Medical expert of the article
New publications
Chemical burns of the esophagus - Symptoms
Last reviewed: 04.07.2025

All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
The symptoms and clinical course of chemical burns of the esophagus are closely related to the dynamics of pathological changes in the affected sections of the esophagus and the time that has passed since the caustic liquid entered it. In the debut stage, corresponding to the acute pathological stage, symptoms of acute esophagitis are observed. In the latent, or "light" stage, symptoms of subacute esophagitis are observed. In the chronic stage, symptoms of chronic esophagitis dominate.
The acute stage is characterized by a dramatic clinical picture: sharp burning pain in the mouth, pharynx, esophagus and epigastric region; cough or temporary respiratory arrest due to spasm of the larynx, vomiting with an admixture of blood depending on the liquid taken: brown or black in case of alkali poisoning, greenish (hydrochloric acid), yellowish (nitric acid). The patient rushes about, instinctively rushes to the water tap to wash the burning liquid out of the mouth, wheezes, there is an expression of indescribable fear on the face, clutches the throat and chest with his hands. The most favorable phenomenon in all this symptomatology is vomiting, which may result in the expulsion of part of the swallowed liquid. After some time (1/2-1 hour), difficulty swallowing or complete inability to do so, hoarseness or complete loss of voice, general weakness, severe thirst, small and frequent pulse appear. In such cases, collapse and death often occur within a few hours.
In this clinical form, characterized as severe, the signs of traumatic (pain) shock dominate, resulting from a sharp irritation of the pain receptors of the oral cavity, pharynx and esophagus. Subsequently, the clinical picture is determined by the toxic effect of catabolites of tissue proteins destroyed by the toxic substance. The victim is pale, lethargic, arterial pressure is low, tachycardia, breathing is frequent and shallow, lips are cyanotic, pupils are dilated. The shock state can progress, and the patient dies within a few days.
Due to numerous chemical burns of the lips, oral cavity and pharynx, the patient experiences severe burning pain in these areas, while damage to the esophagus causes deep pain behind the breastbone, in the epigastric region or in the interscapular region. Other signs characterizing the severe clinical form of chemical burns of the esophagus include high body temperature (39-41°C), bloody vomiting, melena and oliguria with albuminuria. In case of non-fatal poisoning and appropriate treatment, the general condition of the patient gradually improves, the affected areas of the esophageal mucosa are restored and after 12-20 days the patient begins to eat independently. Complications of the severe form include bronchopneumonia, mediastinitis, peritonitis, etc. In case of total dysphagia and severe pain when swallowing, a gastrostomy is applied.
Mild and moderate clinical course in the acute period is much more common. General and local symptoms are less pronounced. After the painful and dysphagic phase, lasting 8-10 days, the patient begins to eat independently, while it is necessary to restrain his excessively large appetite and offer him gentle food for consumption.
The subacute stage (the stage of false recovery) is characterized by a sluggish course, the disappearance of pain. Patients begin to eat almost in full, their body weight and general good condition are quickly restored. This stage is dangerous because, despite the apparent recovery, the process of scarring and stricture formation occurs in the tissues of the esophagus. At this stage, patients often refuse further treatment, believing that complete recovery has occurred. However, after some time they begin to experience difficulties in swallowing food, first dense, then semi-liquid and, finally, liquid. And the esophageal syndrome returns, and the process moves to the third, chronic stage.
The chronic stage of post-burn esophagitis is characterized by a long progressive course of both the local fibrous process leading to cicatricial stenosis of the esophagus and its suprastrictural dilation, as well as the general condition of the body, characterized by general exhaustion, weight loss, and the appearance of signs of alimentary dystrophy. Dysphagia usually reappears 30-60 days after the incident. The final formation of cicatricial post-burn stenosis of the esophagus is completed by the end of the 3rd month after the injury, but there are cases of final formation of stricture after 6 months.
The main symptom of esophageal stricture in this phase is belching of undigested food and saliva, which may appear immediately after eating or after 2-3 hours. No less constant symptom is the progressive weight loss of the patient, the degree of which depends on the diameter of the remaining lumen of the esophagus in the area of the stricture. Usually, with medium strictures, the patient loses up to 20-30 kg within 2-3 months, reaching a state of cachexia by 4-5 months.
Complications of chemical burns of the esophagus are divided into early or immediate, developing within 1-3 days, and late, occurring in the chronic stage. Early complications include laryngeal and tracheal edema, leading to difficulty breathing and even asphyxia, bronchopneumonia, spontaneous or instrumental perforations, periesophagitis, mediastinitis, hemorrhages. Late complications are caused by the development of cicatricial stricture and infection. In the presence of cicatricial stenosis in the hypopharynx and the entrance to the esophagus, dyspnea, asphyxia, dysphagia and aphagia occur. Strictures along the esophagus cause its dilation above them, which maintains its chronic inflammation. Strictures create favorable conditions for the introduction of foreign bodies or fragments of dense food products into them, which leads to obstruction of the esophagus and the development of food blockages. Late spontaneous or probing-induced esophageal perforations lead to the development of mediastinitis, pericarditis, pleurisy, and lung abscess.