bubble_chart Overview

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

bubble_chart Etiology

Disease Cause

Esophageal chemical burns in children are mostly caused by accidental ingestion of household acidic or alkaline chemicals, while in adults, they are mostly due to suicide attempts.

Pathological Changes

After ingesting caustic chemicals, the esophageal tissue is burned. The severity of the injury is related to the type, concentration, quantity of the chemical ingested, and the duration of contact. Alkaline chemicals cause liquefactive necrosis of the tissue and can penetrate deep into the esophageal wall, with severe cases leading to full-thickness ulceration and perforation. Acidic chemicals cause coagulative necrosis, and the damage to esophageal tissue is generally less severe than that caused by alkaline chemicals. However, high-concentration acidic chemicals can also produce grade III damage. The gastric mucosa is more sensitive to acidic chemicals, and damage to the gastric mucosa from contact with strong acid 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 in these areas.

The extent of tissue damage caused by esophageal chemical burns can be classified into three grades. Grade I burns are limited to the esophageal mucosa, causing congestion, edema, and epithelial shedding. After healing, no scar tissue forms, or only a small amount of 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 the full thickness of the esophageal wall and even the surrounding tissues, often leading to esophageal perforation and acute mediastinitis. Scarring and narrowing of the esophagus due to gastroesophageal reflux often occur in the lower esophagus following long-term inflammation and ulceration. Postoperative esophageal scar stenosis occurs at the anastomotic site between the esophagus and the gastrointestinal tract, where granulation tissue forms during the healing process, resulting in annular scar stenosis.

bubble_chart Clinical Manifestations

After ingesting corrosive chemicals such as acids or alkalis, immediate burning pain may occur in the mouth, throat, behind the sternum, and sometimes the upper abdomen, accompanied by drooling, nausea, vomiting, low-grade fever, dysphoria, and restlessness. The patient may refuse to eat. In mild cases of burns, 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 may subside a few days after the burn, temporarily improving swallowing function to grade I. However, 2–3 weeks later, the contraction of scar tissue may cause narrowing of the esophageal lumen, leading to dysphagia again, along with symptoms such as weight loss and dehydration. In cases of severe burns causing esophageal or gastric perforation, symptoms and signs such as shock, high fever, acute mediastinitis, and abdominal infection may appear early after the burn. If the chemicals are inhaled into the larynx, causing laryngeal edema, clinical symptoms may include difficulty breathing. Esophageal stricture caused by gastroesophageal reflux often has a long history of esophagitis. After ulcers form on the esophageal mucosa, there may be minor hematemesis. The narrowing typically occurs in the lower esophagus and is relatively localized. Postoperative esophageal stricture often begins to show symptoms of 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.

Barium swallow X-ray examination can reveal the location, severity, and extent of the stenotic lesion. Esophageal stenosis caused by caustic chemical burns often presents with a narrowed esophageal lumen, a long stenotic segment, irregular edges, uneven thickness, rigid esophageal walls, and barium showing unevenly thick images entering the stomach, or a highly obstructed esophageal lumen where barium cannot pass. Stenosis caused by esophagitis is usually located in the lower esophagus, with a relatively limited lesion range. 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. Performing esophagoscopy within 12 to 48 hours after a chemical burn can confirm the diagnosis and determine the extent of the burn, 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 to 3 weeks after the burn helps assess whether the esophageal lumen is narrowed, as well as the location and severity of the stenosis.

In post-operative cases of esophageal cancer, esophagoscopy and biopsy can help differentiate stenosis caused by tumor recurrence.

bubble_chart Treatment Measures

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

Swallowing alkaline or acidic chemicals immediately causes damage to the esophagus, and taking antidotes such as vinegar or soda water can no longer neutralize them. Emetic medicines or gastric lavage may worsen 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 gastric tube through the nasal cavity can be used for feeding and supporting the esophageal lumen. If esophageal stricture is observed via esophagoscopy and X-ray barium meal examination about 2 weeks after the burn, esophageal dilation may be attempted through esophagoscopy. Cases suitable for dilation require regular and repeated procedures. Severe strictures or long-segment strictures are difficult to successfully dilate via esophagoscopy. Due to difficulty in eating, a gastrostomy is often required 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 also frequently affected, sometimes leading to scar contracture, making high esophageal-gastric anastomosis difficult. The surgical approach typically involves colon replacement of the esophagus. Through a long midline abdominal incision, the right colon is often selected for esophageal replacement, requiring ligation and division of the ileocolic and right colic arteries while 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 divided. If doubts arise about the cecum's blood supply after temporary occlusion, only the ileocolic artery should be ligated and divided, with the colon replacement surgery performed weeks later after further development of vascular anastomotic arches. The appendix is removed, and the ileum is divided about 1 cm proximal to the ileocecal junction, with the distal end sutured. The ileocolic and right colic arteries are ligated and divided 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 pulled into the neck via a retrosternal tunnel created by blunt dissection from the abdominal and cervical incisions. The retrosternal tunnel must be wide enough to avoid compressing the blood supply to the right colon. The cervical esophagus is mobilized, and after dividing it, the distal end is sutured in two layers, while the proximal end is anastomosed to the cecum. The transverse colon is divided at an appropriate site, with its proximal end anastomosed to the anterior gastric wall. The proximal ileal end is then anastomosed end-to-end with the distal transverse colon.