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The authors consider ectopic biliary varices as a possible cause of portal biliopathy in extrahepatic portal hypertension. The main diagnostic methods including ultrasound CT, MRI, endoscopic ultrasonography, cholangioscopy, difficulties of differential diagnosis and clinical manifestations of portal biliopathy are presented. Various treatment options including portosystemic shunting and endoscopic biliary decompression are discussed. The authors emphasize the role of differentiated treatment depending on bile duct lesions. The study not only reviews this problem, but also highlights the issues requiring further analysis for selection of optimal diagnostic and treatment methods.

Bleeding from ectopic varicose veins is a rare life-threatening cause of upper gastrointestinal hemorrhage. Alberti first described duodenal varices in 1931. According to the literature, incidence of duodenal varicose veins in patients with portal hypertension is 1-3% of all varicose veins. Bleeding from duodenal varices makes up 17% of all bleedings from other ectopic varices. Mortality in these patients may be up to 40%. The causes are delayed diagnosis, technical difficulties in endoscopic therapeutic procedures (sclerotherapy, endoscopic ligation), as well as ineffective Blackmore tube for hemorrhage in distal stomach and bowel. We report a rare case of upper gastrointestinal bleeding from ectopic duodenal varices.

Blakemore probe-obturator was previously preferable for primary hemostasis in patients with bleeding from esophageal varices. Currently, Danis self-expanding nitinol stent became an effective alternative. According to some manufacturers, Danis stent has some advantages over balloon tamponade. We report implantation of nitinol stent for hemostasis in a patient with multiple recurrent bleeding and ineffective endoscopic manipulations. A method of stent fixation for prevention of distal migration as the most common complication is described.

In spite of a great number of publications, as yet there is no agreement that which of the detected morphological changes should be considered pathognomonic in portal hypertensive gastropathy (PHG). The study of the pathogenesis of PHG suggested a diversity of mechanisms involved in varying degrees in the development of this abnormality. The paper summarizes the data available in the literature on the role of endothelial dysfunction, apoptosis, damaging factors, and H. pylori infection in the development of this abnormality. A differential diagnosis was made between PHG and GAVE syndrome and histological features in both groups were revealed.

The article highlights modern approaches to the treatment of portal hypertension. The differential tactics is based on the type of portal hypertension, functional liver state, urgency of the situation and severity of blood loss, localization and stage of varices, concomitant diseases, etc. The role of miniinvasive methods is stressed. The reasonability of general treatment algorithm of portal hypertention in specialized centers is proved.

The direct transcutaneous transhepatic portography was performed in 85 patients with hystologically confirmed liver cirrhosis, portal hypertension and varices of the esophagus and stomach. It was found out, that the left gastric vein partakes the varicous transformation in 100% of cases. The least had an isolated division in 27% of the studied patients. 68% had the significant dilatation of the posterior gastric vein, whereas 19 (22%) patients had the combined posterior, left and short gastric veins dilatation. The study allowed the modification of the M.D. Patsiora's operation (the azygo-portal disintegration), by supplementing it with the gastric devascularization. The new method increased the 2-years survival from 77 to 97%, improved the hemostatic effect from 51 to 89% and decrease the recurrences from 25 to 5%.

Portal hypertensive gastropathy (PHG) is a complex of secondary macroscopic and microscopic changes in the mucous layer of the stomach, resulting from portal hypertension of any origin. The overall prevalence of PHG ranges from 9.1 to 80%. PHG is a potential cause of an acute or chronic gastric bleeding. The presence of PHG is associated with prognosis deterioration that dictates the need for improved diagnosis and treatment strategy. The article summarizes literature on the pathological changes, diagnosis and classification of portal hypertensive gastropathy.

Research Objective: studying the features of the collateral venous blood flow and the basic ways of the formation of gastroesophageal varices in patients with cirrhosis and portal hypertension., Methods: The following analysis is based on the interpretation of results from percutaneous transhepatic splenoportography in 85 patients. It has been established that in all 85 patients the left gastric vein plays a key role in the formation of gastroesophageal varices., Results: It is established that a leading collector in 100% of observations participating in formation gastroesophageal varices, is the left gastric vein. In work the attention is focused on an insufficient estimation of a role of a back gastric vein in a pathogenesis of varicose transformation. From 85 observations its presence is taped in 58 (68%) cases, and, at 19 (22%) patients its expansion isn'ted in a combination to expansion left gastric vein, and at 39 (46%) patients - in a combination with left gastric vein and short veins of a stomach., Conclusion: The obtained data on the formation mechanism of varicose expanded veins of an esophagus and a stomach defines necessity of changes for algorithm of inspection of patients for the purpose of diagnostics of features of a venous blood flow of a stomach and an esophagus and definition of surgical tactics concerning volume pre- or intraoperational blockade of the basic venous collectors.

Aneurysms of a chest department of an aorta with esophageal perforation two cases are presented and a lethal outcome. Difficulties in diagnostics have been caused by rare occurrence of the given pathology, insufficient experience of clinical physicians, and also absence during supervision of characteristic attributes Aortoesophageal Fistula.

Clinical supervision of successful conservative treatment of the patient with a huge stomach ulcer with use in the course of performance endoscopic a metabolic homeostasis of solutions of glucose and ascorbic acid of 5%, and also pH-chromoscopy and capillary gastrointestinal a tube is presented.

Clinical supervision diffuse large B-cell lymphoma of the stomach at the patient of young age is presented. Difficulties of the differential diagnostics of lymphom have been caused by macroscopical polyphormism. With the purpose of verification of disease are used the chromoendoscopy and immunohistochemical research.

A new direction with the use of endoscopic hemostasis (EH) was offered in the complex program of metabolic rehabilitation of patients with ulcerous gastroduodenal bleedings (UGDB) and hemorrhagic shock (HS). There was a study of the results of treatment of 44 patients (29 men and 15 women at the age from 61 to 77) with severe concurrent diseases and UGDB complicated with HS. Recurrences of UGDB in case of HS are a factor of high operative-anesthetic risk. Endoscopic preventive metabolic hemostasis is a prospective direction in rehabilitation of patients with UGDB complicated with HS. It is necessary to improve the EH methods for treatment of continued arterial bleedings from giant gastroduodenal ulcers.

The trial of a gastrointestinal tube in gastroduodenal ulcer indicates its high efficiency for enteral tube feeding in serious ulcer cases and as a therapeutic modality in noncomplicated cases. The tube introduction in 55 patients out of 89 promoted the defect healing within 2-3 weeks, in 30 out of 36 cicatrization occurred on week 3-5. The presence of the tube produced no effect on acid production in the stomach, cicatrization of the ulcer took place without basic therapy in remaining hypo-achlorhydria and hyperchlorhydria. Clinico-endoscopic evidence and data on gastroduodenal motility and evacuation suggest the conclusion on the neuro-reflex mechanism of the tube action which eliminates painful syndrome and motor-evacuatory abnormalities which are believed essential in pathogenesis of peptic ulcer.