Chemical burns of the upper digestive tract with corrosive substances occupy one of the leading positions among acute poisonings. It is a serious health problem worldwide due to high morbidity and mortality among people of working age [1, 2]. The cause of this event is oral intake of organic and inorganic acids, alkalis, oxidizing agents and electrolyte solutions [3]. One of the most common complications of chemical burns of the upper digestive tract is cicatricial stenosis of the esophagus following circular damage to the muscle layer of the esophageal wall [4–6]. Incidence of esophageal stenosis among patients with burns grade IIb-III can reach 70-100% [7].

Esophagogastroduodenoscopy is the gold standard for diagnosing gastrointestinal chemical burns [8, 9]. Esophagogastroduodenoscopy within 24 hours after poisoning visualizes injury, its localization and extent [10]. However, standard endoscopic examination has a significant drawback, since it is useless to determine depth of esophageal wall damage early after poisoning [11]. Since the 2000s, introduction of endoscopic ultrasonography (EUS) into diagnostic algorithm allows the most accurate analysis of depth of damage to esophageal wall. In addition, some authors believe that EUS can be used as a prognostic tool to determine the risk of esophageal stenosis [12].

The purpose of this report was to improve treatment outcomes in patients with chemical burns of the esophagus by using of EUS and preventive gastrostomy.

We present a clinical case showing the role of endoscopic diagnosis in chemical burns of the esophagus.

A 66-year-old patient P. admitted to the department of acute poisonings with complaints of sore throat and difficult swallowing. Five days before hospitalization, the patient accidentally drank a sip of alkali (liquid drain cleaner). Upon admission (5 days after injury), diagnostic esophagogastroduodenoscopy revealed overlays of light dense fibrin along posterior pharyngeal wall extending to the mouth of the esophagus. The last one was circularly covered with light dense fibrin. Circular overlays of dirty-gray loose necrotic masses covered esophageal walls from the mouth of the esophagus and up to 33 cm distally (Fig. 1A). There was no peristalsis. Mucous membrane of the esophagus distal to 33 cm was slightly hyperemic

Thus, acute poisoning with corrosive substance followed by ulcerative-necrotic esophagitis was diagnosed. There were no indications for emergency surgery.

In 6 days after injury (the 2^nd day after admission), EUS of the esophagus was performed using 20-MHz mini-transducer. Scanning of the esophagus throughout 33 cm after its mouth revealed undifferentiated muscle layer of the esophageal wall and impaired layering of the wall. The entire esophageal wall had a heterogeneous hyperechoic structure. Less hyperechoic circular zones were observed closer to the lumen of the esophagus, and enhanced US signal was noted outward. The outer boundaries of the esophageal wall were not visualized (Fig. 1B).

Distal scanning up to cardia visualized all layers of the esophageal wall with intact boundaries (Fig. 1C).

Fig. 1. Endoscopy in 5 and 6 days after oral administration of alkali.

a — endoscopic image of the esophagus in 5 days after chemical burn: 1 — esophageal wall is covered with loose dirty gray necrotic masses, 2 —lumen of the esophagus; b — ultrasonography of the esophagus in 6 days after chemical burn with a mini-sensor (double arrow) in the area of damage, impaired layering of esophageal wall, muscle layers are not detected, 2 — lumen of the esophagus; c — ultrasonography of intact esophagus with a mini-sensor (double arrow), intact muscle layers (single arrow), 2 — lumen of the esophagus..

In 7 days after chemical burn (the 3^rd day after admission), contrast-enhanced X-ray examination of the esophagus was performed. Swallowing was not disturbed. Esophagus was patent for contrast agent. Contours of the esophagus were clear. There were periodic spasms in the middle and lower thirds. Diameter of the esophagus between the mouth and the middle third (Th_VI) was reduced to 1.2 cm. Diameter of distal segments was 2 cm. All volume of contrast agent entered the stomach (Fig. 2). X-ray data also confirmed early stage of cicatricial narrowing of the esophagus.

Fig. 2. X-ray examination of the esophagus in 7 days after chemical burn.

Narrowing of the esophagus (single arrow), intact lumen of the esophagus (double arrow).

