Chronic pancreatitis: about some complications and features of their pathogenesis and course

The review article provides up-to-date information on the complications of pancreatitis that are important for the tactics and strategy of patient management both at the inpatient and outpatient stages of observation. The purpose of the review was to emphasize the importance of complications for the course and life of patients with chronic pancreatitis. The authors draw the attention of internists to the course of such complications as pseudocysts, cysts, fistulas, thrombohemorrhagic, cholestatic syndromes, compression syndrome of adjacent organs, pancreatic encephalopathy (acute and chronic). The symptomatology of complications of chronic pancreatitis is discussed in detail, which is very important for differential diagnosis with the corresponding diseases. Such complications include the formation of erosive and ulcerative lesions, varicose veins of the esophagus and bleeding from varicose veins of the esophagus and stomach, portal hypertension syndrome with pancreatic ascites and chronic pancreatic encephalopathy, idio­pathic non-cirrhotic portal hypertension, pancreatic cancer. The authors emphasize the need to analyze the corresponding symptoms, indicating the possibility of complications, negative consequences with each recurrence or exacerbation of chronic pancreatitis, since it concerns the prognosis and life of the patient.

Clinical and pathogenetic aspects of acute pancreatic encephalopathy

Pancreatic encephalopathy is a formidable complication of acute pancreatitis, significantly aggravating the course and increasing the mortality rate in this disease. For pancreatic encephalopathy, an acute onset and fluctuating course with subsequent cyclic progression are typical, and the severity of neurological symptoms may be directly dependent on the activity of the pancreatic process. The risk of having residual symptoms, primarily in the form of cognitive impairment, increases with repeated episodes of acute pancreatic encephalopathy. In the pathogenesis of pancreatic encephalopathy, an important role is played by a combination of enzymatic and hormonal dysfunction of the pancreas, systemic microcirculation disorders due to hypovolemia, typical for acute pancreatitis, and changes in glucose metabolism associated with the effects of secondary hepatocellular insufficiency and pancreonecrosis. Microscopically, gross changes in the vascular link are revealed in the form of plasmorrhages and diapedesic hemorrhages in the Virchow-Robin spaces and the white matter of the brain, desquamation and dystrophy of endothelial cells, swelling of the adventitia membrane, sludge of blood corpuscles, plasma impregnation and segmental necrosis of the vascular wall with predominant involvement and small caliber. The presence of pancreatic encephalopathy should be suspected if neurological symptoms are detected in patients with symptoms of acute pancreatitis, such as psychomotor agitation, visual and auditory hallucinations, delirium, followed by episodes of deafness, adynamia, drowsiness, up to a state of catatonia and coma. In most cases, psychomotor agitation is combined with manifestations of the syndrome of irritation of the meninges. Focal neurological symptoms, myoclonia, hyperkinesis may be associated with mental and general cerebral symptoms. Mortality in acute pancreatic encephalopathy is due to shock, hemorrhagic complications, ketoacidosis, fatty embolism of cerebral vessels or renal failure (bibliography: 35 refs)

Acute pancreatitis complicated by encephalopathy

Pancreatic encephalopathy is a frequently under-diagnosed and rare complication of acute pancreatitis. It denotes the occurrence of neuropsychiatric abnormalities in the setting of acute pancreatic inflammation, and presents with neurological symptoms that may persist even after the resolution of all metabolic parameters. Here we present the case of a 42 year old male patient presenting with altered sensorium and focal neurological deficit during the course of acute pancreatitis. The patient was treated conservatively, and later improved with supportive care.

Pancreatic encephalopathy: clinical, pathogenetic and diagnostic aspects

Pancreatic encephalopathy occurs in 9–35% of patients with pancreatic diseases and is characterized by a variety of focal neurological symptoms. Neuropsychiatric disorders are observed both during the acute and latent period of the pancreatic diseases. The presence of pancreatic encephalopathy should be suspected if patients with symptoms of acute pancreatitis have neurological symptoms. The course of acute pancreatic encephalopathy is cyclical, fluctuating, being in direct proportion to the pancreatic process. Leading mechanism in the development of pancreatic encephalopathy is a combination of hyperenzymemia with insulin imbalance which leads to changes of water-electrolyte balance and carbohydrate metabolism. Infectious complications, that often accompany acute pancreatitis, lead to the increasing intoxication syndrome.

The clinical diagnostic aspects of acute pancreatic encephalopathy

The pancreatic encephalopathy is characterized by various focal neurological symptomatic and sporadic fast development of dementia is considered as a rare complication of acute pancreatitis developing in 9-35% of patients with diseases of pancreas. Factually every patient with acute pancreatitis has a risk of development of pancreatic encephalopathy that significantly makes severer course of disease and increases lethality. The review article considers particular aspects of clinical manifestations and probable diagnostic algorithm of neurological disorders observed in patients with acute pancreatitis. The actuality of development of diagnostic algorithm of pancreatic encephalopathy is emphasized. This algorithm will permit ultimately early, probably at pre-clinical stage, discover the mentioned complication of acute pancreatitis with the purpose of not only ultimate early detection of pancreatic encephalopathy but also development of pathogenically conditioned therapeutic algorithm considering all chains of pathogenesis.