Chemical Burn of the Esophagus: Clinical Guidelines

List of Abbreviations

ALT – Alanine aminotransferase

AST – Aspartate aminotransferase

AEF – Aortoesophageal fistula

CS – Caustic substances

DIC – Disseminated intravascular coagulation

GI – Gastrointestinal tract

ICD-10 – International Classification of Diseases 10th Revision

MSCT – Multislice computed tomography

OMC – Organo-mineral complex

BV – Blood Volume

LLLT – Low-level laser therapy

RCT – Randomized controlled trial

ESES – Esophageal scar stricture

TEF – Tracheoesophageal fistula

Ultrasound – Ultrasound Investigation

CEB – Caustic esophageal burn

CVP – Central venous pressure

CNS – Central nervous system

EGD – Esophagogastroduodenoscopy

ETS – Exotoxic shock

Terms and Definitions

Caustic esophageal burn (CEB) – local damage to the esophageal wall resulting from accidental or intentional ingestion of a caustic chemical substance.

Caustic substances (CS) – chemical substances or mixtures thereof that cause a chemical burn upon contact with mucous membranes or skin.

Post-burn esophageal stricture – narrowing of the esophageal lumen and deformation of its wall of varying extent and at various levels due to scar tissue formation in the esophageal wall at the site of exposure to exogenous factors.

1. Brief information on the disease or condition

1.1 Definition of the disease or condition

Chemical burn of the gastrointestinal tract (GIT) - local damage to the oral cavity, pharynx, esophagus, and stomach resulting from accidental or intentional ingestion of a caustic substance (CS) [1,3,4,11,68].

Chemical burn of the gastrointestinal tract is accompanied by toxic resorptive effects.

1.2 Etiology and pathogenesis of the disease or condition (group of diseases or conditions)

The cause of a chemical burn is the accidental or intentional ingestion of caustic chemical agents [2,4–9]. The pathogenesis of burns depends on the type of chemical agent. The main groups of substances that cause chemical burns.

Alkalis – this group of substances is part of detergents, including grease removers, pipe cleaners, and limescale removers. Alkalis are also used as electrolytes in various batteries and may be components of fertilizers used in suburban plots. Alkalis saponify fats and loosen tissues, forming water-soluble proteinates with the formation of a soft eschar – liquefactive necrosis (from Latin *colliquatio* – liquefaction, melting). Alkalis deeply damage the esophageal wall, up to transmural necrosis and perforation.

Acids – a group of substances actively used in households as preservatives, and as components of bleaching and descaling agents. Acids are also widely used in the production of paints and varnishes. Acids cause protein denaturation by removing water from tissues, and form water-insoluble acid proteinates with the formation of a dense eschar – coagulation necrosis (from Latin *coagulatio* – coagulation, thickening, enlargement). Acids destroy cell membranes and vascular wall membranes, leading to the absorption of the toxin into the systemic circulation.

Strong oxidizing agents (potassium permanganate, hydrogen peroxide, and other oxidizers found in numerous modern detergents, cleaning agents, and bleaches). Potassium permanganate crystals are of particular danger as they are powerful oxidizing agents that, upon contact with and fixation on the mucous membrane, exert a local caustic effect. In addition to the esophagus, the crystals damage the upper digestive tract (pharynx) and respiratory tract (epiglottis, vocal cords) [10].

Ingestion of button batteries in children, used as a power source including in toys and household appliances, should be identified as a separate type of injury. A battery lodged in the esophageal lumen, besides its chemical effect, can cause complete or partial esophageal obstruction and mechanical damage to the esophageal wall (pressure necrosis) if it remains in place for a prolonged period. The primary mechanism of injury is the electrolysis reaction [11]: generation of an external electric field in which hydrolysis of the body's liquid media occurs, producing alkalis (OH-) at the negative pole and acids (H+) at the positive pole. Secondary effects may include leakage of the battery's alkaline electrolyte, which reacts with body fluids and tissues, and disintegration and fragmentation of the battery with release of heavy metals – mercury, zinc, lead, lithium, and others – into the gastrointestinal tract. Heavy metals are released in microdoses, and their toxic potential is minimal.

The severity of the burn directly depends on the nature of the chemical substance, its concentration, quantity, and contact time with the mucosa. In the case of button batteries, burn severity also directly correlates with the battery type (lithium, zinc-air cell, etc.) [11].

1.3 Epidemiology of the Disease or Condition

The incidence of esophageal burns in children across different age groups is: from 1 month to 1 year – 7.3%; from 1 to 3 years – 80.3%; from 4 to 18 years – 12.4% [12], whereas in adults they are most commonly seen between the ages of 30 and 40 (13, 14).

The main causes of esophageal burns in children are: unintentional ingestion of household chemical agents due to inattention of adults who leave dangerous substances in places accessible to children (including galvanic cells); storage of chemicals in food containers without labeling, in bottles or jugs previously used for food or beverages; lack of supervision over a child while adults are handling chemicals. Young children (under 3 years of age) are at the highest risk. The ingestion of household chemical agents and button batteries in this category of children is most often unintentional. In such cases, children take large gulps of liquid, leading to extensive and severe chemical burns of not only the esophagus but also the stomach. In the overwhelming majority of adolescent patients, ingestion of household chemicals occurs intentionally with suicidal intent [13, 14].

In the vast majority of men and women, the ingestion of caustic liquid is unintentional and occurs in a state of alcohol intoxication (85–87%), when careless storage of poisonous liquids leads to their mistaken consumption as alcohol. In such cases, people take large gulps of this liquid, resulting in extensive and severe chemical burns of both the esophagus and the stomach.

In women, suicidal attempts predominate as the cause of caustic liquid ingestion. They are most frequently observed in young women and are seasonal in nature (spring and autumn). In some patients, the realization of potential death and the nature of the liquid induce fear. The first gulp of poison leads to esophageal spasm, and the caustic liquid is spit out of the mouth. In such cases, the burn is limited to a vivid, demonstrative picture of damage to the lips, oral mucosa, pharynx, and upper esophagus.

Patients who decide on serious suicidal acts swallow a large amount at once—over 50–100 ml of a caustic liquid—resulting in deep burns not only of the oral cavity, pharynx, and esophagus, but also of the stomach, duodenum, and jejunum. Such patients die within the first two to three days from severe general intoxication and extensive tissue necrosis [3, 6, 15].

1.4 Features of Coding the Disease or Condition

T28.5 Chemical burn of mouth and pharynx

T28.6 Chemical burn of esophagus

T28.7 Chemical burn of other parts of digestive tract

1.5 Classification of the disease or condition

Clinical practice utilizes disease classifications based on clinical, endoscopic, and radiological findings, which help determine patient management tactics (15, 92).

By etiology

1. Acid burns.

2. Alkali burns.

3. Other.

By burn depth

• Grade I – catarrhal involvement (edema and hyperemia of the mucous membrane);

• Grade II – erosive involvement (not extending beyond the muscularis mucosae);

• Grade III – ulcerative involvement of the mucosa and submucosa;

• Grade IV – ulceronecrotic involvement (mucosal, submucosal, and muscular layers of the esophagus).

By time of obstruction development

1. Early (up to 3–4 weeks).

2. Late (after 1 month).

By degree of stenosis

• First (selective). Stricture diameter 1.0–1.5 cm. Almost all food passes through, except coarse food.

• Second (compensated). Stricture diameter 0.3–0.5 cm. Semiliquid and thoroughly processed food passes through. Suprastenotic esophageal dilation appears.

• Third (subcompensated). Diameter less than 0.3 cm. Only liquids and oil pass through.

• Fourth (reversible). Complete cessation of food and liquid passage through the esophagus, but patency is restored after a course of treatment.

• Fifth (complete obliteration).

By length

• Short (membranous or web-like). A single fold-like scar.

• Circular. Length up to 3 cm.

• Tubular. Length over 3 cm.

• Moniliform. Alternation of narrowed segments with normal ones.

• Total involvement of the esophagus.

By localization

• High strictures. Entrance to the esophagus and cervical region.

• Mid-level strictures. Lower part of the cervical region, aortic arch, and tracheal bifurcation.

• Low strictures (cardiac).

• Combined strictures.

By presence of complications

• Pseudodiverticula.

• False passages.

• Cicatricial shortening.

• Fistulas (esophagobronchial, esophagotracheal).

By combination of upper GI tract injuries:

• Isolated esophageal burn.

• Combined burn of the esophagus and stomach/duodenum.

By stages of the clinical course:

• Acute (toxicogenic) stage;

• Stage of necrotic tissue sloughing;

• Stage of post-burn cicatricial changes formation;

• Long-term outcomes after esophageal burn.

Zargar S.A. Endoscopic Classification

In global clinical practice, the endoscopic classification by Zargar S.A. [6, 16, 17] (Appendix A3) is the most widely used, allowing prediction of post-burn stricture development [18].

1.6 Clinical presentation of the disease or condition

The severity of clinical manifestations of esophageal burns depends on the nature of the chemical agent, its concentration, volume, and duration of exposure to the esophageal wall. In cases where button batteries enter the esophagus, their size and electrical potential are significant. The severity of the patient's condition can range from moderate to extremely severe. Therefore, the clinical presentation should be evaluated according to the stage of the pathological disease process (condition). The following stages of esophageal burns are distinguished [6,13,19].

a) Acute toxicogenic stage (first 3–7 days)

In the acute stage, the clinical manifestations of the disease are characterized by both local changes and somatotropic effects developing immediately after ingestion of the toxicant. The severity of clinical manifestations and the patient's condition directly depends on the type of toxic agent (acid, alkali, or oxidizing agent), the dose of the ingested substance, and its exposure time.

Immediately after contact with caustic substances, pain, voice hoarseness, hypersalivation, and difficulty swallowing (dysphagia) develop within a short period; children experience severe agitation. Hyperthermia up to febrile levels is possible. The cause of dysphagia is edema of the oral, pharyngeal, and esophageal mucosa, as well as pain during swallowing resulting from a chemical burn. Chemical burn lesions may be localized on the face, neck, and anterior chest wall, and less commonly on the extremities. The absence of burns in the oral mucosa and oropharynx does not exclude the possibility of an esophageal burn. In addition to local manifestations, the clinical picture may include the following syndromes: exotoxic shock (ETS), respiratory failure, acute hemolysis, toxic coagulo- and nephropathy, and liver failure.

The pathophysiological basis of ETS upon contact with caustic substances includes the following factors: a decrease in circulating blood volume (fluid loss from the wound surface and pathological pooling of plasma liquid and proteins in the interstitial sector), formation of low cardiac output syndrome, microcirculatory disorders, changes in blood viscosity, and microthrombosis.

Respiratory failure in caustic burns is typically caused by aspiration syndrome with subsequent development of pneumonia or upper airway obstruction (edema and laryngeal stenosis). Some caustic agents, especially organic acids, possess a resorptive effect in addition to their local destructive action, which is most pronounced in acetic acid. Undissociated acetic acid enters the bloodstream and causes erythrocyte hemolysis with subsequent formation of hemin compounds. The transport of free hemoglobin and destroyed erythrocyte membranes through the renal tubules leads to the development of nephropathy up to acute hemoglobinuric nephrosis. Clinically, hemolysis manifests as a change in urine color, which becomes red-brown or cherry-colored.

The absorption and entry of acids and acidic metabolites into the bloodstream leads to metabolic acidosis.

Upon contact with oxalic acid, active binding of calcium ions occurs with the formation of poorly soluble metabolites; consequently, patients show a decrease in ionized calcium levels in blood plasma and tissues.

The resorptive effect of alkalis is less pronounced. An excess of OH- ions in the blood causes alkalosis, leading to cellular metabolism disorders, central nervous system damage, and the development of collapse in severe forms of the disease.

Acetic acid poisoning may lead to the development of bronchospasm and asphyxia. Upon entering the stomach, a general resorptive effect develops, characterized by coagulopathy, nephropathy, and hepatopathy.

