Author: Ildar Indusovich Khairullin Head of the Surgery Department, City Hospital #2, Candidate of Medical Sciences, Naberezhnye Chelny Introduction Gastric phlegmon (phlegmonous gastritis) is a purulent inflammation of the gastric wall with predominant damage to the submucosal layer. The first mention of gastric phlegmon was found in the works of Galen and dates back to 160 AD. The first description of this disease dates back to 1590 (Piso) (7). In Russia, gastric phlegmon was described in 1841 by N. M. Svarnitsky, and the term "gastric phlegmon" was introduced by P. Konovalov in 1888 (3). Most foreign authors believe that Cruveilhier J. in 1862 first reported on this disease in his work Traite d`anatomie pathologique generale. The disease is rare and occurs in 0.003-0.03% of patients undergoing hospital treatment. At autopsy, its frequency reaches 0.03-0.8%. In 50% of cases, the disease is diagnosed at autopsy. (17). The disease has been described in patients of different ages: from 3 months to 67 years, mainly affecting people over 40 years of age. Some authors believe that the majority of them are men (2), others - women (20). Overall mortality reaches 19-92%, postoperative mortality is 18% (4, 20). Such high figures are associated with the difficulties in diagnosing this disease, which does not have a specific clinical picture. Classification The most convenient classification of gastric phlegmon was proposed by Minkov S.I. (1972): 1. Primary phlegmon of the stomach: - Acute - limited, total; - Subacute; - Chronic. 2. Secondary phlegmon of the stomach: - Acute; — Subacute; — Chronic. In this review, we will focus on acute gastric phlegmon, a disease whose diagnosis is extremely difficult, mortality is high, and treatment tactics have not yet been determined. Subacute and chronic forms of gastric phlegmon have a more benign course and are often incidental findings during routine treatment of patients. Etiology and predisposing factors: In 45-75% of cases, the etiologic cause of gastric phlegmon is alpha-hemolytic streptococcus. Other microbial agents include staphylococcus, Escherichia coli, pneumococcus, Proteus, and Clostridia. Sometimes, the causative agent cannot be identified (1, 13, 15). Predisposing factors for the development of gastric phlegmon are: hypoacid state of the stomach, chronic gastritis, ulcer or stomach cancer, pancreatitis, recent upper respiratory tract infections, diabetes mellitus, chronic alcoholism, low social status, states of immunosuppression and immunodeficiency, T-cell leukemia, systemic amyloidosis (20, 25). A case of gastric phlegmon during pregnancy is described (11). Direct causes that cause the development of primary gastric phlegmon include gastric surgery, endoscopic interventions (polypectomy, biopsy), damage to the mucosa by sharp foreign bodies (needles, fish bones) (3, 18). Clinical presentation The clinical picture is nonspecific. It includes three syndromes: pain syndrome, dyspeptic syndrome, and intoxication syndrome. Patients complain of severe pain in the epigastrium, constant in nature, increasing dynamically. The pain may radiate to the back, right shoulder blade, and behind the sternum. The intensity of the pain is not reduced by taking analgesics. A characteristic symptom is Deninger's: increased abdominal pain when the patient is in a horizontal position and decreased in a vertical position (2). With the addition of peritonitis, the pain spreads throughout the abdomen. At the beginning of the process, patients note belching, nausea, salivation, and an unpleasant odor from the mouth. Then comes repeated, painful, excruciating vomiting, which does not bring relief. In advanced cases, the vomit contains pus and blood (21). Sometimes diarrhea or constipation is observed, alternating with diarrhea. This disease is characterized by high temperature (up to 39-40C) and chills, which occur almost from the moment the pain begins. The appearance of patients is typical of patients with an intra-abdominal catastrophe: they are adynamic, have a suffering expression on their face, the tongue is dry, coated with a gray coating; breathing is shallow; There is a tendency to tachycardia and hypotension. In the early stages of the disease, the abdomen is not distended, symmetrical, there is tension in the epigastrium, and symptoms of peritoneal irritation are negative. With the addition of peritonitis and paresis, the abdomen is distended, and symptoms of peritoneal irritation are positive. Sometimes a noticeable bulge can be detected in the epigastric region. At the site of greatest