Esophageal stricture of the esophagus
Esophageal stricture of the esophagus is believed to be the result of fibrosis, when inflammation and damage extend below the mucous membrane due to chronic gastroesophageal reflux. It seems that 11% of patients with gastroesophageal reflux disease develop strictures.
Factors predisposing to the formation of stricture include prolonged gastroesophageal reflux, supine reflux, nasogastric intubation, duodenal ulcer, hypersecretory stomach conditions, conditions after gastrectomy, scleroderma, and treated achalasia. An annular stricture in the distal esophagus at the EG junction is called the Schatsky ring.
The strictures are usually located in the distal third of the esophagus. On the esophagogram of barium, they usually have a smooth conical shape and have a variable length. In some cases, Barrett’s esophagus stricture is located in the middle third or, less commonly, in the proximal third of the esophagus.
Peptic strictures usually do not cause symptoms until the luminal diameter of the esophagus decreases to less than 12 mm. Initially, dysphagia is mainly for solids, but with progressive narrowing, fluid swallowing also becomes a problem. The patient often notices an improvement in the usual symptoms of reflux, as dysphagia develops with a narrowing of the stricture area. Some patients do not even remember the symptoms of gastroesophageal reflux.
After carrying out the appropriate diagnostic tests (barium esophagram, endoscopy and biopsy), to make sure that the stricture is not associated with the malignant process, intensive drug therapy of reflux esophagitis begins. With the resolution of edema and inflammation, some patients may have symptomatic relief. However, most patients require additional therapy in the form of dilatation, surgery, or both.
In the past, progressive dilations with graduated rubbers filled with mercury (Maloney or Hurst dilators) were used to alleviate symptoms in the past. Savary expanders passing through a wire guide or endoscopic inflatable balloon expanders offer safer and more efficient expansion methods.
The main complications of dilatation are perforation and bleeding. Perforations are rare, but should be suspected if the patient complains of persistent pain after dilatation. Perforations identified using x-ray contrast studies. Patients receive intravenous nutrition and antibiotics to protect organisms from the oral flora. Surgical drainage and repair should be considered early, since mortality associated with large esophageal perforations is high.
Stricture dilatation and drug therapy for reflux give good results in 65-85% of patients. Esophageal lumen patency is supported by additional dilations at intervals of weeks to months.
For 15–40% of patients in whom dilatation and drug therapy fail, surgery is indicated. The preferred surgical approach to strictures is pre- or intraoperative dilatation combined with antireflux surgery, such as Nissen fundoplication. If the stricture cannot be expanded or too extensive, a resection and a through anastomosis or the location of a segment of the colon or small intestine can be used. They can be combined with Nissen fundoplication to avoid leakage of anastomosis or relapses of strictures.
Esophageal ulcers and bleeding
A small percentage of patients with gastroesophageal reflux disease, in addition to severe esophagitis, have deep peptic ulcers penetrating the muscle layers. These ulcers sometimes perforate or cause massive bleeding. Most of these ulcers respond to intensive drug therapy, but some require surgical intervention. Deep ulcers are often found in the Barrett metaplastic epithelium. These ulcers should be biopsied before starting therapy to exclude the possibility of malignant neoplasms.
Respiratory problems associated with gastroesophageal reflux include laryngitis, hoarseness, chronic cough, asthma, bronchitis, bronchiectasis, aspiration pneumonitis, atelectasis, and hemoptysis. Although most of these patients experience symptoms of gastroesophageal reflux disease, these symptoms are not always present.
Documenting pulmonary aspiration of gastric contents is difficult. A lung scan using radionuclides can be used to document pulmonary aspiration after technetium 99m sulfur colloid is placed in the stomach. If a positive result is found, this may be useful; however, a negative result does not exclude the desire or lack of connection between lung disease and gastroesophageal reflux.
Prolonged pH monitoring may be useful for some patients. Numerous studies have shown an increase in the frequency of reflux in patients with acute and chronic obstructive pulmonary disease. It is generally accepted that gastroesophageal reflux with or without aspiration causes increased airway resistance. Strict antireflux therapy with constant suppression of gastric acid secretion using high doses of proton pump inhibitors. Some patients may need fundoplication (e.g., refractory asthma, apnea associated with gastroesophageal reflux, recurrent aspiration pneumonitis).
Intensive care for gastroesophageal reflux may be beneficial for these patients. Many of the drugs used to treat asthma reduce pressure in the lower sphincter of the esophagus and increase the likelihood of gastroesophageal reflux. Therefore, the medicines used in these patients should be carefully monitored. In addition, patients should not smoke. Patients who fail to improve medical therapy with proton pump inhibitors may require antireflux surgery.
In some patients, chronic reflux esophagitis leads to the replacement of the normal squamous epithelium of the distal esophagus with a specialized metaplastic columnar epithelium called Barrett’s epithelium. Depending on the length of the abnormal tissue, Barrett’s esophagus may be subdivided into Barrett’s esophagus with a short or long segment. The prevalence of Barrett’s esophagus can reach 10-20%. Although Barrett’s esophagus can be seen at any age, most cases go to the doctor after the fourth decade of life.
Barrett’s epithelium consists of a complex mixture of various types of cells, glands and surface architecture, which is usually observed in the small intestine with varying degrees of atrophy.
Stomach ulcer, stricture and adenocarcinoma are complications associated with Barrett’s esophagus. Strictures are characteristic of the middle and lower esophagus with squamous epithelium above and columnar epithelium below the stricture. Esophageal dysplasia and adenocarcinoma were found in Barrett’s epithelium with a prevalence of 3% to 9%.
Changes in the tumor can be multi-focal and can represent the main pathway in the genesis of adenocarcinoma of the lower esophagus and gastric cardia. In any patient with a narrowing of the middle of the esophagus and the formation of stricture, a malignant lesion should be suspected. However, dysplastic and malignant changes may be present in any patient with Barrett’s esophagus.
Most patients with Barrett’s esophagus are treated for reflux esophagitis with high doses of proton pump inhibitors. Despite strict intensive drug therapy, the regression of this metaplastic change has not been documented. Esophagectomy or ablation of the mucous membrane is recommended if severe dysplasia is detected. Removal of the mucous membrane can be achieved by photodynamic therapy followed by laser ablation or cauterization of the probe using a laser or bipolar heater. These procedures are still not widespread and not available, with the exception of a special tertiary medical center.
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