Toxic coagulopathy caused by hemolysis manifests as hypercoagulation, which is replaced by hypocoagulation. In severe cases, disseminated intravascular coagulation (DIC) may develop.

Toxic nephropathy, depending on the severity of poisoning, is expressed by microhematuria, decreased glomerular filtration rate, elevated creatinine levels, or the development of acute renal failure.

Toxic hepatopathy, depending on the severity of poisoning, is expressed by scleral icterus with elevated aspartate aminotransferase and lactate dehydrogenase or the development of acute liver failure.

In extensive stage III–IV burns, the symptoms of exotoxic shock escalate, and without treatment, patients die within the first one to two days following the burn.

b) Stage of necrotic mass sloughing or the stage of false well-being (1–3 weeks)

This stage is characterized mainly by a reduction in the clinical manifestations of the burn and stabilization of the patient's condition. It is precisely during the stage of false well-being that establishing the severity of esophageal wall damage and choosing the correct management tactics for the patient are extremely crucial. It is especially important to prevent discharging the patient from the hospital without an established burn grade, even in the absence of pronounced clinical manifestations. This stage is characterized by the following features:

• Reduction of edema and hypersalivation: the patient's condition stabilizes; the child gradually begins first to swallow saliva, and then starts to drink water and consume liquid and pureed food;

• Normalization of body temperature: in the absence of complications from the esophageal burn (e.g., pneumonia, mediastinitis, esophageal perforation, etc.), body temperature normalizes and typically does not exceed subfebrile levels. If high fever persists, additional examination is required to rule out the development of complications;

• The patient begins to take food: at this stage, adequate enteral feeding of the patient can often be established. In some cases, the patient may consume not only pureed but also solid food, which can deceptively create the impression of recovery and lead to unjustified hospital discharge.

It should also be remembered that in severe burns caused by technical acids (caustic soda, sulfuric acid, hydrochloric acid), concentrated alkalis, and other aggressive substances, as well as in the event of complications and systemic intoxication phenomena, the stage of false well-being may be absent.

Toxicologists distinguish the acute somatogenic stage of chemical esophageal burns (first 2 weeks).

In this stage of acute poisoning, early (1–2 days) or late (after 3 days) somatogenic complications occur.

Early complications include mechanical asphyxia from burns of the mouth and upper respiratory tract, intoxication delirium, and acute pancreatitis.

Late complications include tracheobronchitis, pneumonia, and late intoxication psychosis.

c) Stage of post-burn scar formation (4–6 weeks)

Clinically, the formation of cicatricial strictures as an outcome of a chemical esophageal burn manifests as the gradual development of impaired patency for food and water. First, a sensation of solid food getting stuck in the esophagus appears, followed by thick and then liquid food; the patient is forced to eat slowly, in small sips, and wash it down with water.

Timely initiated treatment helps reduce the risk of complications. Clinical manifestations of post-burn scar changes:

• Progressive dysphagia: typically, this symptom appears by the end of the 3rd week after the burn. Dysphagia is the sensation of difficulty or complete inability for food and/or water to pass through the esophagus, accompanied by a feeling of difficulty swallowing, pain, a lump in the throat, or an obstruction in the esophagus. Dysphagia usually debuts as difficulty swallowing dense and solid food, a fact the child may not notice or may conceal. As dysphagia progresses, the patient begins to experience difficulties with pureed food as well. In severe cases, a clinical picture of complete esophageal obstruction eventually develops, meaning the inability to swallow water and subsequently even saliva.

• Esophageal vomiting: occurs when a large piece of food gets stuck, clogging the esophageal lumen, or when complete esophageal obstruction develops, and manifests as vomiting immediately after feeding or some time later. The vomitus does not have an acid odor (clarifying this fact has high differential diagnostic value). Vomiting can be persistent until food masses are completely evacuated from the esophageal lumen.

• Weight loss is primarily caused by the inability to provide adequate enteral feeding. Weight loss is especially pronounced in older children and can range from mild protein-energy malnutrition to cachexia in patients with complete esophageal obstruction. If water consumption is impossible, dehydration phenomena may also join in, and if passing saliva is difficult, electrolyte disturbances of varying degrees of severity may develop.

d) Long-term period following a chemical esophageal burn.

Squamous cell carcinoma frequently develops in the scar tissues and the suprastenotic part of the esophagus 15–20 years later [90].

When the tumor reaches a large size and invades adjacent organs, a constant dull pain appears in the interscapular region, to which patients with post-burn esophageal changes do not pay much attention.

Clinical features in children with esophageal burns caused by button batteries and potassium permanganate crystals

Special attention should be paid to the clinical presentation of button battery or potassium permanganate crystal ingestion. For pediatric surgeons and pediatricians, it is critically important to correctly suspect and diagnose the condition within the first few hours after ingestion, as this determines the further prognosis of the disease. The clinical presentation is characterized by the following features:

Acute stage – lasts no more than 24 hours from the moment of ingestion. The main manifestations are hypersalivation and dysphagia, as well as child anxiety, refusal to drink and eat. In case of button battery ingestion, dysphagia may go unnoticed due to its mild expression. Manifestations such as fever appear towards the end of the first day. Ingestion of potassium permanganate crystals is characterized by a characteristic dark purple staining of the oral mucosa.

The stage of false well-being is often absent. If the agent remains unnoticed, the child develops a fever, increased salivation, coughing, and distant wheezing that mimic the clinical picture of bronchitis or pneumonia, and the general condition worsens due to intoxication phenomena.

In the stage of post-burn changes, the clinical presentation depends on the developed complications: after a button battery burn – esophageal stenosis, vocal cord paresis, esophageal perforation, mediastinitis, tracheoesophageal fistula, aorto-esophageal fistula; after a potassium permanganate crystal burn – pharyngeal stenosis, laryngeal stenosis.

2. Diagnostics, medical indications and contraindications for diagnostic methods

Criteria for Establishing the Diagnosis/Condition

The diagnosis of chemical gastrointestinal burns is established based on medical history (history of oral intake of a chemical substance), complaints, physical examination (burns of the facial area, oral cavity, presence of a specific odor), and instrumental diagnostic methods [4,13,19,20].

2.1 Complaints and Anamnesis

• If a chemical burn of the esophagus (gastrointestinal tract) is suspected, it is recommended to pay attention to the patient's complaints: pain in the oral cavity, abdomen, dysphagia, and hypersalivation [4,6,19,20].

GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)

Comments: Typical complaints include burning acute pain in the oral cavity, interscapular and epigastric regions, pain upon swallowing, salivation, hoarseness, and vomiting [4,6,19–21]. The suicide attempt has its own motivation known to the patient.

2.2 Physical Examination

• In all patients with suspected caustic esophageal injury (gastrointestinal tract), it is recommended to check for burn traces in the chin area and corners of the lips, evaluate the oral mucosa to identify local signs of burns, and measure pulse and blood pressure [4,19,20,22].

GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)

Comments:

a) Acute stage of the burn

Upon examination, the patient is restless with pale skin. In severe poisoning, acrocyanosis is present.

On the chin and in the corners of the lips, there are burn traces in the form of hyperemia, edema, and foci of skin necrosis.

Examination of the oral cavity reveals edema and hyperemia of the mucous membranes of the tongue, cheeks, uvula, and faucial pillars, with patchy necrosis in the form of gray, yellow, or black films.

In poisoning with acetic acid, formalin, or ammonia, a specific odor is distinctly perceived. Respiration is spontaneous. In poisonings not accompanied by exotoxic shock, there is no dyspnea. Marked tachycardia is present.

In cases of exotoxic shock – dyspnea, pallor, cold sweat, thready pulse, hypotension.

The abdomen is soft, tender upon deep palpation. With a concomitant gastric burn, deep palpation is not accessible, muscular defense is present; within a few hours, due to reactive effusion in the epigastric region, symptoms of peritoneal irritation are detected. Vomitus may contain admixtures of blood.

b) Somatogenic phase

The clinical presentation is due to the development of complications. The most demonstrative is the clinical picture of gastrointestinal bleeding.

c) Stage of cicatricial changes

Physical examination findings are non-specific. Patients with this pathology are generally undernourished.

• During the initial examination of the patient at the admission department level, consultation (examination, consultation) with an otorhinolaryngologist and consultation (examination, consultation) with a toxicologist (or, in their absence, an intensive care physician) are recommended to assess involvement of the upper airway and identify the toxic agent [19].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

2.3 Laboratory Diagnostics

2.3.1. Clinical and biochemical examination

• Patients with signs of caustic esophageal injury (gastrointestinal tract) are recommended to undergo a complete blood count (detailed clinical blood test), general urinalysis, general clinical blood biochemistry (testing blood total bilirubin, blood conjugated (direct) bilirubin, blood unconjugated (indirect) bilirubin, blood alanine aminotransferase activity, blood aspartate aminotransferase activity, blood urea, blood creatinine, blood total protein, blood glucose, blood sodium, blood potassium, blood chlorides, blood total calcium) to obtain information on the state of the body's main life-support systems and homeostasis parameters [4,19,20,23–26].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Expanding the scope of biochemical tests depending on the severity of the patient's condition is within the competence of the attending physician.

• In patients with signs of caustic esophageal injury (gastrointestinal tract) who develop nephropathy, hepatopathy, hepatorenal failure, and other pathologies, it is recommended as additional methods to determine blood amylase activity, blood alkaline phosphatase activity, blood gamma-glutamyl transferase activity, blood total protein, and blood albumin [19,23].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. The frequency of these tests depends on the severity of poisoning and the duration of the patient's hospital stay.

2.3.2. Chemical-toxicological laboratory diagnostics

• In patients with acetic acid poisoning, it is recommended to test for free hemoglobin levels in blood plasma and urine to assess the severity of damage [2,27].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. It is not possible to detect acid or alkali in the body's biological fluids. The free hemoglobin content in blood for mild hemolysis is 5 g/L, for moderate severity – 5–10 g/L, and for severe cases – over 10 g/L. Free hemoglobin appears in the urine when its plasma concentration exceeds 1–1.5 g/L, manifesting as urine discoloration ranging from red to cherry-red depending on the degree of hemoglobinuria. It should be kept in mind that the absence of hemolysis in the presence of other signs does not rule out acetic acid poisoning.

2.4 Instrumental Diagnostics

• In patients with caustic esophageal injury (gastrointestinal tract) in the acute phase presenting with pain syndrome, it is recommended to administer pre-medication with analgesics and antispasmodic drugs (ATC: papaverine and its derivatives) in standard dosages prior to instrumental endoscopic procedures [2,11,73,74].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

2.4.1. Endoscopic examination method

• Patients with clinical signs of caustic esophageal injury (gastrointestinal tract) are recommended to undergo esophagogastroduodenoscopy (EGD) to assess the extent and depth of the lesion [4,6,13,28,29].

Level of Recommendations CLevel of Evidence 3Level of Recommendation C (Level of Evidence – 3)

Comment. EGD is considered the decisive method in the diagnosis of caustic esophageal injury and is generally recommended within the first 12–48 hours after ingestion of a corrosive chemical into the gastrointestinal tract, although endoscopy is safe and reliable up to 96 hours post-injury [33,93,94]. According to some data, EGD was performed without consequences at later periods – from 5 to 15 days after chemical burns [95]; nevertheless, endoscopy during this period is potentially hazardous for esophageal wall perforation due to tissue thinning.

At the same time, the insufficient accuracy of the endoscopic method in determining the depth of chemical damage can lead to erroneous management tactics with unpredictable consequences [3,4,13,15,17,31,32,96,97]. According to a number of studies, the need for emergency endoscopic assessment of the degree of esophageal and gastric burns is limited to situations where CT cannot be used (unavailable in the medical facility, intravenous contrast is contraindicated, in pediatric patients, and when CT suggests transmural esophageal necrosis but data interpretation is difficult/doubtful) [4,13].