Considering EUS and X-ray examination data, we established high risk of decompensated esophageal stricture. The indications for preventive percutaneous endoscopic gastrostomy for adequate nutrition after esophageal obstruction were defined.

In 8 days after injury (the 4^th day after admission), endoscopy with subsequent percutaneous gastrostomy was performed. Necrotic masses disappeared from the esophageal walls. There were multiple bright red small granulations and overlays of dense light fibrin. The lumen of the esophagus was narrowed to 1.2 cm that corresponded to X-ray data. There was no peristalsis of the esophagus in the damaged area (Fig. 3).

Fig. 3. Endoscopic image of the esophagus in 8 days after chemical burn.

1 — narrowing of the esophagus, small granulations (single arrows), fibrin overlay (double arrow).

Endoscopic percutaneous gastrostomy was performed in the middle third of the stomach along anterior wall as close as possible to the lesser curvature.

In 15 days after chemical burn (the 11^th day after admission), the patient underwent contrast-enhanced X-ray examination of the esophagus with barium sulfate. The esophagus was patent, and swallowing was not disturbed. The upper third of the thoracic esophagus along thoracic vertebrae I-VII was circularly narrowed (maximum internal diameter 0.7 cm). Distal diameter of the esophagus was 2.5 cm. There was a large amount of mucus in the esophagus. We also visualized periodic spasm of the esophageal walls at the level of stenosis. Contours of the esophagus were clear. The narrowed segment was characterized by reduced elasticity of the esophageal walls (Fig. 4).

Fig. 4. X-ray examination of the esophagus in 15 days after chemical burn.

Narrowing of the esophagus (single arrow), intact lumen of the esophagus (double arrow).

The patient required infusion, anti-ulcerative, antisecretory and symptomatic therapy. She was discharged in 16 days after chemical burn (the 12^th day after admission). Impaired passage of mushy food was observed in 3 weeks after chemical burn, liquid — after 4 weeks. Thus, decompensated stricture with complete obstruction of the esophagus developed. Enteral nutrition was continued through a preventive gastrostomy.

After 14 months, the patient admitted to the Sklifosovsky Research Institute for Emergency Care for reconstruction of the esophagus.

Serum total protein 73 g/l and albumin 38 g/l indicated effective enteral nutrition through gastrostomy. Preoperative examination included chest and abdominal CT, contrast-enhanced X-ray examination of the esophagus and esophagoscopy.

CT revealed narrowing of the esophagus at the level of Th_I-II and Th_VII-VIII, as well as thickened walls up to 5-7 mm. The esophagus was enlarged up to 17×20 mm above stenosis. There was a heterogeneous content with contrast agent in this esophageal segment (Fig. 5A).

X-ray examination of the esophagus revealed not disturbed but difficult swallowing. The esophagus was narrowed up to 0.5 cm at the level of Th_I-II throughout 1.3 cm with suprastenotic enlargement up to 2.8 cm and up to 0.1-0.2 cm at the level of Th_VII-VIII throughout 4.2 cm with suprastenotic enlargement up to 2.3 cm. There was contrast agent retention above the narrowing (Fig. 5B).

Fig. 5. Cicatricial narrowing of the esophagus (preoperative examinations).

a — contrast-enhanced chest CT: cicatricial narrowing of the upper thoracic (1) and middle thoracic (2) esophagus; b — contrast-enhanced X-ray examination of the esophagus: cicatricial narrowing of the cervical (1) and mid-thoracic (2) esophagus, 1 — endoscopic image photo of cicatricial stenosis of the cervical esophagus, 2 — middle thoracic esophagus, narrowing is indicated by the arrow.

Endoscopic examination

The first circular cicatricial narrowing of the esophagus up to 0.6 cm and length of 1.0 cm was visualized at a distance of 2 cm from the mouth of the esophagus (cicatricial constriction with recess, Fig. 5, 1). A 4.9-mm endoscope was passed behind the first constriction. At a distance of 20-29 cm, esophageal lumen was somewhat dilated with multiple circular and longitudinal scars. Mucous membrane was whitish at this level. There was the second circular narrowing of the esophagus up to 0.2 cm at a distance of 29 cm impassable for endoscope (Fig. 5, 2).

