Introduction. Cerebral microangiopathy (CMA), being the leading cause of vascular cognitive impairment and strokes, has a number of causes, among which chronic kidney disease (CKD) and programmed hemodialysis (HD) are the least studied.Purpose of the study: to determine the frequency of CMA neuroimaging markers and risk factors for its development in patients receiving renal replacement therapy for a long time using the programmed HD.Material and methods: the study involved 70 patients who had been on programmed HD for 10 months or more. Clinical neurological examination, laboratory tests and brain MRI were performed. The analysis of CMA neuroimaging markers was carried out in accordance with the STRIVE recommendations. Cerebral Small Vessel Disease Score (CSVDS) was used to quantify the overall severity of MR imaging markers of CMA.Results. Among 70 examined (29 men and 41 women) aged 53.0 ± 14.2 years, average HD experience – 70.0 ± 39.5 months, the main clinical manifestations of CMA were cognitive impairment (82.9%, n = 58), emotional disorders (61.4%, n = 43), sleep disorders (38.6%, n = 27), pseudobulbar syndrome (17.1%, n = 12), walking disorders (8.6%, n = 6), acute lacunar syndromes (7.1%, n = 5) and pelvic dysfunction (4.3%, n = 3). CMA neuroimaging markers of varying severity were found in 100% of cases. Expansion of perivascular spaces (100%, n = 70) and white matter hyperintensities (81.4%, n = 57) prevailed in the structure of CMA imaging markers. Cortical atrophy (67%, n = 47), cerebral microbleeds (47%, n = 33), asymptomatic lacunae (35.7%, n = 25) and minor subcortical infarctions (2.9%, n = 3) were less common. Mild CMA (1–2 points on the CSVDS scale) was determined in 38 patients (54.3%), severe CMA (3–4 points on the CSVDS scale) – in 32 patients (45.7%). The presence of uncontrolled arterial hypertension (OR 1.85, p < 0.05), intradialysis hypertension (OR 2.8, p < 0.05), dialysis vegetative polyneuropathies (OR 2.75, p < 0.05), type 2 diabetes mellitus (OR 5.7, p < 0.05) and the experience of programmed HD (more than 50 months) (OR 3.1, p < 0.05) were prognostic signifi cance for the development of severe CMA in dialysis patients.Conclusion. All patients with end-stage CKD who have been on programmed HD for a long time are shown to undergo the brain MRI in order to timely diagnose CMA imaging markers and possible correction of therapy.

Only a few studies have investigated the complications of laparoscopic cholecystectomy in children. Therefore, relevant case reports will be of interest to pediatric surgeons. The patient was a 10-month-old boy diagnosed with calculous cholecystitis who underwent laparoscopic cholecystectomy. He had peripheral edema and adhesions in the neck of the gallbladder. After 10 h, a clinical picture of intra-abdominal bleeding developed. During relaparoscopy in the area of the gallbladder bed, arterial bleeding from the liver vessel was noted, which was eliminated by coagulation. The postoperative period was uneventful, and the child was discharged on day 8. In the second case, a 10-year-old girl was admitted for chronic calculous cholecystitis, and laparoscopic cholecystectomy was performed, in which a pronounced adhesion process was noted in the gallbladder neck region. On day 8, the child was discharged home; however, after 26 days, the patient was admitted again, with a clinical picture of diffuse biliary peritonitis. During laparoscopy, bile outflow from the gallbladder bed was noted, which only partially eliminated by monopolar electrocoagulation. Drainages were installed, through which bile began to be abundantly secreted in the postoperative period. Laparoscopy with a transition to open surgery was performed, during which a perforation in the wall of the common bile duct was found, and stenting and suturing of the defect were performed. In the postoperative period, active infusional infusion and antibacterial therapy were given. The patient was discharged on day 29. Postoperative complications of the ClavienDindo type IIIb are associated both with the presence of congenital anatomical features and inflammatory-adhesive changes in the Calo triangle zone and with the possibility of latent lesions during monopolar coagulation in both cases. The evaluation of the tactics of eliminating biliary peritonitis in the second patient emphasized the necessity to switch to open laparotomy during the second operation. These cases indicate the need to comply with the principles of safe laparoscopic cholecystectomy, including the availability of modern endoscopic equipment and the experience of surgeons in endosurgery. This requires the concentration of patients with cholelithiasis in specialized clinics.

A review article is devoted to diagnostical etiopathogenetic criteria of hepatoblastoma in pediatric patients. There is a distinguished cytogenetic analysis that detects only a limited amount of structural and numerical anomalies in hepatoblastomas; histopathological assessment of liver bioptats which facilitates treatment tactics. Distinctive laboratory findings in pediatric hepatoblastoma are microcytic anaemia, reactive thrombocytosis, and elevated alpha-fetoprotein. The immunohistochemical analysis allows the assessment of the nuclear expression of INI1 (SMARCB1) and the exclusion of malignant rhabdoid liver tumours. There is recommended hepatic doppler ultrasonography, as well as a three-dimensional assessment of primary tumour sizes and tumour volume to reveal the extent of hepatoblastoma according to the PRETEXT system. Radiography and computed tomography of the chest organs are advised to determine hepatoblastoma’s metastases.