In general, the timing of EGD is determined individually and depends on the patient's condition. With minimal clinical manifestations, the procedure is performed as soon as possible. With severe clinical manifestations, EGD is performed after the patient's condition has stabilized. These conditions do not apply to burns caused by button batteries or potassium permanganate crystals, where EGD must be performed on an emergency basis [4,30,31].

• In patients with clinical signs of upper gastrointestinal caustic injury, diagnostic endoscopy (EGD) is not recommended in the presence of unstable hemodynamics, radiologic signs of esophageal perforation and mediastinitis, epiglottic burn with edema, third-degree burn of the larynx and pharynx, as well as airway burns requiring tracheal intubation or temporary tracheostomy [4,31–35]. In such cases, EGD is performed once the patient's condition stabilizes.

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. Epiglottic burn with edema, and third-degree burn of the larynx and pharynx can cause asphyxia due to vocal cord edema (especially in burns caused by potassium permanganate crystals).

• In patients with signs of chemical burn during endoscopic examination, it is recommended to use S.A. Zargar's endoscopic classification to determine the degree of esophageal and gastric burn, as well as to predict the further course of the disease [18].

GCR BLEL 3Grade of Recommendation B (Level of Evidence – 3)

Commentary. On the first day after a grade I–II burn, whitish coagulation films are noted on the mucosa, which repeat the relief (folds) of the mucosal membrane and cannot be removed mechanically. Necrotic foci are dark brown or black. In the lower esophagus, necrotic tissues stain dark yellow or dark green in the presence of bile reflux.

Upon sloughing of the eschar (days 3–4), dark red granulation tissue becomes visible. Following esophageal hemorrhage, small thrombi are visible in the lumen of submucosal vessels on the surface of the granulations.

Data obtained during endoscopic examination largely predict the likelihood of post-burn esophageal stenosis development.

• In patients with grade 1 caustic injury of the gastrointestinal tract, follow-up EGD is not recommended if the condition is stable and there are no complaints [36,58].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

• For patients with grade 2-3 chemical esophageal burn (ХОП) in a stable condition and without complaints, a follow-up EGD is recommended within 4 to 6 weeks to assess the recovery processes and detect the development of post-burn esophageal stenosis [36,58].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

• As an alternative, patients with caustic gastrointestinal injury may be recommended to determine the degree of esophageal and gastric burn according to the endoscopic classification proposed by S.V. Volkov (1997) and supplemented by E.A. Pesnya-Prosolova (2006) in order to determine the depth and extent of the lesion [15].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Commentary. On the first day after a grade I–II burn, whitish coagulation films are noted on the mucosa, which repeat the relief (folds) of the mucosal membrane and cannot be removed mechanically. Necrotic foci are dark brown or black. In the lower esophagus, necrotic tissues stain dark yellow or dark green in the presence of bile reflux.

Upon sloughing of the eschar (days 3–4), dark red granulation tissue becomes visible. Following esophageal hemorrhage, small thrombi are visible in the lumen of submucosal vessels on the surface of the granulations.

Beyond this timeframe, uneven granulation growth with excessive formation at the edges of post-burn ulcers serves as a sign of developing cicatricial deformations and strictures.

Data obtained during endoscopic examination largely predict the severity and duration of the acute phase of esophageal and gastric burns.

Endoscopy during the stage of granulation tissue development, scar formation, and persistent post-burn changes.

• In all patients with caustic gastrointestinal injury in the stage of granulation tissue development, scar formation, and persistent post-burn changes, EGD is recommended 3 weeks after the injury to assess the localization and extent of stenosis and to determine indications for therapeutic manipulations (esophageal bougienage, balloon dilation of esophageal stenosis, esophageal stenting) [4,15,33].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. Three weeks after a caustic injury, dense fibrous tissues typically form, and performing an endoscopic examination becomes safer (the procedure may be performed under local anesthesia) [4,15,33].

The endoscopic classification of cicatricial esophageal stenoses (Yu.I. Gallinger et al., 2000) distinguishes four degrees of narrowing [57]:

1. Grade 1 — the diameter of the esophagus in the stenotic zone is 9–11 mm (a medium-caliber gastrointestinal endoscope passes through the stricture);

2. Grade 2 — the esophageal lumen in the stenotic zone is 6–8 mm (a fiberoptic bronchoscope 5.5–7 mm in diameter passes through);

3. Grade 3 — the diameter of the esophagus in the stenotic zone is 3–5 mm (an ultra-thin endoscope 2.4–2.8 mm in diameter passes through; if not used, the lumen of the stricture is estimated by the diameter of a guidewire or catheter);

4. Grade 4 — the lumen of the stricture is 1–2 mm or completely absent (only a guidewire can be passed beyond the stenosis zone, except for cases of complete obliteration).

In patients with gastric cicatricial stenosis, endoscopy allows for determining the exact diameter of the stricture and evaluating the severity and extent of morphological changes in the suprastenotic part of the stomach to determine the extent of organ resection, the site for bypass anastomosis formation, or the feasibility of any stomach-draining operation.

• In patients with dysphagia, to assess changes in the oropharynx, pharyngoesophageal junction, and suprastenotic part of the esophagus, endoscopic examination is recommended to begin with medium-caliber gastrointestinal endoscopes [15].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. Initial use of small-diameter endoscopes may lead to missing mild cicatricial changes, usually small in extent, located in the area of the esophageal inlet.

The endoscope should be inserted only under direct visual control. Folds in the pharyngeal sinuses and pharyngoesophageal junction are spread apart by the distal tip of the endoscope with gradual air insufflation. In cases where pronounced cicatricial changes in the pharynx and esophageal inlet are absent and the endoscope can be passed into the cervical esophagus, the state of the mucosa and the diameter of the suprastenotic part of the esophagus should be assessed up to the zone of maximal narrowing; the upper boundary of the cicatricial process should be established by the distance from the incisors, and the diameter of the narrowing should be estimated by comparing it with the endoscope that can be passed through the entire narrowing or part of it, or with an instrument of known size (guidewire, catheter, biopsy forceps). The esophageal lumen in the stenosis zone is an objective criterion that largely determines the severity of dysphagia. If the medium-caliber gastrointestinal endoscope successfully traverses the stricture area, the mucosal condition and stricture length are evaluated, and the lower parts of the esophagus, stomach, and duodenum are examined. Areas of cicatricial changes in the esophageal wall may alternate with unaffected areas; in such cases, double or multiple strictures should be diagnosed. At the slightest suspicion of a malignant process, tissue samples should be taken for histological and cytological examination.

If it is impossible to pass the gastrointestinal endoscope through the stricture for further examination, small-caliber endoscopes must be used (small-diameter gastroscopes ranging from 4.8 to 5.9 mm, ureteroscopes 3.5–3.7 mm in diameter, choledochoscopes, specifically SpyGlass, 3 mm in diameter) to assess the length of the stenosis, its severity at various levels, localization, number of strictures, diagnosis of possible complications (fistulas, malignant transformation), and the condition of the mucosa both within the stenosis zone and in the underlying parts of the esophagus, stomach, and duodenum. Instruments not intended for gastrointestinal tract examination are not equipped with an air and water pump; therefore, air must be supplied manually in portions using a rubber bulb attached to the biopsy channel port. If the endoscope is successfully passed below the stenosis zone, it allows for a safe and reliable passage of a guidewire for subsequent endoscopic treatment. However, even in cases where the entire stenotic segment cannot be traversed, the use of small-caliber endoscopes after medium-caliber ones can in many cases allow the operator to approach closely to the upper edge of the main stenosis zone in double and multiple strictures and pass a guidewire under visual control of the upper edge, especially if the entry into the second stricture is eccentric or if diverticulum-like pockets exist between the two strictures.

If it is impossible to pass the endoscope through the stricture zone in the presence of a gastrostomy for a full examination of the post-stenotic part of the esophagus, it is advisable to perform retrograde gastroesophagoscopy. With the patient in the left lateral position, after removing the gastrostomy tube, the endoscope is inserted through the stoma into the stomach and advanced upward along the lesser curvature towards the cardia. Then, the distal end of the endoscope is pressed against the cardia, and with slight air insufflation, the device is advanced into the esophagus up to the lower edge of the stricture. After that, the stomach and duodenum should be examined, which is accessible in most cases. Determining the position of the placed gastrostomy is quite important: in cases where there is no gross cicatricial deformation of the stomach and the gastrostomy is placed close to the lesser curvature, the greater curvature can be used to harvest a graft when deciding in favor of esophagoplasty [15,98].

2.4.2. X-ray examination

• Patients with clinical signs of chemical burn of the upper gastrointestinal tract are recommended to undergo plain chest radiography (targeted chest radiography / digital chest radiography) and plain abdominal radiography to detect air in the mediastinum, which suggests esophageal perforation, as well as free air under the diaphragm, indicating gastric perforation [4].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

• Patients with clinical signs of chemical burn of the upper gastrointestinal tract are recommended to undergo radiopaque examination of the esophagus (contrast esophagography, double-contrast esophagography) to determine the extent and depth of esophageal and gastric lesions [99].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Commentary. Radiopaque examination of the esophagus is a non-invasive and highly informative diagnostic method. If it is necessary to confirm a clinically suspected perforation, water-soluble iodine-containing radiopaque agents can be used, which are less irritating than barium sulfate ** [100]. Conversely, barium sulfate ** should be the preferred contrast agent in delayed examinations, providing greater radiographic detail than water-soluble iodine-containing radiopaque agents [101, 102].

X-ray examination technique in the stage of burn esophagitis (gastritis) and rejection of necrotic tissues.

After plain chest radiography (targeted chest radiography) and abdominal radiography (plain abdominal radiography), the patient is given a swallow of a water-soluble iodine-containing radiopaque agent, monitoring the function of the epiglottis and the act of swallowing. In the absence of aspiration, the examination is continued with a suspension of barium sulfate**, which well outlines the relief of the esophageal and gastric walls.

Radiological signs of esophageal burn

1st degree burn. Swallowing is not difficult, the esophageal lumen is normal, the folds of the mucous membrane are clearly visible, but locally thickened up to 5 mm. Peristalsis is preserved, isolated signs of regurgitation.

2nd degree burn. Swallowing is painful, in small portions. The esophageal lumen is narrowed, mucosal folds are smoothed, locally undefined. The esophageal wall is inelastic and akinetic. Spasm at various levels and frequent regurgitation are noted.

3rd–4th degree burns. Swallowing is extremely painful and difficult. The esophageal lumen is widened up to 4–6 cm in transverse diameter, containing fluid. Esophageal walls are atonic and akinetic. The mucosal relief is not defined, with flat niches at the sites of tissue rejection.

Radiological signs of gastric burn

1st degree burn. The stomach is hypotonic, containing fluid and mucus. Contours are smooth, peristalsis is distinct. Mucosal folds are thickened. A short-term pyloric spasm is noted.

2nd degree burn. The stomach is hypotonic, containing a large amount of fluid and mucus. Contours are smooth, but peristalsis is sluggish. Mucosal folds are thickened and smoothed. Multiple persistent barium sulfate** pools. Evacuation is delayed.

3rd–4th degree burns. The stomach is atonic, overfilled with contents. Peristalsis is absent. Mucosal folds are sharply thickened or not traceable. Multiple barium sulfate** pools – flat (erosions) and deep (ulcers). Prolonged pyloric spasm.

X-ray examination technique in the stage of granulation tissue development, scar formation, and persistent post-burn changes

• Patients with a chemical burn of the esophagus (GI tract) in the stage of granulation tissue development, scar formation, and persistent post-burn changes are recommended to undergo esophagography supplemented by mandatory radiography of the stomach and duodenum to localize strictures, determine their extent, and detect signs of gastric and duodenal lesions [3].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Commentary. The type and consistency of the contrast agent are used depending on the degree of esophageal narrowing. In case of esophageal obstruction for a liquid suspension of barium sulfate** or the clinical picture of an esophagotracheal (esophagobronchial) fistula, water-soluble iodine-containing radiopaque agents are used. The examination is performed in the vertical and horizontal positions of the patient.

