophageal defect then can be closed in two layers. Our preference is to use interrupted 4-0 Vicryl sutures for the mucosal layer and silk for the muscular layer. Suture choices vary according to surgeon's preference. A pedicled strap muscle then is mobilized and tacked over the esophageal closure to provide a layer of tissue between the esophageal and tracheal suture lines and prevent breakdown of the repair. The importance of this step cannot be overemphasized. Finally, the trachea is reapproximated using interrupted 4-0 Vicryl suture with removal of the armored tube and careful guidance of the orotracheal tube through the anastomosis as the anterior cartilaginous wall is being completed. The neck is flexed to minimize tension on the anastomosis, and a stitch can be brought from the chin to the chest to prevent neck extension in the perioperative period.17 A nasogastric tube is left in briefly after the repair and then is removed.


Other uncommon benign disorders leading to TEF are classified as traumatic TEF and inflammatory TEF. Inflammatory TEF is usually caused by granulomatous disease. Traumatic TEF can result from either blunt or penetrating trauma or iatrogenic injury.20 The diagnosis of TEF secondary to penetrating injury is usually made early. The location of the injury in the neck or chest usually prompts an aggressive workup including radiologic and endoscopic evaluation. However, diagnosis of TEF after blunt trauma can occur in a delayed fashion. Barium esophagram, CT scanning, and endoscopy are all useful diagnostic tools. TEF should be considered after blunt chest trauma with the appearance of pneumomediastinum, unexplained fever, leukocytosis, or pleural effusion. Management is founded on the principles of debridement of infected tissue followed by definitive repair of the esophagus and trachea with interposition of tissue between the suture lines.

Inflammatory processes leading to TEF are quite rare. In one small series of TEF, the most frequent etiology was histoplasmosis.21 The pathology of TEF in this setting provides a technical challenge, particularly when associated with esophageal diverticula. Presentation can be subtle. An esophagram is useful for demonstrating the fistula. Bronchoscopy is critical. Repair of the TEF for granulomatous disease follows the same principles prescribed for other etiologies, although identification and management of the fistula in inflamed mediastinal tissue can be difficult.


Malignant TEF develops in advanced stages of disease. It is most often due to esophageal or bronchogenic carcinoma, although rarely it may be associated with lymphoma. TEF occurs in 10-15% of patients with esophageal cancer and in 1% of patients with bronchogenic carcinoma.22 The fistula occurs as a result of primary tumor invasion or as an effect of various treatments, including chemotherapy and radiation therapy, laser therapy, photodynamic therapy, and self-expandable stent placement. Patients undergoing therapies such as esophageal stent placement followed by chemoradiation therapy are at particularly high risk for developing TEF.23 Given the advanced stage of malignancy of patients who present with TEF and the palliative nature of its management, intervention must be carefully individualized.

Patients with malignant TEF have an extremely poor prognosis, with an expected lifespan at diagnosis that is usually measured in weeks. Focus should be on quality of life with symptom control. The primary goals are control of aspiration and establishing or maintaining oral intake. For this reason, traditional surgical intervention is not indicated. Palliative surgery should remain historic. Morbidity and mortality are high, and the recovery period is prolonged such that the patient is unlikely to survive long enough to benefit from the operation. Some patients may be too ill for any intervention and should be considered for comfort care.

Fortunately, endoscopic management of malignant TEF has improved and shown significant promise. It is minimally invasive and can be tolerated by most patients. Frequently, it can be performed in an outpatient setting. Studies have demonstrated the efficacy of self-expanding metallic stents in palliating TEFs from esophageal or bronchogenic carcinoma.23,24 Deployment of self-expanding esophageal stents has been shown to prevent aspiration and improve dysphagia in most patients. Complication rates are acceptable, and major complications are unusual. One of the largest published series treated 101 patients with malignant dysphagia and fistula secondary to esophageal malignancy or bronchogenic carcinoma. Success in sealing a fistula using a coated expandable metal stent was 100%. The complication rate was 38%, and the rate of life-threatening complications was 8%. There were no procedure-related deaths. While 99 of 101 patients were dead at a mean follow-up of 201 days, no death was due to a stent-related complication. Rather, this poor survival reflected the advanced stage of malignancy of this patient population.25

The technical aspects of stent placement are beyond the scope of this chapter but have been reviewed in Chapter 46. Multiple stent options exist. Covered Nitinol self-expanding esophageal stents are deployed most commonly. Covered stents prevent tumor ingrowth but are more prone to migration. Debate continues on the optimal stent choice. In addition to esophageal stents, TEFs also can be stented from the airway side. We have found that TEFs are more difficult to seal using this technique, and management of airway secretions is more problematic. Some espouse double stenting (stenting of both the trachea and the esophagus) to achieve the best symptom relief. This technique runs the risk of enlarging the fistula but has been employed successfully in carefully selected patients.26


TEF represents the manifestation of a wide spectrum of benign and malignant diseases. These diseases range from the congenital malformation of a neonate to the advanced esophageal or lung cancer of an adult. A clear understanding of the pathophysiology of each TEF is critical to choosing an appropriate therapy. Prompt diagnosis and intervention are the cornerstones of successful outcome.


The management of an acquired TEF in an adult depends on the size of the defect and the respiratory status of the patient. If the defect is small and minimal pulmonary soilage has occurred, primary repair with tracheal resection and muscle coverage is indicated. The problem is compounded in patients who had a previous esophagectomy and who have a fistula between the conduit and the trachea. In these patients, tracheal resection is fraught with danger as a result of blood supply considerations. I have treated patients who have pulmonary compromise or those with large defects with removable stents to stabilize them prior to definitive resectional or reparative surgery. On occasion, omental flaps have been used as part of the repair.



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