ABSTRACT
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.