When contrasting the esophagus, it is necessary to establish the presence of a stricture, its localization and extent (upper and lower boundaries relative to the vertebral bodies), minimum and maximum diameter of the stenosis and suprastenotic dilatation, and the location of the stricture entrance (central or eccentric). In patients with multiple strictures, their localization, extent, and the diameter of the esophagus between the strictures are indicated. Cicatricial changes appear as narrowings of the esophageal lumen with irregular, jagged edges.

The stomach may be normal in size, reduced, or enlarged, depending on the localization and prevalence of cicatricial changes. With stenosis in the body, subtotal, and total narrowing, the stomach looks "shrunken". With isolated outlet stenosis, its lumen is dilated. With severe stenosis, cicatricial tissues look like a narrow tube with irregular edges, resembling the radiological picture of gastric cancer. With complete outlet obstruction, the suprastenotic part looks like a bag with a cone facing the pylorus. In patients with complete esophageal obstruction, the examination is performed through the gastrostomy.

• In patients with chemical burns of the esophagus and clinical signs of exotoxic shock, as well as impaired swallowing and esophageal patency, radiopaque examination (contrast esophagoscopy / double-contrast esophagography) is not recommended due to the risk of aspiration [99].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

2.4.3. Computed tomography

MSCT with intravenous contrast enhancement provides a more detailed assessment of intrathoracic changes associated with esophageal perforation and the formation of an esophagorespiratory or esophago-vascular fistula [32,39–43].

• Patients aged 18 years and older with clinical signs of a chemical burn of the upper gastrointestinal tract are recommended to undergo emergency CT of the chest and abdomen (computed tomography of the chest and abdomen with intravenous bolus contrast enhancement, multiplanar and three-dimensional reconstruction, computed tomography of the esophagus with oral contrast) to clarify the localization, volume, and depth of the lesion, provided adequate renal function [13,32].

GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)

Commentary. Emergency CT of the esophagus has a number of advantages over endoscopy in the early diagnosis of chemical injuries of the esophagus and stomach. These include: non-invasiveness, the ability to assess the blood supply to all layers of the esophagus and stomach, and the state of the surrounding adipose tissue and tissues [4,103]. CT provides a more detailed assessment of transmural damage to the esophageal and gastric walls and the degree of necrosis than early endoscopy [32,40], and is more valuable than endoscopy in assessing the threat or established gastric perforation [39].

The application of the method is limited in patients with acute renal failure due to the low information content of the native scan and contraindications to intravenous contrast enhancement.

A CT scoring system has been proposed to predict esophageal stricture [4].

The sensitivity and specificity of CT in determining the severity of chemical injuries of the esophagus are moderately higher compared to endoscopy, which allows for more accurate prediction of post-burn complications.

CT data of the chest organs in burn trauma of the esophagus make it possible to predict both early and late complications and develop treatment tactics [4,39].

With a 1st-degree burn, the development of complications is unlikely. With a 2nd-degree burn, there is a probability of esophageal strictures developing, which requires preventive measures. With a 3rd-degree burn, stricture development is inevitable. 4th-degree changes indicate transmural esophageal injury with an extremely high risk of necrosis and perforation, requiring emergency esophagectomy.

CT is a more effective tool for the early diagnosis of irreversible esophageal and gastric changes following chemical trauma than a strategy based on endoscopic findings and clinical and laboratory parameters [104].

The decision on the need for emergency esophagectomy in chemical esophageal injuries should be based on CT results indicating transmural necrosis (blurring of the esophageal wall and periesophageal tissue, absence of contrast enhancement in the esophageal wall). This approach helps avoid unjustified esophagectomies and diagnostic laparotomies [103].

Thus, CT should be considered a more sensitive method in diagnosing esophageal and gastric injuries from chemical burns. At the same time, the correlation between endoscopy and CT regarding injury grading is not high enough to completely rule out the need for endoscopic examination, especially in the first 12–48 hours after ingestion of caustic substances [32].

In the stage of granulation tissue development, scar formation, and persistent post-burn changes, CT makes it possible to determine the severity of inflammatory and cicatricial post-burn changes in the esophageal wall and periesophageal tissue [13].

• There is no data on the efficacy of CT (computed tomography of the chest and abdominopelvic cavities with intravenous bolus contrast enhancement, multiplanar and three-dimensional reconstruction, and computed tomography of the esophagus with oral contrast) in diagnosing caustic esophageal injury in children; therefore, its routine use cannot be recommended in this group due to the rarity of severe injuries and lifelong risks of radiation exposure [13, 32].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. CT (computed tomography of the chest and abdominopelvic cavities with intravenous bolus contrast enhancement, multiplanar and three-dimensional reconstruction, and computed tomography of the esophagus with oral contrast) may be useful in children with clinical and endoscopic signs of extensive esophageal involvement who are scheduled for surgery.

2.5 Other Procedures

• In patients with caustic gastrointestinal injury at high risk of gastric perforation according to endoscopy, diagnostic laparoscopy is recommended to rule out peritonitis [105, 106].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. Diagnostic laparoscopy is a useful adjunct in evaluating patients with a high risk of gastric perforation observed during EGD, or patients with severe esophageal injury in whom esophagogastroduodenoscopy to assess the state of the stomach is impossible [105, 106].

3. Treatment, including drug and non-drug therapies, diet therapy, and pain management

3.1. Treatment in the acute stage of caustic poisoning

3.1.1. Conservative treatment

• Patients with caustic gastrointestinal injury in the acute stage of caustic substance poisoning are recommended immediate comprehensive treatment, including pain management, removal of the toxicant from the gastrointestinal tract (gastric lavage), local treatment, and detoxification therapy with correction of organ and system dysfunctions [2–4, 20, 35, 39, 44–46]. To neutralize burns caused by potassium permanganate crystals, solutions of weak acids (ascorbic acid**) can be used, which significantly reduces the degree of damage.

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Management of pain syndrome includes administration of opioids, nonsteroidal anti-inflammatory and antirheumatic drugs, and antispasmodics. The choice of drug depends on the patient's age and the severity of pain. In adults, pain management includes the administration of opioids (morphine**, trimeperidine**, codeine + morphine + noscapine + papaverine + thebaine) or nonsteroidal anti-inflammatory and antirheumatic drugs (ketorolac**), other analgesics and antipyretics (metamizole sodium 1 ml 3–4 times daily), belladonna alkaloids, tertiary amines (A03BA) (1 ml of 0.1% atropine** solution 2 times daily), papaverine and its derivatives (2 ml of 2% papaverine solution or 2 ml of drotaverine** intramuscularly, or 1 ml of 0.2% platifylline** solution) subcutaneously up to 4 times daily, and glucose-novocaine mixture (500 ml of 5% dextrose** solution and 50 ml of 2% procaine** solution) 2–3 times daily intravenously.

• In compensated laryngeal stenosis, patients with caustic esophageal injury are recommended intravenous and inhalation administration of glucocorticoids, and intravenous administration of anticholinergics (atropine**) to reduce inflammatory changes, eliminate edema, and restore bronchial patency [1–4, 19, 39, 47–49].

GCR CLoE 3Grade of Recommendation C (Level of Evidence – 3)

Comment. The dose of a specific drug is selected individually according to the severity of the burn [1, 47–49]. The duration of treatment is determined by the severity of the burn: for 1st-degree caustic esophageal injury, glucocorticoid therapy is not prescribed; for 2nd–3rd degree, a short course (5–7 days) is prescribed.

• In patients with caustic esophageal injury, gastric lavage without a tube and with artificially induced vomiting to remove the toxicant is not recommended [4].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Gastric lavage without a tube with artificially induced vomiting is extremely dangerous, as the repeated passage of the toxicant through the esophagus increases the degree of its burn. In addition, there is a risk of aspirating the caustic liquid and developing a respiratory tract burn [4].

Gastric lavage via a tube is most effective, safe, and has no contraindications in the first 2–3 hours after ingestion of a caustic substance; thereafter, efficacy decreases significantly due to the completion of the substance's resorption, and after 12 hours, gastric lavage is ineffective [2, 46].

• In emergency care for patients with caustic esophageal injury, the use of neutralizers is not recommended [1, 2, 4].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

• In patients with caustic esophageal injury in the event of progressive airway edema and the threat of asphyxia, tracheal intubation is recommended to ensure adequate oxygenation and active aspiration of secretions from the trachea and large bronchi. If tracheal intubation is impossible, placement of a temporary tracheostomy is recommended [1–4, 13, 15, 19, 39, 45, 50, 51].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

• In patients with signs of caustic substance poisoning and exotoxin shock, to eliminate extracellular fluid volume deficit and rehydrate the interstitial space in the first hours of the disease, intravenous administration of balanced electrolyte solutions (solutions affecting water-electrolyte balance, initial therapy) is recommended, subsequently including dextrose solutions** [111].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. If crystalloid solutions (solutions affecting water-electrolyte balance) are ineffective, colloid solutions (blood substitutes and plasma preparations - human albumin** 5% or 10%) can be added to the infusion therapy. To reduce manifestations of metabolic acidosis in the first 6 hours of infusion therapy, the use of succinic acid-based drugs (meglumine sodium succinate 1.5%) is not excluded [19, 52]. The use of hydroxyethyl starch-based solutions in patients with burn disease is contraindicated due to increased risks of kidney injury [53]. In case of progressive heart failure, inotropic support (preferably dobutamine**) is recommended to maintain effective blood pressure [54].

In general, the treatment of patients with signs of exotoxic shock complies with the general principles of critical care management for patients in a state of shock. The volume of infusion therapy is determined by the severity of hemodynamic disorders and the degree of restoration of hemodynamic parameters, hematocrit, and central venous pressure. Patients with decompensated shock undergo rapid bolus administration of colloid solutions (blood substitutes and plasma protein fractions). Intensive fluid administration continues until hemodynamic parameters increase by 45–50% compared to baseline.

Severe hemodynamic disorders typically lead to renal dysfunction in the form of oliguria or anuria; therefore, monitoring urine output is recommended from diagnostic and therapeutic perspectives. A urine output of 0.5–1.0 ml/kg/h is considered optimal.

Special attention is paid to correcting metabolic disorders. To correct acidosis, plasma alkalinization and intravenous administration of 4% sodium bicarbonate solution** are used [1–3, 15, 19, 45, 50, 51].

• In patients with caustic esophageal injury, to treat early secondary bleeding, measures to enhance hemostasis at the bleeding site and inhibit intravascular coagulation to prevent microthrombosis are recommended, whereas the administration of heparin sodium** is recommended only on condition of local hemostasis [1–3, 15, 19, 50].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Early primary hemorrhage due to compensatory hypercoagulation stops quickly. Treatment of early secondary hemorrhages involves two directions: enhancement of hemostasis at the bleeding site and simultaneous suppression of general intravascular coagulation using heparin group agents. The best local hemostatic effect is provided by local hypothermia of the esophagus and stomach using special devices and probes. It reduces blood flow through the gastric vessels (by 67%), promotes the aggregation of formed elements, and locally reduces fibrinolytic activity, which creates favorable conditions for local thrombus formation.

Administration of heparin group drugs for the prevention of microthrombosis is indicated only under the condition of local arrest of bleeding. Local gastric hypothermia is ineffective if the patient develops afibrinogenemia. In such cases, freezing of the gastric mucosa can be used to stop the bleeding.

• In late hemorrhages in patients with caustic substance poisoning, heparin therapy is not recommended; standard hemostatic therapy is recommended [1,3,50,99].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. In late hemorrhages, heparin therapy is contraindicated, and local gastric hypothermia is less effective. Standard hemostatic therapy is performed: fasting, fractionated transfusion of red blood cells, blood plasma, and fibrinogen.

