[Trends in endovascular treatment and prevention of portal bleeding]. / Tendentsii v rentgenendovaskulyarnom lechenii i profilaktike portal'nykh krovotechenii (obzor literatury).

Bleeding from esophageal and gastric varices is a major factor of mortality in patients with portal hypertension. The gold standard for diagnosis of portal hypertension is hepatic venous pressure gradient determining the treatment algorithms and risk of recurrent bleeding. Combination of endoscopic methods and therapy is limited by varix localization and not always effective. In these cases, endovascular bypass and decoupling techniques are preferred. Early endovascular treatment of portal bleeding is effective for hemostasis and higher transplantation-free survival of patients. Early transjugular intrahepatic portosystemic bypass should be associated with 8-mm covered stents of controlled dilation. Combination of endovascular techniques reduces the complications of each technique and potentiates their positive effect. Endovascular treatment and prevention of portal bleeding should be determined by anatomical features of portal venous system.

[Influence of early surgery and endoscopic interventions on the risk of infection in patients with pancreatic necrosis]. / Vliyanie rannikh operativnykh i endoskopicheskikh vmeshatel'stv na risk infitsirovaniya u patsientov s pankreonekrozom.

OBJECTIVE: To prevent purulent-septic complications in patients with destructive pancreatitis. MATERIAL AND METHODS: A cohort study included 488 patients with pancreatic necrosis: group 1 (n=331) - active surgical strategy, group 2 (n=157) - follow-up and therapy. We used binary logistic regression to predict purulent-septic complications. RESULTS: Original model of independent variables significantly (p<0.001) revealed 5.3 times higher risk of infectious complications after laparotomy within the first week after hospitalization. Incidence of these events increased by 2.8 times in patients biliary pancreatitis compared to alcohol-alimentary pancreatitis. Complication rate was higher in older patients (by 2.1% for each year). Risk of purulent-septic complications decreased by 57.4% in women compared to men. There was no significant correlation between risk of infectious complications and endoscopic procedures. Specificity and sensitivity of the model was 74.2 and 72.6%, respectively. CONCLUSION: Original model significantly predicts the risk of purulent-septic complications within the first week after hospitalization. Refusal of early active surgical strategy in these patients will significantly reduce the likelihood of purulent-septic complications.

[Prediction and diagnosis of pancreatogenic encephalopathy in patients with destructive pancreatitis]. / Diagnostika i prognozirovanie pankreatogennoi entsefalopatii u bol'nykh destruktivnym pankreatitom (obzor literatury).

OBJECTIVE: To study the literature data on pancreatogenic encephalopathy in patients with destructive pancreatitis. MATERIAL AND METHODS: Searching for Russian- and English-language literature data was carried out in electronic databases: elibrary, PubMed, the Cochrane Library. We planned a systematic review if studies with evidence level 1 and 2 were available. If these trials were absent, descriptive review was considered. RESULTS: No studies with evidence level 1 and 2 were found in available literature. Therefore, a descriptive review was carried out. Analysis of primary sources showed that the incidence of pancreatogenic encephalopathy is 9-35% and has no direct correlation with etiology of destructive pancreatitis. Major factors of pathogenesis are high serum enzymes, activation of proinflammatory cytokines and hypoxemia, which are accompanied by damage to myelin sheath of the white matter and cytotoxic brain edema. Clinical manifestation of pancreatogenic encephalopathy occurs within two weeks. Acute onset and various symptoms are typical. Possible laboratory predictors of encephalopathy are persistent hyperglycemia, increased hematocrit, fibrinogen-like protein 2 (FPB-2), proinflammatory cytokines TNF-αand interleukin-1-beta. Pancreatogenic encephalopathy is a factor of unfavorable prognosis of treatment. Mortality in patients with pancreatogenic encephalopathy is 57-70%. Favorable course of pancreatic necrosis is followed by regression of cerebral disorders in most cases while residual cognitive disorders are possible in elderly patients. CONCLUSION: Pancreatogenic encephalopathy accompanies severe destructive pancreatitis. It is an unfavorable factor for treatment outcomes requiring further research.