Experimental substantiation of esophage stitches inefficiency with Boerhaave syndrome

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1 Research Article Experimental substantiation of esophage stitches inefficiency with Boerhaave syndrome Svetlana G. Gorelik 1 *, Md All Rayhan 2, Vladimir D. Lutsenko 1, Victor V. Bulynin 2, Yuri A. Parkhisenko 2 ABSTRACT Aim: The modeling of Boerhaave syndrome among experimental animals (rats), the study of an esophageal wall state at various times after its rupture and the reasons for the failure of the esophagus stitches, which can form the basis for the development of surgical treatment new methods among the patients with Boerhaave syndrome. Materials and Methods: The experiment was carried out using 3-month-old male rats with the weight of g. The study was conducted in two stages: The first stage (experimental) - the modeling of Boerhaave syndrome, the second stage is the study of the esophageal wall pathology at various times after its rupture and the strength of the stitches applied to the esophagus. Original devices were developed for the experiment; the device for the modeling of Boerhaave syndrome and the device for esophagus stitch strength determination. Study Results: The data obtained by us showed that after the wall esophagus rupture and in the esophagus surrounding organs, the inflammatory phenomena increases synchronously and progressively with the increase of the time interval that has passed since the moment of rupture. In parallel with the increase of changes in the chest organs, bacterial contamination of the mediastinum and pleural cavities increases, this explains esophagus, lungs, and trachea inflammatory response and destruction. Conclusion: In our opinion, the increase of infiltration and destructive changes in an esophageal wall, pleura, and adjacent organs is the main reason for the frequent failure of joints among experimental animals, which allows to suggest that the patients with the Boerhaave syndrome have the same reasons for the failure of stitches. KEY WORDS: Boerhaave syndrome, Experiment, Modeling, Surgery INTRODUCTION Boerhaave syndrome is the disease at which a spontaneous rupture of all layers of the esophagus wall takes place. The first description of this condition was given by Dutch physician Hermann Boerhaave in [1,2] The diagnosis of this syndrome was first made by V. Myers in [3,4] Spontaneous esophageal rupture is a rare disease, accounting for 2 3% of all cases of esophageal injury, and it is more likely to occur among men over 50. An immediate cause of a rupture is a sudden increase of pressure inside an esophagus with a closed pharyngeal esophageal sphincter in combination with negative intrathoracic pressure, which occurs at intense vomiting after a heavy meal, liquid, alcohol, the vomiting of the central genesis Access this article online Website: jprsolutions.info ISSN: (due to the vomiting center disruption), an increased intragastric, and intraepithelial pressure due to weight lifting. As a rule, large defects of an esophageal wall (from 4 5 to cm) occur with this disease. Most often (in 90%), the ruptures are localized in the lower third of the esophagus. Despite the advances in esophageal surgery, a high percentage of stitch insufficiency applied during the spontaneous rupture of the esophagus takes place, which ranges from 30% to 90%. [4-8] The methods of surgical treatment do not have an unambiguous approach and solution. This circumstance was the basis for our scientific and practical research in this direction. Purpose The modeling of Boerhaave syndrome among experimental animals (rats), the study of an esophageal wall state at various times after its rupture and the reasons for the failure of the esophagus stitches, which can form the basis for the development of surgical 1 Department of General Surgery with Course of Topographic Anatomy and Operative Surgery, Belgorod National Research University, Belgorod, Russia, 2 Department of Hospital Surgery, Voronezh State Medical University Named by N. N. Burdenko, Voronezh, Russia *Corresponding author: Svetlana G. Gorelik, Belgorod National Research University, 85, Pobedy Street, Belgorod , Russia. gorelik@bsu.edu.ru Received on: ; Revised on: ; Accepted on:

2 Svetlana G. Gorelik, et al. treatment new methods among the patients with Boerhaave syndrome. MATERIALS AND METHODS 3-month-old male rats were used for the experiment, the weight of which was grams. The experiments were carried out in accordance with the European Convention on the protection of vertebrate animals rights used for experimental or other scientific purposes (ETS No. 123 issued on ). An original device for Boerhaave syndrome modeling was developed to perform an experiment [Figure 1]. [2,9,10] The catheter of an original design, shown on Figure 1, is a tube with the total length of 200 mm, the diameter of 1 mm, which has the marking with an interval of 10 mm. The distal end has the vessel made of natural high-quality latex, which communicates with the tube lumen. The vessel has a cylindrical shape, the length and the width of which make 20 mm, and the wall thickness makes 0.07 mm. The volume of the vessel makes 4.2 ml/cm 3. The catheter tube is connected to the syringe by the connector. An original device works as follows: The catheter is guided into an esophagus so that a vessel is located in the lower third of the esophagus, after which air is injected into the catheter by a syringe with a volume of about 4 5 ml. When the air is pumped up to this volume, the esophagus ruptures accompanied by a specific sound resembling a vessel explosion. Further, an autopsy of the animal chest was performed to ascertain the rupture of the esophagus [Figure 2]. The second stage of the study was the following one. After the modeling of the Boerhaave syndrome, the ruptured esophagus was sutured with nodular sutures with a gap of 2 mm and 1 mm indentation from the rupture edge with atraumatic sutures [Figure 3]. Determination of the stitch strength was carried out during 1, 2, and 3 days using the device of an original design [Figure 4]. [2,9,10] The measurement of the joint strength was carried out in the following way: The esophagus was removed from the deceased animal; the catheter of the device was used to determine the strength of the stitches [Figure 4] Figure 1: Boerhaave syndrome modeling device (1 - vessel, 2 - connection point of the tube with the vessel, 3 - marking, 4 - connection point of the tube to the connector, 5 - connector, 6 - tube) The study was conducted in two stages: The first stage (experimental) is the modeling of Boerhaave syndrome, the second stage is the study of the esophageal wall pathology at various times after its rupture and the strength of the stitches applied to the esophagus. The first stage of the study: The experiment was performed under inhalation anesthesia (isoflurane). When the animal was anesthetized, a distance from the larynx to the xiphoid process was used to calculate the depth of introduction of a special catheter of an original design into the esophagus for the esophagus rupture. Then, the catheter was introduced in the esophagus through the animal s mouth. The vessel was injected to the lower third of the esophagus (according to the catheter markers, 5 6 cm approximately). Then, the catheter was fixed by the clamp so that it would not migrate during a vessel inflation. Then, a medical syringe (10 ml) was connected to the catheter connector, and air was injected into it. The volume of the collected air made 4.2 ml on the average. Thus, a faint sound was heard resembling the sound of a burst ball. After that, the syringe cleaned the area from the collected air. Figure 2: Boerhaave syndrome modeling among rats (1 - esophageal rupture) Figure 3: Suture of the esophagus (1 - catheter, 2 - ligated proximal esophagus department, 3 - esophagus, 4 - sewn part of esophagus, 5 - ligature-stranded distal esophagus department) 1482

