Chemical burns of the esophagus - Causes and pathogenesis

Causes of chemical burns of the esophagus. Most often, chemical burns of the esophagus are caused by swallowing acids (acetic, hydrochloric, sulfuric, nitric) or alkalis (potassium hydroxide, sodium hydroxide). According to V.O. Danilov (1962), sodium hydroxide burns are most common (98 cases out of 115). According to Romanian authors, children under 7 years of age are most often affected (43.7%), 9.1% between the ages of 7 and 16, 9.1% between the ages of 7 and 16, 25.8% between the ages of 16 and 30, and the remaining 21.4% are at an older age. Most often, chemical burns of the esophagus occur as a result of an accident (all victims under 16; after 16 - in 78.2% of cases). Intentional consumption of a caustic liquid (which is also morphologically the most severe) accounts for 19.3% of the total number of victims, of which 94.2% are women and 5.8% are men aged 16 to 30 years.

Pathogenesis and pathological anatomy. The severity of chemical burns depends on the amount of the caustic liquid 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 forming a demarcation border. Such a chemical burn of the mucous membrane spreads in breadth and depth like a spreading oil stain, while with an acid burn, which forms a coagulation crust and, accordingly, a demarcation border of the lesion, the lesion is limited by the size of the contact of the caustic liquid with the affected tissue. From the moment the caustic liquid enters the esophagus, a reflex spasm of its muscles occurs, especially strongly expressed in the area of physiological constrictions. This spasm delays the flow of liquid into the stomach and increases the exposure of its action on the mucous membrane, which leads to deeper burns with the subsequent formation of cicatricial strictures of the esophagus. A particularly pronounced spasm occurs in the area of the cardia, where the caustic fluid is retained for a long time, until emergency care is provided. Penetration of the fluid into the stomach causes a burn, which is especially active when affected by acids, since the alkali is partially neutralized upon contact with the acidic contents of the stomach. Chemicals, upon contact with the mucous membrane, depending on the pH value, either coagulate proteins (acids) or melt them (alkalis).

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

1. reflex spasm phase;
2. the lucid interval phase, when the severity of dysphagia symptoms is significantly reduced;
3. the phase of progressive esophageal stenosis caused by the occurrence of a cicatricial process leading to the formation of a persistent stricture and dilation of the esophagus above it.

The severity of chemical damage to the mucous membrane of the gastrointestinal tract depends on the anatomical area of damage. In the oral cavity, cicatricial changes do not form, since the contact of the mucous membrane with the liquid here is short-lived, and the liquid itself quickly dissolves and is washed away with profuse salivation. In the pharynx, a stenotic cicatricial process rarely occurs for the same reasons, but the ingress of caustic liquid into the hypopharynx can lead to stenosis and edema of the entrance to the larynx, to stenosis of the larynx itself, which can cause respiratory failure, up to asphyxia, and the need for emergency tracheotomy. Most often, cicatricial changes occur, as already noted above, in the area of physiological narrowing of the esophagus and in the stomach, when caustic liquid enters it.

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

In the acute stage, hyperemia, edema and ulceration of the mucous membrane covered with fibrinous films are observed. In cases of widespread damage, these films (dead layer of the mucous membrane) can be rejected in the form of a cast of the inner surface of the esophagus.

In the subacute (reparative) stage, granulation tissue appears, which covers the ulcerated areas of the mucous membrane. The morphological changes in the affected tissues of the esophagus that occur at this stage determine the further clinical course of a chemical burn of the esophagus and the treatment tactics. Granulocytes, plasma cells and fibroblasts appear in the affected tissues. Starting from the 15th day, fibroblasts participate in the formation of collagen fibers that replace the affected tissues; this process is especially pronounced in the muscular layer of the esophagus, in the affected section of which the wall becomes dense, rigid with a complete absence of peristalsis. In shallow burns affecting only the epithelial layer of the mucous membrane, the resulting erosions are soon covered with new epithelium, and no scars or narrowing remain. If necrosis of the mucous membrane and submucous layer occurs over a significant area, they are rejected. Dead tissues are released through vomiting, and sometimes, after passing through the entire gastrointestinal tract, with feces. With deeper burns, necrosis of the mucous membrane, submucous layer and muscular membrane occurs with subsequent formation of ulcers. With very severe burns, necrotic changes of the entire thickness of the esophagus wall with bleeding and perforation, periesophagitis, mediastinitis and pleurisy can occur immediately in the acute stage. Such patients usually die.

In the chronic stage, collagen fibers formed in the affected area, having the property of reducing their length during the development process, ultimately lead to cicatricial stricture of the lumen of the esophagus.

The frequency of localization of cicatricial post-burn stenosis of the esophagus is distributed as follows: most often these stenoses occur in the area of the bronchoaortic stenosis, then in the area of the entrance to the esophagus and less often in the area of the diaphragmatic stenosis. In terms of length and quantity, cicatricial stenosis of the esophagus caused by a chemical burn can be diffuse, total, limited, single and multiple. Above the chronic stenosis, dilation of the esophagus develops, and under the stenosis - its hypoplasia, sometimes affecting the stomach. In the periesophageal 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 chemical burns of the esophagus, an important role is played by the phenomena of general intoxication of varying severity depending on the toxicity and absorption of the swallowed liquid. Most often, the signs of this intoxication are caused by the toxic-resistive effect of the poisonous liquid that has entered the body, which can also affect the kidneys, liver, central nervous system and other organs and systems.

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