pain, a doughy tumor can sometimes be palpated (1, 2, 13). Blood tests reveal leukocytosis, a left shift in the leukocyte formula. Protein, leukocytes, erythrocytes, and casts are detected in the urine. Pus can sometimes be detected in vomit or lavage water. The initial period of this disease is characterized by a discrepancy between the severity of the patient's general condition and objective data confirming pathological findings. Diagnostics In the diagnosis of gastric phlegmon, X-ray examination of the stomach, fibrogastroscopy, ultrasound examination of the abdominal cavity, and computed tomography are used. Gastric X-ray: the gastric wall, thickening as a result of phlegmonous inflammation, loses its elasticity, the inflammatory infiltrate of the submucosa protrudes like a tumor into the lumen of the organ, forming a narrowing and filling defect. It is also important to consider the discrepancy between the clinical data (sudden onset, acute pain, high temperature) and the presence of filling defects, peristaltic disorders, which quickly regress under the influence of conservative therapy (6). FGDS reveals a loose, edematous, hyperemic mucosa. In some cases, the endoscopic picture is consistent with an ulcerative-necrotic process (12). A mucosal biopsy allows us to verify the diagnosis (22). Ultrasound reveals a circular thickening of the gastric wall up to 2.5 cm with a narrowing of its lumen (18, 23, 24). Computed tomography reveals local or diffuse thickening and layering of the stomach walls, sometimes with air bubbles. Crus et al. (1992) describe a low-density area of ??the gastric wall in patients with gastric phlegmon complicated by intramural abscesses. Other authors believe that low-density areas are edematous thickened submucosal layer (16). The lumen of the stomach is narrowed. The information content of the method increases with additional oral and intravenous contrast (13). Treatment. There is no generally accepted treatment tactics for patients with gastric phlegmon. When choosing a treatment method, the localization of the process, its prevalence, stage of the disease, its complications, as well as the patient's age and the presence of concomitant diseases are taken into account. Fundamentally, three approaches to the treatment of this disease can be distinguished: conservative; laparotomy with various options for omentogastropexy; Gastric resection, including gastrectomy Conservative treatment of gastric phlegmon includes antibiotics, gastric decompression, and detoxification, and is indicated in the initial stage of the disease without clinical signs of peritonitis, in patients with severe concomitant diseases (13, 19). Laparotomy with various versions of omentogastropexy, according to a number of authors, is indicated for the diffuse form of the disease and severe condition of the patient, especially with severe peritonitis. In addition, the walls and ligaments of the stomach are infiltrated with antibiotics, and the abdominal cavity is drained. Intensive therapy for peritonitis is administered in the postoperative period (2, 10). There are reports of successful gastrectomy performed in patients with diffuse gastric phlegmon (8, 22). Gastric resection is indicated for limited gastric phlegmon. Gastric resection within the unaffected tissues provides a good outcome if the operation was performed in the absence of peritonitis (3, 9). Complications. Gastric phlegmon is complicated by peritonitis resulting from purulent impregnation of the stomach wall and (or) perforation, acute gastric dilatation, gastric bleeding, gastric gangrene, abscesses of the liver, pancreas and spleen, pylephlebitis. (3, 26). Sakhri J, Youssef S. et al. (1999) report two successful gastrectomies performed for gastric phlegmon complicated by profuse gastric bleeding. Prognosis. The prognosis depends on the severity of the inflammatory process and the correct choice of treatment tactics. Without treatment or if patients seek medical help late, most of them die. Our observation. We have an observation of successful treatment of a patient with gastric phlegmon that developed after endoscopic polypectomy. For the purpose of early diagnosis, diagnostic laparoscopy was used, which significantly reduced the diagnostic stage. We did not find any mentions of using this method in diagnosing gastric phlegmon in the literature available to us. Patient S., born in 1956, was admitted to the surgical department of Naberezhnye Chelny City Hospital #2 on November 4, 2000, at 11:50 a.m., complaining of epigastric pain, weakness, and