• For the prevention of late hemorrhages in patients with caustic substance poisoning, it is recommended to use proton pump inhibitors and antacids [1,3,50,99].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

• In the event of late hemorrhages in patients with caustic substance poisoning, it is recommended to use endoscopic hemostasis methods (Endoscopic arrest of bleeding from a peripheral vessel using electrocoagulation (thermocoagulation) [1,3,50,99].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Since the sources of bleeding are small vessels of the submucosal layer, the bleeding is stopped by endoscopic laser coagulation, which does not cause significant additional damage to the esophageal wall [1,3,50,99].

• In adult patients with signs of caustic substance poisoning, for the treatment of toxic coagulopathy and the prevention of microthrombosis, the use of antithrombotic agents (anticoagulants) is recommended [1,3,50,99].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Antithrombotic agents (anticoagulants) are recommended to be used even before the development of severe toxic coagulopathy syndrome in doses corresponding to the instructions for use. In stage I toxic coagulopathy (hypercoagulation), treatment with antithrombotic agents is carried out with monitoring of clotting time before each injection.

In stages II (hypocoagulation) and III (fibrinolysis), treatment is carried out with monitoring of fibrinogen levels and platelet count every 4 hours until these parameters begin to rise. Subsequently, daily throughout the entire period of treatment with antithrombotic agents (e.g., heparin group drugs), monitoring is performed using an expanded coagulogram (exploratory hemostasis system assay) [107].

• For the prevention of infectious complications in patients with chemical burns of the upper gastrointestinal tract, the administration of systemic broad-spectrum antibacterial drugs is recommended, subsequently adjusted according to the microbiological status [2,19] under the control of laboratory blood parameters and bacteriological monitoring. Consultation with a clinical pharmacologist is indicated as needed.

GDR CLE 5Grade of recommendation C (level of evidence – 5)

• Patients with signs of chemical burns of the upper gastrointestinal tract are recommended early adequate nutritional support to prevent or correct protein and energy metabolism disorders [1–3,15,19].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Early adequate nutritional support is the most effective method for correcting protein and energy metabolism disorders in critical conditions. Nutritional therapy is recommended to be initiated within the first 12 hours after trauma. Oral feeding acts as a kind of "bougienage" procedure for the esophagus. Food should be mechanically, thermally, and chemically sparing. Undesirable consequences can occur both with too early expansion of the diet and with its excessively prolonged restriction. If it is impossible to meet the required daily nutrient requirements, parenteral nutrition is recommended in combination with enteral nutrition. Total parenteral nutrition is prescribed when enteral feeding is not feasible. If enteral feeding is impossible, the issue of gastrostomy placement must be addressed.

• Patients with signs of chronic upper gastrointestinal diseases are recommended to be prescribed proton pump inhibitors to relieve reflux esophagitis symptoms, enveloping agents with a local healing effect (sea buckthorn oil), and antacids [1–3,15,19].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Since chemical burns of the esophagus are usually accompanied by reflux esophagitis, proton pump inhibitors should be used to control hyperacidity. In the acute period, when swallowing is impaired, the drug is administered intravenously followed by a transition to oral administration.

• For the prevention of cicatricial narrowing of the esophagus or stomach in patients with corrosive poisoning, glucocorticoid administration is recommended; the dose of the specific medicinal product is selected individually according to the instructions and depending on the severity of poisoning [1].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. The duration of treatment is determined by the severity of the burn: for a mild burn, 7 days; moderate, up to 20 days; severe, at least 30 days. The specified course of treatment must be carried out in a hospital setting; further treatment may be continued on an outpatient basis: for a mild burn, 3 weeks; a moderate burn, 1 month; a severe burn, up to 2 months [1,3,50,998].

3.1.2. Surgical treatment

• In patients with clinical and instrumental signs of esophageal and/or gastric perforation due to a chemical burn, emergency measures are recommended, the scope of which is determined by the localization, size of the perforation, and verified complications [3,4,13,50,55,112,113].

LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)

Comment: In the acute stage of grade 4 acute corrosive esophagitis (ACE), perforation of the esophagus and stomach may occur either as a result of transmural necrosis or instrumental intervention (gastric intubation, EGD). The surgical management strategy in such situations should be based on X-ray imaging data with water-soluble contrast of the esophagus and stomach and/or (if technically feasible) on the basis of MSCT data with contrast enhancement.

When esophageal perforation is established, the management strategy depends on the localization, defect size, and the presence or absence of clinical manifestations of mediastinitis:

In esophageal perforation without prominent clinical manifestations of mediastinitis, oral feeding is completely discontinued. A nasogastric feeding tube is placed. Parenteral nutrition is prescribed if necessary. Intravenous administration of systemic antibacterial drugs targeting Gram-negative, Gram-positive, and anaerobic microorganisms is indicated. For this purpose, a combination of several antibacterial agents is prescribed (cephalosporins, metronidazole**, penicillin combinations, including beta-lactamase inhibitor combinations, etc.). In some cases, gastrostomy is performed. Gastrostomy can be performed via laparotomy or laparoscopic approach. Intensive care is carried out under clinical, laboratory, and instrumental monitoring. If clinical symptoms of mediastinitis, pneumomediastinum, pneumo- and hydrothorax, or subcutaneous emphysema appear and progress, it is recommended to consider expanding the scope of surgical treatment (cervical esophagostomy, anti-reflux surgery and gastrostomy, drainage of the mediastinum and pleural cavity depending on the level of esophageal perforation).

In esophageal perforation with clinical manifestations of mediastinitis, emergency surgery is recommended. The operation can be performed via either a thoracotomy or thoracoscopic approach. The scope of the surgery includes adequate debridement of the mediastinum, assessment of the condition of the esophagus, and localization and size of the defect(s) to decide on organ preservation. The surgical intervention is completed with adequate drainage of the mediastinum and other fluid collections, if present. A gastrostomy is performed along with an anti-reflux procedure.

Recently, endoscopic vacuum therapy has been widely used for esophageal perforation; it has proven effective in adult practice, but its application in children requires further study [56].

Esophagectomy with creation of an esophagostomy and gastrostomy is performed extremely rarely: in cases of irreversible changes in the esophagus.

In adults, esophagogastrectomy (esophagectomy, gastrectomy) performed via a combined abdominal and cervical approach is the most common emergency surgery performed to treat severe upper aerodigestive tract burns, with a mortality rate reaching 25-34% [13]. If necrosis is confined to the stomach, stomach-preserving gastrectomy should be considered. Gastric resection should be avoided, as ongoing necrosis can adversely affect outcomes. The rationale for esophagus-preserving gastrectomy based on isolated esophageal necrosis is questionable. Concomitant necrosis of other abdominal organs (duodenum, pancreas, spleen, small and large bowel) justifies extended resections in 20% of patients undergoing esophagogastrectomy. Total duodenopancreatectomy or duodenectomy can be performed in a small number (6%) of patients with duodenal necrosis (pancreatic involvement is rare). Total duodenopancreatectomy for chemical injuries is associated with high mortality (39–50%). The presence of extensive intestinal necrosis warrants a case-by-case discussion of withholding surgery due to low survival rates [13].

3.2. Treatment in the stage of scar stricture formation (up to 4 weeks)

• For patients following a chemical burn with severe dysphagia and rapidly developing cicatricial changes of the esophagus, prophylactic esophageal bougienage is recommended [36,57,58,108].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Commentary. In the case of developing esophageal stricture, early prophylactic bougienage tactics can be used. Thermoplastic or silicone bougies are used for bougienage, the sizes of which are presented in the table below. It is recommended to select a bougie with a diameter equal to or exceeding the age-appropriate size of the esophagus. Prophylactic bougienage is performed in an inpatient setting 3 times a week using the guidewire-guided bougienage method, transitioning to direct bougienage. After 3 weeks, a repeat EGD is performed; if complete epithelialization is observed upon inspection, bougienage is discontinued, and the patient can be discharged for outpatient follow-up with recommendations for endoscopic control in 2-3 months. For third-degree burns, bougienage is continued 3 times a week for 3 weeks. Then a control EGD is performed, and the patient may be discharged for outpatient bougienage with a frequency of 1 time per week for 2-3 months, then 2 times a month for 2-3 months, then 1 time per month for half a year. The course of the burn process in the esophagus is monitored by endoscopy every 3 months.

3.3. Treatment in the stage of established scar strictures

• In established esophageal strictures causing impaired patency and preventing normal nutrition, it is recommended to perform maintenance esophageal bougienage for 12 months. In cases of persistent positive dynamics requiring maintenance esophageal bougienage in the absence of dysphagia no more than once every 6 months, extending the bougienage period is possible, but for no more than 24 months. If ineffective, it is recommended to revise the bougienage program or consider reconstructive surgery [58,59].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. Most esophageal strictures caused by chemical burns can be resolved using bougienage. There are several methods: "blind" bougienage, thread-guided bougienage, and guidewire-guided bougienage. Thermoplastic or silicone bougies of various diameters can be used. For patients with esophageal stricture, it is recommended to start dilation 4-6 weeks after the burn using the guidewire-guided bougienage method [36].

Guidewire-guided bougienage is the most effective method for dilating cicatricial esophageal stricture. The bougienage procedure must be performed under endotracheal anesthesia. Special hollow bougies are used for bougienage. The guidewire with an atraumatic tip is passed through the esophagus into the stomach. Bougienage should begin with a bougie corresponding to the diameter of the stricture. The bougie is threaded over the guidewire and advanced into the stomach along it. Then the bougie is slowly withdrawn while simultaneously monitoring the position of the guidewire in the stomach. Next, dilation of the stricture is continued with bougies 2-3 sizes larger than the previous one. It is recommended to use no more than 3 bougies per session. This procedure is repeated in 2-3 days. Usually, 1-3 bougienage procedures are sufficient to achieve the age-appropriate bougie size. Thereafter, "blind" bougienage is recommended. After several sessions of "blind" bougienage in the hospital 2-3 times a week, a transition to outpatient bougienage is possible. The technology of guidewire-guided esophageal bougienage spares the patient from gastrostomy, which is an important socially significant factor.

Table – Bougie sizes (French scale):

Outpatient maintenance bougienage is performed 1 time per week for 3 months. If follow-up EGD at 3 months reveals epithelialization of the burn surface and an esophageal lumen of at least 10-12 mm, bougienage is discontinued. Ifesophagitis or cicatricial deformity persists, esophageal bougienage is continued once every 2 weeks. Bougienage is stopped after complete epithelialization of the esophageal mucosa and an esophageal lumen of at least 10-12 mm are detected. The course of esophageal bougienage should not exceed 6-12 months. In certain cases, prolongation of treatment is possible, but for no more than 24 months. After bougienage is discontinued, dysphagia should be absent, and the patient should consume carefully mechanically processed food. Such results are achieved in the vast majority of patients. Ineffectiveness of bougienage may manifest early if it is not possible to dilate the esophageal stenosis with bougies, or significantly later when, after the cessation of bougienage, stenosis relapses at various intervals.

Another method for dilating esophageal stenosis is string bougienage. This method of bougienage is safe and results in a low number of esophageal perforations. Mainly, this method of esophageal stenosis dilation is indicated in patients with long esophageal strictures caused by alkali or technical acids, and in children with laryngopharyngeal lesions caused by potassium permanganate crystals. Performing this type of bougienage requires the creation of a gastrostomy (gastrostomy), in adults using Kader's method. A gastrostomy is also necessary for adequate nutrition of the patient and further examination of the esophagus. Two weeks after gastrostomy placement, using endoscopic forceps passed through the instrument channel of the endoscope, a bougienage string is retrogradely passed through the stenotic segment. Using the passed string, counter-contrast esophagography can be performed, which provides a complete picture of the length of the stenosis, largely determining the prognosis. Bougienage is started with the smallest bougie that passes through the esophageal stenosis. For string bougienage, thermoplastic bougies of the following sizes on the Charrière scale are used: No. 17, 22, 24, 28, 33, 36, 38, 40, 42, 44, 46, 50. String bougienage is performed in a hospital setting 2 times a week. Once the bougie is advanced to the maximum possible size, the patient can be switched to outpatient maintenance string bougienage once a week, then once every 2 weeks. Follow-up EGD must be performed every 3 months. After complete epithelialization of the burn surface, elimination of the cicatricial stenosis, and an esophageal lumen of at least 10-12 mm, bougienage is discontinued. The course of esophageal bougienage is carried out for no more than 12 months. In certain cases, prolongation of treatment is possible, but for no more than 24 months. The manipulations are performed 2-3 times a week, bringing the size of the bougie to one exceeding the age norm. After the stenosis is eliminated, patients begin to eat orally, and the gastrostomy tube is removed.

