Abstract

The aim of clinical case presentation. To analyze the options of autonomous intestinal neuropathy treatment in critical state patients. Key points. The clinical cases of autonomous intestinal neuropathy of various etiology are presented. Patient A., 19-year-old patient presented with constipation for up to 3 days, progressive feeling of abdominal distention and general weakness. In the past history patient underwent surgery for chronic left-side achillobursitis. In postoperative period antibacterial treatment was prescribed that included first-generation cephalosporin. At the 4thday after onset of antibiotic treatment the patient developed chronic abdominal pain that increased progressively, diarrhea up to 10 times per day and fever of 39 °C. Subsequent investigation revealed positive stool test for C. difficile toxins A and B. Urgent colonoscopy detected pseudomembranes at colonic mucosa. Histological examination of biopsy specimens from affected sites demonstrated focal cystic dilation of crypts with epithelium desquamation, severe edema of lamina propria. Pseudomembranous colitis was diagnosed and vancomycin 125 mg qid in combined to metronidazole 500 mg tid for 10 days were prescribed. At the background of treatment stool frequency gradually decreased up to 2 times per day, hematochezia stopped. However at the 7-8th days patient developed constipation, feeling of abdominal distention and progressive general weakness. The state was regarded as development of C. difficile toxin-associated autonomous intestinal neuropathy. Patient I., 54 year-old admitted to the hospital; presenting complaints included flatulence, constipation for up to three days and severe general weakness. According to the past history in 2014 patient was diagnosed to have adenocarcinoma of the right breast gland with subsequent right-sided radical mastectomy followed by radiation therapy and chemotherapy. In May 2017 patient developed boring pain in the right lumbar area, frequent small-volume urination, febrile fever and progressive general weakness. Laboratory and instrumental investigation revealed obstructive right-sided abscessing pyelohephritis with development of sepsis; antibacterial therapy included meropenem in daily dose of 3.0 g along with correction of hypoalbuminemia and detoxication therapy. At the 3rd day of treatment patient noticed improvement in the state of health: decrease in right-sided lumbar pain and general weakness, decrease in body temperature up to subfebrile level. Catheter-collected urine sample contained no admixture of pus. However in the same day patient developed constipation along with progressive abdominal distention. The most likely cause for development of ileus in this case is development of autonomous intestinal neuropathy associated to severe intoxication. Basic mechanisms for development of autonomous intestinal neuropathy are discussed: suppression of smooth muscular contractility by C. difficile toxins A and B (in the first of presented cases) and combined autoimmune neuronal damage by immune cells due to expression of proteins by neoplastic cells (in the second case). Therapeutic approaches including prescription of prokinetic drug prucalopride and multistrain probiotic containing bifido-and lactobacilli are presented (Bifidobacterium bifidum, B. longum, B. infantis, Lactobacillus rhamnosus). Prescription of prucalopride and multistrain probiotic provided resolution of neuropathy and recovery of adequate intestinal motility due to resumption neuromuscular intestinal complex activity and correction of intestinal microbiota spectrum. Conclusion. Combination of prokinetic drug (prucalopride) and multistrain probiotic medication (Bifidobacterium bifidum, B. longum, B. infantis, Lactobacillus rhamnosus) can be effective in the treatment of autonomous intestinal neuropathy in critical care.

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