nausea. History: on November 2, 2000, while in the gastroenterology department, an endoscopic polypectomy was performed for a gastric antral polyp. She was discharged on November 3 in a satisfactory condition. Concomitant diseases: in 1984 she underwent surgery for kidney and ureteral stones on the right. On November 3, in the evening, epigastric pain, high temperature (39.5C), and then vomiting appeared. At the time of examination: general condition is severe. Skin and mucous membranes are of physiological color. Heart sounds are clear, pulse is 68 beats per minute, blood pressure is 120/80 mmHg. The tongue is dry, coated with a white coating. The abdomen is symmetrical, participates in the act of breathing, upon palpation there is moderate tension and tenderness in the epigastrium, where there is a weakly positive Shchetkin-Blumberg symptom. The patient was hospitalized with a diagnosis of gastric phlegmon. Due to the impossibility of excluding iatrogenic gastric perforation, a decision was made to carry out a series of diagnostic measures. Complete blood count: ESR 41 mm / h, leukocytosis-18.5, Gb-111 g / l, EC-3.65. Leukocyte formula: metamyelocytes-2, band neutrophils-24, segmented neutrophils-68, monocytes-1, lymphocytes-5, anisochromia, toxic granularity. General urine analysis: proteinuria 0.198%0, leukocyturia up to 20 in clusters. During plain radiography of the abdominal cavity, there is no data on the presence of free gas in the abdominal cavity. Ultrasound of the abdominal organs: No free fluid is detected in sloping parts of the abdominal cavity. The stomach is partially filled with fluid, there is sediment. The liver - the structure is homogeneous, the echogenicity is increased. The vascular pattern is preserved. Gallbladder - the walls are compacted, the contents are homogeneous. The pancreas is poorly visualized. Fibrogastroduodenoscopy: The esophagus is normal. There is mucus in the stomach, tortuous folds. The mucosa is pale. The folds are of normal caliber. On the lesser curvature, starting from the angle of the stomach and to the pylorus, there is a mucosal defect, approximately 2.5 by 3.5 cm in size, covered with necrotic tissue. There is no obvious defect in the stomach wall, air remains in the stomach. The duodenum is expanded. Pneumogastrography revealed no evidence of free gas in the abdominal cavity. The clinical picture was characterized by a rapid increase in peritonitis symptoms, despite objectively confirmed evidence of the absence of free fluid and gas in the abdominal cavity. Therefore, after short-term preoperative therapy, with a diagnosis of "Peritonitis. Gastric phlegmon?", the patient was offered diagnostic laparoscopy, having previously discussed the possibility of expanding the scope of the surgical intervention. Consent was obtained. Diagnostic laparoscopy: a 10 mm trocar was typically inserted in the periumbilical region. Laparoscopy revealed no fluid or pathological impurities in the abdominal cavity. An increase in size, edema, and hyperemia of the antrum are noted. The pyloroduodenal junction has a "step" appearance. Instrumental palpation reveals a doughy consistency of the gastric wall. The areas of the greater and lesser omentum adjacent to the antrum of the stomach are edematous and infiltrated. This laparoscopic picture is considered pathognomonic for antral phlegmon. Given the localization of the lesion and the absence of peritonitis, a decision was made to perform resection of the affected area. A B-1 gastric resection was performed with the formation of an intussusceptional precision gastroduodenal anastomosis. The surgery was completed with nasointestinal intubation with a double-lumen active probe and "fascine" (insertion of two drains through a single puncture) drainage with active double-lumen drains. Gross specimen: a 12-cm-long section of the stomach. Mucosal folds are smoothed. The wall is up to 3 cm thick, edematous, and of a gelatinous consistency. Purulent infiltration of the submucosa; purulent fluid is released from the incision surface when pressure is applied. Superficial mucosal defect 1.5 by 1.2 cm. Microscopy: Gastric walls - severe edema of all layers, vascular paresis, lymphostasis, anemia. Diffuse lymphohisteocytic and plasmatic infiltrates of all layers. Focal necrosis. Areas of necrobiosis, red thrombi in some vessels. Bacteriological examination revealed: Hafhiae alvei. Postoperative diagnosis: Phlegmon of the antrum of the stomach, condition after endoscopic polypectomy, atrophic gastritis. 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