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Chemical burn of the esophagus: causes and pathogenesis

 
, medical expert
Last reviewed: 23.04.2024
 
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The cause of chemical burns of the esophagus. Most often, chemical burns of the esophagus are caused by ingestion of acids (acetic, hydrochloric, sulfuric, nitric) or alkalis (potassium hydroxide, sodium hydroxide). According to VO Danilov (1962), sodium hydroxide burns are more common (98 cases out of 115). According to Romanian authors, children under 7 years old (43.7%), children aged 7 to 16 years old - 9.1%, children aged 7 to 16 years - 9.1%, from 16 to 30 years - 25.8%, the remaining 21.4% fall to the older age. Most often, chemical burns of the esophagus arise as a result of an accident (all victims under 16 years old, after 16 years - in 78.2% of cases). Intentional use of caustic liquid (the same morphologically and most severe) among the total number of victims is 19.3%, of which for ages from 16 to 30 years, 94.2% among women and 5.8% among men.

Pathogenesis and pathological anatomy. The severity of chemical burns depends on the amount of acetic fluid taken, its viscosity, concentration and exposure. The deepest and most extensive burns of the esophagus and stomach are caused by alkalis, which have the ability to melt tissues without the formation of a demarcation boundary. Such a chemical burn of the mucous membrane extends in breadth and in depth as a spreading oil stain, while in the same way as when burned with an acid that forms a coagulative crust and, accordingly, the demarcation border of the lesion, the lesion is limited by the contact size of the corrosive liquid with the affected tissue. Since the arrival of caustic fluid in the esophagus, reflex spasm of his muscles arises, especially pronounced in the field of physiological constrictions. This spasm delays the flow of fluid into the stomach and increases the exposure of its action to the mucous membrane, which leads to deeper burns followed by the formation of cicatrical strictures of the esophagus. Especially pronounced spasm occurs in the area of the cardia, where the caustic fluid retention occurs for a long time, up to the provision of emergency care. Penetration of fluid into the stomach causes it to burn, especially active in case of acid damage, since alkali, when in contact with the acid content of the stomach, is partially neutralized. Chemicals in contact with the mucous membrane, depending on the pH value, either coagulate proteins (acids) or melt them (alkalis).

The pathophysiological process with a chemical burn can be divided into 3 phases:

  1. the phase of reflex spasm;
  2. phase of the light interval, when the severity of the phenomena of dysphagia is significantly reduced;
  3. the phase of progressive stenosis of the esophagus, caused by the appearance of a scar process leading to the formation of permanent stricture and dilatation of the esophagus above it.

The severity of chemical damage to the mucosa of the esophagus pathways depends on the anatomical lesion. There are no cicatricial changes in the oral cavity, since the contact of the mucous membrane with the liquid is short-lived, and the liquid itself dissolves quickly and is washed away with excessive salivation. In the throat the stenosing scar process arises rarely for the same reasons, but getting a caustic liquid into the hypopharyngs can lead to stenosis and edema of the entrance to the larynx, to stenosis of the larynx itself, which can cause breathing disorders, up to asphyxia, and the need for an emergency tracheotomy. Most often, cicatricial changes occur, as already noted above, in the field of physiological narrowing of the esophagus and in the stomach, when a corrosive liquid enters it.

Pathological changes in the chemical burns of the esophagus are divided into 3 stages - acute, subacute and chronic.

In the acute stage, there are hyperemia, edema and ulceration of the mucous membrane, covered with fibrinous films. In cases of widespread damage, these films (the necrosis layer of the mucous membrane) can be rejected as a mold of the internal surface of the esophagus.

In the subacute (reparative) stage, a granulation tissue appears that covers the exposed sections of the mucous membrane. The morphological changes in the affected esophagus tissues that occur in this stage determine the further clinical course of the chemical burn of the esophagus and therapeutic tactics. In the affected tissues, granulocytes, plasmocytes and fibroblasts appear. Starting from the 15th day, fibroblasts take part in the formation of collagen fibers that replace the affected tissue; this process is especially pronounced in the muscular layer of the esophagus, on the affected segment of which the wall becomes dense, rigid with complete absence of peristalsis. With shallow burns that affect only the epithelial layer of the mucosa, the erosions that arise are soon covered with a new epithelium, there is no scarring or constriction. If necrosis of the mucous membrane and submucosal layer occurs in a significant area, then their rejection occurs. Dead tissues are released outwardly when vomiting, and sometimes, having passed the whole gastrointestinal tract, - and with calves. With deeper burns, necrosis of the mucous membrane, the submucosal layer and the muscular membrane, followed by the formation of ulcers. With very severe burns, necrotic changes in the entire thickness of the esophagus wall with bleeding and perforation, pereezophagitis, mediastinitis and pleurisy can occur immediately, in an acute stage. Such patients usually die.

In the chronic stage, the collagen fibers formed in the lesion area, possessing the property of shortening their length in the course of development, eventually lead to cicatricial stricture of the esophagus.

The frequency of localization of cicatricial post-burn stenosis of the esophagus is distributed as follows: most often these stenoses arise in the area of bronchial and aortic narrowing, then in the region of the entrance to the esophagus and less frequently in the diaphragmatic narrowing. By the extent and amount of cicatricial esophageal stenosis caused by a chemical burn, they can be diffuse, total, limited, single and multiple. Over the chronic stenosis develops the esophagus, and under the stenosis - its hypoplasia, sometimes exciting and stomach. In the periesophagic region, an inflammatory process often develops, which can spread to nearby organs, the edema and infiltration of which compress the esophagus and sharply worsen its patency.

In the pathogenesis of a chemical burn of the esophagus, an important role is played by the phenomena of general intoxication of different severity, depending on the toxicity and absorption of the swallowed liquid. Most often, the signs of this intoxication are due to the toxic-resonant effect of the toxic liquid that has entered the body, which can also affect the kidneys, liver, central nervous system and other organs and systems.

trusted-source[1], [2], [3], [4], [5], [6], [7]

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