bubble_chart Overview

The most common disease cause of esophageal scar stricture is the ingestion of strong alkalis or acids, leading to chemical burns of the esophagus. After healing, scar tissue contracts, resulting in narrowing of the esophageal lumen. Additionally, gastroesophageal reflux esophagitis can form ulcers and scar contraction. Trauma to the esophagus and post-surgical conditions may also lead to scar strictures.

bubble_chart Etiology

Chemical burns of the esophagus in children are mostly caused by accidental ingestion of household acidic or alkaline chemicals, while in adults, they are often the result of suicide attempts.

bubble_chart Pathological Changes

After ingesting caustic chemicals, the esophageal tissue is immediately burned. The severity of the injury is related to the type, concentration, quantity of the ingested chemical, and the duration of contact. Alkaline chemicals cause liquefactive necrosis of the tissue and can penetrate deep into the layers of the esophageal wall. In severe cases, they may lead to full-thickness ulceration and perforation of the esophageal wall. Acidic chemicals cause coagulative necrosis of the tissue, and the damage to the esophageal tissue is generally less severe than that caused by alkaline chemicals. However, highly concentrated acidic chemicals can also produce grade III injuries. The gastric mucosa is more sensitive to acidic chemicals, and damage to the gastric mucosa caused by contact with strong acids on an empty stomach is often more severe than that to the esophagus. Caustic chemicals tend to linger longer at the natural narrow points of the esophagus, resulting in more severe damage at these locations.

The extent of tissue damage caused by chemical burns in the esophagus can be classified into three grades. Grade I burns are limited to the esophageal mucosa, causing congestion, edema, and epithelial sloughing. After healing, no scar tissue forms, or only minimal scar tissue remains, and the esophageal lumen may not narrow. Grade II burns (dyspepsia) involve injury to the esophageal tissue extending deep into the mucosa and submucosa, forming ulcers. Granulation tissue grows 2–3 weeks after the burn, and healing results in scar formation, leading to narrowing of the esophageal lumen. Grade III burns involve damage to the full thickness of the esophageal wall and even surrounding tissues, often resulting in esophageal perforation and acute mediastinitis. Scar-induced esophageal strictures due to gastroesophageal reflux often occur in the lower esophagus following long-term inflammation and ulceration. Postoperative esophageal strictures occur at the anastomotic site between the esophagus and the gastrointestinal tract, where granulation tissue forms during healing, leading to circumferential scar strictures.

bubble_chart Clinical Manifestations

After ingesting corrosive chemicals such as acids or alkalis, the mouth, throat, and area behind the sternum—sometimes the upper abdomen—immediately experience a burning pain, accompanied by drooling, nausea, vomiting, low-grade fever, dysphoria, and restlessness. The patient refuses to eat. In mild cases of burns, the mucosal edema gradually subsides after a few days, allowing the patient to start consuming liquid foods. If the burns are more severe and scar tissue forms during the healing process, the edema and spasms subside a few days after the injury, temporarily improving swallowing function to grade I. However, 2–3 weeks later, the contraction of scar tissue leads to esophageal stricture, causing dysphagia again, along with symptoms such as weight loss and dehydration. In cases where severe burns result in esophageal or gastric perforation, symptoms such as shock, high fever, acute mediastinitis, and abdominal infection appear early after the injury. If the chemicals are inhaled into the throat, causing laryngeal edema, clinical symptoms include difficulty breathing. Esophageal stricture caused by gastroesophageal reflux often has a long history of esophagitis. After ulcers form on the esophageal mucosa, slight hematemesis may occur. The stricture is usually located in the lower esophagus and is relatively limited in scope. Postoperative esophageal stricture often manifests as dysphagia 2–3 weeks after surgery.

bubble_chart Diagnosis

All cases of esophageal scar stenosis have a history of ingesting acidic or alkaline chemicals, esophagitis, or esophageal surgery, followed by symptoms of dysphagia.

Esophageal barium meal contrast X-ray examination can reveal the location, severity, and extent of the stenosis. Stenosis caused by corrosive chemical burns often presents as a narrowed esophageal lumen, with a long stenotic segment, irregular edges, uneven thickness, and rigid esophageal walls. The barium contrast may appear as uneven streaks entering the stomach, or the esophageal lumen may be highly obstructed, preventing the passage of barium. Stenosis caused by esophagitis is usually located in the lower esophagus, with a relatively localized lesion. In cases with a long disease course and severe stenosis, the upper esophagus may dilate. Postoperative esophageal stenosis often manifests as a localized annular narrowing of the esophageal lumen.