Certain difficulties arise in the management of children with pharyngeal burns caused by potassium permanganate crystals. In this category of children, string bougienage with large-sized bougies (No. 44-60 on the Charrière scale) must be performed. The large sizes of the bougies correspond to the size of the child's pharynx. Direct bougienage in pharyngeal burns with bougies of such sizes is impossible in children.

There are other methods for eliminating esophageal stenosis. These include endoscopic electrosection or cryodestruction, forced esophageal bougienage, stenosis resection with esophago-esophagostomy, etc. However, these methods have limited application.

Short tubular esophageal strictures respond best to bougienage, especially during the first year after the burn. In long strictures, particularly after burns caused by alkalis and mineral acids, bougienage is often ineffective.

Criteria for ineffectiveness of esophageal bougienage:

1. Inability to achieve the maximum possible bougie size;

2. The patient cannot tolerate the intervals between bougienages (dysphagia and/or stenosis recurs);

3. Unable to proceed to the next stage of bougienage (when switching to less frequent bougienage, dysphagia and/or stenosis recurs);

4. Dysphagia symptoms increase after the end of the bougienage course.

Criteria for good results of esophageal bougienage:

1. The patient can eat any food (with no dysphagia present);

2. There is no need for maintenance esophageal bougienage;

3. The esophageal lumen in the stenosis area is at least 10–12 mm.

The course of esophageal bougienage should not exceed 6–12 months. In certain cases, treatment prolongation is possible, but for no more than 24 months. The ineffectiveness of dilatation therapy within this period is an indication for surgical treatment.

After completing the course of bougienage, the patient should be under dispensary follow-up by a surgeon (pediatric surgeon) at their place of residence with dynamic EGDS monitoring. Dispensary follow-up should aim to monitor the esophageal diameter, as well as the presence and severity of gastroesophageal reflux manifestations. Monitoring is carried out based on the clinical picture, endoscopic (EGDS), and radiopaque studies (contrast esophagoscopy/double-contrast esophagography). In the first year after completing bougienage, examinations are performed every 3–6 months, and thereafter as clinically indicated.

For the dilatation of an esophageal stricture up to 5 cm in length, fluoroscopy-assisted hydrostatic balloon dilatation may be used as an alternative standalone method [58,60,109].

All procedures of this treatment method must be performed in an operating room equipped with fluoroscopic equipment, under general anesthesia (total intravenous anesthesia, anesthetic management including early postoperative care). An endoscope of the smallest diameter is used to confirm the presence of stenosis and subsequently introduce a radiopaque guide wire with a soft atraumatic tip through the working channel of the endoscope. Under fluoroscopic guidance, the guide wire is passed beyond the distal edge of the esophageal stenosis and then positioned along the greater curvature of the stomach. The endoscope is then gradually withdrawn above the stricture zone while carefully advancing the guide wire through the working channel to a distance equal to the length of the withdrawn endoscope. Selection of a balloon of the required diameter is carried out taking into account the patient's age-related esophageal diameter and the severity of the stenotic area. A mandatory condition is the presence of radiopaque markers on the balloon, which allows it to be positioned strictly in the middle of the stricture. Before using the balloon dilator, the balloon is lubricated with prednisolone ointment to reduce mechanical impact on the esophageal mucosa during the passage of the balloon into the stenosis zone, as well as to reduce inflammatory changes in the esophageal mucosa after the procedure. Over the guidewire, the balloon is advanced to the stenosis zone and positioned so that the stricture "waist" is in the middle of the balloon's length. Under fluoroscopic guidance, the balloon is inflated by injecting distilled water or saline with a water-soluble contrast agent (in a 1:1 ratio) using an inflation device that allows monitoring and metered pressure increases in the balloon. With the onset of the flattening of the stricture "waist", the increase in balloon pressure is stopped. An exposure time of 60 to 120 seconds is maintained in this state, after which the balloon is deflated and extracted from the esophageal lumen with maximum caution. To rule out complications, a control chest X-ray is performed. To reduce traumatic impact on the esophageal mucosa, a control endoscopic examination is not performed [4,13,15,61–63].

• For patients with scarring strictures developing after a chemical burn, esophageal stenting is not recommended due to the lack of positive results from its use at present [7,13,64–67,110].

GCR BLEL 2Grade of Recommendations B (Level of Evidence – 2)

Comment. Stenting may be accompanied by complications such as granulation stenosis, stricture above and/or below the stent, obturation by food masses, detachment of its inner lining with occlusion of the lumen, fragmentation and migration of the stent, ingrowth of the prosthesis into the esophageal wall with subsequent necrosis, formation of pressure ulcers and fistulas with prolonged stenting, and unsafety of removal [7,64–67].

3.4. Reconstructive and plastic surgeries for complications of caustic esophageal burn

Timely and systemic treatment of patients with ECP described above in the vast majority of cases (up to 96%) allows achieving satisfactory results and resolving cicatricial esophageal stenosis [68–70]. In some cases, even with compliance with the clinical guidelines presented above, the formation of rigid scars cannot be avoided. This depends on the chemical composition and concentration of the damaging agent, as well as the duration of its exposure. In these cases, it is necessary to resort to reconstructive plastic surgery, which is recommended to be performed in specialized institutions.

• Surgical treatment of patients with post-burn esophageal strictures is recommended in the following cases:

1. complete obliteration of the esophageal lumen;

2. presence of a tortuous lumen of one or several strictures with suprastenotic expansions, blind pouches, and diverticula;

3. inability to pass #28–30 bougies (Charrière scale) due to dense, recurrent strictures;

4. post-burn strictures complicated by esophageal fistulas;

5. history of esophageal perforation;

6. long-term (more than 15 years) existence of scar tissues with a high risk of their malignancy;

7. post-burn esophageal shortening with the development of a secondary hiatal hernia and reflux esophagitis [57,97,98].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

3.4.1. Pharyngoplasty for isolated pharyngeal involvement

• For isolated cicatricial strictures of the pharynx due to upper respiratory tract damage, it is recommended to perform pharyngoplasty with a free intestinal segment [71–74, 118].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Comment. Isolated cicatricial strictures of the pharynx in 100% of cases are caused by manganese crystal burns, while the esophagus remains undamaged. Manganese crystals tend to tightly fixate on the mucosa of the oropharynx and laryngopharynx. In these cases, concentric scarring occurs not only at the pharyngeal entry, but also into the larynx, since the epiglottis is completely lysed and scars together with the arytenoid cartilages, turning the laryngeal inlet into a pinpoint opening. At the same time, both swallowing and breathing through natural pathways are impossible. In the acute stage of the burn, these patients survive only if emergency tracheostomy is performed. As a rule, all patients are carriers of tracheostomas and gastrostomas [71–74]. In isolated cicatricial strictures, pharyngoplasty with a free intestinal segment with revascularization of the intestinal graft to the common carotid artery and internal jugular vein end-to-side is performed (pharyngeal reconstruction). This type of surgery allows achieving a good result in all cases with complete resection of all scar tissues of the laryngopharynx, including the altered epiglottis, replacing these defects with a revascularized intestinal graft dissected along the antimesenteric border [72,74].

3.4.2. Pharyngoplasty and pharyngoesophagoplasty

• In case of cicatricial stenosis of the pharynx and cervical esophagus due to upper respiratory tract damage, it is recommended to perform plasty with a free intestinal segment [71–74]. In subtotal damage to the pharynx, cervical and lower parts of the esophagus, it is recommended to perform esophagoplasty with the colon [75,114,115,119].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Comment. A similar operation is also performed for stenosis of the pharynx and cervical esophagus when the lower parts of the esophagus are undamaged. Such lesions occur when concentrated acids and alkalis are ingested. In this case, a tubular revascularized intestinal segment is used. In subtotal damage to the pharynx, cervical and lower parts of the esophagus, preference should be given to coloesophagoplasty. The colonic graft can be brought up to the level of the pharynx and simultaneous reconstruction of the laryngopharynx and the entire esophagus can be performed [75].

3.4.3. Esophagoplasty for extensive and/or multiple scar strictures

• If there are indications for surgical treatment of patients with post-burn strictures, esophageal plasty is recommended in combination with single-stage extirpation of the compromised native esophagus, or these interventions are performed separately [57,97,98].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Comments: The choice of intervention method and its scope depends on the patient's general condition, the extent of scar changes (pharyngeal entry, stomach). Depending on these factors, surgical intervention can be performed in one or several stages. Key issues of reconstructive esophageal surgery—the variant of esophagoplasty (replacement, bypass, delayed), plastic material (stomach, colon), approach (transhiatal, transthoracic), method of graft placement (posterior mediastinal, retrosternal)—are the prerogative of surgeons in specialized centers [57,97,98].

• For children with extended and/or multiple cicatricial strictures of the esophagus resulting from caustic upper digestive tract injury, coloesophagoplasty with retrosternal graft placement (colon interposition) is recommended [76–82].

GCR BLEL 3Grade of Recommendation B (Level of Evidence – 3)

Commentary. Performing segmental esophageal resections with primary anastomosis or using other intestinal grafts in the mediastinum is impractical due to the high rate of anastomotic leakage and the development of mediastinitis. These complications arise from the constant intermittent pressure gradient that occurs in the thoracic cavity during respiration. An abdominocervical approach without thoracotomy is generally used for esophageal replacement.

• In patients with extended post-burn cicatricial strictures of the esophagus refractory to bougienage, provided there are no residual effects of chemical burns in the stomach, it is recommended to perform esophageal resection via an abdominocervical approach with simultaneous gastric pull-up esophagoplasty [57,97,98].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. In coloesophagoplasty, a colonic graft based on the left colic vessels with isoperistaltic placement to the neck is used. There are two methods for routing the graft to the neck: posterior mediastinal (after extirpation of the damaged esophagus in its bed) and retrosternal. The posterior mediastinal route for graft placement to the neck is the shortest, most direct, and most physiological. Posterior mediastinal graft placement eliminates the likelihood of additional loops in the graft, which often occur with retrosternal esophagoplasty. The posterior mediastinal route does not cause inconvenience if a sternotomy becomes necessary for cardiovascular diseases requiring surgical treatment [76–80]. Disadvantages of posterior mediastinal esophagoplasty include: surgical trauma, the possibility of massive hemorrhage, and injury to the thoracic duct, trachea, or bronchus [78,79]. These complications are primarily associated with the complexity of the anatomical region and the limited surgical field.

In cicatricial esophageal stenoses resulting from perifocal inflammation, the esophagus becomes intimately fused with the surrounding tissues. All of this makes esophageal extirpation in such cases either very difficult or impossible. Consequently, contraindications to esophageal extirpation have been defined in the literature: sclerosing mediastinitis, subtotal or total cicatricial esophageal stenosis, a history of esophageal perforation, and esophagorespiratory fistulas [78,79]. Thus, in total or subtotal cicatricial esophageal stenosis and/or following mediastinitis associated with esophageal pathology, performing esophageal extirpation should be considered impractical. Anesthesia and intensive care during posterior mediastinal esophagoplasty are more complex compared to retrosternal esophagoplasty.