Thus, the patient was diagnosed with decompensated cicatricial post-burn two-level narrowing of the upper and middle thoracic esophagus. Elective reconstruction was scheduled. In 441 days after acute poisoning with a corrosive substance, the patient underwent esophagectomy with gastric conduit reconstruction and end-to-end anastomosis. The resected esophagus is shown in Fig. 6.

Fig. 6. Resected esophagus (postoperative image).

Proximal (1) and distal (2) edge of cicatricial narrowing of the cervical esophagus, proximal (3) and distal (4) edge of cicatricial narrowing of the middle thoracic esophagus.

There were no postoperative complications. Contrast-enhanced X-ray examination of the esophagus was performed after 12 postoperative days. Swallowing was not disturbed. Esophagus and gastric conduit were patent for liquid suspension of barium sulfate. Diameter of esophagogastrostomy was at least 1 cm. No contrast agent leakage beyond the esophagus was detected. Passage through the graft was normal (Fig. 7).

Fig. 7. X-ray examination of the esophagus after reconstructive surgery.

1 — enlarged esophagus proximal to resection line; 2 — end-to-end esophagogastrostomy; 3 — esophagus de novo from the greater curvature of the stomach.

The patient was discharged in 15 days after reconstructive surgery.

Discussion

Endoscopic examination is essential in diagnosis of esophageal chemical burns [13]. The concept of endoscopic diagnosis of esophageal chemical burns includes analysis of general signs of chemical burn, as well as depth of damage to the esophageal wall. Identification of general signs of burns is not difficult (hyperemia, mucosal edema, fibrinous-necrotic films and ulcerations). It is difficult to clarify the depth of lesion due to the absence of direct endoscopic signs of damage to the muscle layer [14]. According to some data, EUS with mini-transducer 12/20 MHz is used to assess the depth of lesion [12, 14]. Surinder S. Rana et al. [15] found more accurate data of EUS on depth of damage to the esophageal wall compared to endoscopy. In several studies, the authors analyzed the role of EUS in chemical burns of esophagus and concluded that EUS-confirmed damage to the muscle layer is a significant sign of stricture [7, 16].

Yoshito Kamijo analyzed diagnostic efficacy of EUS in chemical burns of the esophagus. The authors observed stenosis in patients with damage to circular layer and total damage to 2 muscle layers of the esophageal wall [17]. In our case, EUS revealed that muscle layer of the esophageal wall was not differentiated over a large extent and wall layering was disturbed. The entire wall of the esophagus had a heterogeneous hyperechoic structure, and muscle layers were not clearly visualized. EUS indicated high risk of esophageal stenosis that was confirmed by contrast-enhanced X-ray examination of the esophagus with barium suspension in 7 days after chemical burn.

Indirect endoscopic sign of damage to the muscular layer may be wall rigidity during insufflation, as well as absence of peristaltic waves [18]. Yuichi Okata believe that stricture following chemical burn is due to impaired innervation of the esophageal wall and disturbed relaxation of damaged esophageal segment [19]. Periodic spasm in the middle and lower thirds of the esophagus in 7 days after burn indicated impairment of peristalsis. Many authors believe that preventive gastrostomy is necessary in patients with dysphagia and intoxication in acute period of injury indicating deep lesion of the esophagus and extended stenosis [18].

In our case, total circular damage to the muscular layer confirmed by EUS and contrast-enhanced X-ray examination predicted further course of disease and need for preventive percutaneous gastrostomy before severe esophageal stenosis. This made it possible to provide enteral nutrition under decompensated cicatricial stenosis, avoid open surgery and significantly reduce cicatricial lesions of the stomach wall. We placed the gastrostomy along the anterior wall of the lower third of the stomach as close as possible to the lesser curvature. This arrangement of gastrostomy tube allowed us to avoid cicatricial changes in the greater curvature and form gastric conduit for subsequent reconstruction.

Conclusion

This case demonstrates high efficiency and expediency of EUS to predict cicatricial stenosis of the esophagus after oral intake of corrosive substances. This allows timely prediction of course of disease and preventive gastrostomy if necessary. Minimally invasive procedure is valuable to support nutritional status and prepare the patient for reconstructive surgery.

The authors declare no conflicts of interest.