3 Svetlana G. Gorelik, et al. so that the vessel was on the esophagus at the level of the applied stitches. The distal and the proximal part of the esophagus were fixed to the catheter by means of ligatures. The syringe was pumped into the catheter, thereby inflating the vessel. During the rupture of the esophagus stitches, the pressure was fixed on the manometer. After the rupture of the esophagus stitches, the air was evacuated from the vessel with a syringe, and the device was removed from the esophagus, the material was taken for histological and bacteriological examination. The sowing from the pleural cavity was performed for bacterial study. Results of Histological Examination Histological examination of animals that died during the 1 st day [Figures 5-8]. Preparation: Ruptured esophagus [Figure 5]. Conclusion: The edemas, pronounced plethora, diffuse inflammatory infiltration of the esophagus muscles, infiltration of the esophagus outer wall, penetrates into the cellulose, some vessels are injured, and focal hemorrhages in a rupture zone the development of an abscess in the wall. RESULTS AND DISCUSSION The data on the mortality study of experimental animals after the modeling of the Boerhaave syndrome were presented in Table 1. The measurement of pressure by the manometer during the break of esophagus stitches showed the decrease of the esophagus stitch strength on the 3 rd day after the modeling of Boerhaave syndrome [Table 2]. The bacteriological study data from the pleural cavity of experimental animals showed bacterial contamination increase of the mediastinum and pleural cavities [Table 3]. Figure 4: The device which determines the strength of the esophagus stitches (1 - manometer, 2 - tee, 3 - vessel, 4 - distal catheter section, 5 - tube joint with the vessel, 6 - catheter, 7 - syringe) Table 1: Lethality of experimental animals (rats) after Boerhaave syndrome modeling Term Abs. (%) during the 1 st day Abs. (%) during the 2 nd day Abs. (%) during the 3 rd day Absolute amount (%) 54 rats (54%) 37 rats (37%) 9 rats (9%) Table 2: Measurement of pressure by manometer (mmhg) Pressure (mm Hg) 1 st day (mmhg) 2 nd day (mmhg) 3 rd day (mmhg) Average pressure Table 3: Bacteriogram from the pleural cavity of experimental animals died at different periods of the experiment Time Number of animals Pathogenes On the 1 st day 21 Proteus vulgaris 10*3 33 Proteus vulgaris 10*3 Enterococcus spp. 10*4 On the 2 nd day 10 Proteus vulgaris 10*3 Staphylococcus epidermidis 10*4 12 Proteus vulgaris 10*3 Enterococcus spp. 10*3 Staphylococcus epidermidis 10*5 15 Proteus vulgaris 10*4 Enterococcus spp. 10*5 Staphylococcus epidermidis 10*5 Escherichia coli 10*4 On the 3 rd day 3 Proteus vulgaris 10*4 Staphylococcus epidermidis 10*6 Enterococcus spp. 10*6 6 Proteus vulgaris 10*5 Staphylococcus epidermidis 10*5 Enterococcus spp. 10*8 Escherichia coli 10*8 1483

4 Svetlana G. Gorelik, et al. Preparation: Lungs [Figure 6]. Conclusion: Extensive hemorrhages, the areas of distelectases and emphysema with the rupture of interalveolar septa and the development of foci, bronchospasm, blood overflow in microcirculatory bed with distelectases and atelectasis, and shock lungs. Preparation: Trachea [Figure 7]. Conclusion: Inflammatory infiltrate penetrates into the trachea wall, breaks through the lumen of the trachea along the intercartilaginous spaces. Preparation: Mediastinum [Figure 8]. Conclusion: Diffuse inflammatory infiltration (decay of leukocytes). Histological examination of the animals that died during the 2nd day [Figures 9-12] Figure 5: The esophagus (increase 10, Hematoxylin and eosin Preparation: Ruptured esophagus [Figure 9]. Conclusion: Extensive hemorrhages, venous thrombosis, non-focal spot diffuse infiltration, edematous wall, a pronounced congestion, diffuse inflammatory infiltration of the esophagus muscles, infiltration of the esophagus outer wall, and penetrating into the cellulose. Some vessels are injured. Focal hemorrhages in the rupture zone the development of an abscess in the wall. Figure 6: The lungs (increase 10, Hematoxylin and eosin Figure 8: The mediastinum (increase 10, Hematoxylin and eosin Figure 7: The trachea (increase 5, Hematoxylin and eosin Figure 9: The esophagus (increase 5, Hematoxylin and eosin 1484

