rentradВестник рентгенологии и радиологииJournal of radiology and nuclear medicine0042-46762619-0478Limited Liability Company "LUCHEVAYA DIAGNOSTIKA", Russian Association of Radiologists10.20862/0042-4676-2016-97-2-110-117rentrad-120Research ArticleОБЗОРЫ ЛИТЕРАТУРЫREVIEWS OF LITERATUREДИСКИНЕЗИЯ СФИНКТЕРА ОКСНЕРА КАК ПРИЧИНА СИНДРОМА ВЕРХНЕЙ БРЫЖЕЕЧНОЙ АРТЕРИИSPHINCTER OCHSNER DYSKINESIA AS A CAUSE OF SUPERIOR MESENTERIC ARTERY SYNDROMEЛевинМ. Д.LevinM. D.

д. м. н., рентгенолог

MD, PhD, DSc, Radiologist Diagnosis

nivel70@hotmail.comГосударственный гериатрический центрИзраильState Geriatric CenterIsrael201627052016972110117Copyright © Левин М.Д., 20162016Левин М.Д.Levin M.D.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://www.russianradiology.ru/jour/article/view/120

Цель исследования – изучить патологическую физиологию синдрома верхней брыжеечной артерии (СВБА). Материал и методы. Проведен рентгенометрический анализ рентгенограмм, срезов, полученных при выполнении компьютерной томографии и магнитно-резонансной томографии, по материалам 35 статей, посвященных СВБА, которые были опубликованы в 1990–2014 гг. На снимках измерялось сужение третьей (горизонтальной) части двенадцатиперстной кишки (ДПК) от границы расширенного сегмента до уровня ВБА. Результаты. Только в 6 (17%) из 35 случаев участок су- жения находился непосредственно между аортой и ВБА и его длина была в пределах 1 см. В остальных 29 случаях начало суженного сегмента находилось на расстоянии 2,5–4,6 см (в среднем 3,30±0,15 см) краниальнее ВБА, то есть большая часть суженной ДПК локализовалась вне аортомезентериального угла. По расположению и длине суженный сегмент ДПК соответствовал расположению и длине (3,2 ± 0,15 см) (Р>0,2) функционального сфинктера Окснера. Заключение. Приведенные данные свидетельствуют, что в большинстве случаев СВБА причиной заболевания является дискинезия сфинктера Окснера. Вероятно, в качестве триггера выступают тяжелые, фактически стрессовые состояния, которые вызывают резкое и стойкое снижение рН желудочного сока, что и является причиной спазма сфинктера Окснера. При большой длительности заболевания стенки спазмированного участка гипертрофируются, после чего мышечные волокна начинают замещаться соединительной тканью. Это может приводить к ригидности узкого сегмента ДПК.

 

Objective – to investigate the pathological physiology of superior mesenteric artery syndrome (SMAS). Material and methods. We selected 35 articles devoted to SMAS, which were published from 1990 to 2014, and performed radiometric analysis of X-rays, CT scans and MRI slices found in these articles. In pictures the narrowing in the third part of the duodenum was measured from the boundary of the expanded segment to the level of the superior mesenteric artery (SMA). Results. Only in 6 (17%) of 35 cases the narrowing portion of duodenum was located directly between aorta and SMA, and its length was about 1 cm. In the remaining 29 cases, the beginning of the narrow segment was 2.5–4.6 cm (average 3.30 ± 0.15 cm) proximal to SMA, ie, most of the narrowed duodenum was out of aortomesenteric angle. Location and length of the narrowed segment of duodenum corresponded to the location and length (3.2 ± 0.15 cm) (P>0.2) of the functional Ochsner sphincter. Conclusion. These data indicate that in most cases of SMAS the sphincter Ochsner dyskinesia causes the disease. It is likely that the disease is triggered by heavy stressful conditions that cause a sharp and sustained reduction in the pH of gastric secretions, which in turn leads to the spasms of the sphincter Ochsner. With time this condition progresses to hypertrophy of the contracted wall of the duodenum with subsequent replacement of the muscle fibers by connective tissue. This can lead to the rigidity of the wall.

 

 

 

 

 

 

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The authors declare that there are no conflicts of interest present.