Corrosive esophageal scar stenosis is often the result of burns from accidental ingestion of acids, alkalis, and other chemicals. Immediately after accidental ingestion of corrosives, severe pain in the mouth, lips, pharynx, posterior sternum, and upper abdomen is caused, with reflex vomiting, and the vomit is often bloody. If the burn involves the epiglottis, larynx and respiratory tract, coughing, hoarseness and difficulty in breathing can occur. In severe cases, coma, deficiency, fever and other toxic symptoms may occur. The formation of scar stenosis can lead to partial or complete obstruction of the esophagus, and even saliva can be difficult to swallow. Because of the inability to eat, malnutrition, dehydration, emaciation, anemia, etc. can occur, and the growth and development of children are affected. After swallowing chemical corrosives, burns are often not limited to the esophagus, but can also include the oropharynx, larynx, stomach, or duodenum. The severity of chemical burns in the esophagus depends on the type, concentration, dose, accompanying vomiting, and the duration of contact between the corrosive agent and the tissue, usually with three anatomically and physiologically narrow segments of the esophagus. I. The pathology of burns is generally classified as degree III: degree I: superficial congestion and edema of the esophageal mucosa, which heals in 7 to 8 days after the debridement period without leaving a scar. Grade II: Involving the esophageal muscular layer, the acute phase of tissue congestion, edema, exudation, and ulcer formation after tissue necrosis and debridement. granulation tissue proliferation occurs within 3-6 weeks, and later the fibrous tissue forms a scar and leads to stenosis. Degree III: Coagulation necrosis of the whole esophagus and its surrounding tissues can lead to esophageal perforation and mediastinitis. Second, the pathological process after burns can be roughly divided into three stages: Stage I: inflammation, edema or necrosis occur within the first few days after injury, and early esophageal obstruction symptoms often appear. Stage 2: About 1 to 2 weeks after the injury, the necrotic tissue begins to fall off and soft, red granulation tissue appears. Obstructive symptoms can often be reduced. The esophageal wall is weakest at this time and lasts for about 3 to 4 weeks. Stage 3: Scar and stricture formation and progressive worsening. The pathological evolution can proceed for weeks to months, but it is rare for stenosis to reoccur after more than 1 year. The preferred site of scar stenosis is often at the physiological narrowing of the esophagus, i.e., at the entrance of the esophagus, at the plane of the tracheal bifurcation, and at the lower end of the esophagus. Early management: First, keep the airway open, tracheotomy if necessary; establish intravenous access as soon as possible; actively manage complications, including laryngeal edema, shock, gastric perforation, mediastinitis, etc. Immediately take vegetable oil or protein water orally, or even swallow saline or water to dilute the corrosive agent and protect the esophageal and gastric mucosa. The previous practice of using weak acid solution or weak alkali solution to neutralize the corrosive agent is very controversial, because the heat generated by the chemical reaction can cause re-injury, which is not only unhelpful but also harmful. Appropriate application of adrenocorticotropic hormones and antimicrobials can reduce the inflammatory response, prevent infection, fibrous tissue proliferation and scar formation, but hormones should be used with caution in suspected esophageal and gastric perforation. Eat as early as possible when you can to maintain the patency of the digestive tract. D. Esophageal dilation: Patients with milder injury and shorter stenosed esophagus can undergo balloon and esophageal probe dilation after acute inflammation and edema of the esophagus begin to subside 2 to 3 weeks after the burn, or use swallowed wire to pull out through the gastrostomy opening and traction dilator in a downward or reverse circulation type of dilation, weekly or biweekly until feeding is satisfactory, and most patients can be cured. However, esophageal dilatation needs to be repeated periodically. V. Esophageal stents: For malignant esophageal strictures without surgical conditions, esophageal stents can be chosen to relieve feeding difficulties and improve the quality of life, and for patients with esophageal perforation, placement of a stent with membrane can close the fistula to relieve symptoms. However, for benign esophageal strictures, especially corrosive strictures, stenting is very ineffective and often causes severe chest pain, reflux, stent displacement, esophageal perforation, and other problems that are often overlooked in patients with malignancy. Moreover, because of stent stimulation, it can cause sarcoidosis and restenosis rate as high as 40% to 50% or even higher. Among the nearly 100 cases of benign esophageal stenosis treated in our hospital, 8 cases were patients who had been restenosed after stent placement outside the hospital. Granulation tissue grew from the stent mesh into the lumen of the esophagus, and even in patients who used a retrievable stent with membrane, the stent still formed a stenosis with patchy tissue proximally to the stent, and the stent could not be removed, and the esophagus was closely adhered to the surrounding tissue during surgery, making separation difficult. If restenosis occurs after stent placement for corrosive esophageal strictures, the digestive tract should be reconstructed with aggressive surgical treatment. Even if the stent is reinserted again, it will only provide temporary relief and not a real cure, but will further extend the stenosis to the entrance of the esophagus, making surgical reconstruction of the digestive tract difficult to treat. If the entrance to the esophagus is already narrowed, the only way to reconstruct the digestive tract is to perform an anastomosis at the base of the pharynx. Therefore, we believe that patients with corrosive esophageal stenosis should not be treated with stents. Surgical treatment: In patients with severe esophageal stenosis or long stenosis, unsatisfactory dilatation or recurrence of stenosis, or complications during dilatation, or restenosis after stenting, as well as in young children who cannot cooperate with dilatation, further treatment is difficult and often requires surgical treatment by cutting off the esophagus above the stenosis, leaving the stenotic segment of the esophagus open or removing it, and reconstructing it with gastric, jejunal or colonic anastomosis, depending on the specific situation. The gastrointestinal tract is reconstructed by anastomosis with the proximal esophagus; the transplanted colon is ascending transverse colon, with fewer complications when cis-peristalsis is used; the anastomosis site is mostly in the neck, and patients with high stenosis need to perform pharyngeal base anastomosis; the route of lifting the stomach or intestinal segment can be via the esophageal bed, thoracic cavity, posterior sternum or anterior sternum subcutaneously, depending on the patient’s condition.