5 Svetlana G. Gorelik, et al. Figure 10: The lungs (increase 10, Hematoxylin and eosin Figure 12: The mediastinum (increase 10, Hematoxylin and eosin Figure 11: The trachea (increase 5, Hematoxylin and eosin Figure 13: The esophagus (increase 20, Hematoxylin and eosin Preparation: Lung [Figure 10]. Conclusion: Extensive hemorrhages persist, the areas of distelectases and emphysema with the rupture of interalveolar septa and the development of foci, bronchospasm, microcirculatory bed blood overflow with distelectases and atelectasis, and shock lungs. Preparation: Trachea [Figure 11]. Conclusion: The inflammatory infiltrate persists, penetrates into the trachea wall, and breaks through the lumen of the trachea along interchillage spaces. Preparation: Mediastinum [Figure 12]. Conclusion: Diffuse inflammatory infiltration persists (decay of leukocytes). Histological examination of animals that died during the 3rd day [Figures 13-16] Preparation: Ruptured esophagus [Figure 13]. Conclusion: The edemas retained, pronounced inflammatory infiltration, pronounced plethora, diffuse inflammatory infiltration of the esophagus muscles, Figure 14: The lungs (increase 20, Hematoxylin and eosin esophagus outer wall infiltration, and penetrating into the cellulose. Some vessels are injured, focal hemorrhages in the rupture zone the development of an abscess in the esophagus wall. 1485

6 Svetlana G. Gorelik, et al. in the surrounding organs of the esophagus increase synchronously. In parallel with the increase of changes in the chest organs, bacterial contamination of the mediastinum and pleural cavities increases, which explains the increase of the inflammatory response and the destruction of the esophagus, lungs, and trachea. Through the rupture, the edible masses enter the mediastinal fiber, which in its turn explains the titer increase of the microflora that causes the inflammatory response of the mediastinum and adjacent organs. CONCLUSIONS Figure 15: The trachea (increase 5, Hematoxylin and eosin Figure 16: The mediastinum (increase 10, Hematoxylin and eosin Preparation: Lung [Figure 14]. Conclusion: Bronchospasm persists; there are some white blood clots in some branches of the pulmonary vein, pronounced emphysema with intermalveolar septal ruptures, and interstitial pneumonia. Preparation: Trachea [Figure 15]. Conclusion: The inflammatory infiltrates penetrating into a trachea wall, breaking out in the lumen of a trachea along interchillage spaces persists. Preparation: Mediastinum [Figure 16]. Conclusion: Diffuse inflammatory infiltration persists (leukocyte decay). SUMMARY After the rupture of the esophagus, the inflammatory phenomena in esophagus wall increases progressively and synchronously with the increase in the time interval that has passed since the moment of rupture. Furthermore, the destructive phenomena 1. The bacterial colonization of the pleural cavity at rupture of the esophagus occurs from monoculture during the 1 st day, until the appearance of polyflora in the next 24 h with the titer of microorganism increase. 2. Inflammatory reaction and destruction in the mediastinum and surrounding organs progress with time, which is the cause of animal death. 3. The strength of the stitches applied on the esophagus rupture line decreases inversely with the time elapsed since the rupture. 4. In our opinion, the increase of infiltration and destructive changes in the esophagus wall, pleura, and adjacent organs is the main reason for the frequent failure of stitches among experimental animals, which allows to that the patients with Boerhaave syndrome have the same reasons for the failure of stitches. REFERENCES 1. Flynn AE, Verrier ED, Way LW, Thomas AN, Pellegrini CA. Esophageal perforation. Arch Surg 1989;124: Bulynin VV, Rayhan MD, Urgeles IV. Model of the boerhaave syndrome in the experiment. Bull Surg Gastroenterol 2016;3:8. 3. Kochakov VP. Spontaneous rupture of the esophagus (syndrome Boerhaave). Surgery 2012;7: Mason GR. Esophageal perforations, anastomotic leaks, and strictures: The role of prostheses. Am J Surg 2001;181: Angies BA, Hadzhibaev AM, Ligai RE. Povrezhdenie of the esophagus: Diagnosis and treatment. J Surg 2003;162: Rayhan MD, Bulynin VV, Zhdanov AI. Comparative Results Treatment of Spontaneous Esophageal Rupture. Saint-Petersburg: 7 th International Congress Current Trends of Modern Cardiothoracic Surgery; p Dosios T, Safioleas M, Xipolitas N. Surgical treatment of esophageal perforation. Hepatogastroenterology 2003;50: Landen S, El Nakadi I. Minimally invasive approach to boerhaave s syndrome: A pilot study of three cases. Surg Endosc 2002;16: Rayhan MD, Bulynin VV, Leibowitz, BE. Model of the boerhaave syndrome in the experiment. Youth innov Gaz 2017;5: Rayhan MD, Bulynin VV. Model of the Boerhaave syndrome in the experiment. Saint-Petersburg: 7 th International Congress Current trends of modern cardiothoracic surgery; p