Thus, in coloesophagoplasty, retrosternal graft placement should be considered the most optimal approach. However, this operation does not eliminate the occurrence of complications in the "left-behind esophagus", such as gastroesophageal reflux into the "left-behind esophagus" with the development of pain syndrome, erosions, ulcers, bleeding, and Barrett's metaplasia. All these changes in the "left-behind esophagus" contribute to the development of Barrett's adenocarcinoma and esophageal squamous cell carcinoma within 4–52 years after surgery [80]. Furthermore, diagnosing these complications is difficult because endoscopic examination is extremely challenging or impossible. Currently, an opinion is forming in favor of performing thoracoscopic esophageal extirpation after primary reconstruction. The purpose of this surgery is to prevent the likelihood of the complications listed above. This approach adheres to the principle of oncological vigilance.

Gastric pull-up esophagoplasty should be recognized as a technically simpler procedure. It can also be performed laparoscopically with the graft pulled up to the neck. The graft has a good blood supply and requires only a single anastomosis in the neck. It is precisely these circumstances that have made this operation the most preferred. However, studies [81,82] on long-term outcomes comparing gastric pull-up and coloesophagoplasty indicate a significant number of complications with the gastric procedure that impair functional results and reliably reduce patients' quality of life. Following gastric pull-up esophagoplasty, Barrett's esophagus and adenocarcinoma may develop at the site of the gastroesophageal anastomosis in the neck. All this narrows the indications for gastric pull-up esophagoplasty to cases where anatomical variations preclude mobilizing a colonic graft of sufficient length, in cases of primary coloesophagoplasty failure, and in chronic diseases of the colon [74,81–83].

Small bowel esophagoplasty is more frequently used in adult practice. Scientific studies are underway in children to evaluate the effectiveness of this technique, but the results have not yet been published. This type of surgery involves two stages. In the first stage, "conditioning" of the graft is performed by dividing the arcade vessels to create a graft of the necessary length for retrosternal esophagoplasty.

3.4.4. Pyloric stenosis

• For patients with pyloric stenosis resulting from caustic upper digestive tract injury, it is recommended to perform surgical or endoscopic intervention depending on the localization and extent of the stenosis [84, 116, 117].

LeRR CLoE 4Level of recommendation confidence C (level of evidence – 4)

Commentary. Pyloric stenosis can occur due to exposure to either acids or alkalis and is frequently associated with esophageal stenoses. In severe gastric injury, gastric outlet obstruction can manifest as early as 3–10 weeks. Surgical correction may be required depending on the localization and extent of the stenosis. The creation of a posterior gastrojejunostomy on a long loop with a Braun enteroenterostomy is recommended. Gastric resection is not recommended. In some cases, endoscopic balloon dilation has been successfully utilized [84].

3.4.5. Reconstructive surgery for tracheoesophageal fistula

• In the event of a post-burn tracheoesophageal fistula, it is recommended to adhere to a conservative management strategy (laparoscopic fundoplication and gastrostomy with conservative therapy) in the absence of respiratory failure and if the patient is in a stable condition [85,120].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Commentary. Closure of a tracheoesophageal fistula following a burn in the acute period entails early postoperative complications: suture leakage of the esophagus or trachea, fistula recanalization, esophageal stenosis, and tracheal stenosis. Conservative management demonstrates better results with a minimized rate of postoperative complications (16.7%) and good long-term outcomes [85]. It has been reliably established that with this technique, the incidence of postoperative complications is much lower, while the average number of months for spontaneous fistula closure is up to 5 months. Additionally, this technique significantly reduces operative time and the time to initiation of enteral nutrition via the gastrostomy. In cases of incomplete fistula closure within the observed timeframe, scheduled surgical disconnection is performed.

• In children who develop a large post-burn tracheoesophageal fistula with respiratory failure requiring emergency surgical intervention, it is recommended to perform tracheoplasty using an esophageal flap with esophageal extirpation and subsequent planned esophageal reconstruction [85].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Commentary. To resolve the management dilemma in children in an extremely unstable condition with a large tracheal and esophageal defect and respiratory failure, a technique of tracheoplasty using an esophageal flap was developed, which requires esophageal extirpation followed by a second-stage colonic esophagoplasty [86]. This approach increases operative time and complexity, but it is the technique of choice for children with respiratory instability requiring emergency correction of the tracheoesophageal fistula.

3.4.6. Aortoesophageal fistulae

• For patients with a diagnosed aortoesophageal fistula resulting from caustic upper digestive tract injury, emergency surgical intervention is recommended even in the absence of visible bleeding [76–79,87].

GCR CLEL 5Grade of Recommendation C (Level of Evidence – 5)

Commentary. Aorto-esophageal fistula (AEF) in children is an extremely rare condition that in most cases results in death within the first 24 hours after the formation of the communication. The high mortality rate is largely due both to the lack of physicians' awareness regarding the existence of such a complication in children with corrosive esophageal burns and to the lack of treatment experience. AEF can be subdivided into primary, where the underlying pathology is a developmental defect—congenital aneurysm, double aortic arch, or coarctation of the aorta, and secondary AEFs, resulting from trauma and foreign bodies in this area, inflammatory diseases with the development of aortitis or mediastinitis [76–79,87].

The esophagus is a fairly mobile organ, and its deviation during compression often occurs, although aneurysm penetration into the lumen of the hollow organ does not happen in all cases. This is explained by the anatomical features of the bronchial segment of the esophagus, where it is intimately connected by fibro-muscular bands to the aorta, the tracheal bifurcation, and the left main bronchus [77,78]. It is known that during esophageal extirpation, it is precisely in these parts that one has to resort to sharp dissection [78,79,87]. The literature describes cases where damage to the membranous wall of the trachea occurred during esophageal extirpation for the aforementioned reason [75,80,87]. The mechanism of AEF development in foreign bodies and trauma is associated with compression of the esophageal wall by a foreign body or with a burn (in the case of button batteries). It should be particularly emphasized that children with AEF must receive treatment in specialized medical centers equipped with a cardiosurgical department and/or having prior experience in performing such surgeries. The classic clinical manifestations of AEF are Chiari's triad: progressive retrosternal pain, minor periodic bleeding, and finally, massive bleeding following a "silent interval" [87].

Among imaging methods, contrast-enhanced computed tomography (computed tomography of the chest organs with intravenous bolus contrast enhancement, multiplanar and three-dimensional reconstruction) should be considered the most informative, allowing for the detection of an aneurysm, double aortic arch, and coarctation of the aorta, identification of the inflammatory process in the mediastinum, and contrast extravasation during ongoing bleeding [87].

Esophagoscopy should be considered the most effective diagnostic method for AEF. In secondary AEFs, the zone of communication with the aorta is represented only by a mucosal defect in the projection of the aorta. Endoscopic examination allows for the identification and removal of foreign bodies, or visualization of the consequences of trauma to the esophageal mucosa. Tissue biopsy in these cases is contraindicated [87].

If the diagnosis is established, any procedures must be immediately stopped, and the patient should be prepared for emergency surgery [87]. In case of ongoing bleeding, the placement of a Sengstaken-Blakemore tube is recommended, with the esophageal part of the balloon projected onto the middle third of the esophagus, and there is no need to inflate its gastric part. Preoperative preparation should be aimed at correcting the hemostatic system, replenishing blood and fluid loss, and administering broad-spectrum antibiotics.

The surgical treatment strategy for AEF consists of two components. The first is the disconnection of the AEF with hemostasis, and the second is the reconstruction of the esophagus and aorta. After stopping the blood loss, the question of treatment tactics arises. In cases where the defect is minor, management is limited to the disconnection of the fistula and closure of the aortic and esophageal defects. This area should be reinforced with vascularized tissue, such as a fragment of the pleura, pericardium, intercostal muscle, omentum, xenopericardium, or synthetic material. In case of a significant esophageal defect, esophageal resection with the creation of an esophagostomy and gastrostomy should be performed [87]. The damaged wall of the aorta should be sutured. Esophageal plastic surgery should be postponed until the resolution of mediastinitis and the normalization of the child's condition. At the same time, preference should be given to retrosternal graft placement in order to separate the injury zone. Attempting to clip the bleeding site should be considered an error, as only surgical intervention gives hope for saving the patient's life. For such defects in adult surgery, endostents are used; however, their efficacy in pediatric surgery is not high, and their placement is considered a palliative procedure in a growing organism [87]. Another option—resection of the affected aortic segment with the placement of a synthetic prosthesis—is possible only in a specialized cardiac surgery hospital.

4. Medical Rehabilitation and Sanatorium-Resort Treatment

• Medical rehabilitation for patients after corrosive esophageal burns is recommended to be started as early as possible and carried out simultaneously with treatment [4,13,23,88,89].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Commentary. Medical rehabilitation is represented by a complex of physiotherapeutic treatment methods [88,89]. In the absence of contraindications in the acute stage, inductothermy using the UHF therapy apparatus "70-01-R strela" and zinc electrophoresis on the esophagogastric region are recommended. Inductorthermy is performed using a eddy current electrode, which generates an ultra-high-frequency alternating electromagnetic field with a predominance of the magnetic component. The design of the electrode allows focusing energy directly onto the projection area of the esophagus, which provides the possibility of local exposure to magnetic oscillations for anti-inflammatory and anti-edematous purposes. The dose is weakly thermal, daily, with an exposure of 7-10 minutes, for a course of up to 5 procedures depending on the child's age. Electrophoresis of OMC (organo-mineral complex, wipes) is recommended using a transverse technique in age-appropriate dosages for anti-inflammatory and trophic-stimulating purposes. In the absence of contraindications, a course of low-level infrared laser therapy (LLLT) using the "ULAN BL-20" device on the esophagogastric and reflex-segmental regions is recommended. Laser exposure is performed over the lesion site (frequency 1500-800 Hz), with an exposure of no more than 6-8 minutes, and a course of up to 7 exposures. LLLT has a high penetrating property (up to 6 cm into tissues) and exerts anti-inflammatory, analgesic, and trophic-stimulating effects. In the scar formation stage, after bougienage, the administration of magnetotherapy in courses of 5-7 sessions is recommended.

The complex of physiotherapeutic treatment for corrosive esophageal burns allows for a reduction in the hospital stay of patients, achieving complete resolution of the inflammatory process and epithelialization of the mucosa, avoiding complications, and thereby improving the prognosis of the disease and reducing the rate of disability in children.

• Patients with grade I corrosive esophageal burns are recommended to be fed immediately and discharged from the medical organization within 24–48 hours [13].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. These patients do not require long-term monitoring, as the risk of stricture formation is zero [13].

• Patients who have ingested caustic substances with suicidal intent are recommended to undergo a psychiatric examination (admission (examination, consultation) by a psychotherapist) before discharge from the medical organization [13,14,23].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. Monitoring of the mental state and psychological support are mandatory before discharge from the medical organization, regardless of the severity of corrosive injuries [23]. To prevent the recurrence of a suicide attempt, long-term follow-up by a psychotherapist is advisable [13,14].

5. Prevention and Dispensary Observation

Public health programs aimed at public education and the adoption of effective measures to restrict access to strong corrosive agents are of paramount importance for reducing the frequency and severity of caustic ingestions. Preventive strategies such as the introduction of child-resistant bottle caps, proper labeling and packaging, and extensive media coverage of potential complications have proven effective [13].

• Patients with corrosive esophageal burns (gastrointestinal tract) after discharge from the hospital are recommended to undergo dispensary follow-up by a surgeon (pediatric surgeon) at the outpatient clinic at their place of residence in order to monitor the patient's condition, early detection, and timely treatment of complications [13,36].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

Comment. For the early detection and timely treatment of complications such as esophageal stricture, all patients with a history of chemical burn of the esophagus are recommended to undergo dispensary follow-up by a surgeon (pediatric surgeon) at the outpatient clinic at their place of residence for 3 years from the moment of the chemical injury.

• 1 month after initial discharge, all patients with a history of grade III chemical burn of the esophagus are recommended a scheduled hospitalization for inpatient endoscopic control (EGD). In the absence of endoscopic signs of esophageal stricture, subsequent scheduled hospitalizations for endoscopic control should be carried out sequentially at 3 and 6 months, respectively [13,36].

