*2.12.2 Late complications*

*Pediatric Surgery, Flowcharts and Clinical Algorithms*

*Complications associated with oesophageal atresia repair.*

delayed oesophageal replacement would be required.

in the pathogenesis of oesophageal stricture.

*2.12.1.3 Recurrent tracheo-oesophageal fistula*

*2.12.1.2 Anastomotic stricture*

**Table 9.**

usually leads to the formation of a stricture at the site and may be associated with a recurrent TOF. Only 3–5% of anastomotic leaks are known to result from major disruptions of the oesophageal anastomosis. They are found to be typically seen within 24–48 h after repair. Patients usually deteriorate as result of tension pneumothorax or mediastinitis. Hence, prompt reoperation with adequate drainage is imperative. Repair of the leak may be attempted, and this may be buttressed with the help of a pleural or pericardial patch, with or without intercostal muscle flap. Contributing factors to anastomotic leak include poor surgical technique, ischemia of the oesophageal ends, the use of myotomy and excessive tension at the anastomotic site [63, 64]. If reanastomosis is not possible, cervical oesophagostomy and

Anastomotic stricture is found to be a common complication after repair of OA. It is characterised by dysphagia and recurrent respiratory problems due to aspiration or foreign body obstruction. The narrowing is noted on endoscopy or contrast oesophagography. Poor anastomotic technique (excessive tension, twolayered anastomosis and silk suture material), long gap, ischemia at the ends of the oesophagus, gastro-oesophageal reflux and anastomotic leak are factors implicated

Anastomotic stricture is treated by dilatation. However, a stricture resistant to repeated dilatations will require resection and reanastomosis or oesophageal replacement. Triamcinolone injection may be used at the stricture site. However, repeated injections may lead to adrenal suppression. Application of mitomycin C to the stricture under endoscopic control has also been reported to reduce stricture formation after dilation. It is important to determine whether the oesophageal stricture is associated with gastro-oesophageal reflux. This can be determined using contrast oesophagography, endoscopy, pH monitoring or a combination of these studies. The presence of gastro-oesophageal reflux is initially managed medically with proton pump inhibitors. Failure of medical management may warrant antireflux procedure.

Recurrent TOF commonly results from anastomotic leak with local inflammation and erosion through the previous site of TOF repair. Recurrent TOF can be minimised by the use of a pleural flap, vascularized pericardial flap or azygous vein flap interposed between the oesophageal and tracheal suture lines. Symptoms of recurrent TOF can be typical of those seen with a congenital H-type TOF (coughing with feedings and recurrent respiratory distress). However, less obvious symptoms such as recurrent pulmonary infections are more common. Air-filled oesophagus on plain radiographs of the chest is suggestive of the diagnosis. As done in patients with congenital H-type fistula, contrast oesophagography performed in the prone position under videofluoroscopy is a reliable method of establishing the diagnosis. Another reliable diagnostic approach is bronchoscopy with cannulation of the fistula with a 2- to 3-French catheter. It is invaluable in locating the fistula

**62**
