Tracheo-esophageal fistulas

Abstract

Tracheoesophageal fistulas are pathological connections that occur between the trachea and esophagus in the cervical region and mediastinum due to their close proximity. These fistulas can be caused by embryological developmental abnormalities or trauma and can be life-threatening. It is important to determine the etiology and pathophysiology in order to successfully diagnose and treat them. The esophagus and trachea develop from the embryonic foregut. During the third week of gestation, diverticula buds from the esophagus called tracheobronchial diverticula form. By the fourth week, the esophagus and trachea, which were continuously connected, begin to separate from each other starting from the thorax. A failure in this embryological process leads to congenital TEF. In acquired TEFs discussed in this section, the mechanism is different. The formation of acquired fistulas varies depending on the etiology. Acquired TEFs can be divided into two main groups: malignant and benign. The leading cause of malignant TEFs (mTEF) is esophageal cancer. Esophageal cancer accounts for over 50% of malignant TEFs. The incidence of TEF in esophageal cancer is approximately 5-10%. In one of the large case series studies on mTEF by Martini et al., TEF was found to occur in 4.94% (n=1943) of patients with esophageal cancer. Another study by Balazs et al. found that mTEF developed in 12.5% (264/2113) of patients with primary or secondary esophageal malignancies. Both the esophagus and trachea are channels with thin walls. The wall thickness is approximately 4 mm. In esophageal cancer, the tumor progresses directly to the trachea through the membranous wall, which is more resistant to tumor infiltration than the cartilaginous wall of the trachea. Local tumor invasion results in tumor necrosis, leading to the formation of mTEF. Palliative treatments are preferred in advanced stage esophageal cancer. Treatment options include radiotherapy or esophageal stent placement. Unfortunately, both treatment modalities induce tumor necrosis and predispose to the development of TEF. The risk of developing TEF is higher in tumors with high radiosensitivity. It is known that TEF can also occur in lung, trachea, larynx, thyroid, and lymph node malignancies due to their proximity to the trachea and esophagus, especially in the subcarinal region, proximal airway, and adjacent esophageal areas, malignant-metastatic lymph nodes can cause erosion. The most common cause of benign TEF is the use of endotracheal tubes during prolonged intubation. It was first described by Flege in 1967. Cooper and Grillo, who examined the pathological damage caused by cuffed tubes used in mechanical ventilation, examined autopsy samples and tracheal segments removed during surgical resection. They found a specific pattern of damage in the region where the cuff was placed. Initially, tracheal mucosa developed ulceration under the cuff within 3 to 5 days, and the ulcer deepened and affected more cartilage rings. It was observed that tracheal destruction increased with the accumulation of infection. When exposed to high cuff pressure for a short period, the depth of damage is limited to the mucosa; after intubation, tracheal stenosis occurs with a peripheral scar in the damaged tracheal segment. However, when exposed to high cuff pressure continues, cartilage destruction increases and tracheomalacia develops with the destruction of surrounding supportive tissue. With continued cuff exposure, fistulization to adjacent organs is observed due to erosion of the damaged tissue. In addition to pressure necrosis in the tracheal wall due to the inflated balloon of the endotracheal tube, excessive cuff pressure can cause tracheal damage.