Esophagoscopy can reveal a narrowed esophageal lumen, with the esophageal wall replaced by scar tissue. Early esophagoscopy within 12–48 hours after a chemical burn can confirm the diagnosis and extent of the injury, but during this period, the esophageal wall is fragile due to acute inflammation and edema, making it prone to perforation during examination. Esophagoscopy performed 2–3 weeks after the burn helps assess whether the esophageal lumen is narrowed, as well as the location and severity of the stenosis.

In postoperative cases of esophageal cancer, esophagoscopy and biopsy can help differentiate stenosis caused by cancer recurrence.

bubble_chart Treatment Measures

Corrosive chemicals should be specially marked, stored separately and carefully, and strictly managed in households and workplaces to prevent accidental ingestion incidents.

Ingestion of alkaline or acidic chemicals immediately causes damage to the esophagus, and taking antidotes such as vinegar or soda water can no longer neutralize the effect. Emetic medications or gastric lavage may exacerbate esophageal injury and should not be used. Early application of antibiotics and adrenal corticosteroids after esophageal burns may prevent or reduce infection and inflammatory reactions, minimizing future scar formation. Early placement of a nasogastric tube can be used for feeding and to support the esophageal lumen. If esophageal stricture is observed via esophagoscopy and X-ray barium meal examination about two weeks after the burn, esophageal dilation may be attempted via esophagoscopy. Cases suitable for dilation require regular and repeated procedures. Severe strictures or long stricture segments are difficult to treat successfully with endoscopic dilation. Due to difficulty in eating, a gastrostomy is often necessary first. If a thick thread is swallowed beforehand and can be pulled out through the gastrostomy opening, retrograde esophageal dilation can be performed under the guidance of the thread. Cases unsuitable for dilation require surgical treatment after improving overall nutritional status. Chemical burns of the esophagus often result in long-segment strictures, with the stomach frequently affected as well, or even scar contracture, making high esophageal-gastric anastomosis difficult. The surgical approach typically involves colon replacement of the esophagus. A long midline abdominal incision is made to enter the abdominal cavity. If the right colon is chosen for esophageal replacement, the ileocolic and right colic arteries are usually ligated and severed, preserving the middle colic artery as the blood supply for the right colon. Before ligating the ileocolic and right colic arteries, a non-traumatic vascular clamp should temporarily occlude the vessels for 10 minutes. If the cecum's blood supply remains normal, the two arteries can be ligated and severed. If there is doubt about the cecum's blood supply after temporary occlusion, only the ileocolic artery should be ligated and severed, with the colon replacement surgery performed weeks later after further development of vascular anastomotic arches. The appendix is removed, and the ileum is severed about 1 cm proximal to the ileocecal junction, with the distal end sutured. The ileocolic and right colic arteries are ligated and severed at their origins, and the mesentery is incised while protecting the vascular anastomotic arches from injury. After mobilizing the ascending colon and right transverse colon, the right colon is placed behind the stomach through an opening in the lesser omentum and then pulled into the neck via a bluntly dissected retrosternal tunnel from the abdominal and neck incisions. The retrosternal tunnel must be wide enough to avoid compressing the blood supply to the right colon. The cervical esophagus is mobilized through the neck incision. After severing the cervical esophagus, the distal end is sutured in two layers, and the proximal end is anastomosed to the cecum. The transverse colon is severed at an appropriate location, with the proximal end anastomosed to the anterior gastric wall. The proximal end of the ileum is anastomosed end-to-end with the distal end of the transverse colon (Figure 1).

Figure 1 Right colon replacement of the esophagus

(1) Extent of esophageal resection (2) Blood supply to the right colon

(3) Completion of esophageal-colonic, colonic-gastric, and ileal-colonic anastomoses

If the pyloric region of the stomach has scar lesions, a pyloroplasty is required. Patients without prior gastrostomy should undergo an additional gastrostomy, with tubes placed in the retrosternal colon segment and stomach for postoperative decompression. Decompression of the colon segment helps improve the survival rate of the mobilized segment. The gastric tube can be used for feeding several days postoperatively. Drainage is placed in the neck and removed after a few days. A postoperative chest X-ray should confirm no rupture of the pleura.