GDR CLE 5Grade of recommendation C (level of evidence – 5)

• In the absence of signs of esophageal stricture formation, further follow-up is recommended to be continued under the supervision of a pediatric surgeon or general surgeon at the local outpatient clinic; follow-up visits are scheduled every 6 months in the absence of symptoms of dysphagia (disorder of the swallowing act that impedes the passage of liquid, solid food, or both from the pharynx to the stomach) for a total duration of up to 3 years from the time of the injury. In cases where dysphagia develops, hospitalization is advisable for EGDS. Patients with cicatricial esophageal deformity without signs of narrowing (including after treatment) are recommended to undergo EGDS every 3 years following discharge from the hospital due to the risk of malignant transformation of the altered esophageal tissues [90].

GRC CLEL 4Grade of Recommendation C (Level of Evidence – 4)

Commentary. 10 or more years after the burn, squamous cell carcinoma or adenocarcinoma may develop in the esophagus. When the tumor reaches a large size and invades adjacent organs, a persistent dull pain appears in the interscapular region, which patients with post-burn esophageal changes tend to ignore. To detect cancer at an early stage, it is necessary to perform EGDS at scheduled follow-up intervals [90].

6. Organization of Medical Care

Indications for hospital admission to a medical organization:

• clinical and anamnestical signs of chemical burn of the gastrointestinal tract.

Indications for discharging the patient from the medical organization: clinical and laboratory normalization of the general somatic status, endoscopic absence of signs of erosive and ulcerative esophagitis, absence of complications, normalization of nutritional status, and the ability to receive enteral nutrition (naturally or via gastrostomy).

Organization of dietary nutrition for patients during inpatient treatment in medical organizations is carried out in accordance with Appendix 3 of the Order of the Russian Ministry of Health No. 1008n dated September 23, 2020, "On approval of the procedure for providing patients with therapeutic nutrition"

7. Additional Information

At the pre-hospital stage, it is extremely critical to confirm the ingestion of a foreign body/substance and identify the chemical agent, assess the causes (accidental or intentional) and the time elapsed since ingestion, as well as comorbid conditions [4,23,39,91].

Actions that may cause re-passage of the foreign body/substance through the esophagus or lead to aspiration of the chemical agent (supine patient position, administration of diluting agents) should be avoided, as well as attempts to neutralize the pH of the gastric contents, as they may exacerbate the injury.

Emergency care for the ingestion of foreign bodies/substances, as well as the management of late complications, requires a multidisciplinary approach [4,23,39,91].

Surgical management of esophageal perforation must be based on the results of contrast esophagography (water-soluble contrast, fluoroscopic examination of the esophagus with contrast / double-contrast esophagography), contrast MSCT (computed tomography of the chest organs with intravenous bolus contrast enhancement, multiplanar and three-dimensional reconstruction, computed tomography of the esophagus with oral contrast), which can save the patient's life and must be performed in specialized level-1 surgical hospitals.

In resource-constrained settings, simple solutions that can save lives by addressing critical problems are preferred.

The treatment of late consequences of chemical burns of the esophagus is mainly based on bougienage, endoscopy (dilation, stenting), or complex surgical reconstructive interventions and should be performed in specialized centers [13].

Criteria for Evaluating the Quality of Medical Care

References

Appendix A1. Working Group Composition

1. Razumovsky A.Yu. – Corresponding Member of the Russian Academy of Sciences, Doctor of Medical Sciences, Professor

2. Abakumov M.M. – Doctor of Medical Sciences, Professor

3. Allakhverdyan A.S. – Doctor of Medical Sciences, Professor

4. Alkhasov A.B. – Doctor of Medical Sciences, Professor

5. Baranov A.A. – Academician of the RAS, Doctor of Medical Sciences, Professor

6. Barova N.K. – Candidate of Medical Sciences, Associate Professor.

7. Bataev S.M. – Doctor of Medical Sciences, Professor.

8. Belokonev V.I. – Doctor of Medical Sciences, Professor.

9. Godzhelo E.A. – Doctor of Medical Sciences, Professor

10. Gurova M.M. – Doctor of Medical Sciences, Professor

11. Drobyazgin E.A. – Doctor of Medical Sciences

12. Eredzhibokova M.Yu. – Physiotherapist of the Highest Qualification Category, Head of Department.

13. Zavyalova A.N. – Doctor of Medical Sciences, Professor

14. Ilyashenko K.K. – Doctor of Medical Sciences, Professor

15. Kaitukova E.V. – Candidate of Medical Sciences, Associate Professor

16. Kovalenko L.A. – Candidate of Medical Sciences, Associate Professor

17. Komarova E.V. – Doctor of Medical Sciences, Professor

18. Kuznetsova Yu.V. – Candidate of Medical Sciences, Associate Professor

19. Lodyagin A.N. – Doctor of Medical Sciences, Professor

20. Meshkov A.V. – Pediatric Surgeon of the Highest Qualification Category, Thoracic Surgeon, Head of the Endoscopy Department, Assistant Professor at the Department of General Medical Practice, St. Petersburg State Pediatric Medical University

21. Mitupov Z.B. – Doctor of Medical Sciences, Professor

22. Namazova-Baranova L.S. – Academician of the RAS, Doctor of Medical Sciences, Professor

23. Novikova V.P. – Doctor of Medical Sciences, Professor

24. Pelipenko N.V. – Pediatric Surgeon of the Highest Qualification Category, Department Assistant

25. Pushkin S.Yu. – Doctor of Medical Sciences, Professor

26. Rachkov V.E. – Doctor of Medical Sciences

27. Ruchkin D.V. – Doctor of Medical Sciences

28. Savelyeva M.S. – Candidate of Medical Sciences, Associate Professor

29. Surkov A.N. – Candidate of Medical Sciences, Professor

30. Teplov V.O. – Candidate of Medical Sciences

31. Khavkin A.I. – Doctor of Medical Sciences, Professor

32. Khorobrykh T.V. – Doctor of Medical Sciences, Professor

33. Cherkasov M.F. – Doctor of Medical Sciences, Professor

34. Chikinev Yu.V. – Doctor of Medical Sciences, Professor

35. Shulutko A.M. – Doctor of Medical Sciences, Professor

36. Shadrina E.M. – Candidate of Medical Sciences, Associate Professor

37. Yablonsky P.K. – Doctor of Medical Sciences, Professor.

There is no conflict of interest.

Appendix A2. Methodology for Developing Clinical Guidelines

In these clinical guidelines, all data are ranked by level of reliability (evidence) depending on the quantity and quality of studies on the issue.

Target audience of these clinical guidelines:

1. surgeons

2. pediatric surgeons

3. thoracic surgeons

4. endoscopists

5. radiologists

6. anesthesiologists-resuscitators

7. pediatricians

8. general practitioners (family physicians)

9. general practitioners

10. gastroenterologists

11. toxicologists

12. emergency physicians

13. medical students and residents

Table 1. Scale for grading levels of evidence (LE) for diagnostic methods (diagnostic interventions)

Table 2. Scale for evaluating the levels of evidence (LE) for prevention, treatment, and rehabilitation methods (preventive, therapeutic, and rehabilitative interventions)

Table 3. Scale for grading the grades of recommendation (GR) for prevention, diagnostic, treatment, and rehabilitation methods (preventive, diagnostic, therapeutic, rehabilitation interventions)

Procedure for updating clinical guidelines.

The mechanism for updating clinical guidelines provides for their systematic revision at least once every three years, as well as upon the emergence of new evidence-based medicine data on the diagnosis, treatment, prevention, and rehabilitation of specific diseases, or in the presence of justified additions/comments to previously approved clinical guidelines, but no more frequently than once every 6 months.

Appendix A3. Reference Materials

Zargar SA Endoscopic Classification of Chemical Esophageal Burns

Zargar SA, Kochhar R, Mehta S, Mehta SK. The role of fiberoptic endoscopy in the management of corrosive ingestion and modified endoscopic classification of burns. Gastrointest Endosc. 1991;37:165-169. doi:10.1016/s0016-5107(91)70678-0 

Endoscopic images according to the Zargar classification.

A: Grade 0: Normal, B: Grade I; C: Grade IIA; D: Grade IIB; E: Grade IIIB; F: Grade IV.

Volkov S.V. Endoscopic Classification, supplemented by Pesnya-Prasolova E.A.

Pesnya-Prasolova E.A., Ilyashenko K.K., Pinchuk T.P., Gulyaev A.A. Comprehensive evaluation of esophageal and gastric injuries in acute corrosive poisonings // Clinical Perspectives in Gastroenterology, Hepatology – 2006. – N 5. – P. 32 – 35

By burn depth

Grade I – catarrhal lesion (edema and hyperemia of the mucous membrane).

Grade II – erosive lesion (not extending beyond the muscularis mucosae).

Grade III – ulcerative lesion of the mucosa and submucosa.

Grade IV – ulcerative-necrotic lesion (mucosal, submucosal, and muscular layers of the esophagus).

By burn extent

Focal (in the esophagus – extending to 1/2 of the wall and occupying no more than 1/3 of its length; in the stomach – localized in only one anatomical region and extending to no more than 2 walls).

Limited (in the esophagus – involving all walls, i.e., circumferential, and extending to no more than 1/2 of its length; in the stomach – circumferential and semi-circumferential, localized in one anatomical region);

Widespread (in the esophagus – circumferential, involving more than half of the esophagus; in the stomach – extending to 2 or more anatomical regions, can be circumferential or semi-circumferential, or present as multiple foci across all walls).

By lesion localization, taking into account the anatomical regions of the esophagus and stomach:

esophagus – lower, middle, and upper thirds

stomach: cardia, fundus, body, and antrum

Appendix B. Physician Action Algorithms

Appendix C. Patient Information

Substances and items that can cause esophageal burns (acids, alkalis, including cleaning agents [degreasers, oven, drain, and toilet bowl cleaners], potassium permanganate, vinegar, bleach, dishwasher detergents, hair straighteners, batteries [including button cells], etc.) should be stored separately from food and drinking water, in labeled containers, in places inaccessible to children or individuals with intellectual disabilities to prevent accidental ingestion.

If accidental or intentional ingestion of caustic chemicals is suspected, call an ambulance immediately. Do not induce vomiting under any circumstances, and do not give any medications or liquids.

Practically all patients with grade I and IIA burns recover without sequelae. The majority of patients with more severe chemical burns develop esophageal or gastric scarring. Early serious complications and death typically occur in patients with grade III–IV burns.

Cicatricial stenosis occurs more frequently in the esophagus than in the stomach and usually develops within 4–6 months after ingestion of a caustic substance.

For early detection and timely treatment of complications such as esophageal stricture, all patients with a history of grade III chemical esophageal burn are recommended to undergo dispensary follow-up by a surgeon or pediatric surgeon at the outpatient clinic of their place of residence for 3 years from the date of the chemical injury. One month after initial discharge, a scheduled hospitalization for inpatient endoscopic monitoring is recommended. In the absence of endoscopic signs of esophageal stricture, subsequent scheduled hospitalizations for endoscopic monitoring should be performed sequentially at 3 and 6 months, respectively. In the absence of signs of esophageal stricture formation, further dispensary follow-up should be continued under the supervision of an outpatient surgeon (pediatric surgeon) at the place of residence, with consultations scheduled every 6 months in the absence of clinical dysphagia (disorder of the swallowing act that impedes the passage of liquid, solid food, or both from the pharynx to the stomach) for a total duration of up to 3 years from the moment of injury.

The primary symptom of cicatricial esophageal stenosis is dysphagia (difficulty swallowing food). If signs of dysphagia appear, it is necessary to consult a physician (pediatric surgeon) immediately for an examination of the upper gastrointestinal tract.

All patients with cicatricial post-burn esophageal strictures, taking into account the risk of malignancy, should be assigned a lifelong multidisciplinary dispensary follow-up by specialists: a surgeon, gastroenterologist, and oncological surgeon. The schedule for endoscopic examinations is 1 time every 3 years.

Appendix G. Assessment Scales, Questionnaires, and Other Evaluation Tools

None provided.