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Chemical burns of the esophagus
Esophageal burns are usually of a chemical nature, with the exception of the rarest cases of thermal burns. Chemical burns of the esophagus occur with the accidental or deliberate (with suicidal purpose) intake of aggressive fluids inside. Currently, the most common cause of such burns is acetic essence (80% solution of acetic acid).
The pathogenesis of a chemical burn of the esophagus is quite typical. As a result of sharp irritation of the receptors of the mucous membrane, an intense spasm of the muscles of the esophagus occurs in places of its physiological constriction, especially in the cervical region and in the cardia, where the aggressive fluid lingers longer and causes the most severe injuries. However, if this liquid is drunk in one gulp, the protective spasm of the cardia is delayed and the caustic substance enters the stomach. Such combined lesions of the esophagus and stomach are found in 1/4 of cases (Ratner G.L., Belokonev V.I., 1982). The mucous membrane of the stomach, compared with the esophagus, is more resistant to the effects of acids, and in case of alkali poisoning, their acidic gastric contents are partially neutralized.
In the pathogenesis of esophageal burns, chemical damage to the esophagus and the resorptive action of the chemical agent itself are considered. Inorganic acids cause protein denaturation and the development of dense coagulation necrosis, which prevents the penetration of acid. However, severe complications may occur due to pain shock and intoxication.
When ingesting vinegar, local changes in the esophagus are less pronounced, however, due to the lack of a dense scab, very severe intoxication develops. There is a sharp acidification of blood and hemolysis of red blood cells (acetic acid - hemolytic poison), which entails the development of hemoglobinuric nephrosis and toxic hepatitis with acute renal and hepatic insufficiency, usually with an unfavorable prognosis.
When burned with alkalis (washing or caustic soda, ammonia, silicate glue, etc.), dehydration and loosening of the esophagus tissue occurs. This allows alkalis to penetrate the wall of the esophagus much deeper than acids, which leads to the formation of extensive necrosis. The scab itself is soft and friable, which often leads to bleeding and even perforation of the esophagus with the development of near-esophageal phlegmon and mediastinitis. With a alkali burn, edema of the epiglottis and vocal folds is also possible, especially when exposed to ammonia. The appearance of metabolic alkalosis is characteristic.
With all burns of the esophagus as a result of intense pain and severe exudation with the development of hemoconcentration, severe hemodynamic disturbances can occur, up to a fatal shock.
Pathological changes that develop in the tissues of the esophagus are usually divided into 4 stages: necrosis, ulcers and granulations, scarring and persistent cicatricial narrowing.
The clinical picture of a burn of the esophagus is characterized by severe pain in the oral cavity, pharynx, along the esophagus with spreading through the chest and with a concomitant burn of the stomach and in the epigastric. The clinical picture of a burn of the esophagus can be complicated by manifestations of toxic toxic shock, expressed to one degree or another.
The diagnosis of a chemical burn of the esophagus can be made on the basis of an anamnesis (it must be borne in mind that sometimes the victim can hide the fact of drinking aggressive liquids or be in a state of severe alcohol intoxication) and the presence of signs of a chemical burn on the skin of the face, lips, on the mucous membrane of the oral cavity and pharynx. In this case, it is often possible to establish the very aggressive liquid itself: acetic acid and ammonia - according to the characteristic odor; sulfuric acid - on a black or gray scab; nitrogen - by the presence of a yellow crust; hydrochloric (hydrochloric) - on the whitish crust.
Permanent salivation, often there is a hoarseness of the voice.
With developed poisoning with acetic acid, the urine is colored from a weak pinkish-red to dark brown; metabolic acidosis and an increased content of free hemoglobin are detected in the blood.
If the burn complicates bleeding, bloody vomiting or melena appears, and with mediastinitis, chest pain increases and fever joins.
The treatment of chemical burns of the esophagus has two goals: the direct saving of the life of the victim and the prevention of narrowing of the esophagus. It should begin immediately at the scene. To anesthetize and fight against shock, promedol or morphine hydrochloride is administered, as well as taking into account the patient's psychoemotional status - and sedatives. Before washing the esophagus and stomach, thoroughly rinsing the mouth with water. Washing of the esophagus and stomach should be done with a thick rubber probe with a large amount of water (at least 1-1.5 buckets, i.e. 12-18 l) until the smell of a chemical substance or a neutral reaction of the washing liquid disappears. For control, litmus paper can be used. It is advisable to use neutralizing solutions (1-2% sodium bicarbonate solution in case of acid burn).
Gastric bleeding during a burn with acids is not a contraindication to gastric lavage. When providing first aid, a probeless flushing of the esophagus and stomach with water or any non-aggressive liquid can also be performed. After washing the stomach, the patient is given 300 - 500 ml of milk.
If there is a risk of asphyxia caused by edema of the epiglottis and vestibular part of the larynx (usually after an alkali burn), an urgent need to make a tracheostomy. A tracheostomy can be used for airway lavage. In case of violation of external respiration, it is necessary to switch to artificial lung ventilation. All patients are shown antibiotic therapy.
From the very beginning, the victim is given an intravenous infusion (preferably through a catheter inserted into the subclavian vein), anti-shock therapy and detoxification therapy under the control of hematocrit, blood pressure, central venous pressure, and acid-base condition. In the severe and moderate condition of the patient, at least 5-6 liters of liquid (glucosonocaine mixture, polyglucin, gelatinol, plasma, donor blood, crystalloid solutions, etc.) is usually administered on the first day, and alkali solutions are also introduced in case of acid poisoning. For the purpose of forced diuresis, diuretics are prescribed (mannitol or urea up to 1.5 g / kg, then lasix 1 mg / kg).
To prevent hemoglobinuric nephrosis and liver damage, hemo-lymphosorption is probably promising (Komarov B.D. et al., 1981). With the development of acute renal failure, indications for hemodialysis may occur.
From the very beginning of treatment, steroid hormones are prescribed (hydrocortisone 125 - 250 mg or prednisone 90 - 150 mg / day, etc.). They not only prevent the drop in blood pressure, but also limit the spread of local inflammatory process and cicatricial stenosis of the esophagus.
Nutrition in the first 2 days is carried out parenterally, but if swallowing is not impaired and there is no risk of aspiration of food masses, it can be supplemented with enteral nutrition. If swallowing does not cause severe pain, then already in the first day a teaspoonful is prescribed every 30 to 40 minutes with a mixture containing 10% emulsion of sunflower oil - 100 ml, 1 g of anestezin and 1 g of tetracycline or ampicillin. A systematic and prolonged use of teaspoons of iodinol or its starch-based analogue, amyloiodine, is useful, which reduces the risk of perforation and, subsequently, esophageal stricture (Mokhnach V.O. and Mokhnach I.V., 1970).
Most authors recommend feeding patients with 3 days of liquid and gruel-like food. Early eating helps to prevent the development of cicatricial narrowing of the esophagus, as if by softly bougienizing it.
Instrumental bougienage is resorted to only with the development of narrowing of the esophagus in specialized clinics. In some cases, it is possible to restore the patency of the esophagus without resorting to complex, multi-stage, plastic surgeries (Ratner G.L., Belokonev V.I., 1982).
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Chemical burns of the esophagus
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